HANDBOOK OF PAIN MEDICINE

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HANDBOOK OF
PAIN MEDICINE
SECOND EDITION

Dr (Prof.) GP Dureja
Former Professor, All India Institute of Medical Sciences, New Delhi
Director, Delhi Pain Management Centre, New Delhi

ELSEVIER
A division of
Reed Elsevier India Private Limited
Handbook of Pain Medicine, 2/e
GP Dureja

ELSEVIER
A division of
Reed Elsevier India Private Limited

Mosby, Saunders, Churchill Livingstone, Butterworth-Heinemann and Hanley &

Belfus are the Health Science imprints of Elsevier.

© 2014 Elsevier.
First edition 2004
Second edition 2014

All rights reserved. No part of this publication may be reproduced, stored in a

retrieval system, or transmitted in any form or by any means, electronic, mechani-
cal, photocopying, recording or otherwise, without the prior permission of the
publisher.

ISBN: 978-81-312-3466-2

Medical knowledge is constantly changing. As new information becomes avail-

able, changes in treatment, procedures, equipment and the use of drugs become
necessary. The authors, editors, contributors and the publisher have, as far as it is
possible, taken care to ensure that the information given in this text is accurate and
up-to-date. However, readers are strongly advised to confirm that the information,
especially with regard to drug dose/usage, complies with current legislation and
standards of practice. Please consult full prescribing information before issuing prescrip-
tions for any product mentioned in this publication.

Published by Elsevier, a division of Reed Elsevier India Private Limited.

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 To My
Parents, Wife and Children

v
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 Preface

Relief of pain and suffering is one of the most important tasks a physician
can undertake. Pain Medicine, a superspeciality devoted to managing
acute and chronic pain conditions, is now a very well-established and rec-
ognized branch. Pain physicians are now exclusively managing difficult
and complex pain syndromes where conventional treatment modalities
have been unsuccessful. Adequate pain management requires an in-depth
understanding and knowledge of evaluating a pain patient, appropriate
assessment and quantification of his pain state, precision diagnosis of
cause of pain and a judicious selection of treatment modalities. In the past
two decades, it has been our constant endeavour to formulate guidelines
and standardize protocols for our population for an effective management
of acute and intractable chronic pain states.
This book has been designed to fill in the void for comprehensive
guidelines on pain practice and to provide information on clinical practice
protocols rather than experimental study data. The highlight of the second
edition of the book is an in-depth description of the management protocols
of common benign and malignant pain states. Nine new chapters have
been included in this book, and all previous chapters have been revised.
Notable inclusion is a chapter on how to set up a pain clinic, particularly
useful for the young pain physicians. The book also includes a separate
section on pain management in rheumatological disorders. Advanced
interventional pain management techniques such as radiofrequency abla-
tion, spinal neuromodulation and spinal augmentation techniques (e.g.
vertebroplasty and kyphoplasty) have been dealt in greater details.
A special feature of the book is its appendices, which provide use-
ful information on commonly used drugs, common pain terminologies,
equipment used in pain management, pain websites and expanded forms
of abbreviations used in pain medicine.
This handbook will be extremely useful for all specialists involved in
chronic pain management, viz. pain physicians, anaesthesiologists, sur-
geons, neurologists, orthopaedic surgeons, neurosurgeons, internists,
rehabilitation experts, psychologists and family practitioners.

GP Dureja

vii
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 Contributors

Dhamodaran Palaniappan MD Anaesthesiologist, East Hartford, CT, USA

Rani Sunder MD Paediatric Anaesthesiologist, Washington University at
St. Louis, 1 Barnes Jewish Hospital Plz, Saint Louis, MO, USA
Prashanth SM MD Anaesthesiologist/Pain Physician, Boston, USA
Rengarajan J MD Pain Physician, Miami, FL, USA
Dhruv Bibra DA DNB FPM Consultant Pain Physician, Delhi Pain Management
Centre, New Delhi, India
Gunjeet Dua MD Anaesthesiologist, Guys and St Thomas NHS Trust, Bromley, UK
Wg Cdr Sunil Chaturvedi MD Senior Consultant Anaesthesiologist,
­Indraprastha Apollo Hospitals, New Delhi, India
Sudesh Prakash MD Senior Consultant Anaesthesiologist, Yashoda Hospital,
Ghaziabad, India
Sushma Limaye DA Anaesthesiologist, Mumbai, India

ix
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 Contents

Preface vii
Contributors ix

I
GENERAL PRINCIPLES OF PAIN MANAGEMENT
1. Evaluation of the Pain Patient 3
2. Pain Measurement and Assessment 19
3. Radiography and Imaging in Pain Medicine 43
4. Ultrasonography in Pain Medicine 61
5. Pharmacotherapeutics (Drugs) in Pain Management 69
6. Neurolytic Agents 97
7. How to Set Up a Pain Clinic? 105
8. Acute Pain Management: Practical Guidelines 113

II
CHRONIC PAIN SYNDROMES
9. Myofascial Pain Syndromes 129
10. Headache 143
11. Neck and Shoulder Pain 157
12. Back Pain 165
13. Facetogenic Pain 181
14. Knee Pain 193
15. Neuropathic Pain: Mechanisms and Management 203
16. Herpetic Neuralgia 217
17. Orofacial Pain 223
18. Scar Neuralgia/Painful Scars 235
19. Complex Regional Pain Syndrome 239
20. Pelvic Pain 253
21. Perineal Pain 267
22. Peripheral Vascular Diseases 273

xi
xii CONTENTS

III
PAIN MANAGEMENT: NEW PERSPECTIVES
23. Pain Management in Rheumatological Diseases 285
24. Pain Management in the Elderly 305
25. Osteoporosis 319
26. Pain Management by Rehabilitative Approaches 329

IV
CANCER PAIN
27. Cancer Pain 341
28. Cancer Pain Management 345

V
ADVANCED INTERVENTIONAL PAIN
MANAGEMENT
29. Advanced Interventional Pain Management Modalities 363
30. Spinal Cord Stimulation for Management of Chronic Intractable Pain 367
31. Continuous Intrathecal Drug Delivery Systems for Management of Cancer and
Nonmalignant Pain 375
32. Radio Frequency Ablation in Pain Management 383
33. Vertebroplasty and Kyphoplasty 391
34. Management of Spasticity 397

APPENDICES
Appendix 1: Definition of Commonly Used Pain Terms 415
Appendix 2: Common Abbreviations in Pain Medicine 423
Appendix 3: Equipment for Pain Management: Interventional and Noninterventional
Techniques 427
Appendix 4: Professional Journals, Magazines and Newsletters on Pain 433

Bibliography and Suggested Further Readings 473

 S E C T I O N I

GENERAL PRINCIPLES
OF PAIN
MANAGEMENT
1 Evaluation of the Pain Patient 3
2 Pain Measurement and Assessment 19
3 Radiography and Imaging in Pain Medicine 43
4 Ultrasonography in Pain Medicine 61
5 Pharmacotherapeutics (Drugs) in Pain Management 69
6 Neurolytic Agents 97
7 How to Set Up a Pain Clinic? 105
8 Acute Pain Management: Practical Guidelines 113
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 C H A P T E R

1
Evaluation of the Pain
Patient

A perceptual phenomenon, like pain, is not accessible to objective vali-

dation. The subjective experience of pain is universal and one of the most
common reasons that a patient seeks a clinician's help. Patients are referred
to pain clinics by other hospital departments wishing to have help in man-
aging their patients in pain. The referring physicians, however, may have
widely varying opinions about what they expect the patients in the pain
clinic to achieve, which they in turn convey to them.
As the saying goes, ‘Healing begins with the history.’ Clinicians should
be able to put the patient at ease and should then ask open-ended ques-
tions that will give the patient an opportunity to describe the pain in their
own terms. A good way to start may be ‘Tell me all about your pain.’
This generally will allow the patient to describe what he or she believes is
important. This is indeed therapeutic in itself.

TAKING HISTORY OF A PAIN PATIENT

Obtaining history is a skill. The cornerstone of accurate pain diag-

nosis is the medical history. In this age of superfast technology, a large
amount of time and energy is often given to investigations at the expense
of time spent with the patient in collecting a coherent and relevant
history.
Enquiries about the nature of the pain have three main purposes.
  

1. T he patient's description of symptoms may be helpful in diagnosing

the cause of the pain.
2. A description of the type of pain may be important in choosing the
most appropriate treatment for that symptom.
3. It may give the pain clinician an idea of the patient's reaction to the
pain, and the effects that it has on his or her life.

3
4 1. EVALUATION OF THE PAIN PATIENT

Common Questions in the Pain Targeted History

1. T he pain clinician finds out if the pain was followed by any physical
or psychological events or trauma in the patient's life.
2. Is there a history of trauma, surgery or other medical illnesses?
3. Has the pain been continuously present, or are there pain-free
periods? Are there any obvious factors that might account for these
fluctuations?
4. Is the pain constant, getting worse or better with time or are there
diurnal variations?
5. How does the patient describe his pain? Visceral pains are usually
described as dull aching, sickening pain, which is difficult to localize.
Neuralgic pain is generally described as stabbing, shooting, lancinating
or lightning-like in some areas. Associated with pain may be other
sensory disturbances such as tenderness, paraesthesias, hyperalgesia,
hyperpathia or anaesthesia. Myofascial pain may be described as
dull, diffuse aching pain with some tender areas. There may also be
associated paraesthesias, and pain on combing the hair or putting a hat.
6. Has the pain been investigated previously; if so, how and what were
the findings? What was the patient told previously about the pain?
What operations, drugs, physical treatments, and so on have been
applied, and what were the results of such treatments?
7. It is also important to enquire about any other major areas of the
patient's medical, psychiatric, social and employment histories.
  

Summing up all the above points, the targeted history in a pain patient
includes the following:
  

1.  ode of onset
M
2. Chronicity and duration
3. Site of pain
4. Tempo (duration and frequency)
5. Character and severity
6. Associated factors
a. Premonitory symptoms and aura
b. Precipitating factors
c. Environmental factors
d. Family history
e. Age at onset
f. Pregnancy and menstruation
g. Gender
h. Past medical and surgical histories
i. Socioeconomic considerations
j. Psychiatric history
k. Medications, drug and alcohol use

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Taking History of a Pain Patient 5

Psychosocial History
The algologist or the pain clinician will find it useful to know about
patient's previous pain experiences and the reaction to them. The anxiet-
ies associated with pain can lead to phobic and avoidance behaviours,
such as kinesiophobia (fear of movement), which must be identified to be
treated and which often persists long after the original conditioning stim-
ulus has become a history. Psychosocial problems, which could be sup-
pressed or managed prior to the onset of pain syndrome, become terrible
barriers to progress and success unless specifically identified as problems.
Such problems are often ignored by insurance adjusters in the mistaken
belief that the physical domain is their only responsibility and the psycho-
logical aspect somehow is the patient's own responsibility. Therefore, it is
important to
  

• C onsider the role of formal or informal psychometric testing

• Know about contributions of family, friends, employers, culture and
others to the pain syndrome
• Estimate the degree of pain augmentation
• Quantify the degree of pain suffering
• Obtain an adequate sexual history
• Ask for any professional or financial problems
• Look for internal versus external locus of pain control

General Aspects
Some valuable aids to enhance the interview output
  

• T he patient should be appropriately gowned and be sitting upright

and at eye level with the interviewer, if possible.
• Old records, investigations and scans are obtained before the
consultation.
• The pain physician pays full attention, listens patiently and does not
interrupt the patient or allow outside interruptions.
• Physician remains nonjudgemental; her/his own moral, religious and
political beliefs are irrelevant to this process.
• The physician is honest and open with the patient.
• Both the patient and the physician can trust the confidentiality of both
the consultations and the medical records.

Physical Examination
Physical examination is an extension of the history providing objec-
tive support if performed efficiently and methodically. The very physical
aspect of examining the patient imparts a reassuring sense of personal
caring to the entire consultation. Patients want to be examined, expect to

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

6 1. EVALUATION OF THE PAIN PATIENT

be examined and ultimately derive benefit from the process. As Goethe

said ‘We see only what we know.’ The faculty with which we examine
patients is ultimately a function of our knowledge, experience and will-
ingness to learn.

A Quick Guide to Pain Examination

General physical examination
  

• H eight/weight and vital signs.

• Entire body for skin lesions, haemangiomas, café au lait spots, surgical
or injury scars, etc.
• Needle marks, skin ulcerations, etc.
• Overall assessment of multiple joints can be done for deformities,
arthritic change, trauma or prior surgery.
• Scan room for assistive devices brought by the patient.

Pain-Related Behaviours
Note facial expression, colour and grimacing. Speech patterns suggest
emotional factors as well as intoxication with alcohol or prescription or
nonprescription drugs. Some patients attempt to convince the practitioner
how much pain they are suffering by augmenting their verbal presenta-
tion with grunting, moaning, twitching, grabbing the painful area, exag-
gerating the antalgic gait or posture or tightening muscle groups.

Systemic Examination
A quick but thorough systemic examination of the cardiorespiratory
system always helps to point towards the diagnosis and the physician
should be aware of it while prescribing drugs or formulating other treat-
ment options.

Neurological Examination
Table 1.1 highlights the efficient approach to the clinical evaluation of
cranial nerves. Specific attention should be given to this portion of the
examination when headache and facial pain are the complaints. The key
concern again is to develop a routine that with practice becomes thorough.
Motor system examination begins with observation of muscle bulk and
tone with a note on hypertrophy and atrophy. Muscle strength is tested in
upper and lower extremities (Table 1.2). Further knowledge can be gath-
ered by testing deep tendon reflexes (Fig. 1.1), clonus and pathological
reflexes such as Babinski (Table 1.3).

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Taking History of a Pain Patient 7

TABLE 1.1 Clinical Evaluation of Cranial Nerve Function

Cranial nerve(s) Evaluation procedure(s)

Number Name

I Olfactory Test ability to identify familiar aromatic odours,

one naris at a time with eyes closed (not
routinely tested).
II Optic Test vision with Snellen chart or Rosenbaum
near-vision chart.
Perform opthalmoscopic examination of fundi.
Be able to recognize papilloedema.
Test fields of vision using confrontation and
double simultaneous stimulation.
Inspect eyelids for drooping (ptosis).
III, IV, VI Oculomotor, trochlear, Inspect pupil size for equality (direct and
abducens consensual response).
Check for nystagmus.
Assess basic fields of gaze.
Note asymmetric extraocular movements.
V Trigeminal Palpate jaw muscles for tone and strength while
patient clenches teeth.
Test superficial pain and touch sensation in each
branch: V1, V2, V3.
VII Facial Test corneal reflex.
Inspect symmetry of facial features.
Have patient smile, frown, puffed cheeks,
wrinkled forehead.
Watch for spasmodic, jerking movements of
face.
VIII Acoustic Test sense of hearing with watch or tuning fork.
Compare bone and air conduction of sound.
IX Glossopharyngeal Test gag reflex and ability to swallow.
X Vagus Inspect palate and uvula for symmetry with gag
reflex.
Observe for swallowing difficulty.
Have patient take small sip of water.
Watch for nasal or hoarse quality of speech.
XI Spinal accessory Test trapezius strength (have patient shrug
shoulders against resistance).
Test sternocleidomastoid muscle strength
(have patient turn head to each side against
resistance).
XII Hypoglossal Inspect tongue in mouth and while protruded
for symmetry, fasciculations and atrophy.
Test tongue strength with index fingers when
tongue is pressed against cheek.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

8 1. EVALUATION OF THE PAIN PATIENT

TABLE 1.2 Grading of Muscle Strength

Clinical finding Grade Normal response (%)

No evidence of contractility 0 0
Slight contractility, no movement 1 10
Full range of motion, gravity eliminated 2 25
Full range of motion, with gravity 3 50
Full range of motion against gravity, some resistance 4 75
Full range of motion against gravity, full resistance 5 100

TABLE 1.3 Deep Tendon Reflex Scale

Grade Deep tendon reflex response

0+ No response
1+ Sluggish
2+ Active or normal
3+ More brisk than expected, slightly hyperactive
4+ Abnormally hyperactive, with intermittent clonus

Triceps

Biceps

Patellar L2
Achilles S1

FIGURE 1.1 A deep tendon reflex examination.

The sensory examination should be kept simple and guided by clues

obtained through history. Figure 1.2 shows the difference between skin
areas innervated by dermatomes and the corresponding peripheral nerve
cutaneous distribution. Boxes 1.1 and 1.2 summarize the localization
of cervical and lumbar radicular nerves. For pain syndromes of upper

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 BOX 1.1

C L I N I C A L D I F F E R E N T I AT I O N O F
C E RV I C A L R O O T S V E R S U S N E RV E
LESIONS IN THE UPPER EXTREMITY
Root lesions
C5 Sensory supply — Lateral border upper arm
Reflex affected — Biceps
Motor loss — Deltoid, infra- and supraspinatus, rhomboids
C6 Sensory supply — Lateral forearm, including first finger
Reflex affected — None
Motor loss — Biceps, brachialis, brachioradialis
C7 Sensory supply — Over triceps, midforearm, and third finger
Reflex affected — Triceps
Motor loss — Latissimus dorsi, pectoralis major, triceps, wrist
extensors and flexors
C8 Sensory supply — Medial forearm to fifth finger
Reflex affected — None
Motor loss — Finger extensors and flexors; flexor carpi ulnaris
T1 Sensory supply — Axilla to elbow
Reflex affected — None
Motor loss — Intrinsic hand muscles (in some cases, thenar muscle
through C8)

Nerve lesions
Axillary Sensory supply — Over deltoid
(C5, C6) Reflex affected — None
Motor loss — Deltoid
C5, C6 Sensory supply — Lateral forearm to wrist
Reflex affected — Biceps
Motor loss — Biceps and brachialis
Radial Sensory supply — Lateral dorsal forearm, back of thumb
(C5–C8) and second finger
Reflex affected — Triceps
Motor loss — Brachioradialis; forearm supinator; finger,
triceps and wrist extensors
Median Sensory supply — Lateral palm and fingers first, second,
(C6–C8, T1) third and half of fourth
Reflex affected — None
Motor loss — Abductor pollicis brevis; long flexors of first,
second & third fingers; pronators of forearm; wrist flexors
Ulnar Sensory supply — Medial palm, fifth finger and medial
(C8, T1) half of fourth finger
Reflex affected — None
Motor loss — Intrinsic hand muscles, flexor carpi ulnaris,
flexors of fourth and fifth fingers
Abbreviations: C, cervical root; T, thoracic root.
10 1. EVALUATION OF THE PAIN PATIENT

Ophthalmic division
Trigeminal
 Mandibular
Maxillary division
division v
Great auricular, C2, C3 C2
C3
Cervical plexus, C4
superficial branches
Intercostal Lateral cutaneous br.
nerves

T2–T11 Anterior cutaneous br.


Axillary
Intercostobrachial T5
C5
Medial cutaneous T6
Musculocutaneous T7 T3
Posterior

 cutaneous T8
Brachial Radial T9 T2 C6
plexus Superficial T10
branch T11 T1
T12
Median
L1
Ulnar C8
C7
S2, S3


L2
Ilioinguinal
Genitofemoral Obturator
Lateral cutaneous


Anterior
Lumbar cutaneous
plexus Femoral L3
rami
Saphenous

L4


Lateral cutaneous L5
nerve of calf

Sacral Sciatic Superficial and

plexus deep peroneal
Sural
S1
Medial plantar

Sural
Lateral plantar
Tibial
Lateral plantar
Saphenous
Medial cutaneous
Lateral
plantar
Medial
plantar

(a) Anterior aspect

FIGURE 1.2 Comparison of spinal segmental and peripheral nerve cutaneous sensory
supply v: Fifth (trigeminal) nerve, br: Branch.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Taking History of a Pain Patient 11

Dermatomes
Ophthalmic division
C2
C2
Maxillary division
Mandibular division
 Trigeminal
Mastoid branch, C2, C3 Superficial
C3 Great auricular branch, C2, C3  cervical plexus
C4 Occipital, C2
Occipital, C3
Occipital, C4
Occipital, C5–C8
 Dorsal
branches

Supraclavicular, C3, C4
T4
T5 Dorsal rami of thoracic nerves
C5 T6
T7
Cutaneous branch of axillary
T3 Lateral cutaneous branches
T8
T9
of intercostal nerves
T2 Medial and lateral cutaneous br. of radial
T10
T11 Medial cutaneous
T12 Intercostobrachial
T1
Musculocutaneous
L1 Anterior branch of radial
C6
L2
Median
C8
L3 S3
Dorsal cutaneous branch of ulnar
C7 Gluteal branch of 12th intercostal
S2 Lateral cutaneous br. of iliohypogastric
 Lateral branches of dorsal
rami of lumbar and sacral
Medial branches of dorsal rami, L1–S6
L3 Perforating branch of
posterior cutaneous  Pudendal plexus
Lateral cutaneous
Obturator
Medial cutaneous
Saphenous Femoral
Posterior cutaneous
 Lumbar plexus


L5

Superficial peroneal Common
Sural peroneal
Sacral plexus
Tibial
L4
Lateral plantar

S1

L5

S1 L4

L5

(b) Posterior aspect

FIGURE 1.2, cont’d

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

12 1. EVALUATION OF THE PAIN PATIENT

BOX 1.2

C L I N I C A L D I F F E R E N T I AT I O N O F
LUMBAR/SACRAL ROOTS VERSUS
N E RV E L E S I O N S I N T H E L OW E R
EXTREMITY
Root lesions
L2 Sensory supply — Across upper thigh
Reflex affected — None
Motor loss — Hip flexion
L3 Sensory supply — Across lower thigh
Reflex affected — None
Motor loss — Knee extension
L4 Sensory supply — Across knee to medial malleolus
Reflex affected — Patellar
Motor loss — Inversion of foot
L5 Sensory supply — Side of leg to dorsum
Reflex affected — None
Motor loss — Dorsiflexion of toes and foot
S1 Sensory supply — Behind lateral malleolus to lateral foot
Reflex affected — Achilles
Motor loss — Plantar flexion and eversion of foot

Nerve lesions
Obturator Sensory supply — Medial thigh
(L2–L4) Reflex affected — None
Motor loss — Adduction of thigh
Femoral (L2–L4) Sensory supply — Anterior thigh to medial
malleolus
Reflex affected — Patellar
Motor loss — Knee extension
Peroneal division of Sensory supply — Anterior leg to dorsum of
sciatic nerve foot
(L4, L5, S1–S3) Reflex affected — None
Motor loss — Dorsiflexion, inversion, and
eversion of foot
Tibial division of Sensory supply — Posterior leg to sole and
sciatic nerve lateral aspect of foot
(L4, L5, S1–S3) Reflex affected — Achilles
Motor loss — Plantar flexion and inversion of
foot
Abbreviations: L, lumbar root; S, sacral root.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Specific Tests 13

extremity, the examiner should be able to differentiate sensory involve-

ment of the radial, median and ulnar nerves from specific roots. Similarly,
for lower extremities one should be able to differentiate the peroneal and
tibial nerve sensory distribution from that of the L4, L5, S1 roots; such
distinctions elucidate most of the common problems.

Sensation
Sensation to light touch, pinprick, hot and cold stimuli is tested. Tactile
sensation can be evaluated quantitatively with cotton. The sharp end of a
broken sterile wooden tip is convenient way for testing pinprick.

Examination of the Musculoskeletal System

This includes inspection of gait and posture. Deformities and devia-
tions from symmetry are observed. Testing active movement will deter-
mine range, muscle strength and willingness of the patient to cooperate.
Passive movements, on the other hand, when performed properly, test for
pain, range and end-feel. Palpation of soft tissues, bony structures and
stationary or moving joints may reveal temperature differences, presence
of oedema, fluid collections, gaps, crepitus, clicks or tenderness. For a
patient with back pain, the suggested sequence of examinations is testing
range of motion of cervical, thoracic and lumbosacral spine, sacroiliac and
hip joints, and SLRT.

SPECIFIC TESTS

SLRT or Lasègue Sign

Tension on the sciatic nerve begins with 15–30° of elevation in the
supine position. This puts traction on the nerve roots from L4 to S2 and
on the dura. The end of the range is normally restricted by hamstring
muscle tension at 60–120°. More than 60° of elevation causes movement
in the sacroiliac joint and therefore may be painful in sacroiliac joint
disorders.

Basic Sacroiliac Tests

Sacroiliac tests are performed to determine when pain occurs in the
buttock.
  

1. P
 ush the ilia outwards and downwards in the supine position with
the examiner's arms crossed. If gluteal pain results, the test is repeated

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

14 1. EVALUATION OF THE PAIN PATIENT

with patient's forearm placed under the lumbar spine to stabilize the
lumbar joints.
2. Forcibly compress the ilia to the midline with the patient lying on the
painless side. This stretches posterior sacroiliac ligaments.
3. Exert forward pressure on the centre of the sacrum with the patient
prone.
4. Patrick's or ‘FABER'S’ test – flex, abduct and externally rotate femur
while holding down contralateral anterior superior iliac spine. This
stretches anterior sacroiliac ligament and reveals pain caused by
ligamentous strain.
5. Force lateral rotation of the hip joint with knee held in 90° of flexion
and the patient in the supine position.

Spinal Flexibility
Spinal flexion, extension, and rotation and lateral bending may be lim-
ited or painful, leading to a diagnosis of zygapophyseal joint, discogenic,
muscular, or ligamentous pain.

Tinel Test
The Tinel test involves percussion of the carpal tunnel. When it is posi-
tive, it gives rise to distal paraesthesias. It can be performed at other loca-
tions (e.g. the cubital or tarsal tunnel), where it might be suggestive of
nerve entrapment.

Phalen Test
The Phalen test is positive for carpal tunnel syndrome when a passive
flexion in the wrist for 1 min, followed by sudden extension, results in
sensation of paraesthesias.

Adson Test
Adson test has been advocated for diagnosis of thoracic outlet syn-
drome. The examiner evaluates the change of radial artery pulsation
in a standing patient with arms resting at the side. Ipsilateral head
rotation during inspiration may cause vascular compression by the
anterior scalene muscle. In modified Adson test, the patient's head is
rotated to the contralateral side. Pulse change suggests compression by
the middle scalene muscle. Both tests are regarded unreliable by some
clinicians, as the results are found positive in about 50% of the normal
population.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Conclusion 15

Fallacies in the History and Examination of the Pain Patient

The frequently quoted Waddell nonorganic signs may raise suspicion
in patients with low back pain. The Waddell nonorganic signs are grouped
into five categories:
  

1. Tenderness
a. Widespread superficial sensitivity to light touch over lumbar spine
b. Bone tenderness over a large lumbar area
2. Simulation
a. Axial loading, during which light pressure is applied to the skull in
the upright position
b. Simulated rotation of lumbar spine with the shoulders and pelvis
remaining in the same plane
3. Distraction
a. Greater than 40° difference in sitting versus supine straight leg
raising
4. Regional disturbance
a. Motor: generalized giving way or cogwheeling resistance in
manual muscle testing of lower extremities
b. Sensory: nondermatomal loss of sensation to pinprick in lower
extremities
5. Overreaction
a. Disproportionate pain response to testing (pain behaviour with
assisted movement using cane or walker, rigid or slow movement,
rubbing or grasping the affected area for more than 3 s, grimacing,
sighing with shoulders rising and falling).

CONCLUSION

’Like an alarm bell stuck in “on” position such is chronic benign pain’
– Bruce Smoller and Brian Schullman.
It is evidently impossible to transmit the impression of pain by teach-
ing, since it is only known to those who have experienced it. Moreover,
we are ignorant of each type of pain before we have felt it. The history
and physical examination are the foundation of pain evaluation and
treatment. Finally, your brilliant ideas conceived after completion of the
above steps and the patient's informed consent equals a good manage-
ment plan.
We can conclude by saying ‘The clinical assessment is the base of the treat-
ment statue.’ If it is narrow, the statue may crash down. If it is broad and
well made, the statue will be stable and reliable.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

16 1. EVALUATION OF THE PAIN PATIENT

ALL INDIA INSTITUTE OF MEDICAL SCIENCES

(AIIMS) PAIN CLINIC
PAIN ASSESSMENT FORM

Date Regd. no. Referred by

Patient's name Address and phone no.
Weight/age/sex Occupation
Present complaints

Description of pain and findings

  

1. D uration of pain
2. Site of pain (please shade the affected area)
3. Type of pain
a. Sharp
b. Dull aching
c. Burning
d. Spasmodic
e. Pricking
f. Freezing
g. Any other words (patient's words)
4. Onset/variations/rhythms
5. Pain continuous/intermittent/momentary
6. Does pain disturb night and daily activities
7. Aggravating or relieving factors
8. Effects of pain
9. Other comments
  

Right Left Right Left Left Right Right Left R L L R

Left Right

Right Left
Left Right

  
Relevant past history/associated diseases
Any drug allergy
General physical examination

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 All India Institute of Medical Sciences (AIIMS) 17

Chest Cardiovascular Central nervous

Musculoskeletal system system
Investigations
Laboratory tests
X-ray CT scan MRI
Diagnosis
Present treatment for pain
• NSAID
• Narcotics
• Sedatives/anxiolytics
• Antidepressants/
Anticonvulsants
• Nerve blocks/Transforaminal
Epidural Injection
• Any other – Advanced
Intervention/acupuncture/
TENS/laser
Treatment
Modality of Response (visual
Date treatment analog scale readings)
Any other treatment modality
details
Treatment-related side effects
Results
Excellent (75% relief in
symptoms)
Good (50–75% relief in
symptoms)
Fair (25–50% relief)
Poor (25% relief)
No relief
Remarks
Clinical studies carried out if any
Visual analog scale

0 1 2 3 4 5 6 7 8 9 10

No pain Mild Discomforting Distressing Horrible Excruciating

  
Signature of Pain Physician

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

This page intentionally left blank

     
 C H A P T E R

2
Pain Measurement
and Assessment

Pain assessment is a multidimensional approach to evaluate pain attri-

butes. These attributes include intensity, duration and location of pain,
its somatosensory qualities, and the accompanying emotions of the pain
experience. Measurement of pain is difficult because of the variation in
individual responses to painful stimuli and the subjective nature of pain.
Nevertheless, numerous methods have been developed for the measure-
ment of pain of which the most commonly used ones are described here.
When choosing a method, one must consider the type of setting, the ease
of administration and patient's educational level. One must also consider
the reliability and validity of the specific device especially when conduct-
ing research.

APPROACHES TO PAIN MEASUREMENT

Major approaches to quantification of pain and description of their

advantages and limitations are presented here.

Pain as Self-Report on a Single Dimension

Category Scale
Verbal or visual descriptors are used as a simple method for the subjec-
tive reporting of the intensity of pain. Melzack pain scale categorizes pain
as mild, discomforting, distressing, horrible and excruciating. Eight-point
facial expression picture scale, picture scales with differently sized famil-
iar objects coins have worked well for scaling pain intensity. These meth-
ods are effective such as in older people unaccustomed to scaling their
experiences, those without language or verbal fluency, the young, and
the poorly educated, because scaling of this sort is not limited to words.

19
20 2. PAIN MEASUREMENT AND ASSESSMENT

The disadvantages of this scaling approach include the compulsion to

remember or have a printed form for the works or pictures, and the limited
possible range of responses to the number of works or pictures in the list.

Category Scale
Instruction: Choose the word below that describes how your pain feels
right now:
Mild  Discomforting  Distressing Horrible  Excruciating

Rupee Analogue Scale

The Rupee analogue scale is the Indian modification of VAS wherein pain
is quantified from 0 to 100 and compared to 0–100 paise. The advantages
are that it is easily understood by both l­iterate and illiterate patients, as also
health care professionals, and is easy to chart (Fig. 2.1).

Numerical Rating Scale

Scale for children uses colour to code sensory intensity and faces with
varying expressions to code affect. The child gives a nonverbal response
on each of these dimensions while the instrument provides the corre-
sponding NRS. This approach demonstrates the possibility of extracting a
numeric score from a measurement device having a nonnumeric interface
(Fig. 2.2(a) and (b)).

Visual Analogue Scale

An equally simple and efficient alternative is the VAS, which usually
consists of a 10 cm line anchored at one end by a label such as ‘no pain’
and at the other end by a label such as ‘the worst pain imaginable’ or
‘pain as bad as can be’. The patient simply marks the line to indicate pain
intensity, and a slide rule-like device with the line on the patient's side and
numeric score on the obverse facilitates clinical assessment (Fig. 2.3).

FIGURE 2.1 Rupee analogue scale.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 21

VAS is the most common method for measuring pain and pain relief in
clinical practice. Unwritten versions of the NRS or VAS work with very
sick patients. The provider instructs them to give a number from 0 to 10 or
asks them to hold fingers from 0 to 10 or if someone runs a pencil slowly
along a VAS the patient nods his or her head at the point that corresponds
to current intensity of pain.

Pain as Self-Report on Multiple Dimensions

McGill Pain Questionnaire
To assess pain in a multidimensional way, McGill pain questionnaire
was developed. It helps in rapidly measuring subjective pain experience.
It measures the sensory, affective, evaluative and other miscellaneous

(a)

0 1 2 3 4 5
No hurt Hurts Hurts Hurts Hurts Hurts
little bit little more even more whole lot worst
(b)
FIGURE 2.2 (a and b) Numeric rating scale.

0–10 Numeric pain intensity scale

0 1 2 3 4 5 6 7 8 9 10
No Moderate Worst
pain pain possible
pain

FIGURE 2.3 Visual analogue scale.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

22 2. PAIN MEASUREMENT AND ASSESSMENT

aspects of pain, thus measuring pain multidimensionally. McGill pain

questionnaire can differentiate various pain syndromes like phantom limb
pain, postherpetic neuralgia, metastatic carcinoma, rheumatoid arthritis,
osteoarthritis, labour pain and menstrual pain, by assessing different val-
ues to different pain syndromes.

How to use McGill Pain Questionnaire

In the questionnaire (see Box 2.1), 1–10 represents sensory aspect of
pain, 11–15 represents affective aspect of pain, 16 represents evaluative
aspect of pain, 17–20 represents other miscellaneous aspects of pain. Each
subunit has two to five words under them, representing increasing degree
of pain and numerical value. For example, under number 1 of sensory
aspect, if a patient points to throbbing, 4 points are given since it is in the
fourth position in subunit one.
The descriptors fall into four major groups: sensory, 1–10; affective,
11–15; evaluative, 16; and miscellaneous, 17–20. The rank value for each
descriptor is based on its position in the word set. The sum of the rank
values is PRI. PPI is based on a scale of 0–5.

BOX 2.1

M C G I L L PA I N Q U E S T I O N N A I R E
Patient Name Date Time am/pm

PRI: S A E M PRI*(T) PPI

(1-10) (11-15) (16) (17-20) (1-20)

1. Flickering Quivering Pulsing Throbbing Beating Pounding Brief Rhythmic Continuous

2. Jumping Flashing Shooting momentary periodic steady
3. Pricking Boring Drilling Stabbing Lancinating transient intermittent constant
4. Sharp Cutting Lacerating
5. Pinching Pressing Gnawing Cramping Crushing
6. Tugging Pulling Wrenching
7. Hot Burning Scalding Searing
8. Tingling Itchy Smarting Stinging
9. Dull Sore Hurting Aching Heavy
10. Tender Taut Rasping Splitting
11. Tiring Exhausting
12. Sickening Suffocating
13. Fearful Frightful Terrifying
14. Punishing Gruelling Cruel Vicious Killing
15. Wretched Blinding
16. Annoying Troublesome Miserable Intense Unbearable
17. Spreading Radiating Penetrating Pierching
18. Tight Numb Drawing Squeezing Tearing
19. Cool Cold Freezing
20. Nagging Nauseating Agonizing Dreadful Torturing

[ Present Pain Intensity (PPI) : 0 - No pain; 1 - Mild; 2 - Discomfort; 3 - Distressing; 4 - Horrible; 5 - Excruciating ]
Sensory 1 - 10; Affective 11 - 15; Evaluating 16; Miscellaneous 17-20.

*Pain Rating Index

Source: Melzack R. Pain 1975;1:277–99.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 23

An example: Cut injury–surgical incision

Sensory aspect of cut is represented by
  

• S tabbing – 4 points
• Cutting – 2 points
• Splitting – 4 points
  

Affective aspect of cut is represented by

  

• Frightful – 2 points
  

Evaluative aspect of cut is represented by

  

• Intense – 4 points
  

Miscellaneous aspect of cut is represented by

  

• Penetrating – 3 points
  

Total = 4 + 2 + 4 + 2 + 4 + 3 = 19 points.
Therefore, PRI = 19.
In this manner, nature of pain is assessed and a particular range of
number given. So, when assessing pain using McGill pain questionnaire
one can correlate the number of points scored to the nature of injury/pain
or pain syndromes.
Line diagram of body with front and back views to map the spatial
distribution of pain are also included.
There is also a column for PPI, which describes the overall present
intensity of pain. The PPI is recorded as a number from 1 to 5, in which
each number is associated with the following words:
  

1. Mild pain
2. Discomforting
3. Distressing
4. Horrible
5. Excruciating pain
  

Because pain is a personal experience, it is impossible for the treat-

ing physician to know precisely what someone else's pain feels like.
No man can possibly know what it is like to have menstrual pain or
labour pain, nor can a psychologically healthy person know what a
psychotic patient is feeling when the patient says he or she has excru-
ciating pain. But the McGill pain questionnaire provides us with an
insight into the qualities of pain that are experienced. Recent studies
indicate that each kind of pain is characterized by a distinct constella-
tion of words.
There is remarkable consistency in the choice of words by patients suf-
fering the same or similar pain syndrome.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

24 2. PAIN MEASUREMENT AND ASSESSMENT

Clinical Pain
Labour pain pain syndromes after accidents
50

Causalgia 40 Amputation of digit

Primiparas
(no training)
Primiparas
(prepared childbirth training) 30
Multiparas
(trained and untrained)
Chronic back pain
Bruise
Cancer pain (nonterminal) 20 Fracture
Phantom limb pain Cut
Postherpetic neuralgia Laceration
Sprain
Toothache 10
Arthritis

FIGURE 2.4 Comparison of pain scores using McGill pain questionnaire obtained from
women during labour, from patients in a general hospital pain clinic and an emergency
­department.

Figure 2.4 shows comparison of pain scores using McGill pain ques-
tionnaire obtained from women during labour and from patients in a gen-
eral hospital pain clinic and an emergency department.
Labour pain – primiparas have higher pain scores on McGill pain ques-
tionnaire compared to multiparas.
Clinical pain syndromes – causalgia and cancer pain have higher scores
than toothache or arthritis on McGill pain questionnaire.
Pain after accident – amputation of a digit is more painful than lacera-
tion or sprain.
McGill pain questionnaire assigns a number or a range of numerical
value to each type of pain. If one studies the numerical value, one can say
what is the nature of pain the patient is feeling when carefully assessed.
Thus, we can see that McGill pain questionnaire is reliable, consistent
and measures the subjective pain experience and differentiates among
acute, chronic and various pain syndromes. Due to its usefulness, it has
been translated into many languages.

Descriptor Differential Scale

DDS is a simple but sophisticated psychophysical technique. It is used
to assess separately the sensory intensity and unpleasantness of pain
(Box 2.2). It provides quantification by ratio scaling procedure. DDS is
­differentially sensitive.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 25

BOX 2.2

DESCRIPTOR DIFFERENTIAL SCALE-I

(DDS-I)
HOW INTENSE IS YOUR PAIN ?

Less intense than The same intensity as More intense than

MILD MILD MILD

More than
MILD MILD MILD

Less than

Source: Doctor JN et al. Pain 1995;61:251–60.

Memorial Pain Assessment Card

The memorial pain assessment card scales pain, pain relief, and mood
on VAS and adds a set of adjectives reflecting pain intensity (see Box
2.3). The advantages of this measurement tool are that it takes only
seconds to use, it is correlated with other, longer measures of pain and
mood, and the provider can fold the card so that the patient sees only
one scale at a time.

Pain as a Multidimensional Experience that Includes

Effects on Daily Living
Pain when it is ongoing and uncontrolled has a detrimental, dete-
riorative effect on virtually every aspect of a patient's life. It produces
anxiety and emotional stress, undermines well-being, interferes with
functional capacity and hinders the ability to fulfil family, social
and vocational roles. There is a dose–response relationship between
pain and quality of life; as one increases the other proportionately
decreases. Clinicians often measure pain to assess the effect of an

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

26 2. PAIN MEASUREMENT AND ASSESSMENT

BOX 2.3

T H E M E M O R I A L PA I N A S S E S S M E N T C A R D
Moderate Strong
2 Just noticeable

Mild Excruciating
No pain
Sevare weak

Relief Scale
No Complete
relief of relief
pain of pain

Mood Scale

Worst Best
mood mood

Pain Scale
Least Worst
possible possible
pain pain

Source: Fishman B, Pasternaks, Wallenstein SL et al. Cancer 1987;60:1151–58.

intervention to relieve it. A single pain rating, or even ratings that

include sensory and affective components, cannot provide a compre-
hensive indicator of a patient's well-being or functional capability.
A cost-effective intervention for pain must relieve the negative effect
of pain on daily living.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 27

Brief Pain Inventory

The goal of pain relief is to reduce:
  

• S ubjective intensity of pain

• Disability that pain causes
  

BPI quantifies both targets (see Box 2.4).

The BPI is a quick, multidimensional pain measurement tool with dem-
onstrated reliability and validity in patients with cancer, AIDS, and arthri-
tis. In 5–15 min, patients provide subjective ratings of pain intensity (pain
worst, pain least, pain average, and pain right now), and importantly, they
also report the effect of pain on multiple functions (general activity, mood,
ability to walk, normal work, socializing with others, enjoyment of life
and sleep). This instrument is available in several languages, including
French, Spanish, and Chinese.

Assessment of Neuropathic Pain

The following scale is used to measure neuropathic pain.

Neuropathic
  
Pain Scale
1. P
 lease use the scale below to tell us how intense your pain is. Place an
‘X’ through the number that best describes the intensity of your pain.
  

No 0 1 2 3 4 5 6 7 8 9 10 The most intense

pain pain sensation
imaginable
  

2. P
 lease use the scale below to tell us how sharp your pain feels. Words
used to describe sharp feelings include ‘like a knife’, ‘like a spike’,
‘jabbing’ or ‘like jolts’.
  

Not 0 1 2 3 4 5 6 7 8 9 10 The sharp-

sharp est sensation
imaginable
(‘like a knife’)
  

3. P
 lease use the scale below to tell us how hot your pain feels. Words
used to describe very hot pain include ‘burning’ and ‘on fire’.
  

Not 0 1 2 3 4 5 6 7 8 9 10 The hottest sen-

hot sation imagin-
able (‘on fire’)
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

28 2. PAIN MEASUREMENT AND ASSESSMENT

BOX 2.4

B R I E F PA I N I N V E N T O R Y
Date_______/________/_________ Time:________ 6. Please rate your pain by circling the one num-
Name:____________ ____________ ____________ ber that tells how much pain you have RIGHT
Last First Middle Initial NOW.
0 1 2 3 4 5 6 7 8 9 10
1. Throughout our lives, most of us have had pain
No Pain Pain as bad as you can imagine
from time to time (such as minor headaches,
sprains, and toothaches). Have you had pain 7. What treatments or medications are you receiv-
ing for your pain?
other than these everyday kinds of pain today?
_________________________________________
1. Yes 2. No
_________________________________________
2. On the diagram, shade in the areas where you 8. In the last 24 hours, how much relief have pain
feel pain. Put an X on the area that hurts the treatments or medications provided? Please
most. circle the one percentage that shows how much
RELIEF you have received.
Right Left Left Right 0% 10 20 30 40 50 60 70 80 90 100%
N o r el i ef Com p l et e r el i ef
9. Circle the one number that describes how, dur-
ing the past 24 hours, pain has interfered with
your:
A. General activity
0 1 2 3 4 5 6 7 8 9 10
Does not interfere Completely interferes
B. Mood
0 1 2 3 4 5 6 7 8 9 10
Does not interfere Completely interferes
C. Walking ability
0 1 2 3 4 5 6 7 8 9 10
3. Please rate your pain by circling the one num-
ber that best describes your pain at its WORST Does not interfere Completely interferes

in the last 24 hours. D. Normal work (includes both work outside

the home and housework)
0 1 2 3 4 5 6 7 8 9 10
0 1 2 3 4 5 6 7 8 9 10
No Pain Pain as bad as you can imagine
Does not interfere Completely interferes
4. Please rate your pain by circling the one num-
ber that best describes your pain at its LEAST in E. Relations with other people
the last 24 hours. 0 1 2 3 4 5 6 7 8 9 10
0 1 2 3 4 5 6 7 8 9 10 Does not interfere Completely interferes
No Pain Pain as bad as you can imagine F. Sleep
5. Please rate your pain by circling the one num- 0 1 2 3 4 5 6 7 8 9 10
ber that best describes your pain on the AVER- Does not interfere Completely interferes
AGE.
G. Enjoyment of life
0 1 2 3 4 5 6 7 8 9 10
0 1 2 3 4 5 6 7 8 9 10
No Pain Pain as bad as you can imagine
Does not interfere Completely interferes
Source: Pain Research group, MD Anderson Cancer Center, University of Texas.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 29

4. P
 lease use the scale below to tell us how dull your pain feels. Words
used to describe dull pain include ‘like a dull toothache’, ‘dull pain’,
‘aching’ and ‘like a bruise’.
  

Not 0 1 2 3 4 5 6 7 8 9 10 The dullest

dull sensation
imaginable
  

5. P
 lease use the scale below to tell us how cold your pain feels. Words
used to describe very cold pain include ‘like ice’ and ‘freezing’.
  

Not 0 1 2 3 4 5 6 7 8 9 10 The coldest

cold sensation
imaginable
(‘freezing’)
  

6. P
 lease use the scale below to tell us how sensitive your skin is to light
touch or clothing. Words used to describe sensitive skin include ‘like
sunburned skin’ and ‘raw skin’.
  

Not 0 1 2 3 4 5 6 7 8 9 10 The most sen-

sensitive sitive sensation
imaginable
(‘raw skin’)
  

7. P
 lease use the scale below to tell us how itchy your pain feels.
Words used to describe itchy pain include ‘like poison oak’ and ‘like
mosquito bite’.
  

Not 0 1 2 3 4 5 6 7 8 9 10 The most itchy

itchy sensation imag-
inable (‘like
poison oak’)
  

8. W
 hich of the following best describes the time quality of your pain?
Please check only one answer.
  

( ) I feel a background pain all the time and occasional flare ups (break-
through pain) some times.
Describe the background pain: ___________________________
Describe the flare up (breakthrough) pain: _____________________
( ) I feel a single type of pain all the time. Describe this pain: __________
___________________________________
( ) I feel a single type of pain only sometimes. Other times, I am pain free.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

30 2. PAIN MEASUREMENT AND ASSESSMENT

Describe this occasional pain: ___________________________

_____________________________________________
  

9. N
 ow that you have told us the different physical aspects of your
pain, the different types of sensations, we want you to tell us overall
how unpleasant your pain is to you. Words used to describe very
unpleasant pain include ‘miserable’ and ‘intolerable’. Remember,
pain can have a low intensity, but still feel extremely unpleasant, and
some kinds of pain can have a high intensity but be very tolerable.
With this scale, please tell us how unpleasant your pain feels.
  

Not 0 1 2 3 4 5 6 7 8 9 10 The most unpleas-

pleasant ant sensation
imaginable
(‘intolerable’)
  

10. L
 astly, we want you to give us an estimate of the severity of your
deep versus surface pain. We want you to rate each location of pain
separately. We realize that it can be difficult to make these estimates,
and most likely it will be a ‘best guess’, but please give us your best
estimate.
  

How intense is your deep pain?

No 0 1 2 3 4 5 6 7 8 9 10 The most
deep intense
pain deep pain
sensation
imaginable
How intense is your surface pain?
No 0 1 2 3 4 5 6 7 8 9 10 The most
surface intense surface
pain pain sensation
imaginable

Assessing Pain in the Elderly

When patients are older, examiners should anticipate a number of fac-
tors that are less often considered in younger adults. The areas to assess
are the same. The selection of instruments may need some adaptation.
The faces pain scale for the elderly has been well validated, better than
VAS or NRS, and demonstrates excellent rank order and test–retest reli-
ability. Fewer instruments should be selected and time pressure avoided
as they may be having difficulty with comprehension or vision. Even

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 31

mild hearing problems can reduce concentration and understanding if

background noise is interfering. Common visual impediments must be
considered in selecting tools. Large, simple, upper and lower case letters
help, as does greater space between lines. Oral response to items or scales
that allow pointing can ease some visual and dexterity difficulties. If self-
report capability is limited, observer reports may be needed. No tools
exist that offer clear, reliable, and sensitive behavioural methods for use
with cognitively impaired elderly.
In summation, pain assessment in the elderly must be undertaken sys-
tematically using the same tools as those for younger patients. These may,
however, be prepared for a wider range of evaluation before assessment
and for adaptation of the assessment strategy if the factors described pre-
viously apply to the individual patient.

Physiological Indicators of Clinical Pain

Pathophysiological changes accompany acute and chronic pain. When
pain is acute, it can be associated with motor reflexes that produce muscle
spasm or spasm or splinting. Surgical or other trauma to chest or abdo-
men impairs ventilation. Autonomic reflexes also accompany acute pain
and can inhibit gastrointestinal and genitourinary function, producing
ileus and smooth muscle spasm. Liberation of catecholamines increases
blood pressure and cardiac output and increases rate of ventilation.
The concentration of endorphins in plasma was negatively correlated
with acute pain. The greater the levels of beta-endorphin, the lower the
reported pain is.
Pathophysiological changes sometimes characterize the area of painful
focus in chronic pain patients. Skin temperature is perhaps the best stud-
ied. Some physicians use thermography, the measurement of skin tem-
perature, in evaluation of certain types of chronic pain. Complex regional
pain syndromes are characterized by temperature changes in the extremi-
ties. Myofascial pain syndrome and cancer pain syndrome manifest as
low skin temperature in the area of painful focus, which is indicative of
altered sympathetic nervous system function. Pain accompanying some
arthritic or rheumatologic conditions is associated with abnormal warmth
because of acute inflammation.
Trophic changes occur with some types of chronic pain. When pain
is related to trigger points in middle-aged and older patients, it is often
accompanied by subtle indicators of autonomic dysfunction, such as
enhanced pilomotor segmental reflex, vasomotor and sudomotor distur-
bances of the skin, and trophedematous changes in subcutaneous tissue.
Pupil dilation occurs with certain types of migraine headache. Clus-
ter headaches classically involve skin flushing in facial areas. None of
these signs, however, proves the presence of pain, nor does the absence

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

32 2. PAIN MEASUREMENT AND ASSESSMENT

of such signs mean that there is no pain. The presence of such a correla-
tion increases the possibility that pain is present, but does not validate or
definitively indicate pain.

Measurement of Pain Behaviour

In chronic pain patients, the measurement of pain behaviours, along
with pain measurement, can be useful in determining the success of treat-
ment. Home recording of physical activity, medication, and pain intensity
on an hour to hour basis in diary form has been described by Fordyce.
Methods of direct observation of pain behaviours also have been devel-
oped. UAB Pain behaviour scale is an objective assessment of following
pain behaviours: verbal vocal complaints, nonverbal vocal complaints,
time spent in lying down, facial grimaces, standing posture, mobility,
body language, use of visible supportive equipment stationary movement
and medication. Both the Fordyce diary and the UAB scale are fairly sim-
ple to use and can provide important information to the clinician treating
patients with chronic pain.

Pain Measurement in Children

Neonates and Infants
Physiological systems are developed at approximately 26 weeks of ges-
tation, for the fetus to perceive pain. It is well known that assessment of
pain in children is rather difficult when compared to adults. Not provid-
ing adequate pain relief to the neonate during surgical anaesthesia may
lead to serious psychological upsets later in childhood.
Neonates and infants cannot express the pain they perceive. They may
not be able to speak (preverbal) or may not have suitable words to express
the degree of pain they are feeling. So, pain in a small child is mostly
assessed in an indirect way such as observing physiological changes or
behavioural responses of the neonate/infant to pain.
Among the physiological changes, an increase in heart rate, respiratory
rate, blood pressure and excessive palmar sweating can be observed in
response to pain.
When considering behavioural changes, changes in facial expression,
body movement and type of cry are looked for. Facial expressions asso-
ciated with pain include eyebrow bulge, eye squeeze, nasolabial fur-
row, open lips, vertical or horizontal stretching of mouth, lip purse, taut
tongue and chin quiver. The facial expression changes with the inten-
sity of pain the child is feeling. So, in assessing pain by observing facial
expression, there will be interobserver variability in quantifying the pain
felt by a child.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 33

When considering body movements, child of 1–30 days responds with

diffuse body movements to a noxious painful stimuli. By 6 months, the
child develops the capacity to purposefully withdraw the affected limb
and by about 1 year, the child develops the capacity to sense and touch the
painful area and tries to rub it with the hand. The child may also kick or
thrash the legs at random.
Caution: The physiological and behavioural changes already discussed
could be either due to pain or due to fear and anxiety owing to separation
from parents, making assessment of pain more difficult.

Summary of pain assessment and measurement

Adults Children

Subjective pain Quality of life Pain AIIMS pain Neonates and

scale BPI behaviour discomfort infants
Single SF 36 measurements scale Preschoolers
dimension Quality of life Fordyce diary Physiological The Oucher
- Category enjoyment UAB pain measure scale
scales and behaviours Happy–sad
- VAS satisfaction scale face scales
- NRS questionnaire Color analogue
Multiple West scale
dimension Haven–Yale Poker chip
- McGill pain multidimensi- tool
questionnaire onal pain Ladder scale
- Memorial pain inventory Linear analogue
assessment scale
card School-aged
- The descriptor 6 point (0–5)
differential Numerical
scale Verbal pain
Score 0 to 100
Numerical
scale
VAS
  

Preschoolers
When assessing pain in preschool children apart from the physiological
and behavioural changes, self-report is significant.
The various self-report methods developed are
  

1. T he Oucher scale
2. Happy–sad face scales
3. Colour analogue scale

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

34 2. PAIN MEASUREMENT AND ASSESSMENT

FIGURE 2.5 Oucher scale: Pictorial representation of pain. Smiling face indicates no pain
and crying face indicates severe pain. On the left is the numerical scale for children who can
count till 100.

4. P oker chip tool

5. Ladder scale
6. Linear analogue scale
  
  

1. The Oucher scale

  

The Oucher scale displays six photographs of a child's face showing

increasing levels of discomfort. On the left is the vertical numerical scale
for older children capable of counting till 100 (Fig. 2.5). The six photo-
graphs of a child on one side are used for children who have not yet learnt
to count till 100. Children select the facial expression that best reflects their
experience of hurt.
  

2. Happy–sad face
  

Happy–sad face scales (Fig. 2.6) are easily understood by children.

They have been used to assess the affective and fear components of pain.
The number of faces usually varies from four to nine.
  

3. Colour analogue scale

  

This tool has a great deal of practical utility in clinical setting. Chil-
dren select colours (crayons or markers) to indicate the ‘worst hurt’
the child has ever had, ‘hurt not quite as much as…’, ‘just a little hurt’
and ‘not hurt at all’. They then colour their degree of hurt on a body
outline. Outline of both boys and girls with front and back views are
available. Colour has special appeal for children and provides an
appropriate way for preschoolers to express themselves about their

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 35

(a) (b) (c)

(d) (e) (f)

(g) (h) (i)

FIGURE 2.6 Line drawing of faces: nine face scale/happy–sad face scores. Faces (a)–(d)
represent varying magnitudes of positive affect. Faces (f)–(i) represent magnitudes of nega-
tive affect. Face (e) was initially assumed to represent a neutral face.

No pain Mild Discomforting Distressing Horrible Excruciating

FIGURE 2.7 Colour analogue scale. Blue = no pain; green = mild pain; orange = moderate
pain; red = severe pain.

subjective experience of pain. But one fallacy is always there, i.e. chil-
dren may have difference of opinion in relating intensity of pain to
colours (Fig. 2.7).
Their way of relating intensity of pain to colour may vary.
  

4. Poker chip tool

  

Hester's poker chip tool is suitable for children less than 4 years. Four
poker chips are placed in front of the child, and the chips are described to
the child as ‘pieces of hurt’ from ‘just a little hurt’ to ‘a lot more hurt’ to
‘more hurt’ to ‘the most hurt you can have’. The child is asked as to how
many pieces of hurt he or she has.
  

5. Ladder scale
  

Ladder scale has been used with both adults and children; children are
asked to choose the level of their pain from a drawing of a ladder, with
higher rungs indicating greater pain (Fig. 2.8).
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

36 2. PAIN MEASUREMENT AND ASSESSMENT

Hurt as bad as
it can be

No hurt

FIGURE 2.8 Ladder scale.

Not hurting Hurting a whole lot

No discomfort Very uncomfortable
No pain Severe pain

FIGURE 2.9 Linear analogue scale. It includes facial expressions at each end of a horizon-
tal line. This is more abstract and therefore requires more advanced cognitive development
than is required for the Oucher and other face scales.

6. Linear analogue scale

  

This scale includes facial expression at each end of a horizontal line

(Fig. 2.9) and requires more advanced cognitive development than that
required for Oucher or face scales.
School-Aged Children
They are usually able to read and write and can comprehend what is
explained to them. Their method/way of assessing pain is better devel-
oped and they can express their feelings better.
Commonly used methods to assess pain in school-aged children are
  

1.  6 point (0–5) numerical verbal pain score

A
2. A 0–100 numerical scale
3. VAS
4. Modified McGill pain questionnaire
  
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Approaches to Pain Measurement 37

No pain
Worst
0 5 10 ever pain
10
Horizontal

Vertical

Curvilinear 5

0 10
No pain Worst
0
ever pain
No pain

FIGURE 2.10 Visual analogue scale. Numerical representation of pain. Patient marks the
degree or pain he/she feels.

1. Six point (0–5) numerical verbal pain score

  

It has been used effectively with children over the age of 9 years to
assess headache on a daily basis.
  

1 = No pain.
2 = Pain – I am only aware of it if I pay attention to it.
3 = Pain – I can ignore it at times.
4 = Pain – I cannot ignore it but I can do my usual activities.
5 = Pain – It is difficult for me to concentrate, I can only do easy
activities.
6 = Pain – Such that I cannot do anything.
  

2. The 0–100 numerical scale

  

In the Oucher scale, to the left is the numerical scale for children who
have learnt to count till 100. The child places a slide on the number corre-
sponding to the degree of pain he or she feels. The child assigns a numeri-
cal value to pain and is very easy to use.
  

3. Visual analogue scale

  

It is the easiest way to measure the intensity of pain. It is simple, effi-

cient and can be analyzed quickly.
It is a very sensitive way to assess the intensity of pain. It assigns a
numerical value to pain; 0 = no pain and 10 = worst ever pain. It could be
horizontal, vertical or curvilinear (Fig. 2.10). A child or an adult places a

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

38 2. PAIN MEASUREMENT AND ASSESSMENT

BOX 2.5

A I I M S PA I N D I S C O M F O RT S C A L E

Parameter Criteria Points

1. Respiratory +<20% of preoperative baseline 0
rate +20–50% of preoperative baseline 1
+>50% of preoperative baseline 2
2. Heart rate +10% of preoperative baseline 0
+20% of preoperative baseline 1
+30% of preoperative baseline 2
3. Discomfort Calm 0
Restless 1
Agitated 2
4. Crying Not crying; responding to water, 0
food and parental presence
Crying but responds to tender 1
loving care (TLC)
Crying but does not respond to TLC 2
5. P
 ain at site No pain 0
of operation State pain – vague 1
Can localize pain 2

slide corresponding to the degree of pain felt. VAS can measure efficiency
of analgesia by a particular analgesic by noting the scores before and after
treatment.
The main drawback of VAS is that it assumes pain to be unidimensional
and measures only the intensity of pain, whereas the nature, location and
psychosocial aspect of pain are not taken into consideration.
AIIMS pain discomfort scale is given in Box 2.5. In this scale, physi-
ological measures are used as indicators of patient pain. It is used mainly
for measuring acute postoperative pain. Score ≥ 4 validates analgesic
administration.

LIMITATIONS AND PROBLEMS IN PAIN

MEASUREMENT
  

• P
 ain is fundamentally a subjective state. This restriction to subjec-
tivity reduces pain to a scientific metaphenomenon and forces the
investigator or clinician to depend on the patient for accurate and
reliable data.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Algorithm for Selection of Pain Measurement Scales 39

• P ain is a multidimensional experience. The clinician can quantify it on

a single dimension using, for example, a single VAS, but this approach
risks potentially significant oversimplification. Pain has sensory, emo-
tional, motivational, cognitive and behavioural dimension.
• No universal index of pain is equally useful for all health care
professionals.

ALGORITHM FOR SELECTION OF PAIN

MEASUREMENT SCALES

Use rapidly
Is pain Yes Is pain Yes or
administered self
VAS NRS
acute? brief? report methods
and observations and or
No No
Drug
Persistent usage CS
acute pain
and

BEHAVE
Use self report OBS
multidimensional
and
scaling, and
observation data
BPI
and
Is pain Acute and
related to Yes chronic
progressive elements are MPQ
disease? mixed
and
and
No
BEHAVE
OBS
Assess patterns in
Is the pain Yes pain scores over
chronic? time along several and and
dimensions VAS MPQ

Assess the
dependence of pain Psychol and BEHAVE
on psychosocial EVAL
environment OBS

Assess functional Pain and

capability diary

BPI Brief pain inventory

BEHAVE OBS Behavioral observations
CS Category scale
MPQ McGill pain questionnaire
NRS Numerical rating scale
EVAL Other psychological evaluations
VAS Visual analog scale
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

40 2. PAIN MEASUREMENT AND ASSESSMENT

AIIMS Pain Questionnaire (For use in Pain Clinics)

Name of the patient :
Age & Sex :
Regn. No. :
Date :
Occupation :
Office – A Housewife – D
Mannual – B Retired/Sedentary – E
Vocal – C
Address:
Socio-economic Status :
LIG (Rs. <2000 pm) MIG (Rs. 2000–5000 pm) HIG (Rs. >5000 pm)
Referred from :
Present complaint :
Duration of pain :
Occurrence : Momentary/Brief/Intermittent/Continuous
Pain Questionnaire
Associated symptoms :
Factors which increase the pain :
decrease the pain :
Provisional diagnosis :
(already offered if any)
Intensity of pain when started : 0 = negligible
Intensity of pain at present : 1 = mild
Intensity of pain after treatment, : 2 = moderate
at PAIN CLINIC : 3 = severe
4 = intolerable
Nature of treatment taken
Medical : Name of the medicine:
(analgesic/antidepressant / sedative -anxiolytic / placebo)
Duration of usage :
Surgical : Type of the surgery done:
Others : Analgesic blocks :
Acupuncture :
TENS :
Physiotherapy :
Psychotherapy :

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Algorithm for Selection of Pain Measurement Scales 41

Outcome :
Medical : 0 1 2 3 4
Surgical : cured 75% 50% 25% no
Others (specify) : relief relief relief relief relief
Changes in the day-to-day activity levels due to pain:
Activity patterns: Scale:
A Occupational 0: no change
B Recreative and 1: disturbed but can
social and cultural manage routine work
C Household routine 2: activity reduced and slight
changes in day-to-day work
3: change in the life style and
adaptation of new jobs
4: gross inactivity
Sleep patterns:
Scale: 0 1 2 3 4
normal slightly moderately significantly no
reduced reduced reduced sleep

What do you think of the reactions of family members, friends and

colleagues about your pain problem?
0 1 2 3 4
sympathetic considerate annoyed disgusted abandoned

How do you feel about your pain problem?

0 1 2 3 4
accepting anxious apprehensive depressed indifferent

mood changes: best mood worst mood

Pain relief obtained at Pain Clinic :
100% complete relief 0% no relief
Observers’ opinions of patient’s pain relief.
(doctors/nurses/relatives/friends etc.)

Pain Descriptors:
1. Pulsing Patient’s own word
Throbbing
Flashing
Shooting
2. Pricking
Stinging
Stabbing
3. Sharp

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

42 2. PAIN MEASUREMENT AND ASSESSMENT

Cutting
Tearing
4. Pinching
Pulling
Cramping
Squeezing
Crushing
5. Tingling
Itchy
Numb
Burning
Hot
6. Tiring
Exhausting
7. Sickening
Suffocating
8. Fearful
Terrifying
9. Spreading
Radiating
Piercing
10. Annoying
Troublesome
TIME TAKEN: Signature of the Pain Physician
  

CONCLUSION

The measurement of pain is important to determine pain intensity and

quality, aid in diagnosis, help in deciding the choice of therapy, and evalu-
ate the relative effectiveness of different therapies. Further development
and refinement of pain measurement technique will lead to increasingly
accurate tools with greater predictive power.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 C H A P T E R

3
Radiography and Imaging
in Pain Medicine

Diagnostic imaging in a patient with acute pain has a clearly defined

role in establishing or confirming the pathological diagnosis, and in
directing medical, surgical or radiological intervention. Patients suffering
from chronic, recurrent or intractable pain from degenerative diseases,
chronic inflammatory conditions, neoplasm and posttraumatic scarring
may benefit from specialized imaging examination for the determination
of aetiology, treatment planning and prediction of the outcome of therapy.
Some of the important imaging techniques used commonly in chronic
pain syndromes are
  

1. O perating room fluoroscopy – aid to interventional procedures/as a

diagnostic modality
2. Epidurography
3. Spinal endoscopy
4. MRI and CT
5. Radionuclide scanning such as triphasic bone scan, whole body scan, etc.
6. Discography (provocative)
7. Ultrasonography as an aid to interventional pain medicine

OPERATING ROOM FLUOROSCOPY

Fluoroscopic imaging for spinal injections and special procedures has

given pain physicians the safest and the most accurate method of achieving
their objective. By fine-tuning the fluoroscope with the patient's position,
imaging provides documentation and confirmation of the exact placement
of the interventional needle.
By far, interventions for relief of spinal pain and those performed
around the spine are essentially done under fluoroscopy. Fluoroscopically,
it is possible to evaluate a functional spine in terms of the anterior and

43
44 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

posterior elements and associated space contents between the two columns.
The most common structures amenable to fluoroscopic evaluation are
Anterior elements (anterior column)
1. Prevertebral zone
2. Vertebral bodies
3. End plates
4. Intervertebral discs
  

Posterior elements (posterior column)

1. P
 osterior arches
2. F acet joints
  

Space components
The defined spaces enclosed between the anterior and posterior columns
can be divided into
1. C
 entral canal
2. N euroforaminal canal
  

Fluoroscopy is thus an essential armamentarium for interventional

injections in a variety of chronic pain syndromes. Some of the interven-
tional procedures that are routinely performed under fluoroscopy are
1.  audal epidural steroids/catheter placement
C
2. Coeliac plexus block
3. Impar plexus block
4. Facet joint injection/denervation
5. Superior hypogastric plexus injection
6. Transforaminal steroid injection
7. Sympathetic plexus blocks
8. Trigeminal ganglion block
9. Stellate ganglion block
10. Epidurography
11. Intradiscal electrothermal therapy
12. Spinal cord stimulation lead placement
13. Radiofrequency ablation
14. Discography
15. Sacroiliac joint injection

Guidelines for Fluoroscopy

Patient
Taking time for accurate patient positioning is one of the most important
aspects of interventional pain procedures. If adequate time is taken for this
step, one can avoid repositioning frustration during the middle of the injec-
tion/procedure. Start by instructing the patient exactly where he or she

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Operating Room Fluoroscopy 45

needs to be on the table. If the radiography needs to avoid certain places on

the table that will create artifacts like radiopaque bed structures, the patient
needs to know exactly where those places are and add a margin of error
in both directions for tilting and rotating the C-arm. Patients tend to shift
into a more comfortable position once they are on the table, so it is impor-
tant to gain their cooperation and explain the importance of staying exactly
where you want them. Safety straps across the patient's legs and a sheet
tucked around the arms (for cervical procedures) are helpful in restraining
patients and keeping them from moving during the injection/procedure.
Sedating the patients can be helpful in relieving their anxiety, as well as
keeping them in the correct position during the injection/procedure.
C-arm: As a pain interventionist, one should become very familiar with
the locks and movements of the C-arm. The C-arm is moved into position
from the prone patient's right side. Keep the C-arm close to perpendicular
to the table to start. Also, keep the arm portion of the C-arm about halfway
from its fully extended reach; this allows ample room for rotation and left
to right side adjustments. The view on the monitor should be oriented so
that the left side of the screen is the prone patient's left. This may require
reversing the image on the control panel. Increasing the distance between
the patient and the image intensifier will increase magnification.
It would be nice to ascribe a 30° tilt and a 15° rotation as an answer for
all routine oblique lumbar scout images, if setting up for routine lumbar
radiographs. These numbers and degrees are not as useful for interven-
tional spinal procedures.
The beauty of live imaging is that the pain physician can view each
patient's unique anatomy and fine-tune movements of the C-arm to view
the target location with ease.
Before activating the fluoroscope, adjust the C-arm so that the image
intensifier is centred over the spine; then tilt caudal or cephalic to an appro-
priate amount for the patient's anatomy. The plane of the image intensifier
surface should be parallel to the curve of the spine at the affected level.
After activating the fluoro for one quick picture, look at the image to see if
the anatomy is in profile and count vertebrae to determine desired location.
Proceed to adjust the C-arm until the scout image gives the physician land-
marks on the spine and a clear target image. The physician may want to
switch to a magnified field once initial needle is introduced. Do not make
C-arm adjustments while the physician is advancing the needle. Always
save a clear image with contrast for documentation (Photograph 3.1).

Contrast Agents
Contrast agents are administered to help visualize the location of the
needle tip, confirm the flow of injectant, or visualize the involved structure,
e.g. joint, bladder, and bursa. Inadvertent vascular uptake in spite of nega-
tive aspiration is not uncommon. The toxicity of local anaesthetics and cor-
ticosteroids increases with intravascular injection, and contrast-enhanced

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

46 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

PHOTOGRAPH 3.1 C-arm fluoroscope.

fluoroscopic guidance helps minimize such toxicities. All contrast agents are
iodinated compounds that allow opacification of structures for visualization.
Contrast media are divided into ionic and nonionic agents. The non-
ionic contrast agents have low osmolality and may decrease the potential
for adverse reactions. Although these nonionic agents decrease minor
reactions such as nausea and urticaria, they have been shown to decrease
the incidence of more severe reactions as well. They do not eliminate the
possibility for severe or fatal anaphylactic reactions. Potential for adverse
reactions can be minimized by limiting the quantity of the contrast media
injected and adequately screening patients.
Patients with a history of prior contrast reactions, significant allergies,
impaired cardiac function/limited cardiac reserve, blood–brain barrier
breakdown, and severe anxiety are at increased risk for generalized reac-
tions, including urticaria, nausea, vomiting and anaphylaxis. Patients
with impaired renal function and paraproteinemias are at increased risk
of renal failure with the administration of contrast agents. Renal complica-
tions can be minimized by limiting the volume of contrast agents, ensuring
adequate hydration before, during and after the procedure, and using the
low-osmolality agents for patients >70 years with a creatinine ≥2 mg/dL.
Ideally, spinal procedures, including epidural steroid injections, facet
joint injections, sympathetic blocks, discography, spinal nerve blocks and
sacroiliac joint injections are all performed with the aid of fluoroscopy
and contrast enhancement. Nonionic contrast agents are used for these
injections because the potential for subarachnoid spread exists with any
of these procedures.
The two most common nonionic agents are (1) iopamidol and
(2) iohexol (Omnipaque).

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Epidurography 47

Both agents are nonionic, readily available as injectable liquid, water

soluble, and quickly cleared. The first of the nonionic contrast agents,
metrizamide, is a powder that must be reconstituted. Metrizamide is
also associated with a higher incidence of seizures than either iohexol or
iopamidol and is rarely used now. Generally, 0.2–2 mL of nonionic contrast
is sufficient for the experienced injectionist to confirm location and spread
of the contrast. Ninety percent of these agents are eliminated through the
kidneys within 24 h. Side effects are uncommon but include nausea, head-
aches and disturbances in central nervous systems. Ionic contrast agents
such as (1) diatrizoate (Urografin) and (2) iothalamate (Conray) may be
used for other contrast-enhanced injections, including arthrograms, cys-
tometrograms, and bursa injections. These agents are well tolerated when
total volume of contrast is limited to ≤15 mL.
Adverse reactions to contrast agents may be minimized by careful
patient selection and monitoring during the procedure. Bronchospasm
and urticarial reactions require symptomatic management and are easily
reversed. Epinephrine (1:1000) sometimes is required in doses of 0.1–1 mL
subcutaneously. Vasovagal reactions respond to atropine 0.3 mg intrave-
nously. Toxic convulsions, although rare, are managed with intravenous
diazepam and continuous monitoring of vital signs.

EPIDUROGRAPHY

In simple words, epidurography is the opacification of the epidural

space with aqueous contrast medium. The initial views of the epidural
spaces were accidentally obtained by Sicard in 1921 using lipoidal contrast
agent. Although several terms have been applied to the procedure, includ-
ing peridurography and canalography, ‘epidurography’ most accurately
describes the procedure anatomically.

Technique
In epidurography, the epidural space is approached at caudal level via
the sacral hiatus. It requires fluoroscopy and should be done in operation
theatre with recovery room facility.
The procedure is explained to the patient and an informed consent is
taken. Once in the operating room, full set of monitoring (noninvasive
blood pressure, O2 saturation and electrocardiogram) is established along
with an intravenous access. Analgesia and sedation may be provided by
fentanyl, midazolam and propofol. The patient is placed in prone position
with pillow under the abdomen and feet internally rotated, which helps
to expose the sacral hiatus. The position of the hiatus is also confirmed by
palpating the sacral cornua, which lie on either side of midline just above

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

48 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

PHOTOGRAPH 3.2 An epidurogram showing a typical Christmas tree appearance.

the natal crease. This is further confirmed by taking posterioanterior and

lateral views by fluoroscopy.
The lumbosacral area is thoroughly scrubbed and draped. Using a 25 G
or smaller needle, local infiltration (3–4 mL 1% lignocaine) into the floor of
the canal is performed. A 17 G Tuohy needle using loss of resistance tech-
nique is then inserted into the canal and advanced cephalad. Fluoroscopic
lateral view is done to confirm the position of the needle in the canal.
At this stage, epidurogram is performed by injecting 5–10 mL of contrast
medium like Omnipaque (Photographs 3.2 and 3.3). Other contrast agents
like Isovue 300 M or diatrizoate may also be used. Posterioanterior fluo-
roscopy is performed at this stage to outline epidural anatomy of nerve
roots, fat and adhesions. Under fluoroscopic control, a flexible needle can
then be introduced to either target the instillation of drugs such as methyl
prednisolone/triamcinolone/hyaluronidase or perform adhesionolysis of
dense epidural adhesions.
At the end of the procedure, methyl prednisolone 80 mg + 5–10 mL lig-
nocaine 0.5% and 10–20 mL normal saline is injected to cause volumetric
adhesionolysis.

Indications and Contraindications

Lumbar epidurography is most useful in evaluating patients with
nondiagnostic physical findings and negative or equivocal lumbar
myelograms. In this clinical situation, a negative lumbar epidurogram

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Epidurography 49

PHOTOGRAPH 3.3 Epidurogram showing a filling defect due to postoperative adhesions.

can obviate unnecessary lumbar disc surgery, where there is suspicion

of lumbar disc herniation. This modality can be used for evaluation
and identification of even lateral disc herniation. It is recommended in
the management of radiculopathy, failed response to epidural steroids,
postlaminectomy failed syndrome, postsurgical irritation lasting longer
than 3 weeks, failed after conservative therapy and patients with pace-
maker where MRI is contraindicated. Epidurography is used as a confir-
mative test for epidural placement of catheter, drugs and as a preliminary
procedure before epiduroscopy.
Epidurography should not be performed in patients with altered
coagulation profile as seen in patients taking warfarin or presenting with
liver or haematological disorders. A cautious approach should be taken
with elderly patients as rise in intracerebral pressures can be caused
by saline flushing system. It is contraindicated in patients allergic to
iodine, history of seizures, alcoholics or patients on phenothiazines or
neuroleptic analgesics.

Complications of Epidurography
There have been reported incidence of direct nerve root injury, which
can be minimized by keeping the patient awake and maintaining verbal
communication. Headache is another possible problem following this
procedure. Other minor side effects could be in the form of temporary

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

50 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

backache, muscle spasm or seizures. Very rarely, macular haemorrhages

or bleeding in internal layers of eye can happen secondary to excessive
volumes of saline flush used during the procedure, causing rapid rise in
intracerebral pressures.

SPINAL ENDOSCOPY

Visualization of spinal canal has travelled a long way spanning a period

of over 60 years. Michael Burmah first visualized the spinal canal by
arthroscopic equipment in 1931, leading to the development of a flexible
fiberoptic epiduroscope technology, introduced by Koki Shimoji in 1991. This
technology protects tissues from heat injury. Smaller size of the equipment
allows simplification of the procedure.
Spinal canal endoscopy (epiduroscopy) is defined as a percutaneous,
minimally invasive endoscopic investigation of the epidural space to enable
colour visualization of anatomical structures inside the spinal canal: dura
mater, blood vessels, connective tissues, nerves, fat and pathological struc-
tures including adhesions (fibrosis), inflammation and stenotic change.

Uses of Spinal Endoscopy

Spinal endoscopy is used for the following purposes:
1.  bservation of pathology and anatomy
O
2. Direct drug application
3. Direct lysis of scarring with blunt dissection and laser
4. Placement of catheter and electrode system
5. An adjunct to minimally invasive surgery

Caudal versus Conventional Approach

The caudal approach to the visualization of epidural space is advan-
tageous over the conventional paramedian approach due to avoidance
of bending of fiberoptic device, easier placement and easier addition
of channels for further surgical procedures or to steer into space. It has
been suggested that caudal route of injection of lumbar epidural space
takes the path of least resistance and does not necessarily deliver steroids
to their intended target in the sacral nerve root beyond the obstruction
(Photograph 3.4).

Indications and Contraindications

Widely accepted indications are neuralgias, recent onset of radioculop-
athy and radiculopathy associated with postlaminectomy pain syndrome.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Spinal Endoscopy 51

(b)
(a)

(c) (d)

PHOTOGRAPH 3.4 Endoscopic views of epidural space showing different structures

such as (a) dura mater; (b) nerves; (c, d) epidural adhesions.

Absolute contraindications are cauda equina syndrome, urinary

dynamic problem, sphincter dysfunction, foot drop, pilonidal cyst, osteo-
myelitis, coagulopathy and unstable angina.

Procedure
Careful physical examination followed by special investigations such as
electromyography, nerve conduction studies, and MRI should document the
findings. Nonsteroidal anti-inflammatory drugs and anticoagulants should
be discontinued as per recommendations for epidural catheter placement.
Patient is placed in prone position and a 17 G Touhy needle is introduced
into epidural space through sacral hiatus. A guidewire is then introduced
followed by a dilator and an introducer. After removing the dilator sheath,
fiberoptic cable is placed through one of the two lumens in the steering
handle. A normal saline irrigation drip is connected to the second steering
handle. Normal saline irrigation is given only for brief periods (1–2 min)
using a pressure bag to minimize the pressure and limit total volume to 60 mL.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

52 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

Complications
Complications of spinal canal endoscopy generally pertain to improper
placement of needle, generation of excessive hydrostatic pressure lead-
ing to retinal haemorrhage, scapular pain and headache. Other reported
potential complications are transient dysesthesias, paresis, paralysis,
blindness, postdural puncture headache, local surgical site bleeding,
infection and allergic reactions.

Advantages of Spinal Endoscopy

Pilot studies that compared return to work in a group of patients man-
aged with spinal canal endoscopy and a second laminectomy group sug-
gested a remarkable difference in outcomes for epiduroscopically managed
group with high cost-effectiveness. The reasons for an easy return to work
following spinal endoscopy are
1. Relatively atraumatic nature of procedure
2. Relatively short recovery time

COMPUTED TOMOGRAPHY

The introduction of CT for clinical use in the early 1970s revolutionized

the practice of neuroradiology and profoundly affected the practices of
pain medicine, neurology and neurosurgery. The application of CT to the
evaluation of the rest of the body soon afterwards paved way for a revo-
lutionary imaging technique, particularly for abdomen and chest. CT is a
computer-based imaging technology that permits direct visualization of
anatomical structures. It provides exquisite cross-sectional images of both
normal anatomy and pathologic lesions.
Advantages of CT over MRI are rapid scan acquisition, superior bone
detail, demonstration of calcium, and the demonstration of acute haemor-
rhage. Acute intracranial haemorrhage is more reliably and easily evalu-
ated with CT than with MRI.
In the chest and abdomen, CT is helpful in tracking these processes:
• Trauma
• Abscess and other manifestations of infection
• Primary neoplasm (benign and malignant)
• Metastases
• Lymphadenopathy
• Aortic aneurysm
  

A differential absorption of 5% or more is generally required to distin-

guish different soft tissues on plain radiographs. On the other hand, CT

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Magnetic Resonance Imaging 53

is able to differentiate among many different soft tissues for which the
differential absorption may be as little as 0.5%. Because of this remark-
able ability to detect and display minute differences in tissue densities,
CT opened up new vistas of radiological diagnosis. It is an outstand-
ing and very accurate modality. The overall accuracy of CT, especially
when performed first without and then with intravenous contrast mate-
rial, approaches 98% for the identification of a lesion (versus no lesion).
Whether CT or MRI is used as the first diagnostic study depends on the
accessibility and availability of these facilities.
CT, when performed without and then with intravenous iodinated
contrast material, allows greater accuracy of diagnosis and localization of
various lesions by better characterizing them according to their patterns
of contrast enhancement. The intrathecal administration of water soluble,
nonionic myelographic contrast agents significantly increases the accuracy
of CT in the evaluation of the intraspinal contents.

MAGNETIC RESONANCE IMAGING

MRI was the major innovation in medical imaging in the 1980s and
1990s. Like CT, MRI is a computer-based imaging tomographic slices of
varying thickness. The MRI is based on a modality technique that depicts
anatomical sections in effects of large magnet and radio signals from the
nuclei of hydrogen atoms present in body tissues. MRI has rapidly estab-
lished itself as a noninvasive technique for evaluating the central nervous
system and other parts of the body that not only rivals CT but surpasses
it in many instances. CT evaluates only a single tissue parameter (X-ray
attenuation), whereas MRI analyzes multiple tissue characteristics. The
soft-tissue contrast provided by MRI is substantially better than that of
any other imaging modality (Photograph 3.5).

L5–S1

L5

PHOTOGRAPH 3.5 MRI of lumbosacral spine showing an L5–S1 intervertebral disk

prolapse.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

54 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

Although MR images are anatomically similar to CT scans, the MRI

information is fundamentally different from that of X-ray and CT. In CT
and in conventional radiography, the grey-scale ordering never changes.
Bones always appear as the whitest tissue, followed by muscle and fat,
and air always appears black. The grey scale ordering on MRI is highly
variable.
Advantages of MRI:
MRI has several advantages over other imaging modalities. These are
1. I t has no known adverse biological effects.
2. MRI does not use ionizing radiation; although the amount of radiation
used by CT is relatively low, it is obviously preferable to avoid
ionizing radiation altogether.
3. MRI produces substantially greater tissue contrast resolution than
any other imaging technique. It has been reported to provide
additional information not available on CT in as many as 50% of the
patients evaluated by both these techniques. Because of the ability of
MRI to detect small changes in the water content of tissues, it may
identify an abnormality or define the extent of one much more readily
than CT.
4. MRI provides significantly more information than CT about tissue
characteristics. The increased sensitivity of MRI over CT applies to
metastatic disease, especially when an intravenous contrast agent is
used.
5. Beam-hardening artifacts seen with CT (for example, in the posterior
fossa, middle cranial fossa and craniocervical junction), which make
diagnosis difficult, if not impossible, in some patients, do not occur
with MRI.
6. With MRI, multiple projections can be obtained with ease. Most CT
images are cross-sectional, although direct coronal images of the head
can be made if the patient can hyperextend the neck.

Indications and Contraindications of MRI

MRI is the imaging procedure of choice for the evaluation of nearly
all abnormalities involving the brain, spine and musculoskeletal system.
Imaging of soft tissues of the extremities is easy with MRI. In addition
to depicting muscles, fat and blood vessels readily, it can also visualize
articular cartilage. MRI is an outstanding modality for evaluating various
joints, such as the shoulder, hip and knee. Articular cartilage of the knee
is difficult to detect with CT because it lies in the plane of the section,
but it can be visualized on coronal and sagittal MR images. Because a
small amount of motion can decrease the spatial resolution of MR images
considerably, and thus can compromise an examination, MRI is not the

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Radionuclide Scanning 55

primary imaging modality for the chest and abdomen, although it can
play an important role in evaluating these areas. The indications for and
contraindications to MRI are summarized below:
Indications for and contraindications of MRI
Body structures and processes for which MRI is indicated
Brain
Spine and its contents
Musculoskeletal system
Bone (neoplasm, trauma)
Bone marrow (osteomyelitis, neoplasm, devascularization)
Soft tissues (neoplasm, haematoma, abscess)
Muscles
Joints
Heart and great vessels
Focal liver masses
Kidney and retroperitoneum
Prostate
Gynaecological disease
Contraindications of MRI
Cardiac pacemaker
Ferromagnetic cerebral aneurysm clips
Metallic foreign body near the eye
Cochlear implants

RADIONUCLIDE SCANNING

Scintigraphy detects the distribution in the body of a radioactive agent

injected into a vein. Nuclear medicine is an integral part of the diagnos-
tic armamentarium of the radiologist and is of immense value to a pain
clinician in difficult situations. The strength of radionuclide scintigraphy
resides in its ability to portray the functional status of an organ or body
part. The speciality of nuclear medicine has grown tremendously in the last
decade through the linkage of new radioactive elements to biological mate-
rials and via progress in the mechanics of detecting radioactivity. The radio-
active biological element complex is localized to certain parts of the body.
For example, radiolabelled sulphur colloid localizes in the liver, whereas
radiolabelled methylene disphosphonate localizes in bone and bypasses
the liver. The radioactivity is detected from outside the body with special-
ized gamma camera placed over the organs and areas of interest. Localized
defects that cause either too much or too little radioactivity to be emitted
from a usually homogeneous area are then detected as pathological lesions.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

56 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

Almost any organ of the body can be investigated by means of radionu-

clide scanning. Such imaging is extensively used in pathological processes
involving the brain, cerebrospinal fluid, lungs, kidneys, musculoskeletal
system, hepatobiliary system, gastrointestinal tract, thyroid, spleen and
testes.

Bone Scanning
The bone scan is an excellent complement to other imaging studies of
the skeletal system and in many instances can be the definitive procedure.
Technetium Tc 99m is an ideal isotope for bone imaging. Radionuclide bone
imaging is an extremely sensitive but nonspecific modality for imaging the
entire skeleton rapidly and inexpensively. The bone scan is a map of osteo-
blastic activity that occurs in response to a variety of benign and malignant
conditions. Areas of increased or decreased bone turnover or remodelling
can be identified by this method anywhere in the skeleton (Photograph
3.6). This technique is exquisitely sensitive to very small differences in bone
turnover caused by disease processes of all kinds and allows the detection
of abnormal areas long before they are visible on plain radiographs.
Indications for bone scintigraphy:
•  valuating bone pain when plain film findings are normal or equivocal
E
• Metastatic disease
• Early osteomyelitis
• Differentiating cellulitis from osteomyelitis
• Stress fractures
• Primary bone tumours
• Staging of known malignancies
• Joint disease
• Early avascular necrosis

(a) (b)

PHOTOGRAPH 3.6 Bone scan showing increased radiotracer uptake in (a) Left hand
and (b) left ankle indicating complex regional pain syndrome type 1.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Discography 57

• D etecting and evaluating Paget disease

• Evaluating painful joint prostheses
• CRPS
  

Technetium Tc 99m-labelled phosphates accumulate at metabolically

active sites within the skeletal system. Deposition of the radioactive iso-
tope occurs in areas of new bone formation. Fully calcified bone takes up
relatively little radioactive tracer.
The most common use of bone scintigraphy is to detect metastatic
disease (most often due to breast, prostate, lung or renal carcinoma).
Lymphoma and neuroblastoma are also commonly evaluated by bone
scintigraphy, and it is very helpful in follow-up during treatment of bone
metastases. Bone scintigraphy is more sensitive than conventional plain
radiographs for detecting lytic bone lesions. Radionuclide bone scans may,
however, demonstrate either no increased uptake or decreased uptake
(‘cold lesion’) by certain aggressive tumours, such as multiple myeloma,
some anaplastic carcinomas and eosinophilic granulomas.
In addition to neoplastic disease, trauma, infection, vascular, metabolic,
dysplastic and degenerative disease of the musculoskeletal system can be
evaluated by bone scintigraphy (Table 3.1). It is a sensitive evaluation in
the initial phase of aseptic necrosis.

DISCOGRAPHY

Diagnostic disc puncture and intradiscal injection of contrast began

over 40 years ago. Provocative discography has since developed into a
powerful tool for investigating the aetiology of chronic lumbar, thoracic
and cervical pain. Intradiscal injection is indicated when the history,
physical examination and imaging studies point to painful internal disc
disruption. Corticosteroid injected into a disc may provide a therapeutic
response in a small group of patients. Response to discography may also
be useful in selecting patients who will benefit from further interventions
for relief from disc pain.
A discogram is obtained by injecting radiopaque contrast into the
central part of the intervertebral disc. The information provided from
well-conducted discography is twofold:
1. T
 he subjective report of pain at the time of disc pressurization is the
single most important aspect of this procedure. Patients may report no
pain, atypical pain or concordant pain during contrast injection. The
type of pain, location of pain and intensity of pain on a 0–10 visual
analogue scale should all be recorded during the injection. To avoid
potentially biased reporting, the patient should be unaware of the
level that is being injected.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

58 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

TABLE 3.1 Diagnostic Value of Imaging Procedures According to Body Region

Body region Recommended imaging procedure(s)

Head

Brain MRI
CT
Angiography

Head and neck Plain films

CT
MRI

Spine Plain films

MRI
CT
Myelography

Extremities

Soft tissues (including muscle, excluding bone) Plain films

Ultrasonography
CT
MRI
Venography

Bone Plain films

Bone scintigraphy
CT
MRI

Joint Plain films

MRI
Arthrography

Chest Plain films

CT
MRI
Radionuclide studies
Coronary arteriography
Aortography

Abdomen Plain films

Ultrasonography
CT
Contrast studies (barium meal or
enema, intravenous pyelography)
MRI
Radionuclide studies

Pelvis Ultrasonography
MRI
CT

CT, computed tomography; MRI, magnetic resonance imaging.

 Guidelines for Radiation Protection 59

2. O
 bjective information on disc anatomy and the presence of
degenerative changes is obtained at the time of contrast injection.
AP, lateral and offset axial fluoroscopic images should be evaluated
for annular tears, contrast extravasation and degenerative changes.
Further anatomic details can be obtained from the postdiscography
CT scan.
  
Discography requires meticulous attention in visualizing the disc. In
cases of degenerative disc disease, the disc space may be very narrow and
difficult to access. Proximal anatomical structures may hinder easy access
to the disc space. Proper fluoroscopic visualization of the disc space and
related landmarks is essential for safe discography. Close attention should
be paid to sterile technique and prophylactic antibiotics should be given.
One potentially disastrous complication of discography is infectious dis-
citis. Strict sterility conditions including masking for the entire injection
team should be maintained to for all disc puncture procedures.
The fluoroscopist should adopt a standard approach to identify the disc
space and landmarks at each level. The typical sequence includes the fol-
lowing steps:
1. I dentify the correct cephalocaudad angle. For cervical discography,
a scout lateral view is useful to give an idea of the cephalocaudad
angle of each disc. For lumbar and thoracic levels the angle should
be optimized to obtain the clearest view of the vertebral end plate.
Cervical discography is typically performed using an initial AP view
and then a lateral view.
2. For lumbar and thoracic disc punctures, the beam should be
rotated to the proper amount of obliquity to visualize posterolateral
access to disc. At lumbar levels, the beam is rotated until the facet
line is between 1/2 and 1/3 of the way superimposed over the
corresponding end plate shadow. At thoracic levels, a radiolucent
‘box’ is visualized between the end plates medial to the rib head
and lateral to the facet process. Intermittent fluoroscopy is used for
guiding the needle. Once the needle is in contact with the annulus,
the beam is directed to identify lateral fluoroscopic anatomy. Once
needle tip position is confirmed by biplanar fluoroscopy, contrast can
be injected. CT scanning of injected levels following the procedure
provides additional anatomical information.

GUIDELINES FOR RADIATION PROTECTION

There are many regulations regarding the use of radiation for diagnostic
procedures. National Council on Radiation Protection and Measurements,
USA, suggests adhering to the ALARA concept: that radiation exposures

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

60 3. RADIOGRAPHY AND IMAGING IN PAIN MEDICINE

be kept ‘as low as reasonably achievable’. This places responsibility on the

pain physician and radiographer to be aware of radiation doses and safety
practices for all patients and health care workers involved in fluoroscopic
procedures. As always, the potential benefits of exposing the patient to
ionizing radiation must outweigh the risks. Annual effective absorbed
dose equivalent limit for whole-body occupational exposure has been set
at 5 rem (50 mSv). The annual public exposure limit is 1 rem (1 mSv).
Guidelines regarding patient exposure:
• P atients should be shielded by placing lead under the patient during
fluoroscopic imaging.
• Use ‘pulse’ mode to activate intermittent Fluoroscopic whenever
­practical to reduce patient exposure.
• Use appropriate collimation by reducing field size with side filters or
iris adjustments.
• Decrease patient exposure by using higher range peak kilovoltage
(85–120 kVp) and lower range milliamperage (1.5–2.0 mA).
• Utilize a minimum source-to-skin distance of 30 cm (12 inches).
• Passive restraints may be used to reduce fluoroscopic motion if
appropriate.
• Maintain log book of patient exposure rate and time.
  

Guidelines regarding occupational exposure:

• A lways wear protective lead apron (minimum 0.5 mm lead
equivalency).
• Stand at a 90° angle to the patient to receive minimum scatter
radiation.
• Utilize appropriate dosimeter monitoring devices for all personnel
exposed to radiation.
  

Guidelines regarding C-arm:

• F or the most effective use and least exposure, X-ray tube should be
positioned below the patient and image intensifier above the patient.
• Whenever the C-arm is moved from a neutral position, radiation dose
increases, so it is preferred to position the patient in an oblique position
versus rotating the C-arm, for less radiation to the physician.
• The option should be established whether the physician or the
radiographer will control activation of fluoroscope. Frugal use of
­Fluoroscopy should be implemented.
• Trained personnel should be able to position the C-arm and make
appropriate adjustments to establish a useable scout image using less
than 5 s of fluoroscope time.
• A laser beam positioning device that attaches to the image intensifier
is helpful in pointing to targeted anatomy on the patient's skin, further
reducing radiation exposure.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 C H A P T E R

4
Ultrasonography in Pain
Medicine

The science of interventional pain medicine has undergone a signifi-

cant change in the last three decades. From performing interventions by
blind anatomical landmark techniques to the use of portable X-rays to
fluoroscopic guidance and later CT guidance, we have now entered an era
of using a safe, radiation-free and technically perfect technique allowing
real-time visualization of soft tissues, bony structures as well as the needle
and spread of injectate with the help of ultrasound-guided interventions.
Application of ultrasound guidance is a rapidly growing medical field in
interventional pain management. Traditional interventional procedures
for pain management are often performed by techniques using either
landmark or imaging guidance (e.g. fluoroscopy and CT scan). Ultra-
sound provides direct visualization of various soft tissues such as muscle
layers, nerves and blood vessels and real-time needle advancement and
avoids exposing both the pain physician and the patient to the risks of
radiation. The machine itself is more affordable than a fluoroscope, CT
scan, or MRI machine. Limitations to current ultrasound technology exist,
including narrow image windows and acoustic shadow artefact, which
results in the inability to view structures deep to bony obstruction. These
issues are being actively looked into by the industry and we can hope for
better probes and images in the near future.
Advanced pain practices usually use fluoroscopy, which is accurate
when bony structures are targeted, but cannot be used to identify soft
­tissue, including nerves and blood vessels. Fluoroscopy is a standard aid
in performing pain-related interventions across the world. In our pain
centres/clinics, almost every selective root epidurals, interlaminar epidur-
als and even caudal epidurals are all performed under fluoroscopic guid-
ance. The use of contrast to confirm position of needle and also spread
of solution is a great boon for the pain physician in targeting the desired
structures for placing the local anaesthetic, steroids and other drugs.

61
62 4. ULTRASONOGRAPHY IN PAIN MEDICINE

In difficult spine cases, fluoroscopy is of great help, contrast deficits

inform about anatomical obstacle and legal aspects are not to be forgotten.
However, the soft tissue cannot be visualized and it also exposes patient
and the provider to the risk of radiation. It also requires more manpower
as radiographer assistance is usually mandatory. CT provides better guid-
ance, but still lacks the ability to identify nuances of anatomy. It is also less
available, is time consuming, and can be problematic in terms of radiation
safety. CT is mainly reserved for coeliac plexus and hypogastric plexus
blocks or known difficult selective nerve root blocks and sacroiliac joint
injections. CT involves huge amount of radiation and the interventional
pain physician has to move in and out of the room frequently. An access
to a CT scanner is difficult in a busy hospital where CT is mainly used as
a diagnostic tool.
Ultrasonography uses high-frequency sound waves (ultrasound) to
produce dynamic visual images. For decades, radiologists, or specially
trained technicians, have used ultrasonography as a standard imaging
tool. Examination of body cavities, glands, blood vessels, and other tissues
has been routinely performed, often in conjunction with nerve blocks, fine-
needle biopsies, joint injections, or vascular catheterization. Compared to
other imaging equipment, ultrasound machines are transportable, free of
radiation or magnetization, and relatively inexpensive.
Ultrasound has now also gathered momentum for widespread applica-
tion in musculoskeletal medicine. Clinicians have demonstrated the role
of musculoskeletal ultrasound in office-based percutaneous injections
evaluating and treating disorders of joints, tendons, bursa, cystic patholo-
gies, as well as injection of neuromas. Diagnostically, the utility of ultra-
sound may potentially be extended to include assessment of chronicity
in sports-related injury. Musculoskeletal disorders constitute the majority
of the problems pain physicians deal with worldwide. Tendinopathies,
arthritis, back and neck pain, nerve injuries and entrapments are exam-
ples. A ‘clinical diagnosis’, based solely on history and physical examina-
tion, may be confusing and inaccurate. At the same time, clinicians should
not routinely send patients for time consuming and expensive tests such
as MRIs. Sonography allows patients to be examined in a more comfort-
able position, avoiding prolonged and sometimes painful immobilization
in the MRI scanner. Patient and practitioner interaction during ultrasound
examination is an invaluable addition to the imaging itself. Pressure from
the transducer may elicit tenderness, providing information that can be
useful to compare with the scan showing the composition of the under-
lying tissue. Dynamic imaging reveals transient conditions that cannot
be visualized by static scanning. Many abnormalities are not detectable
when a patient is at rest. The patient may have a swelling, pain, or click-
ing that occurs only with a certain movement. Examples include shoul-
der impingement, snapping hip syndrome, subluxations, tendon gliding,

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 4. ULTRASONOGRAPHY IN PAIN MEDICINE 63

ulnar nerve dislocation, and muscle hernia. Ultrasound is an excellent

imaging modality to diagnose tendinosis, tendon tears, and bursitis. Accu-
racy in the diagnosis of rotator cuff tears can reach 100% ­(full-thickness
tears) and 91% (partial-thickness tears), depending on the experience of
the individual performing the examination. With sufficient training and
experience, a diagnosis may be established at the point of care during the
first encounter with a patient.
Procedural ultrasound guidance is a useful and practical application.
Real-time control is ideally suited for delivering local anaesthetics, cor-
ticosteroids, botulinum toxin, and other agents. Ultrasound guidance is
intuitively superior to ‘blind injections’ and has been experimentally con-
firmed in joint injections.
A comparison with other imaging modalities makes sense when devel-
oping standards of care. If ultrasound accuracy compares favourably with
fluoroscopy or CT, it should be recommended as a standard, given its
cost-effectiveness and radiation sparing. In India, the use of ultrasound
guidance for regional anaesthesia-related nerve blocks started in 2004 and
caught the imagination of all young and old. The use of ultrasound guid-
ance resulted in a significant reduction of failure rate of regional blocks
to less than 1%. Anaesthesiologists with experience of peripheral nerve
blocks under ultrasound guidance naturally progress to interventions in
field of pain medicine. Ultrasound brings a new dimension to interven-
tional pain management.
Potential advantages of procedural ultrasound are
  

1. V isualization of nerves and surrounding structures: vessels, muscles,

bone and viscera-pleura, lung, peritoneum, bowel
2. Diagnostic – recognizing anatomical variabilities and pathology
3. Real-time visualization of needle trajectory, needle–nerve contact and
injectate spread
  

Below is a list of interventions that pain physicians can perform under

ultrasound guidance:
  

•  tellate ganglion block

S
• Cervical facet block
• Lumbar facet block
• Greater occipital nerve block
• Intercostal nerve block
• Ilioinguinal/iliohypogastric nerves block
• Psoas muscle injection
• Piriformis injection
• Trigger point injections
• Lateral femoral cutaneous nerve injection
• Coeliac plexus block

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

64 4. ULTRASONOGRAPHY IN PAIN MEDICINE

•  uperior hypogastric plexus block

S
• Impar plexus block
• Lumbar sympathetic block
• Sacroiliac joint injection
• Placing peripheral nerve stimulation leads

USEFUL AND COMMON ULTRASOUND-GUIDED

PAIN PROCEDURES

Stellate Ganglion Block

Currently, it is a common intervention in the diagnosis and manage-
ment of sympathetically mediated pain and vascular insufficiency of the
upper extremities. Both surface anatomy-based and fluoroscopy-guided
approaches are insufficiently accurate and may result in complications,
such as retrolaryngeal haematoma, recurrent laryngeal nerve damage,
and infections. An anatomically sound sonography-guided method was
developed to selectively target the cervical sympathetic trunk and to
avoid potential direct damage of the surrounding vascular, neural, and
parenchymal organs. The needle is directed from the lateral side to the
prevertebral fascia anteriorly to the longus colli muscle, where the lower
part of the sympathetic trunk is located. Injection of 3–5 mL of local anaes-
thetic will consistently spread over the fascial plane from C3 to T2 verte-
brae and will result in reliable blockade of the cervicothoracic ganglion.

Intercostal Nerve Block

This procedure has an important role in the management of acute pain
after rib fractures or thoracotomy. It is also valuable as a diagnostic block
or in the management of intercostals neuralgia in pain clinics. The routine
technique carries a risk of pneumothorax as high as 8%. Conventionally,
injections are performed distal to the rib angle, and the lateral cutaneous
branch may not be anaesthetized. Ultrasound guidance provides another
option that is safe and efficient. An approach on the medial side of the rib
angle allows complete block of the corresponding intercostal nerve while
keeping the pleura under direct view, thereby avoiding pneumothorax. In
addition, painful needle contact with the rib periosteum, which has been
utilized in methods that were not guided by imaging, is no longer required.

Anaesthetic Blockade of Peripheral Nerves

Instillation of local anaesthetic adjacent to the nerves of the trunk
and extremities is within the scope of regional anaesthesia. Despite their

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Useful and Common Ultrasound-Guided Pain Procedures 65

effectiveness in providing surgical anaesthesia and postoperative pain

control, these techniques have a role in chronic pain management that is
usually limited to diagnosis of a putative source of ongoing pain. When
analgesic blocks are used for diagnosis, ultrasound guidance is particu-
larly important because usually small nerves (e.g. the superficial radial,
ilioinguinal, lateral femoral cutaneous, saphenous, and plantar nerves)
are targeted, and only a minimal amount of anaesthetic is injected in order
to provide diagnostic precision. Moreover, often regional anatomy is dis-
torted by previous surgery or trauma, and only real-time ultrasound may
help in finding a displaced nerve.

Joint and Bursa Injections

Steroid injections into the joints and bursae are very commonly uti-
lized in any pain or physical medicine and rehabilitation clinic. Tradi-
tionally performed without imaging guidance, these procedures are
perceived as minor and harmless. However, this may not be the case.
First of all, so-called blind injections are inaccurate. Shoulder joint injec-
tions performed by orthopaedic surgeons may have a 73% failure rate,
and hip injections are accurate in only 60–80% of cases. When patients
do not get better after a procedure that was expected to be curative,
another procedure is usually offered to make up for the initial technical
failure. One of the main advantages of performing intra-articular injec-
tions under ultrasound is that the joints are accessed via the synovial
recesses, which prevents painful needle contact with bone or cartilage
(Fig. 4.1).

Needle

Supraspinatus tendon

FIGURE 4.1 Ultrasound Guided Shoulder injection

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

66 4. ULTRASONOGRAPHY IN PAIN MEDICINE

Spine Injections
Perhaps the major advantage in ultrasound-guided spine interventions
is the lack of radiation exposure. Spine procedures constitute the vast
majority of speciality pain medicine invasive methods, and the annual
dose of ionizing radiation can be significant for both patients and person-
nel. On the other hand, given the significant attenuation of an acoustic
signal by bone structures and the considerable depth of the intervention,
these procedures are challenging for sonographers.
Epidural interlaminar steroid injection is the most commonly per-
formed pain management intervention. The main limitation in imple-
menting ultrasound guidance is the acoustic sheltering and thus the
inability to confirm the spread of the injectate, which may be particularly
important if a specific spinal level or root is targeted. Nevertheless, since
the procedure is still performed in an office setting in a majority of pain
clinics worldwide without imaging, ultrasound can effectively facilitate
localization of precise spinal level and help decrease procedure time and
number of attempts by identification of bony landmarks to assist with
needle placement. It may be particularly helpful in patients with difficult
surface anatomy because of obesity, previous lumbar surgery, or scoliosis.
As in the case of interlaminar epidural steroid injections, ultrasound
is helpful in identification of bony landmarks during a caudal epidural
steroid injection; as much as 10% variation in sacral anatomy has been
reported. Up to 25.9% of caudal epidural placements, performed without
image guidance, were misplaced.
Lumbar zygapophysial (facet) intra-articular joint injections were most
likely the first ultrasound-guided spine injections to be validated against
CT-guided injections. The cleft of the zygapophysial joint is usually visu-
alized utilizing the transverse view of the lumbar vertebra.
Sacroiliac joint injections can technically be done under ultrasound
guidance. Two approaches, superior and inferior, were recently described.
Spinal injections under ultrasound have triggered the most intensive
debates concerning procedural accuracy compared with X-ray-based tech-
niques. However, ultrasound techniques have been extensively evaluated
in both the preclinical setting, utilizing imaging with anatomical correla-
tion, and in clinical comparative experimental work. Evidence is therefore
considered conclusive.

Piriformis Injection
In one of the recently outlined technique for ultrasound-guided injec-
tion of the piriformis muscle, the injection was performed with additional
motor stimulation for real-time reproduction of symptoms in patients
with piriformis syndrome.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Useful and Common Ultrasound-Guided Pain Procedures 67

Trigger Point Injections

An ultrasound-guided trigger point injection technique helps confirm
accurate needle placement in the cervicothoracic musculature. This could
help to avoid injection into adipose tissue particularly in morbidly obese
patients, which may otherwise minimize the injection's effectiveness. The
ultrasound guidance also could help to avoid the potential complication
of a pneumothorax or inadvertent intrathecal injection while injecting in
trigger points close to the chest wall. Thus, the use of ultrasound guidance
may increase the efficacy of trigger point injections to reduce or relieve
myofascial pain while reducing the possibility of complications.
Ultrasound has been shown to offer excellent guidance in selective gan-
glion or nerve blocks for invasive pain therapy.

Coeliac Plexus Block

Coeliac plexus block by anterior approach using ultrasound guidance
has been found to be a very effective technique as it is performed in supine
position and is very comfortable for the terminally ill cancer patients in
whom this block is often performed.
Sonoanatomy of several other acute and chronic pain management
interventions is being studied and all the results that have been obtained
so far emphasize the great potential of ultrasound guidance in invasive
pain therapy. Using a high-frequency probe, we can directly visualize
the distribution of local anaesthetics and neurolytic solutions around the
nerves and plexus. This is perhaps the key to success of interventional
techniques as direct visualization of spread of the local anaesthetic and
the neurolytic solution reduces the failure rate significantly. The devel-
opment of hand-held portable ultrasound machines with high-frequency
probes has further helped the cause for use of the technology for pain
medicine.
Will the use of ultrasound guidance for interventional pain management
become the gold standard in future? This question has to be addressed by
all of us involved in interventional pain management. There are signifi-
cant mental obstacles to be overcome and obviously financial consider-
ations as the cost of the machines is still exorbitant. It is, however, justified
to expect all pain physicians to acquire the skills to use ultrasound guid-
ance in clinical practice. With ultrasound imaging playing an increasing
role in vascular access, transoesophageal echocardiography and regional
blockade, the ultrasound machine may become an important component
and an essential armamentarium of interventional pain practice.
Ultrasonography opens a new two-dimensional and grey-scaled win-
dow into the fascinating world of human anatomy. Bedsides, point-of-
care sonographic imaging is an invaluable clinical tool in diagnosis of

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

68 4. ULTRASONOGRAPHY IN PAIN MEDICINE

musculoskeletal and neurological pathology. Procedural ultrasound effec-

tively provides guidance to ensure precise targeted delivery of drugs and
to avoid complications associated with surface anatomy-based injections.
New developments are under way, such as needle navigation systems,
optical recognition of different tissues, photonic needles, and ultrahigh-
definition ultrasound. Validation studies comparing ultrasound with
other traditional radiological methods are necessary to prove the compa-
rability and in many cases the superiority of this rapidly progressing field
of medical imaging. As ultrasonography becomes increasingly accessible
and easier to use, it opens up many treatment and research opportuni-
ties. Importantly, assuming that cost and practicality continue to compare
favourably, diagnostic sonography and ultrasound-guided interventions
could become routine, especially as the technology improves and the
images become easier to interpret.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 C H A P T E R

5
Pharmacotherapeutics
(Drugs) in Pain
Management

Relief from pain and suffering has been the paramount objective of
medical profession throughout history. Use of drugs is the most common
method of treating all types of pain. However, it is necessary to remember
that pain management is a multidisciplinary effort and pharmacotherapy
forms just a small part of it. No single approach should ever be used exclu-
sively for a patient.
Nociceptive pain, where somatic and visceral tissue sustain insult, gen-
erally responds better to anti-inflammatory and opioid medication. Neu-
ropathic pain (due to dysfunction of the nervous system in the absence of
ongoing neural tissue damage) generally responds better to antiepileptics
and antidepressants. Psychological pain usually responds to antidepres-
sants, neuroleptics, lithium and other measures such as psychotherapy,
counselling, etc.
Drug groups used to treat pain include
  

1.  OX inhibitors, acetaminophen (paracetamol)

C
2. Opioids
3. Anticonvulsants
4. Antidepressants
5. Local anaesthetics
6. Depot steroids
7. Muscle relaxants
8. Botulinum toxins
9. NMDA receptor antagonists
10. Miscellaneous – vasodilators, methoxycobalamine, capsaicin,
hyaluronidase, and naloxone

69
70 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

COX INHIBITORS

Whenever cells are damaged, prostaglandins are released in the tissue.

Inhibition of COX, the enzyme responsible for biosynthesis of prostaglan-
dins and certain related autocoids from arachidonic acid, is thought to be
a major facet in the mechanism of action of COX inhibitors.
Most patients, who have mild to moderate pain from acute or
chronic inflammation, arising primarily from integumental struc-
tures, can be managed with COX inhibitors. The following flowchart
depicts ­physiological and pathophysiological roles of COX 1 and COX
2 inhibitors.

Physiological stimulus Tissue damage

Interleukins (+) (–) Glucocorticoids

Constitutively Inducible enzyme

expressed enzyme COX 2 Selective
COX COX 2 inhibitors
Platelets (TXA2), Classical NSAIDs Macrophages,
stomach endothelium, synoviocytes (cells in
intestines (PG12), the urogenital tract
kidneys (PGE2) and in the CNS)

Normal cell functions Inflammation

Homeostasis Regulation of
electrolyte balance
and fertility

  
NSAIDs can be classified into two categories: acidic and nonacidic
(Tables 5.1 and 5.2).

Indications
• M
 ild to moderate pain associated with acute or chronic inflammation
of integumental structures – osteoarthritis, rheumatoid arthritis, anky-
losing spondylitis, early treatment of prolapsed intervertebral disc,
dental pain, fractures, headache, etc.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 COX Inhibitors 71

TABLE 5.1 Classification of Acidic NSAIDs

Oral dose range Paediatric oral
Class Drugs (max) in mg dose (mg/kg)

1. Low 1. Salicylates 1. Aspirin 1. 325–1000 (3600) 1. 10–15

potency/fast 4–6 h
elimination
2. Trilisate 2. 870–1700 (2000)
8–12 h

2. Propionic 1. Ibuprofen 1. 200–800 (1200) 1. 5–10

acid 8–12 h

3. Anthranilic 1. Mefenamic 1. 500 (8–12 h)

acids acid

2. High 1. Propionic 1. Ketoprofen 1. 300–600 (6–8 h) 1. 1.5

potency/fast acids
elimination
2. Phenylacetic 1. Diclofenac 1. 25–75 (200) 12 h 1. 1–2
acid sodium

3. Intermediate 1. Propionic 1. Naproxen 1. 250–500 (1375) 1. 10

potency/ acids 8–12 h
intermediate
elimination

4. High 1. Oxicam 1. Piroxicam 1. 20 (40) 12–24 h 1. 0.4

potency/slow 2. Meloxicam 2. 7–15/24 h
elimination

TABLE 5.2 Classification of Nonacidic NSAIDs

Oral dose range Paediatric oral
Class Drugs (max) in mg dosage (mg/kg)

Aniline derivatives 1. Acetaminophen 1. 250–600 (2400) 1. 10–15

(paracetamol) 4–6 h

COX 2 preferential 1. Nimesulide 1. 100 12 h 1. 5

inhibitors

COX 2-specific 1. Celecoxib 1. 100–200 (400)

inhibitors 12–24 h

2. Valdecoxib 2. 10 (20) 12–24 h

3. Etoricoxib 3. 60–120 (180) 24 h

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

72 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

• C ancer pain arising from bony metastasis, mechanical compression

of integumental structures, mechanical distention of subcutaneous
tissue, inflammation, myalgia or arthralgia, which can result from
radiotherapy
• Gout and postoperative pain

Adverse Effects/Contraindications/Precautions
1. G I – nausea, vomiting, dyspepsia, gastritis, abdominal pain, and
peptic ulceration (avoid in patients with peptic ulcer disease)
2. Renal – sodium retention, changes in tubular functions, interstitial
nephritis (avoid in patients with renal dysfunction). Risk factors
for renal dysfunction and hypovolemia, CCF, hepatic cirrhosis,
creatinine clearance less than 30 mL/min, diabetic and hypertensive
nephropathy, old age, and anaesthesia
3. Inhibition of platelet aggregation and clot formation (avoid in
patients with bleeding diathesis)
4. Allergic reactions
5. Prolonged labour and the associated coagulopathy may cause
problems in third trimester patients
6. Eye and ear (tinnitus) abnormalities with large doses
7. Changes in perception/mentation/mood especially with propionic
acid derivatives
8. Use with caution in patients with allergic rhinitis/bronchial asthma
9. High doses and long-term administration should be avoided
10. Before commencing treatment measure baseline, complete
blood count and serum creatinine, and thereafter, monitor every
3 months

Commonly Used COX Inhibitors at Our Centre

1. A cetaminophen (paracetamol) is the most widely used analgesic for
relieving mild to moderate musculoskeletal pain. It does not produce
as much GI irritation as other NSAIDs nor does it affect blood clotting.
It is often combined with a weak opioid.
2. Naproxen has a favourable GI profile. Its absorption is slowed
by concomitant ingestion of food. Its plasma half-life is 13 h, and
therefore, can be given as twice-a-day dose. It has a role in treatment
of headache, osteoarthritis, rheumatoid arthritis, tendonitis, bursitis,
acute gout and dysmenorrhoea.
3. Piroxicam has a prominent enterohepatic circulation leading to
prolonged half-life. Therefore, it should be used with caution in the
elderly. The dosage is once or twice daily and it may take up to 1 week

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Opioids 73

to achieve steady state concentration. Up to 40% patients experience

GI side effects.
4. Nimesulide is five to six times more potent at inhibiting COX 2 than
COX 1. It produces minimal gastric irritation. Nimesulide (100 mg) is
also used in combination with paracetamol (500 mg).
5. Mefenamic acid is commonly used in arthralgia. Diarrhoea is the most
common side effect. It was to be used with caution in the elderly. It
has been associated with severe pancytopenia and many other side
effects. Therefore, therapy should not be used for more than 1 week.
6. Diclofenac sodium is used when prompt relief of pain is desired.
It accumulates in the synovial fluid and, therefore, is useful in
the treatment of osteoarthritis and rheumatoid arthritis. It has
high therapeutic index as compared to other NSAIDs. However,
GI side effects are very common. Reversible elevation of hepatic
transaminases can occur. It should be avoided in children and
pregnant or nursing women. Combination of diclofenac with
paracetamol or propoxyphene gives good results. We commonly
use diclofenac gel in the treatment of arthritis and neuropathic
pain.
7. Celecoxib, valdecoxib, Etoricoxib (COX 2-specific inhibitors) belong
to the newest class of nonnarcotic analgesics. They are effective in the
treatment of osteoarthritis and rheumatoid arthritis. Their GI profile is
good. They do not inhibit platelet aggregation. Patients on warfarin,
phenytoin or other highly protein-bound drugs should preferably be
given these drugs. Patients with cardiac risk factors on these drugs
should be given low-dose aspirin. These drugs are not recommended
for children and pregnant or nursing women. The commonly
observed adverse reactions are nausea, vomiting, diarrhoea and
oedema of lower extremities. Celecoxib is contraindicated in patients
with a history of allergy to sulfa group of drugs.

OPIOIDS

Opioids are the most effective analgesics known to mankind. As far

back as 3500 BC, in the Sumerian culture, opium plant was referred to as
Hulgil or joy plant. All opioids with morphine-like pharmacological activ-
ity can be antagonized by the opioid antagonist naloxone.
WHO has defined five principles for opioid use in the management of
cancer pain (Fig. 5.1).
  

1. U se oral routes or other noninvasive routes when possible

2. Titrate doses to individual response
3. Utilize analgesics as described on the analgesic ladder 3

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

74 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

Fre
e
can dom f
cer r
pain om
Op
io
to s id for
e m
± N vere oder
±A
ono pain ate
dju pioid
van
3
Pa t
in p
or i ers
ncr isti
eas ng
ing
Op
ioid
mo
d for
± N erate mild 2
± A onopi pain to
dju oid
van
t
Pa
in
or pers
inc
rea isting
sin
g

No 1
± A nopi
dju oid
va
nt

Pa
in

FIGURE 5.1 World Health Organization analgesic ladder.

4. M aintain effective drug concentration while noxious stimulus is

present
5. Use adjuvant medications when indicated

Classification of Opioids
1. W eak opioids for mild to moderate pain – codeine, propoxyphene,
pentazocine, oxycodone, hydrocodone, and meperidine
2. Strong opioids for moderate to severe pain – alfentanil,
buprenorphine, butorphanol, diacetylmorphine (heroin),
dihydromorphine, fentanyl, levorphanol, methadone, morphine, and
sufentanil
  

Morphine is the mainstay in the treatment of moderate to severe pain,

especially cancer pain. Nociceptive pain (moderate–severe) is most respon-
sive to opioids. Neuropathic pain and central pain are less responsive and

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Opioids 75

the response is variable. Psychological pain is generally nonresponsive

and chronic opioid treatment is inappropriate.
Morphine acts on μ-, κ-, δ- and nociceptin (orphan) opioid receptors,
which are mostly concentrated in the substantia gelatinosa of the spinal
cord. μ Receptor is the main molecular target for opioid analgesic activity.
Activation of opioid receptors leads to inhibition of adenylcylase activ-
ity and, therefore, suppresses voltage-gated calcium currents and, thus,
activates inward potassium currents.

Starting a Patient on Oral Morphine

Psychological evaluation prior to initiation of opioids and following
titration to therapeutic doses would decrease the chances of a negative
outcome. Prior to starting morphine an informed ‘consent form’ should
be signed by the patient.
If pain persists despite using maximum dose of nonopioid and a weak
opioid, immediate release oral morphine is started at a dose of 10 mg
every 4–6 h (0.2–0.6 mg/kg/day). After 2 days, reassess the pain relief.
If pain relief is inadequate, step up the dose (taking into account the pre-
vious daily dose + the amount of morphine used for breakthrough pain
per day) till adequate pain relief is obtained or a maximum of 360 mg/
day is reached. A double dose at bedtime negates the need for treatment
during the night. In elderly patients, start on a lower dose – 5 mg/4–6 h
in order to reduce initial drowsiness, confusion, and unsteadiness. Once
the patient is stable on plain morphine, one can change to slow-release
morphine. The 12 h dose will be three times the previous 4 hourly dose
rounded off to a convenient number of tablets.
If plain morphine is not available, start slow-release morphine at
20–30 mg/bd. Use a weak opioid or half the dose of morphine (i.e.
10–15 mg) for breakthrough pain. Dose is titrated every 2 days until ade-
quate pain relief is obtained throughout every 12 h period.

Spinal and Epidural Morphine for Chronic Pain

In patients with chronic intractable pain, who have failed a trial
of systemically administered opioids because of toxic side effects or
because maximum dose has been reached, administration of spinal
or epidural morphine should be considered. A trial of spinal opioids
is given to establish opioid responsiveness prior to intrathecal pump
implantation. Morphine is the drug of choice for intrathecal use because
of its long duration of action, relative ease of use and extensive avail-
able literature.
300 mg of oral morphine = 100 mg of parenteral morphine = 10 mg of
epidural morphine = 1 mg of intrathecal morphine.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

76 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

The dose of intrathecal morphine is 0.01–0.05 mg/kg while the bolus

dose of epidural morphine in adults is 2–6 mg.
Even after treatment, if the problem persists, change to an alternative
opioid. Fortunately, tolerance to most side effects occurs with time except
constipation. Constipation is such a certain consequence that the lack of it,
in part, supports the concern that the opioid dose may be too low or that
opioids may be diverted (Table 5.3).

Opioid Tolerance, Dependence and Addiction

Opioid tolerance and physical dependence are expected with long-term
treatment and should not be confused with psychological dependence
(addiction). Pain is a psychological antagonist to the central depressant
effects of morphine; hence, respiratory depression is rare with increas-
ing doses. For most cancer patients, the first indication of tolerance is the
decrease in the duration of analgesia for a given dose.
Possible causes of pseudotolerance are
  

1.  rogression of the underlying disease

P
2. Onset of second new disorder
3. Increased physical activity
4. Lack of compliance
5. Change in opioid formulation
6. Drug interaction

Determining Treatment End Points during an Opioid Trial

1. P ain reduction, improvement in visual analogue scale (<4).
2. Restoration of function and improvement in quality of life such
as return to work, performance of household chores, increased
socializing and family activities.
  

If the patients on opioids have subjective, marked relief of pain but no

functional gains or have signs of functional loss such as unemployment,
diminished physical activity, dysfunctional interpersonal relationships,
they need to be assessed for possible opioid side effects like sedation, cog-
nitive impairment and possible addiction.

When to Discontinue Opioid Therapy

1. I f treatment is deemed unsatisfactory, then consideration of many
factors such as inadequate dose, inappropriate dosage schedule,
improper drug delivery route, and opioid resistant pain (neuropathic)
is important.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Opioids 77

TABLE 5.3 Adverse Effects of Opioids and Their Management

1. Common Initial 1. Nausea, vomiting Metoclopramide 10–20 mg/6
hourly. Ondansetron 4–8 mg/8
hourly

2. Drowsiness, Decrease the dose of morphine,

unsteadiness consider methyl phenindate 10 mg
od or bd

3. Confusion, delirium Decrease dose of morphine and/or

add haloperidol 3–5 mg od/hs

Ongoing 1. Constipation Increase intake of fluids, cathartics,

stool softeners, osmotic laxatives,
naloxone

2. Nausea, vomiting If movement induced – cyclizine or

promethazine 25–50 mg/8 hourly,
ondansetron 4–8 mg/8–12 hourly,
transdermal scopolamine

3. Tolerance Increase frequency or dose of the

drug, consider switching to another
structurally dissimilar opioid

2. Occasional Dry mouth, sweating, Chlorpheniramine 4 mg/bd or

pruritus, hallucinations tds, naloxone. Decrease dose of
morphine and/or add haloperidol
3–5 mg od/hs

Myoclonus (common Decrease dose of morphine but

with high dose IV/ revert to former dose if pain
spinal morphine) (not recurs, meanwhile consider
reversed by naloxone) benzodiazepine

Urinary retention, Change to another opioid,

common with intrathecal naloxone small doses titrated
epidural morphine

3. Rare Respiratory depression If moderate to severe, give IV

naloxone 0.1–0.4 mg, every
10–15 min slowly over 2–3 min

Psychological IM/IV antihistaminic and

dependence bronchodilator
Bronchoconstriction

2. I n cancer patients, when the cause of pain is eliminated effectively by

antineoplastic treatment or modified by neuroablative or neurolytic
procedures, opioids need to be decreased or discontinued. Slow
systematic tapering of opioids can prevent withdrawal.
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

78 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

On day 1 and day 2 of commencing discontinuation, 50% of the prior

daily dose is given. Thereafter, reduce the daily dose by 25% every 2 days
until the total dose (in morphine equivalents) is 30 mg/day. The drug may
be discontinued after 2 days on 30 mg/day dose.
Codeine phosphate is 1/10 as potent as morphine (Table 5.4). It has
weak affinity for opioid receptor. Codeine is generally used in combi-
nation with nonopioid (ibuprofen) in doses of 20–60 mg; 60 mg codeine
given intramuscular is equianalgesic to 180 mg oral. When given for
prolonged periods, it has high oral efficiency and low incidence and
degree of physical dependence. Constipation and nausea are its common
adverse effects.
Tramadol is a synthetic analogue of codeine. It is a centrally acting
analgesic. When given orally it is 1/5 as potent as morphine. Trama-
dol has high degree of efficacy and low incidence of dependence. It is
mainly used for relief from moderate pain, i.e. radiculopathy, PDN,
fibromyalgia, musculoskeletal pain, and postoperative pain. Sometimes
it is used to relieve breakthrough pain. Dose-related dizziness, sedation
and nausea are seen. Tramadol is better tolerated by slow increase in
the doses. Abrupt discontinuation of tramadol can lead to withdrawal
symptoms.
Fentanyl transdermal is available in four patch sizes – 25, 50, 75, and
100 mcg/h. Its effect lasts for 72 h; thus, dose is increased every 72 h.
Absorption is similar from chest, abdomen and thigh. When applied to
dry noninflamed, nonirradiated, unshaven hairless skin, it may need
micropore on the sides to fix it to the skin (Photograph 5.1).
It avoids the first pass of the liver. It takes about 48 h before steady
state is achieved. Dose is increased every 72 h if pain relief is inade-
quate. Patch position is changed every time. Fentanyl patches are used
in patients with chronic pain, who are unable to take oral opioids and

TABLE 5.4 Dosages and Duration of Action of Opioids

Potency ratio to Duration of
Analgesic oral morphine action (h) Dose in mg

Codeine 1/10 3–6 30–200

(0.5–1.0 mg/kg/day)
PO or IM

Tramadol 1/5 4–6 50 mg OD or tds–Max

200 mg/day, PO or IM

Fentanyl 150 72 25, 50, 75 and 100 mcg/h

transdermal

Propoxyphene 4–6 32–65 PO

IM, intramuscular; OD, once a day; and PO, per oral.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Opioids 79

who do not require a rapid dose titration. All patients should be pro-
vided with oral rapidly acting short-duration opioids for relief from
breakthrough pain. After removal of the patch, serum concentration
decreases by 50% after 16 h. Patients not relieved by morphine will not
be relieved by fentanyl transdermal. It cannot be used in patients who
perspire profusely. Side effects seen are nausea, mental clouding and
skin irritation. Laxatives may or may not be needed as fentanyl pro-
duces far less constipation.
Propoxyphene is structurally related to methadone. Being a weak opi-
oid, it is usually given in combination with aspirin or acetaminophen. It is
cumulative with repeated doses. It causes cardiac conduction system (like
lidocaine), which constitutes a significant risk in case of overdose. Given
in high dose, it can also cause convulsions, which can be reversed with
naloxone (Table 5.5).

PHOTOGRAPH 5.1 Fentanyl patch applied on the chest wall.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

80 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

TABLE 5.5 Important Opioid Drug and Disease Interactions

Opioids Disease state Comment Drugs Comment

All Renal Adjust Antihistamines ↑s Sedation

dysfunction liver dose, Butrophenones
disease, elderly use with
patients caution TCAs ↑ Sedation +
potentiation of
respiratory depression

Controlled Metoclopromide Earlier peak plasma

release concentration, ↑s
sedation

Morphine Where Avoid Amitriptyline ↑s Levels of available

respiration morphine
is affected
Emphysema,
asthma,
increased ICT

Adrenocortical Avoid Cimetidine ↑s Levels of available

insufficiency, morphine
severe liver
disease,
hypothyroidism,
diverticulitis,
biliary colic,
during labour

Codeine MAOIs Avoid

Quinidine Inhibits conversion to
morphine thus
↓s analgesia

Tramadol Risk of seizures, Use with Carbamazepine ↑s Tramadol

epilepsy, head caution concentration, hence
injury higher doses required

Drugs that ↓ Use with caution

seizure threshold:
TCAs, SSRIs,
neuroleptics

MAOIs Avoid

Propoxyphene Carbamazepine ↑s Levels of

carbamazepine to
levels of toxicity

Doxepin ↑s Levels of doxepin,

potential for toxicity

Metoprolol, ↑ Levels of beta blockers

propranolol

ICT, intracranial tension; MAOIs, monoamine oxidase inhibitors; SSRIs, selective serotonin reuptake
inhibitors; and TCAs, tricyclic antidepressants.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Anticonvulsants 81

ANTICONVULSANTS

Anticonvulsants significantly relieve neuropathic pain, especially the

lancinating, burning, dysesthetic pain. Their efficacy in musculoskeletal,
nociceptive or idiopathic pain is not very clear. We commonly use car-
bamazepine, oxcarbazepine and gabapentin. The pain relief obtained is
gradual so an adequate trial of anticonvulsants for 1–2 months should be
given before the anticonvulsant is considered ineffective.
Carbamazepine acts by blocking Na+ channels, which in turn decrease
repetitive spontaneous firing of action potentials in the depolarized neu-
rons of Aδ and C fibres.
It is the first line of treatment for trigeminal neuralgia. It is also used
in the treatment of other neuropathic pains, particularly acute onset of
PDN, postherpetic neuralgia, central pain, phantom limb, and facial
pains. For chronic onset of PDN, amitriptyline would be the choice. Neu-
ropathic pain produced by neural invasion by tumour, radiation fibro-
sis, and surgical scarring may be relieved by carbamazepine. It has been
used with varying success in the treatment of chronic cluster headaches
and prevention of migraine. Dosage – Before starting treatment, monitor
complete blood count and liver function, and thereafter, monitor every
3 months.
Start with 100 mg/bd, increase by 100 mg/bd–tds weekly to
600–800 mg/day in two or three divided doses. Usual maintenance dose
is 600 mg/day. It takes about 1–2 weeks for significant pain relief to occur.
Once the patient is pain free, for an adequate interval, carbamazepine
can be discontinued by slow tapering off. Tapering is very important, if
missed, patients can come back with severe recurrence of pain.
Adverse effects – commonly observed adverse effects are nausea, diz-
ziness and sedation, and less common ones are blurring of vision, skin
rashes, transient leucopenia, thrombocytopenia and aplastic anaemia.
Combination of carbamazepine with other anticonvulsants, tramadol,
propoxyphene, SSRIs and oral contraceptives, isoniazide, and erythromy-
cin need careful monitoring. Cimetidine, valproate, erythromycin, isonia-
zide and verapamil inhibit metabolism of carbamazepine and, therefore,
increase its serum levels.
Oxcarbazepine has actions similar to carbamazepine, but has a better
safety profile. It is a second-line drug for treatment of intractable trigemi-
nal neuralgia, radiculopathy and other neuropathic pains.
The starting dose is 300 mg/h with weekly increments of 300 mg/day
up to a maximum of 1200 mg/day. There is no autoinduction of hepatic
enzymes; thus, dose titration and adjustments are relatively easy. Com-
mon side effects are dizziness, drowsiness, nausea, headache, and blurred
vision. As compared to carbazepine, monitoring of haematologic and
hepatic parameters is not required.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

82 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

Gabapentin has chemical structure similar to GABA. Its mecha-

nism of action is still unclear. It probably acts on aδ-2 subunit of Ca++
channels to suppress spontaneous neuronal firing. It may enhance the
release and/or activity of GABA and inhibit release of excitatory amino
acids.
Gabapentin's relative safety and low side effect profile has gained it
widespread acceptance. It has no documented major drug interactions.
This makes it the first choice drug for treating neuropathic pain in the
elderly. It is the drug of first choice for DPN, postherpetic neuralgia and
radiculopathy. It is also used in the treatment of other neuropathic pains
like trigeminal neuralgia, deafferentation neuralgia, cranial neuralgias,
fibromyalgia, atypical facial pain and CRPS. Efficacy of gabapentin in
prevention of migraine is noteworthy. It is also used in the treatment of
multiple sclerosis.
Dosage – Start at 300 mg hs oral; increase in the first week to 300 mg/
bd; increase in the third week to 300 mg/tds; increase to a maximum of
1200–1600 mg/day or until side effects supervene. Because of its short
half-life, doses should not be given more than 12 h apart. Its effect starts in
3 or 4 days and pain relief occurs in about 2 weeks. Gabapentin is discon-
tinued by slow tapering over 1 week (or longer).
Adverse effects are minimal and dose dependent. Common ones are
dizziness, sedation, nausea, fatigue, and rarely skin rashes.
If possible, antacids should be given 2 h prior to or 2 h after gabapentin
to maximize bioavailability. Gabapentin dose should be reduced by 25% in
kidney disease as excretion is entirely renal, without any liver metabolism.

Pregabalin
Pregabalin is a synthetic molecule and a structural derivative of the
inhibitory neurotransmitter γ-aminobutyric acid. It is an A2-δ (α2-δ) ligand
that has analgesic, anticonvulsant, anxiolytic, and sleep-modulating activ-
ities. Pregabalin binds potently to the α2-δ subunit of calcium channels,
resulting in a reduction in the release of several neurotransmitters, includ-
ing glutamate, noradrenaline, serotonin, dopamine, and substance P.
For painful DPN, the maximum recommended dose of pregabalin is
100 mg thrice a day (300 mg/day). Dosing should begin at 50 mg thrice
a day (150 mg/day) and may be increased to 300 mg/day within 1 week
based on efficacy and tolerability. Because pregabalin is eliminated pri-
marily by renal excretion, the dose should be adjusted for patients with
reduced renal function. Although pregabalin was also studied at 600 mg/
day, which was less well tolerated, there is no evidence that this dose con-
fers additional significant benefit. In view of the dose-dependent adverse
effects, treatment of DPN patients with doses larger than 300 mg/day is
not recommended.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Antidepressants 83

For PHN, dosing should begin at 75 mg twice a day or 50 mg thrice a day

(150 mg/day) and may be increased to 300 mg/day within 1 week based on
efficacy and tolerability. Patients who do not experience sufficient pain relief
after 2–4 weeks of treatment with 300 mg/day, and who are able to tolerate
pregabalin, may be treated with up to 300 mg twice a day, or 200 mg thrice a
day (600 mg/day).
Pregabalin is well tolerated and associated with dose-dependent
adverse effects that are mild to moderate and are usually transient. In
clinical trials, dizziness and somnolence are the most frequently reported
adverse events, with dizziness experienced by 29% of pregabalin-treated
patients compared with 9% with placebo and somnolence experienced
by 22% of pregabalin-treated patients compared with 8% with placebo.
Dose-dependent weight gain has been reported. There have been case
reports of myoclonus aterixis and gynaecomastia, and a single case report
has described encephalopathy and oedema of the corpus callosum after
abrupt discontinuation of pregabalin.

ANTIDEPRESSANTS

These drugs show a direct analgesic effect at a dose lower than the one
needed to produce antidepressant action. Both actions are due to blockade
of presynaptic reuptake of serotonin, norepinephrine or both. Depression
may worsen pain perception. So by treating depression, patients can toler-
ate pain better. They also have improved sleep and appetite.

Indications
Older TCAs (amitriptyline and imipramine) have a more established
track record as analgesics than SSRIs, while SSRIs are more effective
antidepressants (Table 5.6). Generally, antidepressants produce more
than 50% pain relief in 30% of patients with neuropathic pain at the
price of minor adverse reactions in 30% and major side effects in 4%.
TCAs are most useful in patients with neuropathic pains, especially
postherpetic neuralgia and DPN. Other neuropathies in which TCAs
are used are trigeminal neuralgia, causalgia, radiculopathy, phantom
limb, perineal neuralgia and central pain. Analgesic effect is accompa-
nied by sedation, diminished anxiety, muscle relaxation and restored
sleep cycles.
Antidepressants potentiate the action of opioids. In chronic tension
headaches, migraine, fibromyalgia, and atypical facial pain, TCAs are con-
sidered the first line of treatment. Other chronic pain conditions in which
TCAs are used are arthritis, low back pain, malignancy and myofascial
pain.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 84
TABLE 5.6 Classification of Antidepressants
Anticholinergic Orthostatic Initial dose Daily dose range

5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

Class Drug Sedation action hypotension (mg/day) in mg Dosing schedule
I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

Tricyclic Amitriptyline High High Moderate 10–25 25–300 Qd–bid

antidepressants
(TCAs) Clomipramine High High High 12.5–25 25–250 Qd–bid

Desipramine Low Low Low 10–25 50–300 Qd–bid

Doxepin High Moderate Moderate 10–25 75–300 Qd–bid

Imipramine Moderate Moderate High 10–25 75–300 Qd–bid

Nortriptyline Moderate Moderate Low 12.5–25 40–150 Qd–bid

Selective Fluoxetine Very low Very low Very low 10 10–80 Qd–bid
serotonin uptake
inhibitors (SSRIs) Sertraline Very low Very low Very low 25 25–200 Qd–bid

Citalopram Low Very low Very low 10 20–60 Qd–bid

Monoamine Phenelzine Low Very low High 15 45–90 Tid

oxidase inhibitors
(MAOIs) Tranylcypromine – Very low High 10 30–60 Bid

Atypical Venlafaxine Low Very low – 37.5 75–225 Qd

antidepressants
Trazodone High Very low High 50 150–400 Qd
 Antidepressants 85

For psychological pain in which structural damage is not present, but

features of anxiety and depression co-occur with pain, and which exacer-
bates pain-related disability, TCAs are helpful. The more sedating TCAs
(amitriptyline imipramine, and doxepin) can be used at bedtime for
patients with insomnia, agitation and anxiety.
Commonly seen adverse effects of TCAs are palpitations, drowsiness
and delirium, especially with high doses and when combined with anti-
convulsants and neuroleptics. Anticholinergic effects are usually transient.
Given along with carbamazepine, higher doses of TCAs are required
because of hepatic enzyme induction. TCAs can lower the insulin needs
of a diabetic. They are preferably avoided in patients taking SSRIs and/or
other antidepressants.
SSRIs are relatively free from adverse effects. Common ones are nausea,
diarrhoea, anxiety, agitations and sexual dysfunction.

Starting Antidepressants
Prior to starting treatment and during dose escalation, it is prudent to
monitor electrocardiogram (↑ QT interval and conduction abnormalities),
complete blood count and liver function regularly. Carefully noting car-
diovascular status history is also important, i.e. if patient is on diuretics,
nitrates, quinidines, procainamides, and disopyramides. In the elderly,
the starting dose should be reduced by 50% and titrated up very slowly.
When using TCAs, it is important to remember that the analgesic effects
occur at doses 1/5 to 1/3 of those required to treat depression.
We usually start amitriptyline 10 mg/day hs, 1–2 h before bedtime;
increase the dose to 25 mg/day after 1 week. After another 2–3 weeks,
increase the dose to 50 mg/day/bd to a maximum of 75 mg/day or until
patient achieves satisfactory pain relief or troublesome side effects occur.
Pain relief occurs within 2–3 weeks. It is prudent to wait for another
6–8 weeks before determining whether the patient has had an adequate
response to antidepressant therapy. We also use a combination of amitrip-
tyline (12.5 mg/25 mg) and chlordiazepoxide (5 mg/10 mg).
The relatively fewer drug interactions, benign side effects and toxic-
ity profile of SSRIs, when compared to TCAs favour their use in clinical
conditions in which there is no therapeutic advantage of using TCAs
or that TCAs are contraindicated. They are essentially devoid of type
I antiarrhythmic effect of TCAs and rarely cause postural hypoten-
sion. SSRIs given with MAOIs cause life threatening central serotonin
syndrome.
Fluoxetine has a slower onset of action and may cause more agitation,
weight loss, and skin reactions than other SSRIs. Fluoxetine and sertaline
are relatively free of interactions with CNS depressants. Citalopram has
lesser sexual dysfunction than other SSRIs.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

86 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

Duloxetine hydrochloride is a selective serotonin and norepineph-

rine reuptake inhibitor for oral administration. Its chemical designation
is (+)-(S)-N-methyl-gamma-(1-naphthyloxy)-2-thiophenepropylamine
hydrochloride. Although the exact mechanisms of the antidepres-
sant and central pain inhibitory action of duloxetine in humans are
unknown, the antidepressant and pain inhibitory actions are believed
to be related to its potentiation of serotonergic and noradrenergic
activity in the CNS. Duloxetine, with dual effects on serotonin and
norepinephrine, appears to have more consistent benefits than selec-
tive serotonin antidepressants for the treatment of persistent pain asso-
ciated with fibromyalgia. Over 90% of the observed effect on pain in
fibromyalgia is due to a direct analgesic effect rather than an indirect
antidepressant effect.
For diabetic peripheral neuropathic pain, duloxetine should be admin-
istered at a total dose of 60 mg/day given once a day, without regard to
meals. According to a Cochrane Database review of controlled clinical
trials, duloxetine 60 and 120 mg daily are effective for treating pain in
diabetic peripheral neuropathy and fibromyalgia, but 20 mg daily is not.
There is no evidence that a dose of 120 mg/day confers any additional
benefits.
Abrupt discontinuation of a substantial dose of antidepressants may
be associated with withdrawal syndrome (sleep disruption characterized
by vivid colourful dreams, restlessness, and GI distress). This can be pre-
vented by gradually discontinuing the drug over 5–10 days.

Algorithm for Antidepressant Selection

(Gallagher and Pascol 1997 Current Therapies)

Nociceptive pain Neuropathic pain Pain condition plus

major depression

NSAID trial 2° Sleep Secondary Primary

Opioid disturbance
Persists after
Persists after adequate
adequate analgesia
analgesia
Assess medical risks
Medical risks

Yes– No– Anticonvulsants, No– Yes–

Antihistamine Low dose TCA tizanidine TCA SSRI trial
Low dose at bedtime Mexiletine Atypical
benzodiazepine NMDA antidepressants
antagonists

  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Local Anaesthetics 87

LOCAL ANAESTHETICS

Local anaesthetics are competitive Na+ channel blockers that stop

impulse propagation in neural tissues. The local anaesthetics are com-
monly classified by their potency (Table 5.7).
Local anaesthetics can be used for diagnostic and therapeutic pur-
poses. Their greatest advantage is that they allow precise identification
of peripheral nerves, nerve roots and autonomic ganglia, targeted for
destructive procedures. Temporary block lets the patient experience the
sensation of numbness before the numbness becomes permanent. Thus, it
is a good diagnostic tool that obviates, ineffective but everlasting, damage
from inappropriate treatment.
Repeated temporary block with local anaesthetics halts spontaneous
discharge in neurons, and thus, relieves pain effectively far beyond the
few hours duration of action of the drug, i.e. trigger point injections in the
treatment of scar neuromas and reflex sympathetic dystrophy.
Differential neural blockade can be achieved with differing concen-
trations of local anaesthetics. For example, bupivacaine 0.0625–0.125%
usually produces sympathetic blockade, 0.125–0.25% usually produces
sensory blockade and 0.5% usually produces a motor blockade. This is
useful in the diagnosis of the type of pain, whether sympathetically medi-
ated or sympathetically independent.
Local anaesthetics act synergistically with opioids; hence, this combina-
tion is commonly used in spinal and epidural injections.
Lidocaine infusion suppresses both injury-induced nociception and
secondary wind-up sensitization of wide dynamic range neurons in the
dorsal column of the spinal cord. It has been used in the management of
intractable central sensitization. Lidocaine infusion given at 5 mg/kg over
60 min duration has been shown to produce analgesia even up to 3 weeks.
Tachyphylaxis is a thing of the past; instead continuous lidocaine infusion
enhances lidocaine potency by raising the nerve to a supra Cmax steady
state. Over time, lidocaine requirements for a continuous infusion block
decrease as drug absorption matches drug disposition. Gradually decreas-
ing the concentration of infused lidocaine to near Cmax range can main-
tain solid analgesia with little or no motor block for days on end.
Allergy to local anaesthetics is rarely seen. Toxicity can occur because
of overdosage or intravascular injection leading to headache, lighthead-
edness, drowsiness, circumoral paresthesias, tinnitus, blurred vision, and
seizures. Care should be taken while injecting (by repeatedly aspirating),
to check for blood and cerebrospinal fluid. Continuous conversation with
the patient and maintaining eye contact with the patient also helps in early
detection of toxicity. If inadvertently intravascular injection is adminis-
tered, the most important step is to maintain oxygenation. If unable to
adequately ventilate a convulsing patient, a small dose of short-acting

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

88 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

TABLE 5.7 Classification of Local Anaesthetics

Drug Concentration Clinical use Duration

Low potency/ Prilocaine 0.5–1.0% Infiltration

short duration
0.25–0.5% IV regional

1.5–2.0% PNB 2–3 h

2.0–3.0% Epidural 1.5–3 h

2 Chlorprocaine 1.0% Infiltration

2.0% PNB 30–60 h

2.0–3.0% Epidural

Intermediate Lidocaine, max. 0.5–1.0% Infiltration

potency/ dose 4 mg/kg
intermediate
duration with
adrenaline 7 mg/kg 0.25–0.5% IV regional

1.0–1.5% PNB 1–2 h

1.5–2.0% Epidural 45–60 min

4.0% Topical

5.0% Spinal 30–45 min

Procaine 1% Infiltration

1.5–2% PNB

2% Epidural

10% Spinal

Mepivacaine 0.5–1% Infiltration

1–1.5% PNB

1.5–2% Epidural

4% Spinal

High long Bupivacaine, 0.25%

potency/ maximum dose
duration 2 mg/kg 0.25–0.5% PNB, epidural 4–6 h, 2 h or less
infiltration 0.5% Spinal 2 h or less

Tetracaine 0.5% Spinal 2–4 h

2% Topical 30–60 h

Etidocaine 0.5% Infiltration

0.5–1% PNB 3–12 h

1–1.5% Epidural 2–4 h

IV, intravenous and PNB, peripheral nerve block.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Depot Steroids 89

muscle relaxant, i.e. suxamethonium can be given. Benzodiazepines are

commonly used to control local anaesthetic-induced convulsions.

Mexiletine
Mexiletine is an orally active drug similar to lidocaine, which is resis-
tant to hepatic first pass effect.
Response to IV lidocaine infusion is predictive of the analgesic response
to oral mexiletine. Diabetic neuropathy seems to respond well to oral mex-
iletine. It has been reported to be useful in other neuropathies (phantom
limb, chemotherapeutic and postirradiation neuralgias), poststroke pain
and multiple sclerosis.
Mexiletine is commonly used in the dose 10 mg/kg/day. The ini-
tial adult dose is 150–200 mg/day, given along with food. The dose is
increased by 150 mg/week to a maximum of 750 mg/day, given in three
divided doses.
Electrocardiogram, liver function and plasma levels of the drug should be
monitored quarterly in patients on long-term treatment and on higher doses.
It is a class I antiarrhythmic agent used in the treatment of ventricular
arrhythmias. Thus, mexiletine is contraindicated in patients with second-
and third-degree AV blocks. But with first-degree AV block, it can be given
safely.
Commonly seen adverse effects are upper GI distress (40%), tremors,
lightheadedness, incoordination (10% each) and drowsiness.

EMLA Cream
EMLA cream is a mixture of lidocaine and prilocaine in equal amounts,
which acts transdermally and anaesthetizes terminal afferent nerve
fibres.
It has been used with reasonable positive results in the treatment of
postherpetic allodynia, superficial scar neuromas and atypical facial pain.
Application of thick layer of EMLA cream for an hour gives reliable anal-
gesia, which may last up to 5 h.

DEPOT STEROIDS

Steroids relieve pain by

  

1. R educing inflammation (by inhibition of phospholipase A2, which in

turn inhibits conversion of phospholipids to arachadonic acid, and
thus release of prostaglandins and leukotrienes)
2. Blocking transmission of nociceptive C fibre input suppresses ongoing
and ectopic neural discharge
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

90 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

Depot steroids are used for ESIs, trigger point injections, intra-
articular injections, in carpal tunnel syndrome under the flexor reti-
naculum and in perineural blocks along with local anaesthetics. The
potency of Depot steroids in relation to hydrocortisone is as shown in
Table 5.8.
If there is inadequate pain relief with 0.25% bupivacaine at trigger
point, then 20–40 mg Depot steroid should be given with bupivacaine.
In our practice, we commonly use methyl prednisolone in ESIs and
in perineural blocks, and triamcinolone in intra-articular injections
(Table 5.9).
ESI delivers the drug to the affected nerve roots thereby reducing sys-
temic side effects of the Depot steroids.
The indication for ESI is nerve root irritation and inflammation leading
to nerve root oedema, as seen in patients with
  

1. C hronic radicular pain with corresponding sensory change, who fail

4–6 weeks conservative treatment
2. Acute herniated disc (but not an extruded disc) after 4–6 weeks of
conservative treatment
3. Active patients with chronic low backache with radicular features and
poor response to conservative treatment
4. Patients with metastatic carcinoma in whom tumour infiltration of
nerve root has occurred
  

TABLE 5.8 Potency of Depot Steroids Relative to Hydrocortisone

Agent Anti-inflammatory Topical Salt retaining

Hydrocortisone 1 1 1

Methyl prednisolone 5 5 0

Triamcinolone 5 5 0

TABLE 5.9 Methyl Prednisolone and Triamcinolone

Methyl prednisolone acetate (Depomedrol) Triamcinolone diacetate (Kenacort)

1. Available as 40–80 mg/mL suspension Available as 40 mg/mL suspension

2. Never dissolves completely in the epidural Seemingly dissolves with time and
space adequate diluent

3. Has been used in thousands of patients

worldwide without any apparent side effects.
Controlled trial reports are awaited.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Muscle Relaxants 91

The aim of ESI is to produce short-term pain relief so that rehabilitation

and exercises can commence.
In patients with spinal stenosis, spondylosis, spondylolysthesis and
failed back surgery syndrome, the efficacy of ESI is doubtful.
In our pain clinic, we administer epidural steroids in a series of three
injections, given in the OT under fluoroscopic guidance.
Dose of ESI – 80 mg methyl prednisolone + normal saline (10–25 mL).
Local anaesthetics (0.25% bupivacaine 4–5 mL) can be given in the OT, but
should be avoided in the outpatient clinic. Volume of injection depends of
the site of injection.
  

Lumbar level: 10–12 mL

Cervical level: 4–5 mL
Caudal route: 20–25 mL
  

It takes between 2 and 6 days for pain relief to occur, so the patient is
asked to come for the first follow-up after 1 week.
Adverse effects are flushing, insomnia, weight gain, Cushing syndrome
(with frequent Depot steroid injections), suppression of the hypothalamic
pituitary adrenal axis and osteoporosis; behavioural changes like mood
changes and insomnia are usually not seen because of concomitant anti-
depressant therapy.
Inadvertent intrathecal steroid injection can cause arachnoiditis. The
dose of ESI should be reduced when injecting in a patient suffering from
diabetes mellitus.

MUSCLE RELAXANTS
Complex neurological mechanisms combine to maintain muscle tone.
Any malfunction within the system can lead to sustained abnormal mus-
cle contraction, producing marked stiffness and pain. Persistent pain for
any length of time can frustrate a patient.
Certain aspects of spasticity such as control of painful spasms and
decrease in resistance to passive movements can now be reliably addressed
with the help of centrally acting muscle relaxants.
It is not always clear whether in these disorders, the muscle is the pri-
mary source of pain and that muscle relaxants act on the primary pathol-
ogy or that these drugs work solely by relaxing muscles. The muscle
relaxants are classified as shown in Table 5.10.
Baclofen is the most established oral agent in the treatment of spasticity.
It is the most effective in patients with spinal cord lesions, especially mul-
tiple sclerosis or traumatic lesions. Baclofen is not effective in all types of
spasticity, especially spasticity of cerebral origin, nor is it effective against
all symptoms of spasticity.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

92 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

TABLE 5.10 Classification of Muscle Relaxants

Primary indication Pharmacological classification

Acute muscle spasm Antihistamine (orphenadrine)

Benzazol derivative (chlorzoxazone)

Benzodiazipine (diazapam)

Carbamate esters (carisoprodol)

Methyl propiophenone derivative

(tolperisone)

Tricyclic derivative (cyclobenzaprine)

Chronic CNS spasticity Alpha adrenergic agonist (tizanidine)

Benzodiazepine (diazapam)

GABA derivative (baclofen)

Peripherally acting (dantrolene)

Fibromyalgia Tricyclic derivative (cyclobenzaprine)

Nocturnal leg cramps Peripherally acting (quinine)

Its most useful effects are

  

1. R eduction in painful flexor and extensor muscle spasms, which often

wakes up the patient at night or renders voluntary movement difficult.
2. Improvement in resistance to passive movements, thus helping in
physiotherapy.
  

Although baclofen improves muscle tone, it also causes muscle weakness. It

has also been tried in patients with stroke and amyotrophic lateral sclerosis as
an adjuvant in neuropathic pain – trigeminal neuralgia and g­ lossopharyngeal
neuralgia. Adverse effects are common with baclofen but they subside after
a few days. Slow titration of treatment is important. Abrupt cessation may
cause withdrawal syndrome – hallucinations, anxiety, tachycardia, and sei-
zures. It should be avoided in patients with history of seizures (Table 5.11).
In patients with impaired renal function, dose of baclofen should be reduced.
Intrathecal baclofen can be beneficial in patients who are unresponsive
to oral antispastic agents or have intolerable side effects of oral drugs.
Each patient should undergo initial screening with bolus intrathecal
baclofen, followed by careful individualized dose titration, since there is
great variability in the effective individual therapeutic dose. The first dose
should be given in the OT with resuscitation equipment on standby and
patient closely monitored. Usually intrathecal screening dose is 25–50 mg.
Positive response is significant decrease in muscle tone and/or decrease
in frequency and severity of spasms.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Botulinum Toxin Type A 93

TABLE 5.11 Dosage and Adverse Effects of Muscle Relaxants

Usual adult Usual adult Common Uncommon adverse
Drug dose dose adverse effects effects

Baclofen Oral 10 mg/ Intrathecal Drowsiness, Ataxia, respiratory

day tid; start 50–460 mg/day dizziness, depression,
with 5 mg tid Initial test dose is confusion, headache, muscle
and increase by 50 mg weakness pain, paresthesias,
15 mg tid every weight gain,
3 days until a tremors, tinnitus,
max. of 80 mg diplopia, nystagmus,
tid dysarthria,
hallucinations, skin
rashes

Tizanidine 2 mg/day bid-tid. Sedation, Dry mouth, headache,

Start with 2 mg hs; dizziness, insomnia, nausea,
increase by 2 mg asthenia hypotension
every day to a max.
of 8 mg tid

Tizanidine is mainly an α2 receptor agonist, which has noradrenergic

activity in spinal cord and brain.
It should be considered as first-line agent for the management of spas-
ticity and painful spasms resulting from brain and spinal cord diseases
like multiple sclerosis, stroke, traumatic brain injury, spinal cord injury
and cerebral palsy. It is as effective as baclofen in relieving spasticity.
Its greatest advantage is that compared to baclofen it does not cause
muscle weakness despite improvement in muscle tone. Thus, it may be
preferred in patients with spasticity and spasms, who still have marginal
strength. It is more effective than other drugs in reducing clonus. Tiza-
nidine (2 mg/bid/tid) is used with ibuprofen (200 mg/tid), paracetamol,
nimesulide, valdecoxib for treatment of acute low back pain. It is also
effective in the treatment of tension headaches. Tizanidine is tolerated rea-
sonably well when started at a low dose and titrated up slowly.
It should be used cautiously in patients on antihypertensives and
patients with renal dysfunction. It should be avoided in patients taking
other α2 agonists (clonidine) and in patients with impaired liver function.
Serum transaminase levels should be monitored before starting therapy,
and then at 1, 3 and 6 month intervals.

BOTULINUM TOXIN TYPE A

Botulinum toxin is a potent neurotoxin produced by Clostridium botu-

linum. It binds to presynaptic cholinergic nerves and blocks the release of
acetylcholine.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

94 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

It is used in the treatment of spasticity where muscle contraction is

abnormal and painful, and affects one's quality of life. It has been used in
chronic spastic states such as cervical dystonia (torticollis), chronic tension
headaches, central spasticity of various aetiologies, blepharospasm, writ-
er's cramp, myofascial pain syndrome, strabismus and hemifacial spasm.
It is injected into muscles by the palpation technique or under electromyo-
graphic guidance at multiple sites in the same muscle. The effect occurs in
a few days to 2 weeks after injection and usually lasts for 3–4 months, and
sometimes, even up to 6 months. Injections are given every 3 months, with
a dose limit of 300–400 mouse units/3 months. Per muscle dose range is
from 10 to 25 mouse units. The main risk with botulinum toxin injection is
significant atrophy and weakness in a muscle due to overuse of the drug.
Botox is a lyophylized, freeze dried preparation stored at 5°C, diluted
with normal saline (preservative free) to 100 units/2 mL, prior to injection.
It is not recommended to refreeze the prepared solution or to use it after
being at room temperature for more than 48 h.
It is contraindicated in patients with neuromuscular junction diseases
such as myasthenia gravis, myasthenic states, motor neuron disease and
in patients on aminoglycosides as it may increase muscle weakness. It is
to be avoided in pregnancy.

NMDA RECEPTOR ANTAGONISTS

NMDA receptors are involved in central sensitization and windup –

long-term potentiation of pain. They generate plasticity in many systems
such as memory, motor function, vision, spinal and sensory transmission.
Two commonly studied NMDA receptor antagonists are ketamine and
dextromethorphan.
Ketamine is an anaesthetic, sedative, amnesic and analgesic. It is non-
competitive NMDA receptor antagonist. We have used it in patients with
CRPS, with central sensitization to almost completely ameliorate the
symptoms of allodynia and hyperalgesia. A series of placebo-controlled
trials have shown that brief infusions of ketamine reduce pain caused by
peripheral nerve injury, postherpetic neuralgia, chronic trauma, amputa-
tion, spinal cord injury, fibromyalgia, surgery and a variety of other con-
ditions. Ketamine causes induction of hepatic microsomal enzymes, so
patients receiving repeated doses develop tolerance to its analgesic effects.

MISCELLANEOUS DRUGS

Vasodilators are used in the treatment of Raynaud phenomenon,

Buerger disease, intermittent claudication, reflex sympathetic dystrophy,
systemic sclerosis and systemic vasculitis.
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Miscellaneous Drugs 95

1. N ifedipine treatment is started with 5 mg/day tds, increased to a

maximum of 20 mg/day tds or 10 mg (retard)/day bd. Nifedipine
is contraindicated in patients with hypotension, acute myocardial
infarction, CCF, and volume depletion. Headache, flushing,
palpitation and nausea are the commonly seen adverse effects.
2. Xanthinol nicotinate increases blood flow to the periphery and the
brain. It is given as slow release 500 mg/day/bd after meals.
3. Pentoxifyllines improve blood flow. It is given in the dose of
200–400 mg/day/bid to tid.
  

Capsaicin is a topical analgesic cream derived from chilli pepper. It

has been postulated that capsaicin renders the skin insensitive to pain by
depleting and preventing reaccumulation of substance P in peripheral
sensory neurons. Moreover, it produces a counterirritant effect in major-
ity of patients by causing mild to severe burning on application. We use it
in the treatment of postherpetic neuralgia, arthritis, diabetic neuropathy,
causalgia, radiculopathy and other neuropathic pains.
No known systemic side effects or drug interactions are known with
capsaicin.
Mecobalamin (vitamin B12) is a neuron revitalizer, which helps in
regeneration of damaged neurons. Vitamin B12 is used in the treatment
of various neuropathies, including diabetic neuropathy, radiculopathy
and multiple sclerosis. It is prescribed in a dose of 1500 mcg/day or
500 mcg/tds.
Hyaluronidase breaks down hyaluronic acid, a component of connec-
tive tissue and scar tissue. By doing so, it increases the spread of what-
ever drug it is mixed with. Hyaluronidase is commonly used with Depot
steroids for ESIs and intra-articular injections. We also use it for the lysis
of lumbar epidural adhesions, especially in patients with failed back sur-
gery syndrome, in an attempt to spread the steroid into areas around the
­scar-bound nerve roots. It is combined with steroids or local anaesthet-
ics or saline and injected through an epidural catheter, which is placed
against the fibrotic tissue in the epidural space. A dose of hyaluronidase
up to 1500 U is recommended. Allergic hypersensitivity reactions occur in
<1% of patients.
Naloxone is a potent, pure, competitive opioid antagonist, both fast and
short acting. Its most important effect is reversal of opioid-induced respira-
tory depression. It is given in the dose of 0.1–0.4 mg (1–5 mcg/kg), titrated
and given slowly over 2–3 min. If given rapidly to patients on chronic opi-
oid treatment, it can precipitate withdrawal syndrome. Onset of effect is
prompt and duration is 30–45 min. If repeated doses are required, a con-
tinuous infusion of 5 mcg/kg/h is set up.
It should not be used for reversal of drowsiness and/or delirium,
which is not life threatening because of the danger of totally reversing
opioid analgesia and precipitating severe pain with major withdrawal
syndrome.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

96 5. PHARMACOTHERAPEUTICS (DRUGS) IN PAIN MANAGEMENT

Intraspinal opioid often produces urinary retention, pruritus, nausea

and vomiting, which can be treated by giving carefully titrated naloxone
intravenously without significantly affecting analgesia.

CONCLUSION

Optimal drug therapy is often denied to our patients because of inad-

equate knowledge of pharmacology, inordinate fear of side effects, gov-
ernment policies and patient reluctance to use effective therapies.
Current knowledge provides a framework with which one can plan
more effective treatment for relief of pain.
The dramatic increase in information about mechanisms of nocicep-
tion is likely to lead to newer drugs, with higher specificity and hope-
fully fewer side effects, in the coming years, lending a helping hand to the
medical fraternity's efforts to alleviate pain.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 C H A P T E R

6
Neurolytic Agents

Neurolysis implies the destruction of neurons by placing a needle

close to the nerve(s) and either injecting neurodestructive chemicals
or producing neural damage with cold (cryotherapy) or heat (radio
frequency coagulation). Prolonged interruption of painful pathways
may be accomplished by the injection of chemical neurolytic agents.
This form of neurolysis has been performed for many years. The first
reported injection of a neurolytic solution in the treatment of pain was
by Luton, who in 1863 administered subcutaneous injections of irritant
substances into painful areas.
Doppler (1895) was the first to report the use of phenol for neurolysis.
The first use of phenol for subarachnoid neurolysis was reported by Maher
in 1955. Today, phenol and ethyl alcohol are the most commonly used neu-
rolytic agents. Chemical neurolysis is indicated for cancer patients with
limited life expectancy and patients who have recurrent or intractable
benign pain after a series of local analgesic blocks.

DIAGNOSTIC NERVE BLOCKS PRIOR

TO NEUROLYTIC BLOCK

Diagnostic blocks are of prime importance due to the undesirable

side effects of the neurolytic agents combined with a limited duration of
analgesia. Potential side effects of neurolytic agents include neuritis and
deafferentation pain, motor deficit when mixed nerves are ablated and
unintentional damage to nontargeted tissue. Therefore, careful selection
of patients combined with clinical expertise is the essence. The following
criteria should be considered before peripheral neurolysis is performed:
  

• D etermine and document that the pain is severe.

• Document that the pain will not be relieved by less invasive therapies.
• Document that the pain is localized in the distribution of an identifi-
able nerve.

97
98 6. NEUROLYTIC AGENTS

• C onfirm that the pain is relieved with a diagnostic block performed

with local anaesthetic.
• Document the absence of undesirable deficits after the local anaes-
thetic blocks.
  

The neurolytic agents commonly used in clinical practice are

  

1.  thyl alcohol (50% and absolute alcohol)

E
2. Phenol (aqueous 6–8%, phenol in glycerine)
3. Glycerol (anhydrous)
4. Hypertonic saline
5. Ammonium salts and chlorocresol (not used presently)

Ethyl Alcohol
Ethyl alcohol is commercially available as a colourless solution that
can be injected readily through small-bore needles. It is hypobaric with
respect to CSF. However, specific gravity is not of concern when injecting
the peripheral nerve because injection takes place in a nonfluid medium.
It is usually used undiluted (absolute or >95% concentration). The peri-
neural injection of alcohol is followed immediately by severe burning pain
along the nerve, which lasts about a minute before giving way to a warm,
numb sensation. Pain on injection may be diminished by prior injection of
a local anaesthetic.
Despite the inconsistency in results for varying concentrations of alco-
hol, there is consensus regarding maximum and minimum concentrations.
For complete paralysis, the concentration must be stronger than 95%. It
may be concluded that a minimum concentration of 33% alcohol is neces-
sary to obtain satisfactory analgesia without any motor paralysis.

Mechanism of Action of Alcohol

Histopathological studies have shown that alcohol extracts cholesterol,
phospholipids and cerebrosides from the nerve tissue and causes precipi-
tation of lipoproteins and mucoproteins. This results in sclerosis of the
nerve fibres and myelin sheath. Alcohol produces nonselective destruction
of nervous tissue by precipitating cell membrane proteins and extracting
lipid compounds, resulting in demyelination and subsequent Wallerian
degeneration. Because the basal lamina of the Schwann cell tube is often
spared, the axon often regenerates along its former course. If destruction
is into a ganglion, it may cause cell body annihilation without subsequent
regeneration.
For subarachnoid block, concentrations between 50 and 100% are gen-
erally selected. Alcohol is hypobaric in nature relative to CSF. Therefore,
the position of the patient must be in the lateral decubitus position with
the painful site uppermost. Then, the patient must be rolled anteriorly,

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Diagnostic Nerve Blocks Prior to Neurolytic Block 99

approximately 45° to place the dorsal (sensory) root uppermost. The

reported volumes required for neurolysis have ranged from 0.3 mL to
a maximum of 0.7 mL of absolute alcohol per segment to 0.5–1 mL to a
maximum of 1.5 mL per segment. For coeliac plexus block, volumes of
15–30 mL of 50% alcohol bilaterally may be administered for a complete
sympathetic block. Often, 100% alcohol is diluted 1:1 with a local anaes-
thetic (bupivacaine) prior to injection.
The most ominous complication associated with the use of alcohol is
the possible occurrence of alcoholic neuritis. These pains may be more
intense than the original pain. Fortunately, in most instances, these symp-
toms subside within a few weeks or a month.
Another complication associated with alcohol nerve block includes
hypoesthesia or anaesthesia of the dermatomal distribution of the nerve
roots treated with neurolysis. The lack of sensation can overshadow the
pain relief obtained by the procedure; this complication is rare and recov-
ery is relatively quick.

Phenol
Phenol is a combination of carbolic acid, phenic acid, phenylic acid,
phenyl hydroxide, hydroxybenzene and oxybenzene. It is not available
commercially in the injectable form and is always prepared by the hospital
pharmacy. One gram of phenol dissolves in about 15 mL of water (6.67%).
It is highly soluble in alcohol, glycerol and a number of other organic sub-
stances. It is usually mixed with saline or glycerine. It may be mixed with
sterile water or material used for contrast radiography. Because it is highly
soluble in glycerine, it diffuses from it slowly. This is an advantage when
injecting intrathecally because it allows limited spread and highly local-
ized tissue fixation. This also makes it hyperbaric relative to CSF. When
mixed with glycerine, it is so viscid that even when warmed, injection
must be through at least a 20 gauge needle. When phenol is mixed in an
aqueous mixture, it is a far more potent neurolytic. Phenol oxidizes and
turns pink when exposed to air and light. It has a shelf life that is said
to exceed 1 year when preparations are refrigerated and not exposed to
light. Phenol is therefore stored in dark bottles only. Phenol acts as a local
anaesthetic at lower concentrations and as a neurolytic agent at higher
concentrations. It has an advantage over alcohol in that it causes minimal
discomfort on injection. We use 8% aqueous phenol for neurolytic proce-
dures in our clinical practice.

Mechanism of Action of Phenol

Histopathological studies have demonstrated nonselective degenera-
tion in cat rootlets, the severity being parallel to the concentration. There
is evidence of Aδ and Aβ damage in the electrophysiological experiments.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

100 6. NEUROLYTIC AGENTS

At concentrations less than 5%, phenol produces protein denatur-

ation. Concentrations greater than 5% cause protein coagulation and
nonspecific segmental demyelination and orthograde degeneration (i.e.
Wallerian degeneration). Concentrations of 5–6% produce destruction
of nociceptive fibres with minimum side effects. Higher concentrations
result in axonal abnormalities, nerve root damage, spinal cord infarcts
and arachnoiditis or meningitis. These characteristics may explain the
long-lasting results of neurolytic blocks performed with 10% phenol in
the sympathetic axis.
The block produced by phenol tends to be less intense and of shorter
duration than that produced by alcohol (Table 6.1).

Glycerol
Glycerol is used mostly for neurolysis of the Gasserian ganglion to treat
idiopathic trigeminal neuralgia. Considered a mild neurolytic, like other
alcohols, it produces localized perineural damage, whereas intraneural
injection results in Schwann cell oedema, axonolysis and Wallerian degen-
eration. Anhydrous form of glycerol is a selective neurolytic and does not
disperse to adjoining tissues.

TABLE 6.1 Comparison of Phenol and Alcohol as Neurolytic Agents

Property Phenol Alcohol

Physical properties Clear, colourless, pungent Clear, colourless

odour
Poorly soluble in water Absorbs water on exposure
to air
Unstable at room temperature Stable at room temperature
Hyperbaric relative to CSF Hypobaric relative to CSF
Chemical nature Acid Alcohol
Agent concentrations (%) 6–10 50–100
Equipotent neurolytic 5 40
concentration (%)
Complications of use in Neuritis (uncommon) Neuritis (common)
neurolysis Toxicity at higher doses Toxicity at commonly used
doses
Hepatic and cardiac
complications
Sites of use Epidural Intrathecal
Paravertebral Coeliac ganglion
Peripheral nerve roots Lumbar sympathetic chain
Intrathecal Cranial nerves
Cranial nerves Epidural (low concentrations)

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Hypertonic and Hypotonic Solutions 101

Mechanism of Action of Glycerol

The mechanism of action is not clear. It is suggested that glycerol pri-
marily affects small myelinated and unmyelinated fibres. There is an
extensive myelin sheath swelling, axonolysis and severe inflammatory
response after intraneuronal injection.

HYPERTONIC AND HYPOTONIC SOLUTIONS

Hypertonic or hypotonic subarachnoid injections have been used for

achieving neurolysis. The intrathecal injection of cold (2–4°C) 0.9% NaCl
is supposed to have a specific action on the pain-carrying C fibres, sparing
the larger fibres that subserve the sensory, motor and autonomic functions.
Injections of hypertonic saline can be quite painful; therefore, local
anaesthetics are generally injected before the saline injection. The intrathe-
cal injection of hypertonic saline can produce a variety of complications.

Mechanism of Action
Pathological changes due to hypertonic and hypotonic solutions have
been extensively studied. Microscopic changes seen on the peripheral
nerves do not correlate with clinical effects of differential C fibre block.
Hypertonic saline injection causes osmotic swelling of the nerve bundle
and is proposed as the mechanism of nerve conduction block.

Neuraxial Neurolytic Blocks

Injection of a neurolytic agent into the subarachnoid, extradural, or
subdural space is one of the most effective methods of relieving severe
intractable pain caused by advanced or terminal cancer. The use of these
techniques for chronic nonmalignant pain is to be discouraged except in
special circumstances.
Agents that have been used for this purpose include ethyl alcohol, phe-
nol in glycerine, chlorocresol in glycerine, aqueous phenol, hypertonic
saline solution, and ammonium compounds.

Neurolytic Blocks for Control of Spasticity

Although neurolytic nerve blocks are usually used for the control of
chronic pain, they are also important for the treatment of spasticity conse-
quent to injuries to the central nervous system (e.g. stroke, cerebral palsy,
and spinal cord damage secondary to trauma or disease, such as multiple
sclerosis). Such patients often develop spasticity that is uncontrolled and
often produce sporadic spontaneous and uncontrolled flexor or extensor

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

102 6. NEUROLYTIC AGENTS

movements that can severely compromise the patients' ability to sit in a

wheelchair. Sometimes, such spasms of the adductor muscles of the hip in
addition to the painful spasm affect the ability to perform perineal toilet
and to carry out other aspects of nursing care.
Reduction in such profound skeletal muscle spasm by neurolytic block
has been helpful in these patients. Less commonly, such blocks can be
used to treat muscle spasms in the trunk or in the upper extremity associ-
ated with quadriplegia. We are using 8% aqueous phenol for motor nerve
blocks in cerebral palsy children with spasticity. The nerves commonly
blocked are obturator nerves, posterior tibial nerve, musculocutaneous
and median nerves. Phenol nerve blocks are also being used in our centre
for treating spasticity in paraplegic and quadriplegic patients thus mini-
mizing the formation of contractures.

CRYOTHERAPY

It has long been known that cooling causes a reversible conduction

block in nerves. In 1945, Denny-Brown and colleagues reported on pathol-
ogy of nerves subjected to cold and noted the sensitivity of Aδ and C fibres
to damage. Subsequent studies have revealed that a prolonged axonal
potential results when nerve fibres are cooled to 5°C. Early cytopatho-
logical studies revealed abnormalities of Schwann cells and endoneurial
capillaries that were attributed to accelerated enzyme production, which
affected Schwann cell metabolism. More recent studies have shown that
freezing results in the formation of ice crystals and causes necrosis of all
tissue elements, including nerves. Freezing produces a long-lasting clini-
cal deficit and has become a method of neurolysis of intercostals nerves
following thoracotomy for relief from postthoracotomy pain.

CONCLUSION

Neurolytic agents such as alcohol, phenol, and glycerol, injected around

or into a nerve produce pathophysiological changes of varying degree,
depending on the concentration of the agent that comes in direct contact
with the nerve tissue. These agents, applied to the surface of the nerve
or nerve rootlets (in the subarachnoid space), alter perineurial permeabil-
ity causing damage to axons and occasionally to nerve cells. Intraneural
injection of these agents produces severe nerve damage, consisting of sig-
nificant axonal abnormality and Wallerian degeneration. Techniques that
physically damage the nerve with cold (via the cryoprobe) or with heat (via
laser or radio frequency) produce similar results. It has been shown that
a differential block of only Aδ and C fibres, without affecting larger fibres

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Conclusion 103

and with good relief still being obtained, is usually not possible. Although
variations in concentration produce different clinical findings, suggesting
a dose-related response, the nerve needs to be damaged sufficiently to pro-
duce Wallerian degeneration to achieve desirable long-­lasting pain relief.
The persistence of basal lamina around the Schwann cell tube allows the
successful and appropriate regeneration of nerve fibres, thus eliminating
the formation of painful neuroma. This is in contrast to surgical section
of a nerve, which invariably results in neuroma formation. Complete and
permanent transaction of a nerve can only be accomplished with surgical
resection; however, a painful neuroma may result.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

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 C H A P T E R

7
How to Set Up a Pain
Clinic?

For centuries, pain is one of the greatest factors affecting human life.
From mystics to quacks everyone has promised relief but alas has failed.
Pain is now being considered a major health problem. In fact, 80% of
the patients visiting any hospital or doctor have pain as their major
complaint. It can be severe and extensive to the extent of damaging the
nervous system. Pain could be acute, short lived and usually second-
ary to some disease, or chronic, lasting for months/years and leading
to disability. Pain is multidimensional and its severity depends on psy-
chological, emotional, cultural and situational components as well as
physiological inputs. Last two decades have seen tremendous advances
in our understanding of mechanisms that underlie in causation of pain
and the treatment of patients with acute and chronic pain. This has
resulted chiefly due to an extensive experimental and clinical research
being undertaken to understand the pathophysiology of pain. In the
1960s, pain was considered just an inevitable sensory response to tissue
damage and no considerations were given to the affective dimension
of this miserable experience and none whatsoever to the accompanying
anxiety and stress.
Last two decades have seen tremendous advances in our understand-
ing of mechanisms that underlie the causation of pain and the treatment
of patients with acute and chronic pain. This has resulted chiefly due to an
extensive experimental and clinical research being undertaken to under-
stand the pathophysiology of pain. The concept of a Pain Clinic was first
advocated by Bonica in the 1950s and further enriched by inputs from
Fordyce and Sternbach in the 1970s. It is now widely agreed that pain
clinics have an important role to play in the health care systems of the
developing countries and cater to a very large number of chronic pain
patients including those with intractable cancer pain. The pain clinicians
in these countries have the dilemma of providing the best pain treatment

105
106 7. HOW TO SET UP A PAIN CLINIC?

but within the resources available for the purpose. Keeping pace with the
technological advances in pain management worldwide, pain clinics in
developing countries are also employing newer methods of pain assess-
ment, pain imaging and advanced interventional strategies for managing
patients with chronic pain.

PAIN MEDICINE AS A SUPERSPECIALITY

Treatment of acute and chronic pain has always been the major concern
of physicians and superspecialists. Alleviating chronic pain, however,
becomes a major challenge for the treating doctor and requires specialized
physicians for its treatment. Pain medicine – a superspeciality – deals with
the management of these difficult chronic painful disease states includ-
ing treatment of cancer pain. This science and art of pain management
is rapidly approaching the period of responsibility and recognition even
in developing countries like India. Majority of complex chronic painful
states, unsuccessful by conventional treatment, are being successfully
treated at pain clinics. The very concept of a pain clinic is based on the
conviction that the effective management of difficult pain conditions is
possible only through well-coordinated efforts of a specialist possessing
knowledge and skills to diagnose and treat pain.
Millions of people suffer from chronic or intractable pain. Persistent
pain varies in aetiology and presentation. In some cases, symptoms and
signs may be evident within a few weeks to a few months after the occur-
rence of an injury or the onset of disease. The cause of pain is not always
known or apparent. For many patients, initial medical evaluation and
treatments effectively relieve pain that might otherwise become chronic.
Pain is as major a problem in our country as anywhere else but the lack
of a formal treatment strategy has been major lacuna in health care in our
country. Statistics from advanced countries show that 15–20% of popula-
tion has acute pain (medical and surgical emergencies, postoperative pain,
after accidents and injuries) and 25–30% of all population have chronic
pain (as in chronic backache, cancer pain, migraines, arthritis, neuropathic
pain, etc).
Because it impairs the ability to work and have a productive life, pain
has serious economic and social consequences. For example, half to two-
thirds of all chronic pain sufferers are totally or partially disabled for
days (headache, migraine), weeks or months (those with CRPS) and some
permanently (like low backache, cancer pain and arthritis). Like many
illnesses that at one time were not well understood, pain and its many
manifestations may be poorly treated and seriously underestimated. Inap-
propriately treated pain seriously compromises the patient's quality of
life, causing emotional suffering and increasing the risk of lost livelihood

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Role of Pain Clinics 107

and social integration. Severe chronic pain affects both the paediatric and
adult population, and often leads to mood disorders, including depres-
sion and, in rare cases, suicide.
Each physician bears the responsibility to evaluate and treat persistent
pain as a serious medical condition. Principal treatment physicians must
approach each patient with respect and urgency and provide appropriate
and timely referrals to a pain medicine specialist when primary medical
care has not been effective. Such referrals are appropriate because pain
medicine specialists can provide a more advanced level of treatment to
patients suffering from chronic or intractable pain. As physicians, we are
trained to preserve patients' quality of life and relieve their pain and suf-
fering. We must use all available resources to achieve these goals for our
patients.

ROLE OF PAIN CLINICS

Pain clinics are essentially areas/centres established with the pur-

pose of practicing algology – the art and science of pain management.
In India, the concept of pain clinics or pain management centres was
initiated at major institutions in the 1970s and it is only in the last few
years that we have seen more of such centres being set up in major insti-
tutions and in private institutions. In fact, dedicated pain management
centres are also being started to provide a holistic care to patients with
chronic pain. Pain management is an emerging discipline emphasiz-
ing an interdisciplinary approach with a goal of functional restoration,
and reduction of pain and suffering. Pain centres are specialized enti-
ties set up to evaluate and treat patients with complex, intractable, and
disabling problems. It is now widely agreed that pain clinics have an
important role to play in the health care systems of the developing coun-
tries and cater to a very large number of chronic pain patients including
those with intractable cancer pain. The pain clinicians in these countries
have the dilemma of providing the best pain treatment but within the
resources available for the purpose. Keeping pace with the technologi-
cal advances in pain management worldwide, pain clinics in developing
countries are also employing newer methods of pain assessment, pain
imaging and advanced interventional strategies for managing patients
with chronic pain. Because chronic pain is so complex, there are often
multiple treatment goals. These goals may include more comfort (being
‘pain free’ is often not possible when pain has become chronic), better
physical functioning, improved coping and less distress, getting back to
work, helping the family cope, and other positive outcomes. To accom-
plish these goals, chronic pain often is best managed using what is called
a ‘multimodality’ approach.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

108 7. HOW TO SET UP A PAIN CLINIC?

A multimodality approach to chronic pain includes a combination of

therapies selected from eight broad categories:
  

• Drug therapies
• Psychological therapies
• Rehabilitative therapies
• Neurolytic blocks and spinal interventions
• Neurostimulatory therapies (intrathecal pumps and spinal cord
stimulators)
• Surgical therapies
• Lifestyle changes
• Complementary and alternative medicine therapies

IMPORTANT ACTIVITIES OF A PAIN CLINIC/PAIN

MANAGEMENT CENTRE

Pain clinics are involved in three important activities:

  

1. T reatment of painful syndromes: The most important conditions

managed in pain clinics include chronic low back pain, cervical
spondylitis, osteoarthritis, migraines, cancer pain, CRPS and other
neuropathic pain syndromes.
2. Provision of training opportunities for doctors: Patients attending the pain
clinic present a wealth of teaching material in a unique setting and the
trainees benefit a lot from exposure to these patients.
3. Research work benefits from the pain clinic: Tremendous scope for basic
research, clinical research and trial of newer pharmacological agents.
  

Common chronic pain syndromes presenting to a pain clinic or a pain

centre would include
  

1. n europathic pain syndromes: neurogenic and sympathetically

mediated pain, CRPS
2. neuralgic pain: postherpetic, trigeminal, peripheral neuropathies
3. musculoskeletal pain: low back pain, failed back syndrome,
polyarthralgia, fibromyalgia
4. vascular pain: peripheral vascular disease, headaches, Raynaud disease
5. central pain: phantom pain, thalamic pain
6. cancer pain
7. chronic pelvic pain in women
8. unusual pain conditions like human immunodeficiency virus
infection, paediatric and geriatric age groups
  

The most significant advance of a modern pain clinic is the multidisci-

plinary approach to the management of pain to achieve the ultimate goal of

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Important Activities of a Pain Clinic/Pain Management Centre 109

pain relief and restoration of work productivity to the patient. Another sig-
nificant change has been the emergence of a new breed of specialists called
the interventional pain specialists who rely on evidence-based practice
with modern techniques for precision in locating the cause of pain and its
treatment. The services of a physical therapist are judiciously utilized to
augment the result of pain relief achieved by nerve blocks medication and
other modalities. A clinical psychologist helps to assess the expectations
of the patient vis-a-vis the planned treatment, to teach coping strategies.
Interventional pain management involves special procedures to treat
and manage pain. ‘Interventional’ procedures might include an injection
of an anaesthetic medicine or steroid around nerves, tendons, joints or
muscles; spinal cord stimulation; insertion of a drug delivery system; or
a procedure with radiofrequency ablation or cryoablation to stop a nerve
from working for a long period of time. Patients needing interventional
pain management services suffer distress and discomfort caused by a vari-
ety of conditions and disorders, including
  

•  hronic low back and neck pain

C
• Chronic reflex sympathetic dystrophy or CRPS
• Chronic head, mouth and face pain
• Postsurgical procedures
• Malignancy
• Posttraumatic pain syndrome
• Muscle and/or bone pain
  

Interventional pain management provides the most sophisticated and

complex treatments available, including
  

• E pidural/transforaminal injections (cervical, thoracic, lumbar and

caudal)
• Selective epidural and root blocks (cervical, thoracic, lumbar and
sacral)
• Facet injections and medical branch blocks (cervical, thoracic and
lumbar)
• Sympathetic blocks (stellate ganglion, thoracic, lumbar and
hypogastric)
• Discography
• Percutaneous nucleoplasty
• Epiduroscopy
• Ozone discectomy
• Peripheral nerve blocks
• Radiofrequency denervation
• Spinal cord stimulation
• Neurolytic blocks of coeliac plexus in cancer pain
• Intrathecal implantation of pump and epidural infusion systems

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

110 7. HOW TO SET UP A PAIN CLINIC?

BASIC EQUIPMENTS REQUIRED TO SET UP

A PAIN CLINIC/PAIN CENTRE

The advances and sophistication in imaging, nerve location and phar-

macology in the last decade has ushered in the shifting paradigms like evi-
dence-based practice and revolutionary advances in pain treatment. The
recent explosive advances in pain management have pain relief a reality
rather than an aim. The emphasis is on accuracy by abandoning the older
blind techniques of nerve localization.
Enhancing the expertise of an anaesthesiologist involves the manda-
tory use of imaging, use of radiopaque dyes for exact localization and the
use of electrical- and ultrasound-guided nerve locator. Use of continu-
ous plexus and nerve blocks to replace the repetitive intermittent blocks
addresses the windup mechanics of chronic pain. Utilization of radiofre-
quency ablations, intrathecal drug delivery and spinal cord stimulators
has made it possible for total alleviation of pain without the mutilation of
nerve damage from neurolytic blocks of vital nerves, ganglia and central
neuraxis.
Besides a dedicated space for pain clinic, there are few basic equip-
ments that are mandatory for running a modern pain clinic.
  

1. C -arm fluoroscope: The extensive mandatory use of fluoroscopy for

pinpoint accuracy of the nerve blocks so that the patient does not
suffer from indiscriminate destruction of nerves as may happen with
blind techniques.
2. Nerve locator/ultrasound machine for localizing various motor/sensory
nerves/spinal structures when blocking them for diagnostic or
therapeutic purposes.
3. Operating room with a cardiac monitor, defibrillator and a basic anaesthesia
machine and a C-arm compatible operation theatre table.
4. Basic equipments for TENS therapy, laser therapy and other physiotherapy
equipments.
  

Few other types of equipment that are essential but can be added at a
later stage are
  

•  adiofrequency ablation/lesioning machine

R
• Nucleotome for nucleoplasty procedures
• Ozone generator for ozone discectomy
• Hydrocision Discectomy Console for Hydrocision Discectomy
• Epiduroscope
  

Practice of pain management in India is fraught with many pitfalls, dif-

ficulties and frustrations and is at all times a challenge. The need to bal-
ance practical realities with the wish to maintain an academic approach
makes the challenge a tight rope walk. But with all these limitations, it

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Basic Equipments Required to Set Up a Pain Clinic/Pain Centre 111

is exhilarating in its very challenge, and is unparalleled for the intellec-

tual stimulation of solving a pain problem that has remained refractory to
treatment by multiple physicians of various other specialities.
Today, proper management of pain remains one of the most important
and pressing responsibilities of the society in general, the medical insti-
tutions and personnel in particular. How seriously is this responsibility
understood and implemented is a reflection of the quality, sensitivity,
and accountability and of course the economic capability of that partic-
ular society. Specialist pain clinics are the norm in developed countries
with cutting edge technology, dedicated specialists and state-of-the-art
facilities.
From a clinical perspective, pain clinics have survived and grown
because they meet a need unmet by any previously existing medical ser-
vice, i.e. they treat chronic pain effectively. Moreover, pain clinics are cost-
effective as well. A holistic approach to managing pain is followed at the
pain clinics and all aspects, physical, emotional, cognitive, behavioural
vocational and social aspects, of chronic pain are simultaneously treated.
The management of chronic refractory pain of any aetiology is based on
evidence-based protocols that are periodically evaluated and modified as
per patient's requirements and satisfaction. Having a personal experience
of setting up a day care pain management centre in the capital city of the
country, I am very optimistic that the day is not far off when pain clinics
will become an integral and essential part of health care system in India.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

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 C H A P T E R

8
Acute Pain Management:
Practical Guidelines

The relief of acute pain must play a prominent role in the modern prac-
tice of emergency medicine. Triage guidelines should assign a high priority
to patients in pain. The problem of pain relief in the emergency department
should be addressed with a planned approach that incorporates adminis-
trators, nursing staff and clinicians. All emergency department and casu-
alty staff must be aware of the protocols for pain management. Triage
algorithms should consider pain as a medical ­emergency. The degree of
pain and the haemodynamic status should determine the rapidity of care:
pain scales should be used with frequent charting of the patient's subjec-
tive report of degree of pain in a fashion analogous to the recording of
vital signs.
The prompt and effective treatment of acute pain should be important
not only for humanitarian concerns but also for biologic reasons. Evidence
suggests that poorly treated acute pain may exacerbate the underlying
pathophysiology of many illnesses and injuries. In addition, many physi-
cians hypothesize that poorly treated or untreated acute pain may be one
of the actual causes of the development of chronic pain.
The practice of emergency medicine requires expertise in a wide vari-
ety of pharmacologic and nonpharmacologic techniques to treat the acute
pain resulting from a myriad of injuries and illnesses. In short, approaches
to pain relief in emergency medicine must be designed to be safe and
effective in the organized chaos of the prehospital environment or the
emergency department.
For emergency medicine, the approach to analgesia in acute care medi-
cine must emphasize the following:
  

1. S afety: Any analgesic procedure or agent must be administered with

proper technique and monitoring to ensure safety.
2. Speed of onset: The action of the agent should be rapid. The IV and
inhalational routes best fulfill this requirement.

113
114 8. ACUTE PAIN MANAGEMENT: PRACTICAL GUIDELINES

 ase of administration: Techniques used must be suited to the

3. E
emergency department environment and to staff resources. Intraspinal
opioids are effective in the surgical and postoperative setting but are
too cumbersome to be used routinely in the emergency department.
New routes of administration and delivery systems are being
developed for analgesic and anaesthetic agents, and some may be
suitable for use in the acute care setting. The transmucosal route of
absorption using a formulation of fentanyl citrate in a candy matrix
(lollipop) has been shown to provide analgesia in adult and paediatric
patients. The intranasal route can also be used for drugs such as
midazolam, ketamine, butorphanol, and sufentanil.

ACUTE PAIN MANAGEMENT

FOLLOWING TRAUMA

Trauma causes physical and emotional suffering to the victims. The

painful experience associated with it may have ramifications, which
may last a lifetime. Hence, effective management of trauma victims must
include pain management. In the adult trauma patients, it has been found
that pain is poorly managed. According to Whipple et al., 74% of multi-
trauma patients in intensive care units reported poor analgesia and rated
their pain as moderate to severe. Choiniere et al. found that approximately
half the burn patients reported little or no analgesic effect from doses of
drugs they were given for dressing changes. There are reasons to believe
that pain management in children with trauma is also poorly managed.
There are multiple reasons for poor pain management in trauma
patients. These include
  

1. u nderappreciation of pain,
2. concern about haemodynamic instability and respiratory depression
and
3. unfounded fear or addiction.
  

Sometimes pain relief is withheld so as not to reduce the surgeon's abil-

ity to evaluate patient's neurological function.

Causes of Pain following Trauma

Pain in trauma may be attributed to a number of causes. These include
  

1.  ain due to primary tissue damage,

p
2. surgical procedures performed,
3. procedural pain like insertion of drains, tubes and lines,
4. pain and discomfort of restricted movement and
5. presence of tubes and drains.
  

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Acute Pain Management following Trauma 115

The sequelae of inadequate pain relief following trauma are more than
just psychological. Trauma and the tissue damage it causes lead to a stress
response. This response, mediated by metabolic and neurohormonal
mechanisms, leads to hyperglycaemia, lipolysis, protein catabolism,
increased antidiuretic hormone and catecholamine levels, immunosup-
pression, and a hypercoagulable state. It accounts for a large propor-
tion of mortality in a trauma patient. Pain is known to potentiate this
physiological stress response to trauma. In several studies, inadequately
treated pain has been shown to increase this response, resulting in higher
morbidity.
It is now the prevailing opinion that proper pain treatment should
be provided for all trauma victims, even in very small children. There is
mounting evidence that pain treatment in trauma is not only safe but ade-
quate pain control can improve outcome.
Pain control in trauma patients poses some problems. Victims of
trauma often present in a state of cardiovascular and respiratory insta-
bility that mandates immediate life-saving procedures, e.g. endotracheal
intubation, insertion of IV lines and chest tubes without analgesia. Hae-
modynamic instability and respiratory depression can ensue with the
use of injudicious doses of analgesics. The side effect of sedation may
interfere with the monitoring of neurological status after head injury. The
masking effect of analgesia may delay recognition of compartment syn-
dromes, compressive casts or even life-threatening events such as splenic
rupture.
There is a paucity of studies on trauma-related pain; because of this,
our understanding of management of pain in trauma is usually extrapo-
lated from studies of postsurgical pain. One needs to realize that there are
differences between these two types of pain. Unlike accidental trauma,
the extent of surgical trauma is usually controlled and the procedures
themselves are scheduled such that pre-emptive manipulations can be
performed. For victims of trauma, the ablation of initial, painful stimuli
is not an option, because pain has already occurred prior to the patient's
entrance into the medical system.

Evaluation and Documentation of Acute Trauma Pain

Pain is a complex experience – a composite of anatomic, chemical and
psychologic factors that affect people differently. Unfortunately, no test or
physiologic index exists to measure pain objectively and reliably. A visual
analogue scale may be used to evaluate the trend in the patient's subjec-
tive sensation of pain.
The only accurate barometer in treating pain is the patient's verbal
report. Changes in facial expressions or vital signs do not correlate reli-
ably with a patient's subjective sensation of pain. Pain behaviour is unique
to each individual and is a product of many influences, including past

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

116 8. ACUTE PAIN MANAGEMENT: PRACTICAL GUIDELINES

experiences with pain, cultural background, and the psychosocial makeup

of the patient.
One of the best techniques to encourage the use of pain evaluations is to
include a pain scale as a routine part of vital signs and recorded as such.
This simple tool encourages clinicians to frequently communicate with
patients to assess their pain. It also allows charts to be used for continu-
ous quality improvement efforts to improve pain control practices on a
departmental level.

Methods of Pain Relief in Patients with Trauma

The mainstay of moderate to severe acute pain management following
trauma in both adults and children is opioids. The choice of opioid drug,
route and mode of administration will depend on the extent of injury, car-
diopulmonary status, and should be tailored to the individual patient. In
minor injuries, NSAIDs like diclofenac and paracoxib can be given orally
or by IM routes.

Narcotic Analgesics
MORPHINE
Morphine sulfate is the standard against which all opioid drugs are
compared as to route of administration, efficacy, duration, side effects, and
addicting potential. The opioids achieve their analgesic effect by stimulat-
ing opioid receptors in the midbrain and medulla, thus resulting in an
alteration of the patient's perception of pain. Tolerance, physiologic and
psychologic dependence, as well as the other side effects of opioid drugs,
are well known. Morphine is analgesic, reduces anxiety, and is sedating. It
is used in the emergency department for pain of acute myocardial infarc-
tion and other types of severe continuous pain states. The preferred route
is IV with dosage of 0.1 mg/kg titrated to effect. Naloxone will reverse
effects of excessive dosage.
The various narcotic analgesics commonly used in the emergency
department are listed in Table 8.1. The opioid analgesics are indicated
for acute moderate to severe pain, and pain associated with terminal dis-
ease. They are administered alone or in combination with other drugs that
either potentiate their effect or ameliorate a side effect. It is important to
note that those narcotics that are agonist–antagonist must be used with
caution if the patient was previously using a narcotic agonist for pain
relief, because the antagonistic action of the new drug may cause an acute
withdrawal syndrome.

PETHIDINE
Pethidine is the most widely used opioid analgesic agent for acute
pain control in the emergency department. Pethidine seems to have

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Acute Pain Management following Trauma 117

TABLE 8.1 The Opioid Analgesics Used in Emergency Department

Equianalgesic
Name dose (mg) Route Peak (h) Duration (h) Comments

Morphine 10 IV/PO ½–1 3–4 Decreased

ventilation; may
increase asthma
Fentanyl 60 IV ½–2 3–4
Pethidine 100 IV, IM ½–1 2 High potency:
beware of
respiratory arrest
Butorphanol 2 IM ½–1 3–4 Agonist–antagonist;
may precipitate
withdrawal,
psychotomimetic
effects
Pentazocine 60 IM ½–1 3–4 Similar to butorphanol

PO, per os.

TABLE 8.2 Morphine versus Pethidine

Pethidine Morphine

Half-life 2.5–3 h 3–3.5 h

Parenteral potency 1/8 Morphine
Oral/parenteral potency 50% 15%
Respiratory depression Moderate Moderate
Abuse potential High High
Metabolism Hepatic Hepatic
Liver disease Half-life prolonged Half-life unaffected
Renal disease Increased CNS toxicity Relatively unaffected
Histamine release Yes Yes
Biliary tract spasm Significant Significant
Urinary tract spasm Yes Yes
Side effects Similar to morphine but Vomiting, histamine release,
higher CNS toxicity; less constipation
constipation
Cardiovascular system Increased pulse, decreased Decreased PVR, no change
contractility, decreased PVR in pulse

several disadvantages compared with morphine (Table 8.2). The duration

of action of pethidine is only 2–3 h, which is less than that of morphine.
Perhaps the greatest disadvantage of pethidine is CNS toxicity, which is
caused by a metabolite, norpethidine (6-in-desmethylpethidine), a cere-
bral irritant. The adverse CNS actions that can be caused by norpethidine

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

118 8. ACUTE PAIN MANAGEMENT: PRACTICAL GUIDELINES

include anxiety, disorientation, tremors, seizures, hallucinations, and psy-

chosis. Norpethidine is renally excreted and also has a longer half-life in
the elderly. Repeated doses of pethidine should be avoided when possible
in patients with renal insufficiency and in the elderly. In patients with
sickle cell disease treated for several days with pethidine, up to 12% may
experience seizures. Of particular concern is the potentially lethal inter-
action of pethidine with monoamine oxidase inhibitors. Several studies
have shown that pethidine is often administered in inadequate doses and
with an excessive dosing interval.

FENTANYL
Fentanyl is a synthetic opioid of the phenylpiperidine group, which has
some unique properties that make it a useful agent in emergency medi-
cine. The most prominent properties of fentanyl are its short half-life, lack
of histamine release, and lack of decrease in cardiac contractility. Fentanyl
is lipid soluble, which allows it to cross the blood–brain barrier rapidly
and thus have a rapid onset of action (<5 min). The half-life of fentanyl is
90 min but the duration of action is often less because of redistribution,
which makes it an ideal agent for brief procedures (e.g. dislocated joint
relocation and incision and drainage of abscesses).
Fentanyl and its derivatives are the only opioid analgesic agents that do
not release histamine, which makes them ideal for treating pain in patients
with bronchospastic lung disease. High or repeated doses of fentanyl may
produce muscle rigidity. This side effect usually occurs with anaesthetic
doses and may be so severe that it interferes with respiration. This rigid-
ity can be treated with naloxone or muscle relaxants. Fentanyl does not
directly decrease cardiac output, but it may blunt central sympathetic
output, which can potentially decrease cardiac output in selected patients
who depend on sympathetic drive. Combining fentanyl with nitrous oxide
or benzodiazepines may also cause mild cardiovascular compromise.

BUTORPHANOL
Butorphanol is a synthetic opioid with properties similar to nalbuphine.
One major difference, however, is that butorphanol increases systemic and
pulmonary artery pressures. Because it increases cardiac afterload, butor-
phanol is not recommended in myocardial infarction or states of decreased
myocardial contractility.
The most common side effect of butorphanol is sedation. Psychotomi-
metic reactions have been described but are rare. The usual therapeutic
dose is 2–4 mg. The half-life is 3 h; hepatic metabolism and renal excre-
tion both contribute to drug elimination. A transnasal preparation is now
available. The great advantage of the transnasal route is that absorption
is relatively rapid and it can be easily self-titrated by the patient on dis-
charge. Each nasal spray delivers 1 mg.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Acute Pain Management following Trauma 119

TRAMADOL
Tramadol is a unique centrally acting analgesic. Some of its actions are
caused by binding at the mu opiate receptor, whereas other actions are
caused by inhibition of reuptake of norepinephrine and serotonin. Trama-
dol can be administered orally with 60% bioavailability and seems to have
an excellent safety profile. Respiratory depression has not been reported
in recommended dosages. Tramadol has very little potential for abuse or
addiction.

Local and Regional Analgesia for Emergency Patients

Infiltration of tissues with lidocaine is the mainstay of rapid effective
local anaesthesia for use in limited surgical procedures in the emergency
department. For more extensive procedures, regional nerve blocks may
also be achieved using lidocaine. The duration of action of lidocaine is
approximately 90–120 min. Recently, bupivacaine has gained popular-
ity for use in longer procedures because it is approximately four times
as potent as lidocaine and longer acting. Epinephrine 1:100,000 may be
added to the lidocaine to promote vasoconstriction and slow metabolism
of the anaesthetic for procedures in highly vascular areas such as the face.
Because of its vasoconstrictive properties, however, epinephrine should
never be used in digital or toe blocks, or for anaesthesia of the ear lobe
or other relatively poorly vascularized areas. Because of its alpha and
beta effects, epinephrine should be used with caution in patients with
hypertension, cardiac arrhythmias, and those with history of cerebral
haemorrhage.
For local infiltration, a maximum dose of 4.5 mg/kg of lidocaine, not
to exceed 300 mg, may be used. If lidocaine with epinephrine is used, the
dose is 7 mg/kg, not to exceed 500 mg. Beware of significant side effects
(CNS and cardiovascular) that may occur at higher dosages. For children,
a lidocaine-soaked gauze pad (2 or 4% xylocaine) placed on the wound
will result in superficial anaesthesia that will later facilitate less painful
injection of anaesthesia into the deeper layers of the wound.
Neuraxial blocks such as epidural and intrathecal routes for producing
analgesia in the emergency departments are technically not feasible and
should be avoided as far as possible. However, there are few indications of
epidural analgesia in emergency patients and they include chest trauma,
peripheral vascular disease, acute over chronic malignant pain and acute
lumbosacral radiculopathy.
Nerve blocks such as intercostal and intrapleural blocks for chest
trauma and peripheral nerve blocks for upper limb fractures are useful
for ameliorating pain as well as for performing minor procedures such as
manipulations. A 3-in-1 block is useful in patients with fracture of femur
shaft especially during transfer to the stretcher, operation theatre table or
imaging room.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

120 8. ACUTE PAIN MANAGEMENT: PRACTICAL GUIDELINES

NONOPIOID ANALGESIC AGENTS

Nonopioid analgesic agents are the most widely used class of analgesics
in the practice of emergency medicine. The common indications include
musculoskeletal pain, dysmenorrhoea, pleuritis, pharyngitis, and head-
ache. Studies have suggested that they are also effective for renal and biliary
colic. The mechanism of action of this class of drugs is thought to be prosta-
glandin inhibition and possibly a decrease in leukotriene production. These
agents are also used for their antipyretic and anti-inflammatory properties
and are thus classified as NSAIDs. The most commonly used of the nonopi-
oid analgesic agents are aspirin, acetaminophen, and ibuprofen; however,
new drugs are released and heavily promoted each year (Table 8.3).
The widespread use of NSAIDs is largely the result of the perceived
safety of this class of drugs. The lack of respiratory depression and
abuse potential is the major advantage to using these drugs as anal-
gesics. Although these drugs lack the side effects of opioids, they are
not problem free and can cause significant morbidity and even mortal-
ity. Even the safest of the nonnarcotic analgesic agents, acetaminophen,
has serious side effects. Some patients take larger-than-safe doses of
acetaminophen with resultant hepatic toxicity. A recent report showed
the occurrence of hepatic failure in three patients taking the drug. The
major side effects of nonopiod analgesic agents are GI bleeding, renal
failure, anaphylaxis, and platelet dysfunction. Acetaminophen has few
of these possible complications. Aspirin is not recommended as an
antipyretic for children with viral syndromes because of its association
with Reye syndrome. Because NSAIDs are associated with numerous

TABLE 8.3 Nonsteroidal Anti-inflammatory Drugs

Approved as Route; duration
Drug analgesic Indications Adverse effects of action

Aspirin Yes MI, stroke, acute GI bleeding PO; 4 h

arthritis
Paracetamol Yes Mild to Hepatic toxicity PO; 4–6 h
moderate
musculoskeletal
pain
Ibuprofen Yes Musculoskeletal GI bleeding PO; 4–8 h
pain, trauma
Ketorolac Yes Moderate to GI symptoms IM; >6 h
severe pain
Diclofenac Yes Severe pain, GI symptoms IM; >6 h
trauma, colic
Paracoxib Yes Moderate to Oedema, IV; 8 h
severe pain hypertension

PO, per os.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Treatment of Pain in Acute Myocardial Infarction 121

potentially serious side effects, they should be used only when con-
sidered to be particularly effective for a given type of pain and not
automatically prescribed for all pain conditions because they are safer
than opioids.
NSAIDs have become one of the mainstays of therapy in renal colic.
The inhibition of prostaglandin seems to inhibit ureteral peristalsis,
decrease pain, and promote passage of the calculus. Opioid analgesics
have the theoretic disadvantage of increasing ureteral peristalsis. Despite
this potential disadvantage, opioid analgesics have passed the test of
time and should be considered standard treatment along with the use of
NSAIDs.

TREATMENT OF PAIN IN ACUTE

MYOCARDIAL INFARCTION

Patients suffering acute myocardial infarction experience pain and

associated anxiety, which contribute to restlessness and increased activity
of the autonomic nervous system, leading to increased myocardial oxy-
gen demand. Alleviation of pain is therefore an essential component of
treatment. The pain of acute myocardial infarction is believed to be due
to stimulation of afferent fibres from the heart by chemical mediators
released from ischaemic tissue and so anti-ischaemic interventions, such
as oxygen, beta-blockers, nitrates and thrombolytic therapy will contrib-
ute to pain control. The administration of opioids should not, however, be
delayed to allow evaluation of the effects of other therapies.
Guidelines for the early management of patients with acute myocardial
infarction have been developed by the American College of Cardiology
and the American Heart Association, and include discussion of pain-
relieving therapies. Briefly, glyceryl trinitrate (sublingual or IV) should be
given to all patients unless initial systolic blood pressure is <90 mmHg or
right ventricular infarction is suspected. Beta-blockers reduce myocardial
oxygen demand and may improve perfusion of the ischaemic area. Con-
traindications include heart rate <60 beats/min, systolic blood pressure
<100 mmHg, moderate to severe left ventricular failure, signs of periph-
eral hypoperfusion, atrioventricular pulmonary disease. Morphine is the
opioid of choice and should be given in doses of 2–5 mg IV every 5–30 min
as needed. In addition to alleviating pain, morphine reduces myocardial
oxygen demand (Table 8.4). Morphine can cause hypotension associated
with inappropriate bradycardia but this is uncommon. Pethidine has
been recommended for inferior wall infarction with bradycardia due to
its vagolytic properties, but it is doubtful if it offers any advantage over
morphine. It may be used in patients with documented hypersensitivity
to morphine.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

122 8. ACUTE PAIN MANAGEMENT: PRACTICAL GUIDELINES

TABLE 8.4 Effects of Morphine in Acute Myocardial Infarction

1. Blocks sympathetic efferent discharge, leading to
a. peripheral venous and arterial dilation
b. ↓ preload and afterload
c. ↓ myocardial oxygen demand
2. Reduces pain and anxiety, leading to
a. ↓ circulating catecholamines
b. possible reduction in arrhythmias

TABLE 8.5 Recommended Drugs for Severe Acute Migraine Headache

• A ntiemetic + oral analgesic, e.g. metoclopramide and aspirin
• 5-HT1 agonists
• Nonselective, e.g. DHE
• Selective, e.g. sumatriptan
• Chlorpromazine
• NSAIDs, e.g. ketorolac, diclofenac, and nimesulide

PAIN MANAGEMENT IN SEVERE ACUTE MIGRAINE

In contrast to their central place in the control of postoperative pain

and pain due to acute myocardial infarction, the role of opioids in the
treatment of acute migraine attacks is limited. Pethidine has been com-
monly used in the past; however, its use is associated with a high level of
side effects, including nausea and sedation; its frequent use may lead to
iatrogenic drug dependence; and its efficacy is poor. Fortunately, a range
of more effective treatments is available (Table 8.5). Choice of initial treat-
ment depends on a number of factors: drugs already taken by the patient
for the current attack or in the preceding days, presence of GI symptoms,
history of response to previous treatments, coexisting medical conditions,
likelihood of medication misuse, and presence of contraindications to
antimigraine drugs.
Even in the absence of GI symptoms, gastric stasis is usually present
and absorption of oral medication is impaired. Metoclopramide reduces
nausea and vomiting and improves absorption of oral medication as well
as having an intrinsic antimigraine effect. Oral metoclopramide 10 mg
plus lysine acetylsalicylate equivalent to aspirin 900 mg is as effective as
oral sumatriptan 100 mg in the relief of moderate to severe migraine head-
ache. For patients suffering severe nausea or vomiting, administration of
IV fluids plus 10 mg metoclopramide IV, followed by 900 mg aspirin or
1000 mg paracetamol (acetaminophen) is safe and usually effective.
For patients unable to tolerate oral medication, several parenteral agents
are available. 5-HT1 receptor agonists induce vasoconstriction, includ-
ing of the coronary vessels, and contraindications include known or sus-
pected coronary artery disease. Guidelines for the use of ergot derivatives

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Pain Management in the Patient with Acute Abdomen 123

have been developed by a working panel of the American Academy of

Neurology. DHE may be given IV, SC or IM modes. The effective dose
varies among individuals; 0.25–1 mg may be given in repeated doses up to
a maximum of 3 mg in 24 h. DHE is an agonist at dopamine D2 receptors
and may cause or exacerbate GI symptoms; its administration should be
preceded by an antiemetic such as metoclopramide 10 mg. An intranasal
formulation of DHE is now available. The selective 5-HT1 agonist sumat-
riptan may be given at a dose of 6 mg SC; if ineffective, a second dose is
also unlikely to be effective, but the dose may be repeated once in 24 h if
recurrence occurs following successful initial treatment. Sumatriptan is
effective in 70–80% of patients, but, presumably due to its short half-life,
recurrence of headache is more frequent than following DHE. IV chlor-
promazine 0.1 mg/kg is also effective in majority of patients and can be
repeated for up to three doses.

PAIN MANAGEMENT IN THE PATIENT

WITH ACUTE ABDOMEN

The patient presenting with symptoms consistent with an acute abdo-

men is often in extreme pain. The emergency physician is then confronted
with the dilemma of waiting for the surgical consultant to arrive while
the patient remains in a continuous, if not worsening, state of pain and
suffering. This is not only unfair to the patient but also contrary to the
emergency physician's goal and duty to alleviate suffering.
If the diagnosis is fairly certain, as determined from history, physical
examination, radiograph, and laboratory studies, and if there is little doubt
that the patient is to be admitted to the hospital, alleviation of pain should
be a priority. When the exact diagnosis is not certain but there is no doubt
that surgical exploration will have to be performed, pain medications are
certainly warranted after discussion with the consulting surgeon. A decision
to give pain medication in the emergency department under these circum-
stances implies and requires a trusting and confident relationship between
the emergency physician and the surgeon. Because the patient will be moni-
tored in the Casualty as well as after admission, there is absolutely no ben-
efit to the patient to remain in a state of pain. To the contrary, for the anxious
preoperative patient, there is much to be gained by allaying pain and anxi-
ety; this will result in a less stressful and complicated recovery period.
However, patients with abdominal pain who are discharged from the
casualty should not routinely be given analgesics unless a firm diagno-
sis is reached that adequately explains the symptoms (an example of this
is colic secondary to cholelithiasis) or timely follow-up can be assured if
pain persists.
Both opioids and NSAIDs are used in the treatment of abdominal pain.
The dosage of opioid should be titrated to prevent patient suffering but

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

124 8. ACUTE PAIN MANAGEMENT: PRACTICAL GUIDELINES

not to totally alleviate pain. Opioids should be used with caution in ulcer-
ative colitis. In biliary colic, pure agonist opioids such as morphine can
increase intrabiliary pressure; NSAIDs are useful in the treatment of bili-
ary colic. Opioids like tramadol and butorphanol are also effective in treat-
ing acute pain of renal and biliary colic.

ACUTE PAIN MANAGEMENT IN CHILDREN

Several studies show that children are less likely than adults to receive
analgesic agents for the same painful conditions. Although safety should
be a primary concern with any therapeutic intervention, when used prop-
erly, most of the techniques described in this chapter can be adapted to use
in children. Overall, the same general principles that apply to providing
analgesia to adults apply to children. The major difference in providing
analgesia to children is the difficulty of accurately assessing subjective
sensation of pain, particularly in the very young. The most common indi-
cation for providing analgesia in children in an emergency department is
for procedural analgesia and sedation. The same drugs used for analgesia
in adults are safe in children in size-adjusted and age-adjusted doses.
The general approach to a child can be important in developing a trust-
ing relationship with both child and parent. Techniques in communicating
with children should take into account the unique developmental aspects
of each age group. Words chosen carefully, with care taken to avoid a
threatening manner can be invaluable. The decision to separate children
from their parents must be individualized, but many authorities suggest
avoiding the separation when possible. Parents can help distract the child
and reinforce the suggestions of the medical team.
Children deserve even more attention than adults with regard to safe
and effective analgesia because their early experiences will affect their life-
long outlook and trust in the medical profession. Recently, there has been
much interest in providing children analgesia and sedation by less threat-
ening routes of administration. Transmucosal fentanyl in the form of lolli-
pops and transnasal butorphanol and transnasal midazolam are examples
that have shown some promise. Rectal administration of NSAIDs such as
diclofenac is very effective in children for effective pain management fol-
lowing trauma in children.

ACUTE PAIN MANAGEMENT IN THE ELDERLY

Approximately 80% of the elderly have at least one chronic ailment

commonly associated with pain. Many studies have attempted to deter-
mine if the elderly lose pain sensitivity with increasing age, but the results

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 Acute Pain Service 125

have varied with different experimental models. Extra caution must be

taken to avoid side effects when using analgesic agents in the elderly.
This group of patients needs lower dosages of opioid analgesic agents.
In addition, opioids seem to produce sedation and constipation more
often. When a parenteral opioid is used, pethidine should be used only
if renal and hepatic function is normal. When renal and hepatic functions
are unknown, morphine or fentanyl are preferred. NSAIDs must also be
used cautiously in this group because of the many potentially serious side
effects (e.g. worsening renal function and GI bleeding).

ACUTE PAIN SERVICE

Effective pain control in trauma and emergency patients requires not

only an informed choice of drugs, initial dosage regimen and route, but
also frequent assessments of the patient by skilled staff, with modifica-
tions to the analgesic prescription where appropriate. The safety of opioid
administration, particularly by continuous infusion or by the spinal route,
is also contingent upon adequate monitoring of the patient. Establishment
of an acute pain service, commonly including a nurse and an anaesthe-
tist, is one way of facilitating this. The roles of the acute pain service may
include education of patients and staff, formulation of pain management
guidelines and protocols, and audit of efficacy and safety of postoperative
pain management. An acute pain service allows the use of relatively inva-
sive pain management techniques without compromising patient safety.
A number of studies have documented an improvement in management
of trauma-related pain following the introduction of an acute pain service.
Establishment of a multidisciplinary acute pain service may not be fea-
sible in some institutions. However, even the appointment of a dedicated
acute pain nurse in the emergency department can result in improved effi-
cacy and reduced side effects of pain control techniques.
Early advances in acute pain service focused on safe application of aggres-
sive techniques utilizing protocols and standing orders with the monitoring
available on the ward. However, it is the PCA services that paved the way
for the development of true acute pain management services providing
on-demand systemic as well as epidural and intrathecal analgesia. The US
model focused on physician management while the European model put a
greater emphasis on the nursing role.
In recent years, regional anaesthesia has gained popularity because of
its contribution to postoperative pain management. Single and continu-
ous peripheral neural blockages are increasingly practiced in both the
inpatient and outpatient settings. However, effective application of these
techniques requires adequate expertise, surveillance and organization, not
simply placing the particular block or catheter. Multidisciplinary acute

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

126 8. ACUTE PAIN MANAGEMENT: PRACTICAL GUIDELINES

pain teams can monitor and titrate these techniques to maximize pain
relief and safety while minimizing side effects.
More aggressive techniques such as IV-PCA, epidural analgesia, intra-
thecal opioids, and peripheral blocks find their best results when launched
on a multimodal analgesic platform incorporating NSAIDs and cyclooxy-
genase-2 inhibitors as well as other means of nonpharmacologic approaches
to acute pain management. True multimodal analgesia targets multiple
mechanisms of pain to effectively relieve both rest and dynamic pain.
A dedicated acute pain management team enhances implementation
of these above techniques for pain management. The primary goals of
an acute pain management service are to offer a wide variety of services,
provide a high level of patient surveillance and integrate these services
into the overall hospital setting. Optimal analgesia requires judicious dose
adjustment to maximize the benefits and minimize the side effects of ther-
apy. This can only occur if the patient is adequately monitored.
Anaesthesiologists, surgeons, pharmacists and various members of the
nursing team all have important roles when considering the organization
of an acute pain service. Acute pain management requires a multimodal
and multidisciplinary approach with a clear organization framework.
Regional anaesthesia techniques for surgical anaesthesia are a highly
effective component of acute pain management. Maximizing the contribu-
tions of regional anaesthesia to acute pain management requires integrat-
ing these techniques into the larger framework of patient care. Clinicians
must regard their efforts as extending beyond the operating room and
postanaesthesia care unit. This requires an organizational framework
that includes all members of the health care team, standard order sets,
assessment and documentation forms and institution-wide policies and
procedures for the management of aggressive pain techniques. Strong
institutional commitment is imperative.

I. GENERAL PRINCIPLES OF PAIN MANAGEMENT

 S E C T I O N II

CHRONIC PAIN
SYNDROMES
9 Myofascial Pain Syndromes 129
10 Headache 143
11 Neck and Shoulder Pain 157
12 Back Pain 165
13 Facetogenic Pain 181
14 Knee Pain 193
15 Neuropathic Pain: Mechanisms and Management 203
16 Herpetic Neuralgia 217
17 Orofacial Pain 223
18 Scar Neuralgia/Painful Scars 235
19 Complex Regional Pain Syndrome 239
20 Pelvic Pain 253
21 Perineal Pain 267
22 Peripheral Vascular Diseases 273
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 C H A P T E R

9
Myofascial Pain
Syndromes

MPS constitutes a large group of muscle disorders characterized by

the presence of hypersensitive points, called TPs, within one or more
muscles, the investing connective tissue, or both, together with a syn-
drome of pain, muscle spasm, tenderness, stiffness, limitation of motion,
weakness and occasionally autonomic dysfunction. The symptoms are
usually referred to an area distant from the TPs, although local pain may
be present.
Myofascial syndromes are the most common musculoskeletal disabili-
ties of the shoulder girdle, neck, upper back, low back, and to a lesser
extent, chest and ribs. They are certainly among the most frequent causes
of severe disabling pain. Moreover, because of the peculiar symptoms
associated with these syndromes, they were not recognized until recently.
They were often misdiagnosed and treated as bursitis, arthritis or visceral
disease.
Fibrositis, now commonly known as PFS, can be differentiated from
MPSs (see Table 9.1). The difference is based on the fact that MPSs are
characterized by the presence of specific TPs in one or several muscles,
whereas PFS is characterized by local tenderness in more than 11 specified
sites, with widespread aching of more than 3 months duration. This dif-
ference has been recognized by the Committee on Taxonomy of the Inter-
national Association for the Study of Pain.

AETIOPATHOGENESIS OF MPSs

The most easily identifiable causes of MPSs are

1. T rauma to myofascial structures
2. Acute overload of muscles

129
130 9. MYOFASCIAL PAIN SYNDROMES

TABLE 9.1 Differences between Fibromyalgia and Myofascial Pain Syndrome

Fibromyalgia Myofascial pain syndrome

Sex Female/male 10:1 Male/female 2:1

Tender point pain Local Referred

Trigger point distribution Widespread Regional

Trigger point anatomy Muscle tendon junction Muscle belly

Stiffness Widespread Regional

Fatigue Debilitating Usually absent

Treatment Drugs TP injection, stretch

Prognosis Seldom cured Usually good

TP, trigger points.

3. A
 third etiologic pattern for myofascial syndrome is slow onset, in
which the microtraumas of daily activities or repetitive movements
while working result in overload fatigue
  

After acute injury, TPs (small, circumscribed, hypersensitive regions

in muscles or connective tissue) can be identified in some individuals.
These TPs are also known as trigger areas, trigger zones, and myalgic spots.
Impulses arise from these points and bombard the central nervous system
to produce local or referred pain or both and the associated phenomena in
the area of reference or activation. The TP is so named because its stimula-
tion, with pressure or activation of the muscle, is like pulling the trigger of
a gun, producing effects at another place (a target), called the reference zone
or area of reference. The term, then, implies the existence of a relationship
between two different topographic areas, the trigger and the target.
An active TP is associated with spontaneous pain at rest or with motion
that stretches or overloads the muscle. A latent TP does not cause sponta-
neous pain, but it can be diagnosed by applying discrete pressure on the
TP, which is likely to cause pain locally and in the area of reference.

Major Differential Diagnosis of MPS

• CRPS I and II (RSD and causalgia)
• Named MPSs, e.g. scapulocostal syndrome
• Bursitis
• Enthesiopathies, e.g. tennis elbow
• Thoracoabdominal entrapment neuropathies
• Hypothyroidism
• Polymyositis

II. CHRONIC PAIN SYNDROMES

 AETIOPATHOGENESIS OF MPSs 131

• Metabolic myopathies
• Hyperparathyroidism
• Connective tissue disorders, especially in early stages
• Polymyalgia rheumatica (temporal arteritis elderly)
• Osteoarthritis
• Parkinsonism

Symptoms and Signs

Patients with myofascial disorders usually present with persistent pain,
tight or aching muscles, limited ROM, general fatigue or a combination of
these. The patient might not be aware of the muscular involvement and
might complain instead of headache, neck pain, joint pain, backache or
sciatica-like pain in the buttocks or lower extremities.
The intensity of myofascial pain ranges from a low level, felt as a mild
ache, to an excruciating ache or burning pain, or both. The pain can be
either continuous or periodic, but it is usually continuous, debilitating and
limiting. It is usually elicited explosively and spontaneously as soon as the
trigger area is touched (jump sign). The extent of the area of focal and
referred pain apparently depends on the sensitivity of the trigger areas.
If the TP is very sensitive, there is a wide radiation of pain to include the
essential zone of reference as well as a spillover zone.
In a minority of patients, the presenting complaint is not pain but lim-
ited ROM or conditions associated with shortened or guarded muscles.
The search of TPs is best accomplished by palpating the area with the
tip of the finger. The palpation should be systematic so that every square
centimetre of the surface overlying the suspected sensitive zone or site
from which the pain arises is palpated. The patient is instructed to indicate
when the point of exquisite tenderness is not only locally painful, but also
aggravates or reproduces the pain in the reference zone. The patient is
observed closely during the palpation, because pressure on the exquisitely
tender TP usually causes the patient to jump, wince or cry out.
When several areas of exquisite tenderness are found, it is important to
initiate treatment at the most sensitive point.

Search for Tight Bands

To examine the suspected muscle for the objective sign of a tight band,
it is placed on stretch. This manoeuvre places the fibres in a tight band
under increased tension, while uninvolved adjacent fibres remain slack.
This tight band can be felt most readily by rubbing the tip of the finger
(rather than the flat pads) across (perpendicular to) the direction of the
fibres. As the fingertip passes over the tight muscle, it feels tense as a nod-
ule. Another technique of palpating the tight muscle and the TP is to grasp

II. CHRONIC PAIN SYNDROMES

132 9. MYOFASCIAL PAIN SYNDROMES

the belly of the muscle between thumb and forefinger and squeeze the
fibres with a back-and-forth rolling motion to locate taut bands.

Local Twitch Response

LTR is readily observed in superficial muscles when rapidly changing
pressure is applied to the TP by snapping palpation. The greatest LTR is
observed when the TP itself is stimulated and generally, the more active
(hyperirritable) the TP, the stronger its LTR. As one moves further from
the TP, stronger pressure is required and the LTR becomes less and less
vigorous. The referred pain pattern caused by stimulation of a TP is also
invoked when a needle penetrates a TP during injection.

Segmental Clusters
Cluster of myofascial syndromes are common in the neck and shoul-
der and include most frequently the trapezius, levator scapula and
infraspinatous. As the severity and duration of pain increase, clini-
cal findings indicate progressively greater involvement of all other
muscles innervated by the same spinal segment(s). Hypersensitivity at
one level readily involves other muscles with overlapping segmental
innervation.

Multiple Segmental Clusters

As the self-perpetuating myofascial disturbance continues and pro-
gresses, TPs develop further and further from the initial area of stress or
injury. TPs tend to develop with a higher frequency in ipsilateral muscle
groups.

Treatment
Treatment of MPSs revolves around interruption of the pain cycle by
eliminating the TP.

TP Injection Technique
Treatment must be directed primarily towards the trigger area and not
to the zone of reference (Photograph 9.1). Penetration is accomplished
with a 25 gauge, 5 cm needle for deep muscles or a 27 gauge, 2 cm needle
for superficial muscles. The use of such fine needles makes preliminary
intracutaneous injection of the local anaesthetic unnecessary and even
undesirable because the pain caused during injection is usually more than
that caused by the deliberate insertion of a fine needle through the skin.
Solutions used are 2 mL 0.25–0.5% lidocaine, or 0.125–0.25% bupivacaine
along with low-dose steroids (10 mg methyl prednisolone acetate, 0.05%
dexamethasone) (Box 9.1).
Saline alone is very effective in young patients and is the only choice
for pregnant patients.

II. CHRONIC PAIN SYNDROMES

 AETIOPATHOGENESIS OF MPSs 133

(a) (b) (c)

PHOTOGRAPH 9.1 Trigger point injection.

BOX 9.1

OUR PROTOCOL FOR TRIGGER

POINT INJECTION

No. of injections 5–10 per course repeated after 3 months if

required
Solution 0.25% bupivacaine with 5–10 mg of methyl
prednisolone (to a maximum of 120 mg per
course)
Volume 2–5 mL

The needle is directed at the most sensitive TP identified and is advanced

until the TP is penetrated. Penetration of the TP elicits exquisite tenderness
and pain, not locally but also at the zone of reference. The depth of the injec-
tion depends on the region involved and on the site of the TP. Once the TP
is penetrated, a total of 0.5–2 mL of solution is injected under some pressure.
This process usually causes further exaggeration of the local or referred pain
and tenderness and not infrequently brief local spasm.
The needle is then withdrawn slightly and redirected two or three times
to cover the immediate area of the TP with a fanning technique. Exaggera-
tion of pain and tenderness and local spasms is presumptive evidence that
the injection has been properly executed. Confirmation is obtained if the
procedure effects relief of pain and muscle spasm, which is usually dra-
matic. If no relief is obtained, it is most likely that the TP was not injected,
indicating another trial. It is essential to eliminate the TP or points com-
pletely by repeated infiltration because incomplete blockade is not only
partially ineffective, but is followed by increased pain after disappearance
of the effects of the local anaesthetic.
Immediately after the injection therapy, a warm moist pack is applied
to the area to relieve temporary discomfort.

II. CHRONIC PAIN SYNDROMES

134 9. MYOFASCIAL PAIN SYNDROMES

The dominant role of the larger muscles of the lower torso requires that
TPs identified in these areas be treated on the first visit. They are usually
involved in a myofascial syndrome that has been well established. Failure to
treat TPs in the lower trunk concurrent with or before treatment of points in
other parts of the body is likely to result in greater discomfort for the patient.
Relief of pain, tenderness, muscle spasm, and associated phenomena
persists for several hours after treatment, and sometimes for a day or
two. Young patients tend to respond more quickly and positively than
older patients; however, a series of two to five treatments is usually suf-
ficient either to provide prolonged relief or to establish that the patient is
responding to the therapy. Patients with severe pain associated with acti-
vation of latent TPs might require 3–6 weeks of intensive therapy consist-
ing of TP injections and physical therapy.
Patients who have history of severe pain for several years before treat-
ment may not respond to treatments for many months.

Technique of Stretch and Spray

The advantages of this technique are that it is simple, relatively pain-
less, and a rapid way to relieve a single muscle syndrome. It is more effec-
tive in deactivating all TPs in the affected muscles, some of which might
be missed by palpation. Best results are obtained by spraying first, then
stretching and spraying again.

TECHNIQUE
The patient is made comfortable, and the part to be sprayed is well sup-
ported so that the involved muscles are relaxed. One end of the muscle must
be anchored so that the pressure can be applied at the other end to passively
stretch it. A jet or stream (not a diffuse mist) of the vapocoolant spray is
applied to the skin overlying the trigger area and moved slowly in one direc-
tion. The direction is determined by the pain reference pattern of the specific
TPs to be sprayed; the sweep should be started on the skin over the trigger
area and made to travel towards the area of referred pain. A moist hot pack is
applied to rewarm the skin and help further relax the muscle. After the skin
has rewarmed, stretch and spray can be repeated. Several cycles of full ROM
and complete stretch and spray treatment of the muscle may be required.
The patient is cautioned to avoid overloading the muscle after treatment.

Pharmacotherapy
Pharmacotherapy has to be started along with TP injections.
Analgesics – NSAIDs and cyclooxygenase 2 inhibitors or mild oral
opioids such as tramadol are administered depending on the severity of
pain. Muscle relaxants such as tizanidine are indicated in acute phase
when there is significant muscle spasm.

II. CHRONIC PAIN SYNDROMES

 AETIOPATHOGENESIS OF MPSs 135

TCAs – amitriptyline (10–50 mg/day) is an essential drug in patients

with chronic MPSs. (Drug details are given in relevant section.)

BTx A Injection in Refractory MPS

Since many of the treatments for myofascial syndrome are aimed at
blocking the trigger to allow sustained muscle relaxation, the use of botu-
linum toxin represents a logical extension of traditional therapies. BTx
A has been used clinically for relief from pain in a number of disorders
believed to be due to overactive striated or smooth muscles, such as cer-
vical dystonia, blepharospasm, spasticity, achalasia and rectal sphincter
spasm associated with fissure. Pain relief is achieved by reducing muscle
hyperactivity.

Characteristics of BTx A
• Neurotoxin derived from Clostridium botulinum
• Eight subtypes, type A is the one used clinically
• BTx A is a purified neurotoxin and a potent neuromuscular blocking
agent with negligible undesirable effects
• Decreases muscle tone when injected in spastic and hypertrophic muscles
• Dichain polypeptide

Dosage
MPS: 5–10 units at each TP and maximum up to 300 units. The injection
of BTx A into myofascial TPs is carried out in a manner analogous to TP
injection by using a solution containing 10 units/mL (Photograph 9.2).
The smallest possible dose should be used and the therapeutic dose is
significantly less than the toxic dose.
The drug should not be repeated before 6 months for fear of antibodies
formation.

Contraindications
• Coagulation disorders
• Neuromuscular disorders like myasthenia gravis

Side Effects and Complications

• Dull, transient pain in area of injection
• Generalized weakness
• Allergy to toxin
• Haematoma formation

Adjunctive Therapies for Treatment of Myofascial Pain

1. Appropriate forms of exercise. It is essential that the involved muscles
should not be activated too rapidly or moved to a painful degree,

II. CHRONIC PAIN SYNDROMES

136 9. MYOFASCIAL PAIN SYNDROMES

PHOTOGRAPH 9.2 Botulinum toxin injection in upper back myofascial pain.

especially in the early phases of treatment, because severe pain itself is

deleterious and provokes reflex muscle spasm.
2. Pressure and massage (especially deep friction); TENS, ice massage;
cervical or lumbar traction or both; compression; ultrasound; and
biofeedback.
3. Acupuncture.

FIBROMYALGIA SYNDROME

FMS is a disorder of unknown aetiology. It can be classified as a soft-

tissue pain syndrome characterized by widespread pain emanating from
periarticular structures located outside the joint capsule and periosteum
(Box 9.2). There is history of chronic, bilateral, upper and lower body
‘musculoskeletal’ pain combined with typical examination findings of
painful tenderness at 11 or more of 18 anatomically defined soft-tissue
TePs (Fig. 9.1).

Symptoms and Signs

1. T
 he most prominent symptom is chronic, widespread pain in
soft-tissue regions such as the muscles, ligaments, bursae and tendons.
The pain has been described as a persistent, diffuse,
deep, aching, throbbing, sometimes stabbing pain associated
with distal extremity dysesthesias. Patients with FMS typically
exhibit high pain severity scores on the McGill Pain Questionnaire.
They usually indicate bilateral body sites involving the upper and
lower extremities, the neck posteriorly, the anterior chest, and the
low back.

II. CHRONIC PAIN SYNDROMES

 Fibromyalgia Syndrome 137

BOX 9.2

THE AMERICAN COLLEGE OF

R H E U M AT O L O G Y 2 0 1 0 D I A G N O S T I C
C R I T E R I A F O R F I B R O M YA L G I A *
Criteria
A patient satisfies the diagnostic criteria for fibromyalgia if the follow-
ing three conditions are met:
  

1. W idespread pain index (WPI) ≥ 7 and symptom severity (SS) scale

score ≥ 5 or WPI 3–6 and SS scale score ≥ 9.
2. Symptoms have been present at a similar level for at least 3 months.
3. The patient does not have a disorder that would otherwise explain
the pain.

Ascertainment
1. WPI
  

Note the number of areas in which the patient has had pain over the
last week. In how many areas has the patient had pain? The score will be
between 0 and 19.

Shoulder girdle, left Hip (buttock, Jaw, left Upper back

trochanter), left
Shoulder girdle, Hip (buttock, Jaw, right Lower back
right trochanter), right
Upper arm, left Upper leg, left Chest Neck
Upper arm, right Upper leg, right Abdomen
Lower arm, left Lower leg, left
Lower arm, right Lower leg, right
  

2. S
 S scale score
a. Fatigue
b. Waking unfreshed
c. Cognitive symptoms
  

For each of the three symptoms above, indicate the level of severity
over the past week using the following scale:
  

0 = no problem
1 = slight or mild problems, generally mild or intermittent
2 = moderate, considerable problems, often present and/or at a
moderate level
3 = severe: pervasive, continuous, life-disturbing problems
  

Continued

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138 9. MYOFASCIAL PAIN SYNDROMES

BOX 9.2 (cont’d)

Considering somatic symptoms in general, indicate whether the pa-

tient
  
has
0 = no problem
1 = few problems
2 = a moderate number of symptoms
  
3 = a great deal of symptoms
The SS scale score is the sum of the severity of the three symptoms
plus the extent (severity) of somatic symptoms in general. The final score
is between 0 and 12.
*Adapted from Wolfe F, Clauw DJ, Fitzcharles MA, et al. The American College of Rheumatology
preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis
Care Res (Hoboken). 2010;62:600-610.

Occiput:
suboccipital Low cervical:
muscle anterior aspects
insertions of the intertransverse
spaces at C5–C7

Trapezius: Second rib:

midpoint of the second
upper border costochondral
junctions

Supraspinatus:
above the medial Lateral
border of the epicondyle:
scpular spine 2 cm distal to
the epicondyles

Gluteal:
upper outer
quadrants Knee:
of buttocks medial fat pad
proximal to the
joint line

Greater
trochanter:
posterior to
the trochanteric
prominence

FIGURE 9.1 Anatomical locations of tender point sites.

II. CHRONIC PAIN SYNDROMES

 Fibromyalgia Syndrome 139

2. T ePs – The characteristic physical finding of multiple TePs in FMS can

be elicited by pressing firmly (approximately 4 kg of pressure on an
area of approximately 1 cm2 – enough to blanch a thumb nail) over
each of 18 anatomically defined soft-tissue areas called TePs. Diagnosis
is made based on the ACR criteria described above. TePs points differ
from TPs in that they do not demonstrate referred pain distally.
3. Associated clinical symptoms (as given in Box 9.3)

Assessment of Progress
Although TeP score is important for diagnosis, it is not helpful as a mea-
sure of treatment efficiency. We can use the undermentioned tenderness
scale (Box 9.4) to measure the severity at each visit.

Treatment Modalities
Pharmacological
1. NSAIDs: cannot be used as primary agents but only as an adjunct to
centrally acting analgesics (doses as described in pharmacotherapy
chapter).
2. Corticosteroids: low-dose prednisolone as in maintenance therapy
for rheumatoid arthritis.
3. Opioids: results of preliminary report suggest that oral doses of the
weak opioid tramadol have limited benefit (50 mg bd/tds).

BOX 9.3

C L I N I C A L S Y M P T O M S A S S O C I AT E D
WITH FMS
• D epression, anxiety
• Cognitive deficits, short-term memory loss
• Throbbing occipital pain of muscle contraction headache, lighthead-
edness, dizziness, syncope
• Chronic insomnia, nocturnal myoclonus, nocturnal bruxism, daytime
tiredness resembling physical fatigue
• Prolonged morning stiffness as in rheumatoid arthritis
• Chest wall pain mimicking angina pectoris, breast area pain
• Mechanical low back pain or sciatica-like radiation of pain
• Bursitis, tendonitis, myalgias, arthralgias, piriformis syndrome
• Numbness, tingling, dysesthesias in hands and feet
• Irritable bowel, abdominal pain, diarrhoea, constipation
• Interstitial cystitis, frequency, urgency, sterile dysuria

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140 9. MYOFASCIAL PAIN SYNDROMES

BOX 9.4

C L I N I C A L D E T E R M I N AT I O N
OF TENDERNESS SEVERITY –
C A L C U L AT I N G T H E T E N D E R P O I N T
INDEX
1. A pply 4 kg of digital pressure at each tender point.
2. Observe body language, especially the face, for response.
3. Use the following scale to quantify each response:

Not painful 0
Feels painful, no physical response 1+
Feels painful, wince or withdrawal 2+
Feels painful, exaggerated withdrawal 3+
Area deemed too painful to allow pressure 4+
4. Add the individual tenderness severities for all 18 sites

The sum is the tender point index –

The expected range for normal controls 0–5
The expected range for fibromyalgia 11–72

BOX 9.5

D R U G H O L I D AY C O N C E P T F O R U S E
O F L O W- D O S E S E R O T O N I N R E U P TA K E
INHIBITORS
Three to four months of serotonin reuptake inhibition: Amitriptyline,
10–25 mg hs (cyclobenzaprine 5–10 mg hs). Possibly fluoxetine,
10–20 mg, in the morning. Possibly ibuprofen, 800 mg bid, or nonnar-
cotic analgesic possibly tramadol, 50–300 mg, in divided dosages.
One month of serotonin reuptake inhibitor holiday: Alprazolam,
0.5–1.0 mg hs, or clonazepam, 1.0 mg hs. Resume serotonin reuptake
inhibition for another cycle.

4. S edatives: benzodiazepines (zolpidem, diazepam).

5. Antidepressants: TCAs like amitriptyline have been found to be
most useful. In a recent study, a flexible protocol with serotonin-
specific reuptake inhibitors has been found to reduce FMS symptoms
in nondepressed patients. This protocol is as shown in Box 9.5.

II. CHRONIC PAIN SYNDROMES

 Fibromyalgia Syndrome 141

6. I ntravenous lidocaine: 5 mg/kg infusion over 60 min. Can be

repeated for three consecutive daily sittings.
7. TeP injections (as described for MPS earlier).
8. Alpha–2 adrenergic agonists: tizanidine is useful in FMS as
antinociceptive, antispasmodic and sedative.
9. NMDA receptor antagonists: dextromethorphan in adjunct to
tramadol has been found useful. Ketamine infusion intravenously
and as TP injection has shown anecdotal success.
10. Exercise: aerobic exercise and strength training are generally
beneficial in reducing hyperalgesia.
11. Electroacupuncture.
12. Relaxation techniques and biofeedback.

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 C H A P T E R

10
Headache

Headache is the most common medical complaint encountered in clinical

practice. Patients with refractory headaches unresponsive to drug treatment
are often referred to a pain clinic. Headache is broadly classified into chronic
and episodic types. Headache presenting for more than 15 days per month
and lasting more than 4 h per day is classified as chronic daily headache.
About 5% of the general population is affected by chronic daily headache
and the incidence is significantly higher in women. Headaches occurring at
irregular intervals are episodic headaches; the most common being cluster
headaches. Occasionally, tension-type headaches may also be episodic in
nature.

MECHANISMS OF HEADACHES

The mechanisms of head pain include

1. T raction on intracranial structures, i.e. intracranial mass, postlumbar
puncture headache
2. Dilatation of cranial arteries (it is felt that both tension-type and
migraine or vascular headaches have a central brainstem pacemaker
that affects structures in the trigeminal nerve selectively)
a. Intracranial: cluster headaches, anoxia, CO2 intoxication,
pheochromocytoma
b. Extracranial: migraine or cluster
3. Inflammation
a. Intracranial: meningitis
b. Extracranial: temporal arteritis
4. Contraction of the striated muscles of the head or neck, i.e. contraction
headache (this concept has been questioned by the recent discovery of
central-type pacemaker on positron emission tomography scan)
5. Cranial neuralgias
6. Diseases of the eyes, nose, sinus, ears or teeth

143
144 10. HEADACHE

CLASSIFICATION OF TYPES OF HEADACHES

The major categories of headache disorders are given in Box 10.1

(Fig. 10.1).

HEADACHE EVALUATION: HISTORY

The headache evaluation consists of a detailed history, pertinent infor-

mation from the physical examination and pertinent diagnostic studies.
Of these, the most important element is the headache history. ‘If you have
thirty minutes to see a patient, spend twenty-nine on history, one on the
examination’ (Sahs, 1987). Evaluation of a patient with headache requires
the following:
1. D etailed history
2. P  ertinent information from physical examination
3. Pertinent diagnostic laboratory, neurophysiologic and radiographic
studies
  

In the headache evaluation, factors that cause concern are

1.  eadaches associated with neurologic dysfunction
H
2. Exertional headache
3. Headaches that peak rapidly
4. Nocturnal headaches
5. Headaches associated with systemic symptoms
6. Focal headaches
7. Recent headaches
8. A recent change in headache
  

Before evaluating in detail, a simple questionnaire (MIDAS Question-

naire) is administered to grade the disability level of patients with chronic
intractable headache (Box 10.2).
The following are important questions that should always be asked to
a patient with headache.
1.  hat is the character and location?
W
2. What is the onset to peak time?
3. What is the usual time of day it occurs and the total duration?
4. Are there any associated and/or residual neurological phenomena or
sequelae?
5. Is there an aura?
6. What makes the headache worse?
7. What makes the headache better?
8. Is there a family history?
9. Were there headaches in childhood?

II. CHRONIC PAIN SYNDROMES

 Headache Evaluation: History 145

BOX 10.1

C L A S S I F I C AT I O N O F H E A D A C H E S
Primary headache disorders
1. Migraine
Migraine with aura
Migraine without aura
2. Tension-type headache
Episodic tension-type headache
Chronic tension-type headache
Cluster headache and chronic paroxysmal hemicrania
3. Cluster headache
Episodic cluster headache
Chronic cluster headache
4. Miscellaneous headaches unassociated with structural lesion
Idiopathic stabbing headache
External compression headache
Cold stimulus headache
Benign cough headache

Secondary headache disorders

5. H eadache associated with head trauma
Acute posttraumatic headache
Chronic posttraumatic headache
6. Headache associated with vascular disorders
Acute ischaemic cerebrovascular disease
Intracranial haematoma
Subarachnoid haemorrhage
Venous thrombosis
Arterial hypertension
7. Headache associated with nonvascular intracranial disorder
High/low cerebrospinal fluid pressure
Intracranial infection
Headache related to intrathecal injections
Intracranial neoplasm
8. Headache associated with substance withdrawal
9. Headache associated with noncephalic infections
10. Headache associated with metabolic disorders
11. Headache or focal pain associated with disorder of cranium, neck,
eyes, nose, sinuses, teeth, mouth or other facial or cranial structures
12. Cranial neuralgias, nerve trunk pain and deafferentation pain

II. CHRONIC PAIN SYNDROMES

146 10. HEADACHE

Sinus: Cluster: Tension: Migraine:

pain is usually pain is in pain is like pain, nausea
behind the forehead and around a band squeezing and visual changes
and/or cheekbones one eye the head are typical of
classic form

FIGURE 10.1 Common Types of Headaches.

10. W as there motion sickness, cyclical vomiting, dizziness, or

unexplained fever in childhood?
11. Were there any prior diagnostic tests?
12. What were the results of prior medication?
13. Are there any other medical illnesses?
14. Are there any psychiatric illnesses, history of alcohol or substance
abuse and what is the quality of the individual's life?

EVALUATING A PATIENT WITH HEADACHE:

EXAMINATION

A headache patient will commonly show no abnormalities on exami-

nation if he or she has a chronic benign type of headache. Incidental
abnormalities may be encountered that are not germane to the patient's
situation. However, in all patients, a careful general physical and neu-
rological examination should be carried out. In addition to the general
examination, the skull and spine should be examined. The patient should
have a complete examination of the head, eyes, ears, nose and throat for
sinus disease, temporomandibular joint disease and even dental disease.
Often, pain referred to the head will come from the tooth.
In the general examination, attention should be paid to the possible
existence of cafe au lait spots or other stigmata of the phakomatoses.
Examination of the range of motion of the neck as well as a complete
neurovascular examination should be carried out. In the elderly with any
suspicion of temporal arteritis, examination of the joints of the body plus
the temporal arteries is mandatory.

II. CHRONIC PAIN SYNDROMES

 Evaluating a Patient with Headache: Examination 147

BOX 10.2

MIDAS HEADACHE QUESTIONNAIRE

Instructions: Please answer the following questions about all the head-
aches you have had over the last 3 months. Write your answer in the box
next to each question. Write zero if you did not do the activity in the last
3 months.

1. O n how many days in the last 3 months did you days

miss work or school because of your headaches?
2. How many days in the last 3 months was your days
productivity at work reduced by half or more (do
not include days counted in question (1))?
3. On how many days in the last 3 months did you days
not do household work because of your head-
aches?
4. How many days in the last 3 months was your days
productivity in household work reduced by half
or more because of your headaches? (Do not
include days you counted in question (3) where
you did not do household work.)
5. On how many days in the last 3 months did you days
miss family, social or leisure activities because of
your headaches?
Total days
a. O n how many days in the last 3 months did you days
have a headache? (If a headache lasted more
than 1 day, count each day.)
b. On a scale of 0–10, on average, how painful were days
these headaches (where 0 = no pain at all and
10 = pain as bad as it can be)?

Grading system for the MIDAS Questionnaire

Grade Definition Score

I Minimal or infrequent disability 0–5
II Mild or infrequent disability 6–10
III Moderate disability 11–20
IV Severe disability 21+

II. CHRONIC PAIN SYNDROMES

148 10. HEADACHE

The general configuration of the body especially a short neck or a low

hair line may suggest congenital anomalies that may lead to headaches.
Obesity should be considered as a risk factor for the development of pseu-
dotumor cerebri.
The steps to examination of a patient with headache are
1. C heck the patient's gait, noting his arm swing. Check tandem walking
and walking on heels or toes. Remove any high-heeled shoes. It
gives a general idea as to whether or not there is any hemiparesis,
any limp, any postural abnormalities, and will quickly reveal any
extrapyramidal or cerebellar signs.
2. Check the patient's posture with feet together and then have the
patient close the eyes (Romberg test).
3. Have the patient step up and down alternatively with either leg onto a
stool. This is a gross test of the strength of the lower extremity plus the
patient's balance.
4. Test the motor power of the patient, fine finger movements and
alternating hand movements. This is a test for both upper and lower
motor neuron disease.
5. Check the reflexes starting with the jaw jerk, and for the presence of a
snout reflex. Check the biceps, triceps, brachioradialis reflexes, knee
and ankle jerk, and check the foot for possible Babinski respose. Also,
check the abdominal reflexes.
6. Check sensation starting with the face, first with a wisp of cotton,
then with a pin. Use a cotton pledget to test corneal reflexes. Check
vibration and position sense in both upper and lower extremities as
well as the pin prick sensation in both upper and lower extremities.
7. Check cranial nerves. The first cranial nerve can be checked with
common substances such as coffee, perfume, etc. Check the second
cranial nerve by the pupillary light response, optic fundus and field
by confrontation. With eye movements in all directions check the
third, fourth and sixth cranial nerves. The sensory part of the fifth
nerve has already been checked under sensation, so the strength of the
temporalis and masseter muscles should be checked and also whether
the jaw is protruded in the midline.
  

The seventh cranial nerve is conveniently checked by having the patient

close the eyes tightly and bare his or her teeth. The patient can also elevate
the eyebrows and flare the nostrils. At this point, tongue movements can be
checked including whether or not the tongue is protruded in the midline.
The tongue then should push the examiner's finger away in each cheek.
The eighth cranial nerve has been checked already when the vibration
is checked during the sensory examination. The ninth and tenth cranial
nerves should be checked by observing the palate, the palatal movements
and touching the back of the throat on either side with a cotton swab. The
eleventh cranial nerve is checked by resistance of the patient to attempts to

II. CHRONIC PAIN SYNDROMES

 Headache: Factors that Cause Concern 149

turn his head from right to left and left to right. At this point, the strength
of anterior flexion and extension of the neck should be checked. Finally,
shoulder shrugging should be checked.
This entire scheme of the neurological exam should not take more than
5–7 min in a healthy, normal adult.

HEADACHE: FACTORS THAT CAUSE CONCERN

Clues to headaches that are life threatening and that cause concern
come from the history, the physical examination and the diagnostic tests
that are ordered. Four key factors distinguishing physiological (primary)
from secondary (organic) headaches are
1.  bruptness of onset
A
2. Progression of the headache pattern
3. The presence of abnormal neurological and physical findings
4. The nature of the provoking and alleviating factors

Danger Signs in Headache

‘Danger signs’ in headache patients that suggest the need for immedi-
ate attention are
1. H eadache is a new symptom for the individual in the past 3 months, or
the nature of the headache has changed markedly in the past 3 months.
2. Presence of any sensory or motor deficits preceding or accompanying
the headache other than the typical visual prodromata of migraine
with aura. Examples include hands or feet, aphasia or slurred speech.
3. Headache is one sided and has always been on the same side of the
head.
4. Headache is due to trauma, especially if it follows a period of
unconsciousness (even if only momentary).
5. Headache is constant and unremitting.
6. For a patient reporting tension-type headache-like symptoms:
a. Pain intensity has been steadily increasing over a period of weeks
to months with little or no relief.
b. Headache is worse in the morning and becomes less severe during
the day.
c. Headache is accompanied by vomiting.
7. Patient has been treated for any kind of cancer and now has a
complaint of headache (to this may be added any patient who is
immunosuppressed).
8. Patient or significant others report a noticeable change in personality
or behaviour, or a notable decrease in memory or other intellectual
functioning.

II. CHRONIC PAIN SYNDROMES

150 10. HEADACHE

9. T he patient is over 60 years of age, and the headache is a new

complaint.
10. Pain onset is sudden and occurs during conditions of exertion
(such as lifting objects, sexual intercourse or ‘heated’ interpersonal
situation).
11. Patient's family has a history of cerebral aneurysm, other vascular
anomalies or polycystic kidneys.

DIAGNOSTIC TESTING IN A PATIENT WITH

HEADACHE

1. L aboratory testing: complete blood count, erythrocyte sedimentation

rate, blood sugar, renal functions, thyroid functions
2. Radiographic testing: plain skull radiograph
3. Computed tomography of head
4. Magnetic resonance imaging head/cervical spine
5. Electroencephalogram and somatosensory evoked potential testing
6. Arteriography/digital subtraction angiography
7. Electromyography of cranial nerves

MANAGEMENT OF HEADACHES

Primary headaches (migraine, tension-type headache, cluster head-

ache, chronic daily headache) can be very debilitating for the individual.
Unfortunately, there is no ‘magic bullet’ to treat these conditions and as
a pain clinician it will be a challenging task to provide optimal relief to
the sufferer. While a cure for headaches is not currently possible, ade-
quate control can be achieved for the majority of sufferers. The manage-
ment strategies are primarily pharmacological, although few patients do
require nonpharmacological therapies including interventional manage-
ment. Overuse of drugs should be avoided and analgesic intake should
be restricted.

Migraine
Clinical Presentation
Episodic attacks characterized by pulsating and throbbing headache in
association with nausea, photophobia and phonophobia.

Treatment of Acute Attacks

Acute attack of migraine is generally aborted by drugs such as aspi-
rin, paracetamol (650 mg), NSAIDs such as oral or parenteral diclofenac

II. CHRONIC PAIN SYNDROMES

 Management of Headaches 151

75 mg, opioids such as tramadol 50–100 mg IM or butorphanol 1–2 mg

IM. Specific antimigraine drugs such as ergotamine, DHE and the trip-
tans are also effective in aborting the acute attack. Antiemetics such as
metoclopramide may also be useful. All the oral triptans appear to be
equally effective. Sumatriptan by nasal spray or by subcutaneous injec-
tion may be faster acting. DHE appears to be less effective. Tramadol,
although frequently used, is not particularly effective. Combinations
such as acetaminophen, aspirin, and caffeine may be useful in mild cases.
Opiate analgesics including nasal butorphanol appear to be more effec-
tive than oral opiates. Corticosteroids IV plus antiemetics are reasonably
effective.

Doses
1. DHE 1 mg IM to be repeated after every 1 h (maximum up to 3 mg).
Nasal spray of DHE (maximum up to 2 mg).
2. Triptans – Drugs of choice due to their safety profile. Sumatripan
is available as injection, tablets and nasal sprays (50–100 mg orally)
zolmitriptan nasal spray (2.5–5 mg).

Preventive Treatment of Migraine

Prophylactic drugs are indicated when patients have three or more
severe migraine attacks a month and symptomatic medication alone is
not satisfactory. Preventive treatment is taken on daily basis, whether or
not the patient is having an attack of migraine. The response to preventive
treatment is unpredictable. Nonpharmacological treatments such as acu-
puncture, relaxation training and biofeedback have also been found to be
effective in select group of patients with migraine. The six main classes of
drugs that may be used as prophylactics are as shown in Box 10.3.

Tension-Type Headache
It is characterized by pain that is mild to moderate in severity, bilat-
eral in distribution, pressing or tightening in quality and not accompanied
with any neurological sign. There is evidence of sustained contraction of
pericranial muscles in majority of patients with tension-type headaches.
Treatment strategies are aimed at treating an acute episode as well as pro-
phylaxis of chronic headache (Box 10.4).

Cluster Headache
Cluster headache is a well-defined neurovascular entity occurring in
both episodic and chronic varieties. The attacks are extremely intense
and of short duration, occur unilaterally and are accompanied by signs of
autonomic dysfunction.

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152 10. HEADACHE

BOX 10.3

CLASSES OF DRUGS USED IN THE

P R E V E N T I V E T R E AT M E N T O F
MIGRAINE

Class/Substance Adverse events

Beta-adrenoceptor antagonists
Propranolol: 80–160 mg/day Bradycardia
Metoprolol: 100–200 mg/day Hypotension
Atenolol: 50–100 mg/day Sleep disturbance
Calcium channel antagonists
Flunarizine: 5–10 mg/day Sedation
Weight gain
Bradycardia
5-Hydroxytryptamine antagonists
Cyproheptadine: 4 mg tablet × 2–4 Nausea
per day Sleep disturbance
Methysergide: 1–2 mg × 1–3 per day Peripheral
Vasoconstriction
Antiepileptics
Sodium valproate: 300–600 mg × 1–3 Nausea, vomiting
per day Tremor
Weight gain/loss
Divalproex sodium 250–1000 mg/day
Topiramate 25–100 mg/day Hepatotoxicity
Thrombocytopenia
Tricyclics
Amitriptyline: 10–100 mg/day (bedtime) Sedation
Dry mouth
Constipation
Urinary retention
Postural hypotension
NSAIDs
Naproxen: 250–500 mg × 1–2 per day Abdominal pain
Nausea
Headache
Tinnitus

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 Management of Headaches 153

BOX 10.4

A C U T E A N D P R E V E N T I V E T R E AT M E N T
A LT E R N AT I V E S I N T E N S I O N - T Y P E
HEADACHE

Attack treatment: First-line alternatives

Analgesics
Aspirin: Effervescent tablet 500–1000 mg × 1–4 per day
Acetaminophen: Effervescent tablet/supp. 500–1000 mg × 1–4 per day
NSAIDs
Naproxen: Tablet/supp. 250–750 mg × 1–2 per day
Diclofenac-K: Tablet/supp. 50–100 mg × 1–2 per day
Ibuprofen: Tablet 400–800 × 1–2 per day
Combinations
Acetaminophen + codeine: Tablet/supp. 500–1000 mg +
30–60 mg × 1–4 per day
Aspirin + caffeine: Tablet 500–1000 mg + 50–100 mg × 1–4 per day

Preventive therapy: First-line alternative

Amitriptyline: Tablet 10–75 mg × 1 per day

The medical treatment includes both acute therapy and prophylactic

therapy (Box 10.5).

Chronic Daily Headache

Many of these patients are rebound-type patients. When treated with
amitriptyline, there is a 30% improvement, but with the withdrawal of
analgesics, 72% improvement. When not treated with amitriptyline and
analgesics were continued, there was an 18% improvement, with analgesics
withdrawn at 43% improvement.

Botulinum Toxin in the Treatment of Headaches

Recently, botulinum toxin has been under intensive clinical investiga-
tion for the treatment of migraine and other types of headaches. Pain relief
conferred by botulinum toxin is probably due to actions beyond those on
neuromuscular transmission, which may help to explain its effectiveness
in headache.

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154 10. HEADACHE

BOX 10.5

AT T A C K A N D P R E V E N T I V E
T R E AT M E N T A LT E R N AT I V E S I N
CLUSTER HEADACHE

Attack treatment
1. F irst-line alternatives
Sumatriptan: Injection 6 mg × 1–3 alternatively
Oxygen (100% O2) inhalation through a facemask, 6–8 L/min for
10–15 min
2. Second-line alternatives (optional for convenience but less effective)
Sumatriptan: Nasal spray 20 mg × 1–3 alternatively
Zolmitriptan: Tablet 5–10 mg × 1–3 or nasal spray 5 mg × 1–3 or
Lidocaine: Spray 10 mg/dose alternatively
Ergotamine: Tablet 1–2 mg × 1–2

Preventive therapy
1. F irst-line alternative
Verapamil: Tablet 360–720 mg/day
Short-term prophylaxis
Prednisolone: Tablet 45–80 mg/day during 3 days, gradually tapered
by 10–20 mg/week.
Ergotamine: Tablet 3–4 mg/day
Long-term prophylaxis
Lithium sulfate: Tablet 42 mg × 2–3 per day
(Therapeutic plasma concentration 0.3–0.8 mmol/L)
2. Second-line alternatives (optional)
Methysergide: Tablet 3–6 mg/day alternatively
Sodium valproate: Tablet 500–1500 mg/day alternatively
Melatonin: Tablet 6–12 mg at bedtime

Dose: 100–150 units of botulinum toxin are injected at multiple fixed

symmetrical pericranial sites (frontalis, temporalis, corrugator and pro-
cerus muscles) (Fig. 10.2). The headache severity, headache frequency and
acute medication usage is significantly reduced within 2 weeks of inject-
ing the toxin. Botulinum toxin has an extremely favourable toxicity and
safety profile (Box 10.6).

II. CHRONIC PAIN SYNDROMES

 Management of Headaches 155

Frontalis
muscle

Procerus
muscle

Corrugator
muscle

FIGURE 10.2 Botulinum toxin injection sites in headache.

BOX 10.6

S E L E C T I O N O F P AT I E N T S F O R
BOTULINUM TOXIN TYPE A THERAPY
FOR HEADACHE
• Patients with disabling primary headaches
• Patients who have failed to respond adequately to conventional
treatments
• Patients with unacceptable side effects (from existing treatment)
• Patients in whom standard preventive treatments are contraindicated
• Patients in special populations or situations (the elderly, those at risk
of unacceptable side effects from trial drugs or traditional treatments,
aeroplane pilots, students studying and preparing for examinations)
• Patients misusing, abusing or overusing medications
• Patients with coexistent jaw, head or neck muscle spasm
• Patients with disabling primary headaches
• Patients who have failed to respond adequately to conventional
treatments

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 C H A P T E R

11
Neck and Shoulder Pain

The neck, shoulder and upper extremity are composed of numerous

pain-sensitive tissues including nerves, vessels, muscles, ligaments, and
joints. Pain may result from irritation, injury, inflammation, or infection
of any of these tissues. Conditions causing pain in this region are those
of neurogenic, musculoskeletal, soft-tissue, referred, and autonomic
origin.
The patient complaining of neck, shoulder and arm pain should be
examined for anatomical location of the pain, derangement of mechanical
structures, and underlying pathological conditions. A careful history and
examination are needed to reach a diagnosis. Laboratory tests and X-rays
may be necessary but may have limited diagnostic value.

COMMON CAUSES OF NECK AND SHOULDER PAIN

Neurogenic pain
Cervical spinal cord compression
Nerve root compression
Neuritis
Peripheral nerve compression
Peripheral neuropathy
Torticollis
Herpetic neuralgia
Cervical myelopathy
Neoplasm
Meningitis
Neuroma
Soft-tissue pain
Acute cervical strain
Myofascial pain
Fibromyalgia

157
158 11. NECK AND SHOULDER PAIN

Referred pain
Cardiac
Neoplasm
Musculoskeletal pain
Degenerative joint disease
Tendinitis and bursitis
Cervical spondylosis
Degenerative disc disease
Rheumatoid arthritis
Fracture
Osteomyelitis
Periarthritis shoulders
Sympathetic pain
Reflex sympathetic dystrophy (CRPS I)
Causalgia (CRPS II)

DIAGNOSIS OF NECK AND SHOULDER PAIN

Keys to diagnosis in most patients are the history and physical exami-
nation. Imaging is rarely necessary unless the patient has myelopathy or a
gait disorder. Clues from the history are based on
  

•  ircumstances and timing of pain onset

C
• Character of pain
• Factors that make the pain better or worse
• Underlying and coexisting disease
• Family history
• Pattern of medication use
  

When taking the history, ask

  

• W hat was your life like before the pain began?

• What is your life like now?
• What is it that you cannot do now but were able to do
before?
• What do you think is causing the pain?
  

The physical examination comprises a musculoskeletal, neurologic and

general physical examination.
Pay special attention to
  

• N ormal landmarks of the neck

• Skin colouration and temperature
• Areas of swelling or tenderness

II. CHRONIC PAIN SYNDROMES

 Diagnosis of Neck and Shoulder Pain 159

• P osture, movement and facial experiences when the patient is sitting,

standing and supine
• Deviations in spinal curvature
• Asymmetry or prominence in scapular borders
• Atrophy
  

In the physical examination, perform

  

• P alpation of the sternocleidomastoid, trapezius, scalenes, and posteri-

orly situated extensor musculature
• Forward and lateral flexion, extension, and rotation
• Spurling test (applying compression to the head in a position of exten-
sion and rotation to each side)
• Distraction tests
• Valsalva manoeuvre (pain with this manoeuvre suggests a herniated
disc or an intraspinal tumour)
  

Investigation: Diagnostic tests may be helpful in differentiating the

causes of neck and arm pain, but a thorough neurological examination
is one of the most important ways of making a diagnosis. To localize
and establish the nature of lesions causing intraspinal compression,
several diagnostic tests may be used. Roentgenographic investigations
are the most useful, but electrophysiological techniques, radioisotope
scanning, and cerebrospinal fluid examination may also be helpful.
Roentgenographic investigation should begin with the suspected
site of spinal cord or root compression. Frontal, lateral, and oblique
views are required for examination of the cervical spine; frontal and
lateral views are generally satisfactory for examination of the thoracic
and lumbosacral spine. Lateral films of the cervical spine in flexion and
extension are needed if subluxation is suspected. In certain situations,
tomography may be necessary to define a bone lesion more precisely.
X-ray films of the cervical spine, especially lateral and oblique views,
are helpful in evaluating spinal abnormalities. Dumbbell-shaped neu-
rofibromas that enlarge the intervertebral foramen are readily apparent
in X-ray films. Congenital anomalies of the vertebral bodies are at times
associated with intraspinal teratomas or lipomas. Bone caries suggest
an infectious pathology. Vertebral bone destruction from infection often
involves the intervertebral disc; conversely, tumour metastases to the ver-
tebral column spare the discs. Degenerative changes in the spine are fre-
quently seen in asymptomatic individuals, but may be normal in patients
with a herniated disc.
Bone scanning after radioisotope injection may be helpful if metastases
are suspected as the cause of bone destruction. However, fractures, infec-
tion, and ankylosing spondylitis may also cause increased radioisotope
uptake.

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160 11. NECK AND SHOULDER PAIN

DIFFERENTIAL DIAGNOSIS OF NECK

AND SHOULDER PAIN

There are several methods to differentiate the cause of neck pain. Some
of the clues to commonly occurring conditions are the following.
Clues to myofacial pain syndromes are
  

• P resence of trigger points

• Underlying trauma, poor posture, ongoing stress on neck muscles,
degenerative joint disease, or emotional stress
  

Clues to osteoarthritis, which is unusual before age 40 years and rarely

involves the neck alone, are
  

•  enderness of the zygapophyseal joint

T
• Capsular cervical spine motion
• Limited extension and side flexion
• Insidious onset
• Unilateral pain and aching
  

Clues to cervical radiculopathy are

  

•  ain in the neck and/or radiating pain in the arm

P
• Restricted neck movement
• Dermatomal and myotomal distribution of neurologic loss
• Positive Spurling test
  

Clues to cervical facet syndrome are

  

•  istory of turning head to side with resultant pain

H
• Loss of motion
• Palpable discomfort in zygapophyseal joint
• Lack of neurologic findings
  

Clues to ankylosing spondylitis are

  

• Gradual onset
• Morning stiffness that improves with activity
• Involvement of neck motion
• Restricted neck motion
• Reduced chest expansion

CERVICAL PAIN OF NEUROGENIC ORIGIN

Neurogenic pain in the neck and upper extremities may commonly be

caused by spinal cord/nerve root compression, myelopathy, postherpetic
neuralgia, neuritis, peripheral nerve compression, and peripheral neuropathy.

II. CHRONIC PAIN SYNDROMES

 Cervical Pain of Neurogenic Origin 161

When cord or nerve root compression produces only pain, localization

by clinical examination alone is difficult. EMG, CT scan, and MRI are often
more accurate. Pain alone in the neck, shoulder, upper arm, scapula, or
interscapular area is nonlocalizing. Most of the lesions in this area involve
C5, C6, C7, and C8 nerve roots. Pain in the posterior aspect of the arm
may be due to C7 root lesion, whereas medial anterior or lateral arm pain
may be due to C6 or C7 nerve root lesion. Hand pain is more accurately
localized to a particular nerve root. Radiating pain in the thumb is usually
due to C6 nerve root compression. Index and middle finger pain is often
caused by C7 nerve root compression, and pain in ring and little fingers is
due to C8 nerve root compression.
Differential diagnosis of neurogenic cervical pain: The most common
causes of cervical nerve compression are
  

1. C
 ervical spondylosis
2. D isc degeneration
3. A  cute disc herniation
  

Radicular pain is a shooting, radiating type of pain that is accompa-

nied by objective neurological signs such as loss of sensation and changes
in the reflex and muscle strength. Radiculopathy itself may be caused by
other aetiologic factors such as primary or secondary malignancy of the
bone, involvement of the nerve root by carcinoma of the lung, and the
degenerative changes of the cervical spine itself. Compression of the spi-
nal cord from a herniated disc may produce symptoms very similar to
those of nerve root compression.
Compression of the spinal cord in the neck may result in cervical
myelopathy, which produces radicular symptoms in the upper extremi-
ties and long tract signs in the lower extremities. Sensory impairment,
muscle weakness, and loss of tendon reflexes may be found in the upper
extremities. In the lower extremities, spastic weakness, hyperreflexia,
clonus, extensor plantar reflexes, and impaired vibratory and position
sense may be observed. Bowel and bladder functions are not usually
impaired.
Pain associated with degenerative disc disease may be local and limit
neck movement. Pain referred to the upper back, shoulders, and upper
extremity suggests that the pathology lies in the intervertebral foramina
and the adjacent tissues.
Diagnosis: The diagnosis is arrived at after a thorough study of his-
tory and neurological examination. The diagnosis of the exact cause of
neck pain is based on CT, MRI, and EMG to confirm the nerve roots
involved.

II. CHRONIC PAIN SYNDROMES

162 11. NECK AND SHOULDER PAIN

MANAGEMENT

A careful history and physical examination are essential for effective

treatment of pain.
Acute disc herniation is managed conservatively (most commonly with
rest) using a soft collar to minimize the movements of the cervical spine.
Keeping the muscles relaxed during the acute stage may be beneficial, and
drugs such as tizanidine and diazepam may be useful during this stage.
NSAIDs, in addition to decreasing the inflammation, are likely to reduce
the pain and swelling. Muscle spasm associated with acute disc herniation
may be reduced by ice massage or spray or a vapocoolant such as ethyl
chloride. Cervical traction could be applied in the hospital or home. Heat
followed by gentle limbering movements of the neck and arm may also
reduce the pain and muscle spasm.
If symptoms persist despite 8–12 weeks of conservative treatment, a
cervical epidural steroid injection should be considered. Inject methyl
prednisolone (Depo-Medrol) 80 mg or triamcinolone 25–50 mg at the level
of the disc herniation.

Technique of Cervical Epidural Block

The cervical epidural block is given either in sitting, prone or lateral
position. A fluoroscopic control is desirable. In the sitting position, flexed
cervical spine results in widening of lower cervical epidural space.
Vasovagal syncope, however, is commonly seen in sitting position.
Improvement is likely to be seen in 24–48 h. If so, give no further epidural
injections; if there is partial or negligible improvement after 10–14 days, give
a second injection of steroid. Lidocaine (2–5 mL of 1%) or bupivacaine (0.25%)
may be injected before or during steroid injection to confirm the correct place-
ment of the drugs in the epidural space. If two injections of steroids placed
epidurally do not produce any improvement, further injections are unlikely
to be useful. There is no rationale for giving a series of injections if the patient
is free of pain after the first injection. If neurological deficits and pain continue
or worsen despite the conservative treatment, surgical treatment is indicated.
The most commonly performed surgery is anterior cervical discectomy.

NECK AND SHOULDER PAIN DUE TO

MYOFASCIAL PAIN SYNDROME

This is a common pain syndrome causing pain in the neck and upper
back. The pain may even radiate to shoulder and arm. Myofascial pain
is always accompanied with the presence of single or multiple trigger
points in neck muscles. The clinical features, diagnosis and management
­protocols are discussed in detail in a separate chapter in this book.

II. CHRONIC PAIN SYNDROMES

 Painful Shoulder 163

PAINFUL SHOULDER

More than 90% of the lesions resulting in painful shoulder are due to
extracapsular soft-tissue lesions. Shoulder joint is a multiaxial joint that
allows greater mobility and is supported by various ligaments and mus-
cles. Majority of painful, nontraumatic conditions about the shoulder joint
are caused by tendonitis of rotator cuff. A good history and clinical exami-
nation gives the diagnosis.
Periarticular conditions affecting the shoulder can be grouped into
those with and without capsulitis. In capsulitis, there is a generalized
restriction of movements, and if the capsule is not involved only active
movements are restricted.

Management Protocol of Painful Shoulder

• N SAIDs
• I ntralesional/articular methyl prednisolone 20–40 mg with 0.25%
bupivacaine 2–3 mL, to be repeated after 1–2 weeks
• Physiotherapy for gentle mobilization of the affected shoulder
  

A condition called ‘frozen shoulder’ with global restriction of active

and passive movements in all planes may be associated with diabetes,
thyroid disease and pulmonary disorders. These patients may develop a
secondary sympathetic dystrophy, ‘shoulder hand syndrome’, which con-
sists of a frozen shoulder with painful, swollen, cold and dystrophic look-
ing hand. Patients exhibiting features of sympathetic dystrophy should
be administered repeated stellate ganglion blocks with 0.25% bupivacaine
(10 mL) for an early relief of symptoms.

Physical Therapy in Neck and Shoulder Pain

Physical therapy depends on past medical interventions, the
extent of the pathology causing pain, and the stage of recovery. Dur-
ing the acute stage, the patient may be treated with bed rest and
immobilization only. No active form of physical therapy is advisable at
this stage. ­Transcutaneous electrical nerve stimulation may be used at
this stage.
In the subacute stage of the pain state, the patient should begin an
exercise program suited to the level of the existing pain and based on the
pathology causing pain. Aggressive physical therapy begins in the chronic
phase of the disease. Immobilization such as cervical collar at this stage will
promote poor posture, increased muscle weakness and lead to tightening
of soft-tissue structures and should therefore be avoided at all costs. The
therapy techniques commonly advised by us include flexion–extension,
strengthening, and gradual mobilization.

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 C H A P T E R

12
Back Pain

Back pain is an extremely common medical entity and the most com-
mon cause of disability in population younger than 45 years. Studies
have shown that about 80% of the population will suffer low backache
of moderate to severe intensity at some part during their lifetime. It is
a major cause of work absenteeism with significant emotional, physical
and economic ramifications. Fortunately, majority of cases of backache
resolve in 6 weeks with or without treatment. Up to 85% of patients
cannot be given a definite diagnosis because back pain is a symptom
rather than a disease.
The differential diagnosis of back pain is extensive, physical findings
may vary from one examination to the next and investigations are incon-
clusive quite often. It has been surmised that musculoskeletal structures of
the back are rarely the sole cause of back pain; therefore, a thorough and
systematic examination is always indicated.
The goal of pain management therapy in back pain is to reduce the
pain to the extent that the patient is able to cooperate with corrective/
restorative therapy.

COMMON CAUSES OF THORACOLUMBAR PAIN

1.  yofascial lower back pain

M
2. HNP of lumbar spine
3. HNP of thoracic spine
4. Spinal canal stenosis
5. Lumbar spondylolysis
6. Spondylolisthesis
7. Facet syndrome
8. Adult kyphosis and scoliosis
9. Infective pathology of spine, e.g. tuberculosis and osteomyelitis
10. Primary neoplasms of the neural tissues and multiple myeloma
11. Metastatic disease of spine

165
166 12. BACK PAIN

12. R heumatic conditions, e.g. ankylosing spondylitis and fibromyalgia

13. Metabolic causes of back pain
14. FBSS
  

The salient clinical symptoms and signs in some of the common condi-
tions enumerated above are as follows:
1. M
 yofascial lower back pain
a. Nonradiating back pain
b. No clear aetiology
c. Pain referred in a nondermatomal pattern
d. Examination reveals localized tenderness and limitation of
movement (due to pain)
e. Responds to physical therapy
f. No positive diagnostic tests
2. H
 NP of the lumbar spine
a. Displacement of central area of the disc (nucleus) resulting in
impingement of a nerve root
b. Most commonly involves L4–5 disc (L5 nerve root)
c. Symptoms of radicular leg pain present; may or may not have back
pain
d. Signs of motor weakness
– L4 – tibialis anterior weakness
– L5 – EHL weakness
e. Asymmetric reflexes
– Knee jerk (L4)
– Ankle jerk (S1)
f. Patient presents with pain along nerve root distribution (see Fig. 12.1)

FIGURE 12.1 Straight leg raising test.

II. CHRONIC PAIN SYNDROMES

 Common Causes of Thoracolumbar Pain 167

g. S igns of nerve root impingement (tension signs) are positive

– SLRT
– Lasègue manoeuvre
– Crossed leg raise test
– Bowstring signs
– Femoral stretch test
h. Diagnostic tests
– MRI
– EMG
– Nerve conduction studies
– Epidurography (as part of advanced pain management
techniques)
3. H
 NP of thoracic spine
a. Less common than lumbar
b. Mostly involves lower thoracic discs
c. Patient presents with thoracic back pain with or without
circumferential radiating pain around thorax
d. Pain exacerbated by sneezing or coughing
e. Sensory distribution in trapped dermatomal area
f. Diagnostic tests same as for lumbar HNP
4. S
 pinal canal stenosis
a. Involves narrowing of the spinal canal (central stenosis) or neural
(intervertebral) foramen
b. Congenital/acquired (narrowing of the spinal canal from facet joint
hypertrophy or hypertrophy of supporting soft tissues)
c. Presents with insidious pain and paresthesias
d. Diagnosis based on symptoms of neurogenic claudication and CT
and MRI findings
e. Lateral recess stenosis (intervertebral foramen stenosis)
– Commonly due to bony spurs (osteophytes)
– Presents with feature of HNP
– May not respond to conservative management
f. Farout syndrome
– Extraforaminal lateral root compression of L5 root between L5
transverse process and sacral ala
5. Spondylolysis
a. Represents a defect in the pars interarticularis
b. Common cause of back pain in adolescents
c. Precipitated by repeated hyperextension activities (e.g. gymnasts)
d. Diagnosed by X-rays and bone scan
e. CT scan that shows a ‘collar’, i.e. break in the neck of the ‘Scottie dog’
f. Responds to activity restriction, stretching, exercise and bracing

II. CHRONIC PAIN SYNDROMES

168 12. BACK PAIN

6. Spondylolisthesis
a. Forward displacement of one vertebra over the other
b. Severity of slip
– Grade I: 0–25%
– Grade II: 25–50%
– Grade III: 50–75%
– Grade IV: 75–100%
– Grade V: >100%
7. Facet syndrome
a. Inflammation/degeneration of facet joints on MRI
b. Lower back pain becomes worse with extension
c. May have referred pain to buttock and posterior thigh
8. A
 dult scoliosis and kyphosis
a. Presents with progressively increasing back pain and deformity
b. May respond to symptomatic treatment initially
c. May need surgical correction later for cosmetic purpose and
intractable pain due to mechanical compression

THORACOLUMBAR SPINE: ANATOMICAL

CONSIDERATIONS

In normal posture, the anterior vertebral column carries most of the weight
of the low back, and the discs absorb shocks and allow flexion yet limit motion.
The discs comprise one-third of the height of the lumbar vertebral column
and one-fifth in the thoracic region. These discs are composed of viscous gel-
like centre of mucopolysaccharides surrounded by a tough annulus fibrosis.
The thinnest part of the annulus is posterior, which may explain herniation in
that direction with sudden uneven loads on the spine. Also, with increasing
age, discs become less resilient and lose the ability to distribute mechanical
forces evenly. The posterior longitudinal ligament narrows from L2 to L3 and
is thus a poor barrier to prevent posterolateral disc herniation. It is thus not
surprising that maximum disc herniations occur in L4–L5 or L5–S1 regions.
In the cervical region, nerve roots exit the foramina above the corre-
sponding vertebra; the thoracic lumbar and sacral nerve roots exit below
the corresponding vertebra. Therefore, when the L4–L5 disc herniates, it
compresses the S1 nerve root. It is important to remember that only 1–2%
of the patients with back pain have herniated discs.
The posterior structures of the spine include lamina, pedicles, and facet
joints, which together encircle and protect the spinal cord and the emerging
nerve roots.
The posterior elements restrict the range of movements and anchor mus-
cles, ligaments, and tendons. The intervertebral foramina are formed by ped-
icles and apposing articular surfaces of the facet joints. The nerve roots fill

II. CHRONIC PAIN SYNDROMES

 Thoracolumbar Spine: Anatomical Considerations 169

35–50% of the foramina. The facet joint is innervated by articular filaments

from the medial branch of the posterior primary division of the spinal nerve
at and from the level above the joint (may occasionally be from three levels).

Differential Diagnosis of Back Pain

Differential diagnosis of common thoracolumbar spine complaints
1. B
 ack pain with no radiation of pain
a. Musculoskeletal lower back pain
b. Spondylolysis
c. Facet syndrome
d. Adult scoliosis
e. Adult kyphosis
f. Spondylolisthesis
g. Infections
h. Tumours
i. Fractures
j. Dislocations
k. Arthritis
l. Rheumatologic conditions
m. Referred pain from viscera
2. B
 ack pain with radicular lower extremity pain or weakness
a. HNP
b. Spinal stenosis
c. Fractures
d. Dislocation
e. Cauda equina syndrome

Examination of a Patient with Back Pain

• O
 bservation
• Skin
• Redness, skin markings, unusual stain and patches
• Posture
• Curves of the spine
• P
 alpation
• Spinous processes
• Coccyx
• Sacral promontory
• Iliac crest
• Posterior superior iliac spine
• Ischial tuberosities
• S
 oft tissue
• Paraspinal muscle spasm

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170 12. BACK PAIN

• S ciatic nerve (tenderness along its route)

• Psoas muscle
• M
 ovements of the spine
• Flexion (normal – can bend over to touch the toes)
• Extension (normal – 30–40°)
• Lateral bending (normal – 30° to each side)
• Rotation (symmetric)
• R
 eflexes
• L4 – knee jerk
• S1 – ankle jerk
• S2–4 – bulbocavernosus reflex
• M
 otor power
• Iliopsoas – hip flexion (T12–L3)
• Quadriceps – knee extension hip adduction (L2–L4)
• Tibialis anterior – ankle dorsiflexion and inversion (L4)
• Extensor hallucis longus – great toe extension (L5)
• Gluteus maximus – hip abduction (L5)
• Bowel/bladder – (S2–S4)
• T
 ests for nerve compression
• SLRT
– Passive lifting of leg reproduces radicular symptoms especially
of lower lumbar nerve roots L4, L5, and S1
– A positive SLR is defined as one that reproduces sciatica between
30 and 70° of leg elevation
• Lasègue test dorsiflexion of foot during straight leg raising worsens
the symptoms (Fig. 12.2)
• Crossed SLR (Fajersztajn test)
  

FIGURE 12.2 Lasègue test.

II. CHRONIC PAIN SYNDROMES

 Thoracolumbar Spine: Anatomical Considerations 171

Raising the contralateral leg can cause symptoms in affected leg when
there is central disc herniation. This test is highly specific for indicating
symptomatic disc herniation.
• Femoral stretch test
  

This is useful for testing the entrapment of upper lumbar nerve roots
(mostly L2 and L3). With the patient in a complete prone position, with
the hip off the table the knees are flexed as the legs are stretched towards
buttocks. Pain on the front thigh may indicate a femoral nerve problem.
• K
 ernig test: With the patient in a supine position, the thigh is flexed
to 90° and the knee is flexed 90° to the thigh. A positive Kernig test
causes leg pain as a result of nerve root irritation

Tests for Sacroiliac Joint Evaluation

Pathology of the SI joint is relatively uncommon. Tenderness on palpa-
tion of the SI joint does not necessarily signify SI joint dysfunction. The
tests for SI joint disease should be interpreted with care, as their sensitivi-
ties are moderate at best.

Pelvic Rock Test

With the patient lying supine on the table, the examiner should place
both hands on the superior anterior iliac spine and compress the pelvis
towards the midline. Pain can be produced in the SI joint if there is local-
ized pathology.

Gaenslen Test
The patient is supine with the left leg beyond the edge of the table. The
examiner flexes the patient's right knee and hip and presses downwards
over the left thigh to hyperextend the left hip. Pain is present on the left
SI joint in the presence of SI joint dysfunction. The manoeuvre is repeated
on the right side with the right leg by hanging over the edge on the table.

Patrick Test
The patient lies supine on the table and places the foot of the painful
side on the opposite knee. The examiner can stress the SI joint by plac-
ing one hand on the flexed knee joint and the other hand on the anterior
superior iliac spine of the opposite side. This test is also called the FABER
test, as it designates flexion, abduction, and external rotation of involved
SI joint or hip. This test is used to detect pathology in the SI joint as well
as in the hip.

II. CHRONIC PAIN SYNDROMES

172 12. BACK PAIN

Extension Test
The patient is prone and the examiner places one hand under the thigh
above the knee on the affected side. With the other hand, the examiner
presses downwards over the crest of the ileum to elicit the pain in the SI joint.

Investigations
1.  -ray of the thoracolumbosacral spine
X
2. CT scan
3. MRI
4. Discography (provocative)
5. Epidurography
6. Triphasic bone scan
7. Nerve conduction velocity (NCV)
8. EMG
9. Human leucocyte antigen typing, where indicated
10. Appropriate blood investigations for underlying medical conditions
enumerated above

TREATMENT PLAN FOR THORACOLUMBAR

BACKACHE

When a patient reports with an acute attack of back pain he or she should
be evaluated thoroughly both systemic and locoregional for specific joint or
disc pathology, and appropriate investigations ordered (blood and radiology).
In the acute phase, bed rest with analgesics, muscle relaxants and sedatives
is advised for a period of 7 days. Pain becomes chronic when it lasts for more
than 4 weeks. Treatment goals for chronic pain are different from those for
acute pain. There may be structural reasons such as soft-tissue scarring, nerve
root fibrosis, or bony derangement, which do not allow complete recovery.
Therefore, realistic goals for chronic pain management include the
following.
1. D ecrease the frequency and intensity of pain (with medications, nerve
blocks, surgery, stimulation techniques).
2. Improve coping mechanisms to tackle residual pain (psychological
strategies).
3. Optimize functional capacity of the patient.

PHARMACOLOGICAL THERAPY

Pharmacotherapy forms an important part of the multimodal therapy that

is essential for tackling chronic low backache. Detailed pharmacology with

II. CHRONIC PAIN SYNDROMES

 Pharmacological Therapy 173

respect to appropriate drugs is discussed in the relevant section. Here, we

will only outline the pharmacotherapeutic protocol for chronic low backache.
If the pain is predominantly of inflammatory origin in the musculo-
skeletal system, then NSAIDs are advocated. They should be combined
with indirect acting muscle relaxants (cyclobenzaprine, methocarbamol,
tizanidine and baclofen) for short periods. One should be aware of their
sedative effects, which may become additive when used with drugs hav-
ing similar side effects.
Oral narcotics such as tramadol and codeine should be used in the set-
ting of moderate to severe pain unresponsive to NSAIDs.
TCAs and anticonvulsants are useful adjuncts to pharmacotherapy
where neuralgic symptoms are predominant.

Epidural Steroids
Mechanism of Action of Epidural Steroids
Steroids relieve pain by reducing inflammation and by blocking trans-
mission of nociceptive C fibre input. They decrease inflammation by
inhibiting the action of phospholipase A2 (released from the injured disc),
which induces membrane injury and oedema by release of arachadonic
acid. This is the rate-limiting step in the production of prostaglandins and
leukotrienes, which sensitize small neurons and enhance pain generation.
Steroids also produce analgesia by blocking transmission of nociceptive
output. They also prevent the development of ectopic neural discharge foci.

Effectiveness of Epidural Steroid Injections in Different Causes of Back Pain

Causes of back pain Effect of epidural steroid injection
1. Anulus tear Hastens recovery
2. Chronic lumbar degenerative disc Transient relief
disease
3. HNP without neurological deficit Transient relief
4. HNP with nerve root irritation Therapeutic
5. HNP with nerve root compression Therapeutic
6. Spondylolisthesis Therapeutic if there is nerve root irritation
7. Facet arthropathy Injections into the joint are therapeutic
8. Scoliosis Relief if nerve entrapment is present
9. Ankylosing spondylitis Ineffective
10. Spinal stenosis Transient relief
11. Functional low backache Ineffective

Success Rate of Epidural Steroids in Relation to Duration of Symptoms

Duration of symptoms (months) Success rate (%)
<3 83–100
3–6 67–81
6–12 44–69
>12 46–58

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174 12. BACK PAIN

Controversies Regarding Epidural Steroids

1. M
 ethyl prednisolone or triamcinolone?
There has been no study to directly compare the two drugs and they
both seem to be equally effective. Toxicity of polyethylene glycol (preser-
vative in methyl prednisolone) has been noted at concentrations beyond
40% in experimental models. Most commercial preparations contain only
2–3% polyethylene glycol.
  

2. H
 ow soon do you get a positive response?
Most patients take several days to respond (2–7 days). It is therefore
advisable to wait for 1 week before planning further injections.
  

3. W
 here does one ideally site the epidural injection and do large
volumes help?
Although there have been studies indicating that both epidural and
caudal routes to deposit the steroid are equally efficacious, it is recom-
mended to select the interspace corresponding to the radicular symp-
toms. A volume of 8–10 mL is recommended; however, larger volumes are
needed if the caudal route is chosen.
  

4. I s it normal to have discomfort after an epidural injection?

Symptoms may vary from mild heaviness to an exacerbation of symp-
toms for 2–3 days.
  

5. W
 hat is the ideal number for therapeutic epidural injections?
There has been little evidence in the literature to indicate that more than
three injections improve the clinical benefit of this therapy. A minimum
of three injections at intervals of 3–4 weeks is recommended for a better
overall success rate.
  

6. C
 an you add local anaesthetic to the steroid solution?
No clinical advantage has been reported by adding local anaesthetic
to epidural injection, although in dural sleeve foraminal injections local
anaesthetic can be used to diagnose correct needle placement.
  

7. I s fluoroscopic guidance a must for this procedure?

As far as possible, the procedure must be carried out under fluoro-
scopic guidance. Various studies have reported only 30–75% correct
needle placement in blind techniques. Adhesions, especially in the ‘failed
backs’, make it imperative that the procedure be done under fluoroscopy
for optimal results.

Injection Technique and Protocol

Get the standard armamentarium for epidural injection ready. It
should include 18 or 20 gauge Touhy needle, a well-lubricated glass

II. CHRONIC PAIN SYNDROMES

 Pharmacological Therapy 175

syringe or a commercially available LOR syringe, local anaesthetic for

the skin wheal, noniodinated contrast, 80 mg methyl prednisolone or
60 mg triamcinolone, 1500 units of hyalase and 20 mL saline for injection.
The patient is placed in a prone position with a pillow under the hips to
minimize the lumbar curve. The appropriate space is selected by the ‘no
touch technique’ fluoroscopically – the point of entry should correspond to
a point just distal to the spinous process of the upper vertebra of the selected
interspace. After a skin wheal, the Touhy needle is advanced perpendicular
to the skin till the typical LOR of the epidural space is appreciated. Then,
2–5 mL of contrast is injected to confirm the space and for a diagnostic epi-
durography (Photograph 12.1). Epidurography would give us information
about the degree of bilateral spread and the presence of adhesions (appear
as filling defects).
Once the space is confirmed, the steroid with hyalase is deposited. In
the presence of adhesions, special spring-loaded catheters (Racz catheters
Epimed Inc USA) are threaded to negotiate the adhesions and percuta-
neous saline adhesionolysis is done. If an epiduroscope is available, the
patient can be posted for epiduroscopic removal of adhesion bands.
Our institutional protocol for epidural steroids is as follows:
1. First appointment
Epidurography performed; interspace selected according to clinical
presentation coupled with MRI findings
a. Note the epidurography findings – pattern of spread of the dye
b. About 80 mg methyl prednisolone + 1500 units hyalase deposited
epidurally (10 mL volume, saline diluent) after negative aspiration
for blood and CSF
c. If foraminal block is detected, combine transforaminal injection at
the appropriate level in the same sitting (Photograph 12.2)

PHOTOGRAPH 12.1 Epidurogram showing good bilateral spread of contrast.

II. CHRONIC PAIN SYNDROMES

176 12. BACK PAIN

PHOTOGRAPH 12.2 Transforaminal injection showing delineation of the nerve root.

d. I f adhesions are detected, insert epidural catheter for percutaneous

saline neuroplasty
2. R
 eview in OPD (Outpatient department) after a week. Continue with
oral medications prescribed; avoid rigorous exercise
a. If the patient is a responder, i.e. has at least 20% relief in symptoms,
post for a second injection between 2 and 4 weeks and a third after
8–12 weeks from the first injection.
b. If the patient is not a responder, i.e. no relief, reassess, consider a
repeat injection at the earliest; if the patient still does not respond,
consider other modalities

Complications
1. Unintentional dural puncture and its consequences
2. Epidural haematoma
3. Neurotoxicity of methyl prednisolone is a theoretical possibility
4. Steroid-induced arachnoiditis
5. Aseptic meningitis
6. Epidural abscess
7. Systemic effects of steroids – iatrogenic Cushing syndrome and adrenal
suppression. Difficulty in controlling blood sugar of diabetic patients

II. CHRONIC PAIN SYNDROMES

 Failed Back Surgery Syndrome 177

SI Joint Pain and Injection Techniques

The SI joint is a synovial joint that is more mobile in youth than in later
life. The upper two-thirds of the joint becomes fibrotic in adulthood. Liga-
ments and muscle attachments help maintain stability of the pelvic ring.
Further motion is limited by the irregular shape of joint articulation, in
which the ridges and grooves increase resistance friction. Prolonged load-
ing (standing or sitting for long periods) and alterations of sacral base (leg
asymmetry or ligamentous injury) are associated with joint hypermobility
and resultant low backache.
SI joint is also commonly involved with tubercular infections and this
must be ruled out in any patient with history of fever, local tenderness and
loss of appetite. Joint effusion and pain is also commonly seen in rheuma-
tological conditions such as ankylosing spondylitis. Relevant laboratory
investigations can clinch the diagnosis.
Treatment of nonspecific inflammatory conditions of SI joint causing
pain includes physical therapy, stabilization of joint, local heat or ultrason-
ics and anti-inflammatory medications.
The SI joint is densely innervated by several levels of spinal nerves
(L3–S1) and may produce lumbar disc-like symptoms when stimulated.
SI pain is usually located in the gluteus and referred to the groin, hip,
anterior thigh and calf. The pain is more intense in the morning and remits
during the day. Pressure on the joint elicits pain. Specific tests for the SI
have been described earlier in the text.

SI Joint Injection Procedure

The patient lies prone. The fluoroscope is started in the PA view and
rotated towards the oblique view till a clear view of the SI joint is obtained.
The image must show the entire joint for needle entry at the most inferior
aspect. The scope is angled in such a way that the anterior and posterior
aspects of the joint appear to overlap. Injection of contrast spreads the dye
throughout the joint in an inferior to superior fashion (Photograph 12.3).
Once needle position is confirmed, 40 mg of methyl prednisolone + 500
units of hyalase is injected twice weekly for five sittings.
SI joint RF denervation can also be done. Multiple lesions along the
entire posterior joint line must be attempted for good results. The facets
and dorsal root ganglia of S1–3 must be lesioned to complete the therapy.

FAILED BACK SURGERY SYNDROME

FBSS refers to persistent or recurrent chronic pain after one or more sur-
gical procedures on the lumbosacral spine. FBSS refers to both persistence

II. CHRONIC PAIN SYNDROMES

178 12. BACK PAIN

PHOTOGRAPH 12.3 Sacroiliac joint injection.

of back pain and occurrence of a different type of pain following surgery.

It does not necessarily imply failure of treatment or surgery but only a
functional failure of the back. In terms of time duration, it would be rea-
sonable to describe this syndrome if the pain persists or occurs 8–12 weeks
following the surgical procedure. The prevalence of FBSS is in a range of
10–40% of lumbar spine operations.

Aetiology of FBSS
1.  erve injury causing neuropathic pain
N
2. Unrecognized lateral recess stenosis or lateral disc herniation
3. Inappropriate patient selection
4. Postsurgical arachnoid fibrosis or arachnoiditis
5. Extensive fusion causing abnormal position and pain
6. Segmental instability due to generous laminectomy
  

CT and MRI may reveal the causative factor, although few patients may
require detailed neurological evaluation including EMG, NCV, etc. Epi-
durography and CT myelography is helpful in refractory FBSS patients.

Treatment Options in FBSS

FBSS patients are commonly referred to a pain clinic for detailed evalu-
ation and treatment. The pain clinician has to treat these patients skillfully
and with compassion. FBSS can be a difficult and frustrating condition to
treat. Multiple treatments and interventions result in psychosocial prob-
lems thus aggravating pain and suffering. The treatment modalities include

II. CHRONIC PAIN SYNDROMES

 Percutaneous Epidural Adhesionolysis 179

1. R ehabilitation and medical management

2. Anticonvulsants such as gabapentin in patients with neuropathic pain
3. Antidepressant drugs such as serotonin-specific reuptake inhibitor
(fluoxetine) and TCA (amitriptyline)
4. Percutaneous fluoroscopic procedures such as epidural adhesionolysis
5. RF denervation of facet joints, DRG lesioning
6. Neuromodulatory techniques such as spinal cord stimulation and
intrathecal morphine delivery systems

PERCUTANEOUS EPIDURAL ADHESIONOLYSIS

The most common cause of FBSS is epidural fibrosis and adhesions.

Postsurgical bleeding and the associated healing process frequently pro-
duce scarring. Epidural adhesions alone do not cause pain. The associated
irritation or inducement of epidural venous engorgement may contrib-
ute to pain production. Whether by the direct mechanical encasement of
nerve roots within scar tissue or the secondary process of epidural venous
congestion with increasing nerve root oedema, pain is produced by move-
ment of the swollen inflamed nerve root.
MRI can be used to detect epidural fibrosis, but it is not a perfect
test. It has been documented that myelography, CT, and MRI have been
unsuccessful.
Technique of epidural adhesionolysis: The ideal epidural catheter used
for adhesionolysis is a stainless steel, fluoropolymer-coated, spiral-tipped
catheter. Such a catheter is passed through the needle into the scar tissue
by the caudal epidural route. The bevel of the needle should face the ven-
trolateral aspect of the caudal canal on the affected side. This facilitates
passage of the catheter to the desired side and decreases the chance of
shearing the catheter. Because scar formation is usually uneven, multiple
passes may be necessary to place the catheter into the scarred area. For
this reason, it is best to use a 16 gauge epidural needle, which has been
specially designed to allow multiple passes of the catheter. To facilitate
steering of the catheter into the desired location, a 15° bend is placed at
its distal end. After final placement of the catheter and negative aspira-
tion, 5–10 mL of contrast medium is injected through the catheter. This
dye should spread into the area of the previous filling defect and out-
line the targeted nerve root. Then, 1500 units of hyaluronidase in 10 mL of
preservative-free saline is injected rapidly. After negative aspiration, 10 mL
of 0.125% bupivacaine and 40 mg of triamcinolone/methyl prednisolone
are injected through the 0.2 micron bacteriostatic filter; the steroid must be
injected before the in-line filter is installed.
When the procedure is completed, the catheter should be secured to
the skin with 2-0 nylon on a cutting needle. Caution must be exercised to

II. CHRONIC PAIN SYNDROMES

180 12. BACK PAIN

avoid puncturing the catheter with the needle or cutting the catheter coating
while wrapping it.
The catheter is left in place for 3 days. On the second and third days, it
is injected once a day with 10 mL of 0.125% bupivacaine with low dose of
methyl prednisolone after negative aspiration from the catheter. Fifteen
minutes later, 10 mL of 10% saline is infused over 20 min.
The procedure is usually followed by significant improvement in pain
and motor function. As pain is relieved, it is important to initiate aggres-
sive physical therapy to improve muscle strength and tone, which are
usually reduced by disease secondary to pain. Often, it is not possible to
lyse existing epidural adhesions completely because of the extensive scar
tissue. If necessary, we repeat the procedure after 6–8 weeks. Because of
the steroids, a 1- to 2- month delay between procedures is necessary, dur-
ing which time the patient should be encouraged to continue intensive
physical therapy.
Clearly, lysis of adhesions in the epidural space is a procedure that
must be used after simpler procedures, such as rest, nonsteroidal anti-
inflammatory medications, muscle relaxants, physical therapy, activity
programs, two or three single shots of epidural steroid, and transcutane-
ous electrical nerve stimulation. Better informed patients will opt for pro-
cedures such as lysis of adhesions rather than surgery. The results clearly
show a dramatic decline in the need for complete avoidance of surgical
intervention in appropriately selected patients with clearly documented
herniated discs and nerve root compression.
The technique described above overcomes the obstacle of being able to
get the medication to a lesion-specific site by placing the tip of a soft spring
catheter within the scar and letting the injected fluid under pressure find
the path of least resistance within the scar and open up the perineural
space. Thus, steroid can reach the inflamed, angry nerve root and produce
its anti-inflammatory effect.
The addition of hyaluronidase has resulted in threefold reduction of
outright failures in our patients, and this needs to be investigated further
to determine whether we are looking at a volume or if the addition of
hyaluronidase really makes the difference.

II. CHRONIC PAIN SYNDROMES

 C H A P T E R

13
Facetogenic Pain

Chronic LBP affects almost 60–80% of the adult population sometime

in their lives, leading to considerable loss of working man-hours and pro-
ductivity. The most common anatomical structures implicated as possible
sources of chronic LBP are the lumbar facet joints, discs, nerve roots, verte-
bral body and the sacroiliac joints. Contrary to the commonly held belief,
disc herniation contributes to only a small fraction of chronic LBP. A major
source of frustration for clinicians has been the fact that no reliable means
exist to document the exact aetiological diagnosis on the basis of signs and
symptoms, clinical examination or imaging alone or in combination. Since
clinical signs and imaging abnormalities do not correlate with symptoms
of LBP in many cases, patients do not receive a specific diagnosis and con-
tinue to suffer.
Various minimally invasive techniques have been developed to diag-
nose the origin of this pain and attempt to treat it more precisely. In two
large studies employing precision diagnostic injections to locate the cause
of LBP, the source of pain was facet joint(s) in as many as 24–40%, disc
herniation and nerve root irritation in 13–20%, discogenic pain in 26% and
sacroiliac joint pain in 4–6%. In 13–19% patients, the cause of pain still
remained elusive. In cases of postlaminectomy pain syndrome, also called
failed back surgery syndrome, the nonsurgical causes outnumber the surgi-
cal causes with facetal arthropathy noted in as many as 32% and epidural
fibrosis in 45% of cases.
Face syndrome is not a new entity. As early as 1933, Ghormley
described facet joint-mediated pain and also described the facet syn-
drome. Unfortunately, with the advent and increasing popularity of
surgeries for herniated discs, facet syndrome as an entity was largely
ignored.
The facet joints are a pair of joints in the posterior aspect of the spine.
Although these joints are most commonly called the facet joints, they are
more properly termed the zygapophyseal joints (abbreviated as Z-joints),
a term derived from the Greek roots zygos, meaning yoke or bridge, and

181
182 13. FACETOGENIC PAIN

physis, meaning outgrowth. The term facet joint is a misnomer because

the joint occurs between adjoining zygapophyseal processes, rather than
facets, which are the articular cartilage lining small joints in the body
(e.g. phalanges, costotransverse and costovertebral joints). This joint is
also sometimes referred to as the apophyseal joint or the posterior interver-
tebral joint. As is true of any synovial joint, the facet joint is a potential
source of pain. In fact, the facet joint is one of the most common sources
of LBP.

FUNCTIONAL ANATOMY OF FACET JOINTS

The spine is composed of a series of functional units. Each unit consists

of an anterior segment, which is made up of two adjacent vertebral bod-
ies and the intervertebral disc between them, and the posterior segment,
which consists of the laminae and their processes. One joint is formed
between the two vertebral bodies, whereas the other two joints, known
as the facet joints, are formed by the articulation of the superior articular
processes of one vertebra with the inferior articular processes of the verte-
bra above. Thus, the facet joints are part of an interdependent functional
spinal unit consisting of the disc–vertebral body joint and the two facet
joints, with the facet joints paired along the entire posterolateral vertebral
column.
Facet joints are well innervated by the medial branches of the dorsal
rami. In the thoracic and lumbar spine, the facet joints are innervated by
medial branches of the dorsal rami of the spinal nerves except at L5 level.
After the medial branch splits off from the dorsal ramus, it courses cau-
dally around the base of the superior articular process of the level below
towards that level's Z-joint (e.g. the L2 medial branch wraps around
the L3 superior articular process to approach the L2–L3 facet joint). The
medial branch then continues in a groove between the superior articular
process and transverse process (or, in the case of the L5 medial branch,
between the superior articular process of S1 and the sacral ala of S1, which
is the homologous structure to the transverse processes of the lumbar ver-
tebrae). As it makes this course, the medial branch is held in place by a
ligament joining the superior articular process and the transverse process,
termed the mamillo-accessory ligament.
The superior and inferior articular processes of adjacent vertebral lami-
nae form the facet or zygapophyseal joints. These are paired diarthrodial
synovial with a joint space, hyaline cartilage surfaces, a synovial mem-
brane, and a fibrous capsule. The facet joint is innervated by branches of
the dorsal ramus, which arise in the intervertebral foramen, run superior to
the transverse process and then travel medially to reach the base of the
facet joint. A deep branch of the dorsal ramus loops under the transverse

II. CHRONIC PAIN SYNDROMES

 Diagnosis of Facetogenic Pain 183

process and supplies the joint capsule of its superior articular face.
Another more lateral branch of the same dorsal ramus is directed cau-
dally and sends a branch to the joint capsule of the inferior articular facet.
A single lumbar spinal nerve, therefore, supplies two facet joints, and each
facet joint has bisegmental innervation. Facet joints are motion-restricting
joints and have a prominent role in resisting the intervertebral compres-
sive force in extension and protecting the intervertebral disc during
rotation movements.

PATHOPHYSIOLOGY OF FACET ARTHROPATHY/

FACETOGENIC PAIN

As with any synovial joint, degeneration, inflammation and injury of

facet joints can lead to pain upon joint motion. Pain leads to restriction of
motion, which eventually leads to overall physical deconditioning. Irrita-
tion of the facet joint innervation in itself also leads to secondary muscle
spasm. It has been assumed that degeneration of the disc would lead to
associated facet joint degeneration and subsequent spinal pain. These
assumptions were based on the pathogenesis of degenerative cascade in
the context of a three-joint complex that involves the articulation between
two vertebrae consisting of the intervertebral disc and adjacent facet
joints, as changes within each member of this joint complex will result in
changes in others.
The facet joint is a common pain generator in the lower back. The two
common mechanisms for this generation of pain are either (1) direct,
from an arthritic process within the joint itself, or (2) indirect, in which
overgrowth of the joint (e.g. facet joint hypertrophy or a synovial cyst)
impinges on nearby structures.
The facet joints are diarthrodial joints with a synovial lining, the sur-
faces of which are covered with hyaline cartilage, which is susceptible to
arthritic changes and arthropathies. Repetitive stress and osteoarthritic
changes to the facet joint can lead to zygapophyseal hypertrophy. Like any
synovial joint, degeneration, inflammation, and injury can lead to pain
with joint motion, causing restriction of motion secondary to pain and,
thus, deconditioning. In addition, facet joint arthrosis, particularly trophic
changes of the superior articular process, can progress to narrowing of the
neural foramen.

DIAGNOSIS OF FACETOGENIC PAIN

Unfortunately, there are no definite clinical findings to diagnose facet

syndrome and very often facet syndrome is used as a ‘dustbin diagnosis’

II. CHRONIC PAIN SYNDROMES

184 13. FACETOGENIC PAIN

when nothing else fits. However, some clinical features commonly associ-
ated with facetal arthropathy are
  

1. D eep-seated, aching pain that is usually localized to a unilateral or

bilateral paravertebral region
2. Pain that is worse in the morning, aggravated by rest and
hyperextension, and relieved by repeated motion
3. Diffuse referred pain over the buttock and sometimes posterolateral
thigh (pseudoradicular pain)
4. Exacerbation of pain by twisting the back, by stretching, by lateral
bending, and in the presence of a torsional load
5. There is absence of exacerbation with a Valsalva manoeuvre
6. Focal tenderness elicited by digital pressure over facet joint
7. Absence of root pain or neurological deficit
  

Imaging is not reliable for diagnosis since radiographic, CT and MRI

changes of osteoarthritis have been shown to be equally common in
patients with and without LBP. The results of most studies fail to show
a correlation between radiologic imaging findings and facet joint pain,
although some studies report severely degenerated joints as being more
likely to be symptomatic and also more likely to respond to facet joint
interventions. Therefore, controlled diagnostic blocks with two local
anaesthetics (or placebo-controlled) are the only means of confirming the
diagnosis of facet joint pain.

CLINICAL EXAMINATION AND PATIENT SELECTION

Meticulous patient selection is an important factor in achieving a suc-

cessful response to interventional techniques. The following are the main
indications for facet joint interventions:
  

1. C hronic LBA of more than 3 months duration not responding to

conventional drugs, exercise and physiotherapy.
2. Symptoms suggesting pain of facet origin in the form of LBP with or
without radiation to the buttocks, thigh or groin; pain increasing on
hyperextension; pain when initiating movement.
3. Focal tenderness elicited by digital pressure over facet joint.
4. Postlumbar disc surgery patients with persistent pain and no MRI
evidence of arachnoiditis or recurrent disc disease.
5. The clinical assessment is correlated with a review of any pertinent
imaging studies, particularly CT and MRI scans, to make a
presumptive diagnosis of the patient's pain generator. It is essential to
exclude other causes such as disc herniation, spinal stenosis and nerve
entrapment.

II. CHRONIC PAIN SYNDROMES

 Imaging Studies 185

Contraindications
1. N eurological deficit in lower limbs or positive sciatic nerve stretch sign
2. Evidence of nerve root compression on MRI at the expected level of
the pain
3. Clinical or imaging evidence of infection or neoplastic disease
4. Possible pregnancy, bleeding diathesis and anticoagulant therapy
5. History of local anaesthetic sensitivity
  

Facet joint pathology should be considered if the patient describes non-

specific LBP with a deep and achy quality that is usually localized to a
unilateral or bilateral paravertebral area.
The common referral areas for facet joint-mediated pain are flank pain,
buttock pain (often extending into the posterior thigh, but rarely below
the knee), pain overlying the iliac crests, and pain radiating into the groin.
The pain is often exacerbated by twisting the back, by stretching, by
lateral bending, and in the presence of a torsional load. Some patients
describe their pain as worse in the morning, aggravated by rest and hyper-
extension, and relieved by repeated motion. Often, this lumbosacral facet
syndrome may occur after an acute injury (e.g. extension and rotation of
the spine), or it may be chronic in nature.
Unlike other lumbar spine pathologies such as disc herniation, facet
joint-mediated pain likely will not worsen with an increase in intra-
abdominal and thoracic pressures. Therefore, worsening of pain with
coughing, laughing, or a Valsalva manoeuvre is suggestive that the facet
joint is not the primary pain generator.
Neurological Examination
Sensory and motor neurological examination is normal in patients with
facet joint pathology.
STRAIGHT LEG RAISE TEST
This manoeuvre is usually normal for facet joint-mediated pain. How-
ever, if facet joint hypertrophy or a synovial cyst encroaches on the inter-
vertebral foramen, causing nerve root impingement, this manoeuvre may
elicit a positive response.

IMAGING STUDIES

Plain Radiography
Plain radiographs are traditionally ordered as the initial step in the workup
of lumbar spine pain. The main purpose of plain films is to determine under-
lying structural pathologic conditions. These studies are not generally rec-
ommended in the first month of symptoms in the absence of red flags. An

II. CHRONIC PAIN SYNDROMES

186 13. FACETOGENIC PAIN

exception to this would be if the low back symptoms are related to a sports
injury and a fracture is suggested. Three views are commonly obtained, includ-
ing anteroposterior, lateral, and oblique; however, the utility of oblique views
has been questioned. Plain radiographs may reveal degenerative changes, but
these findings have not been found to correlate with facet joint-mediated pain.

Bone Scanning
Bone scanning can be helpful when a tumour, infection, or fracture
(occult or traumatic) is suggested. Bone scanning is not usually indicated
in the initial workup, and the results are normal in persons with lumbo-
sacral facet joint syndrome. Bone scan findings have not been found to
correlate with facet joint-mediated pain.

CT Scanning
A CT scan of the lumbosacral spine provides excellent anatomic imag-
ing of the osseous structures of the spine, especially to rule out fractures
or arthritic changes. With facet joint pathology, one may find arthritic
changes in the facet joints and degenerative disc disease; however, facet
joint pathology is also frequently seen in asymptomatic patients, and,
therefore, abnormal findings on a CT scan are not diagnostic.
Despite the excellent imaging of the bony anatomy of the facet joint, CT
scans are not useful for the diagnosis of the facet joint as a pain generator.
Schwarzer et al. found no correlation between facet joint pathology on a
CT scan and those patients who responded to diagnostic facet joint blocks.
Therefore, the correlation of an abnormal facet joint anatomy as observed
on CT scans with true facet joint-mediated pain is poor.

Magnetic Resonance Imaging

The main utility of MRI is for excluding pathologies other than facet
joint arthropathy, because many degenerative changes in the facet joint
are asymptomatic. Similarly, true facet joint-mediated pain may be pres-
ent despite a normal MRI examination. MRI also may illustrate nerve root
entrapment secondary to facet joint hypertrophy or a synovial cyst and
may help visualize the intervertebral foramen; however, facet joint pathol-
ogy may be present despite normal imaging study findings.

DIAGNOSTIC BLOCKS

It has been postulated that for any structure to be deemed a cause of

back pain, the structure should have been shown to be a source of pain

II. CHRONIC PAIN SYNDROMES

 Diagnostic blocks 187

in patients, using diagnostic techniques of known reliability and validity.

The diagnostic blockade of a structure with a nerve supply with the abil-
ity to generate pain can be performed to test the hypothesis that the target
structure is a source of a patient's pain.
Facet joint injections with local anaesthetic and steroid are the simplest
and most common procedure for facet joint-mediated pain. The injec-
tion of local anaesthetic and steroids into the facet joint is diagnostic and
potentially therapeutic. When optimally performed, the injection is made
directly into the joint space, although many studies have shown relief
with periarticular injections as well. Pain relief following a precise intra-
articular injection confirms the facet joint as the source of pain. The choice
of imaging guidance – whether CT or fluoroscopic – is largely a matter of
personal preference and experience as both are equally effective. Fluoros-
copy is preferred in most centres due to easy availability in the operating
room, shorter procedure duration compared to CT, less exposure to radia-
tion, and lower costs.
Levels for injection are selected on the basis of clinical examination viz.
local pain and tenderness and not on imaging evidence of disease. It is
often difficult to localize the pain to one level, so that generally two and
occasionally three levels are injected. If the pain is bilateral, injections are
performed bilaterally.
The choice between intra-articular blocks and medial branch blocks is
to some extent preference and training of the physician. However, various
considerations apply in choosing either intra-articular injection or medial
branch. Intra-articular injections are more difficult and time consuming
than nerve blocks because they require accurate placement of the needle
within the joint cavity with care not to overdistend the joint. In contrast,
medial branch blocks are expeditious and carry no risk of overdistention.
Furthermore, at times, joint entry may be impossible because of the severe
age-related changes or posttraumatic arthropathy; no such processes affect
access to the nerves. Significant leakage of intra-articular injected fluid into
epidural space and spillage over to the nerve roots has been described.
With appropriate care, this is minimal with medial branch blocks. Finally,
intra-articular blocks are appropriate if intra-articular therapy is proposed
but if RF therapy is proposed, medial branch blocks become the diagnostic
procedure of choice. In addition, in the past only intra-articular injections
were considered as therapeutic. However, recent evidence has shown that
medial branch blocks have better evidence for the therapeutic effective-
ness than intra-articular blocks.
Valid information is only obtained by performing controlled blocks,
either in the form of placebo injections of normal saline or comparative
local anaesthetic blocks, in which, on two separate occasions, the same
joint is anaesthetized using local anaesthetics with different durations of
action. In a double-block protocol, the patient is given an injection with a

II. CHRONIC PAIN SYNDROMES

188 13. FACETOGENIC PAIN

short-acting anaesthetic (e.g. lignocaine) and records the duration of pain

relief in a diary. On a follow-up visit (typically 1–2 weeks later), a second
injection is performed, using an anaesthetic with a different duration of
action (e.g. bupivacaine, which has a longer half-life than lignocaine),
and the patient again should chart pain relief in a diary. A patient is diag-
nosed as having a positive block if they receive pain relief (typically >80%)
for both injections for a length of time corresponding to the duration of
action of the medication. Given the dual innervation of each Z-joint, one
must anaesthetize or block the cephalad and subadjacent medial branches
(e.g. anaesthetize the L3 and L4 medial branches for the L4–L5 Z-joint).
Injections are diagnostic if patients report significant relief of symptoms,
usually at least a 50% reduction in pain.

TREATMENT OF FACETOGENIC PAIN

Therapeutic Interventional Technique

Facet joint pain may be managed by intra-articular injections, medial
branch blocks, or RF ablation of medial branches (facet denervation).

Technique of Fluoroscopy-Guided Facet Joint Infiltration

The patient is placed in the prone position on a radiolucent table with a
pillow under the abdomen to correct the lumbar lordosis and to open up
the facet joint. The back is cleaned and draped. The fluoroscope is posi-
tioned with the tube head under the table. After a scout shoot to count the
level of the vertebrae upwards from the sacrum, the X-ray tube is angled
slowly opposite to the side of facet injection till the joint appears in profile
as two parallel lines. When the joint is visualized with least obliquity, this
point is marked on the skin. The lower lumbar levels typically require a
steep obliquity, while less of an obliquity is required further up the spine
to visualize the joint in profile. After injecting local anaesthetic, a 22 G
spinal needle is inserted in line with the X-ray beam, aiming the inferior
part of the joint, till it contacts bone at the lip of the facet joint. With fine
movements, the needle tip enters the joint with a distinct ‘give’; 0.5 mL of
a nonionic dye (Omnipaque) can be injected to confirm the intra-articular
position of the needle. In experienced hands, confirmation of appropriate
needle placement can be made by feel and by viewing in lateral oblique
projection. Once the needle is in place, 0.5 mL of a mixture of 20 mg of
methyl prednisolone acetate (Depo-Medrol) and l mL of bupivacaine is
injected into each joint.

CT-Guided Facet Joint Infiltration

With CT guidance, the patient is placed in the prone position, and 5 mm
axial sections obtained at the level of interest to determine entry site and

II. CHRONIC PAIN SYNDROMES

 Treatment of Facetogenic Pain 189

angle of approach. The entry site is marked on the skin, and a 22 gauge
needle is advanced into the joint (Fig.13.1) Injections are identical to those
done with fluoroscopic guidance.
CT guidance is especially useful in severely degenerated joints where
access to the joint space is hampered by large osteophytes. In the event of
an intra-articular injection not being possible, many workers resort to a
periarticular injection of the same drugs with acceptable pain relief.
The lumbar facet joint typically has a volume of 0.8–1.2 mL and care
is taken not to inject a larger volume. Overfilling the joint will result in
anterior rupture into the epidural space, which may occur even with small
amounts of fluid, as the anterior ligament is often fenestrated or partially
degenerated.
The patient is observed for 1 h after the procedure to document pain
relief and to monitor for allergic reactions. Pain relief following a precise
intra-articular injection of local anaesthetic confirms the facet joint as the
source of pain. In most patients, the first 15 min is sufficient to determine
whether the injection is successful in alleviating symptoms. In a small sub-
group of patients, there may be no immediate relief, but the pain resolves
over the next few days. So it must not be concluded that the injection is
unsuccessful until 1 week after the injection.
The immediate pain relief after the injection is attributed to the effect
of the long-acting local anaesthetic, which interrupts the pain–spasm
cycle. Corticosteroid action begins by 1 week and takes about 3 weeks
for peak effect to set in. There may be a nonspecific synovitis present in
many of these joints that is relieved by the anti-inflammatory action of

FIGURE 13.1 CT-guided facet injection.

II. CHRONIC PAIN SYNDROMES

190 13. FACETOGENIC PAIN

corticosteroids. In many cases, rupture of the articular capsule during

injection makes the drugs diffuse into the intravenous foramina and thus
act on the adjacent nerves as well. A simple physical effect of clearing of
inflammatory exudates or adhesions from the joint and the nerve root
sleeve may also play a role.

FACET DENERVATION

Denervation of the facet joint is the next logical step in management

of facetal pain and the aim is to achieve pain relief by denervation of the
medial branch of the dorsal ramus by RF ablation. Since the facet joint is
supplied by medial branch nerve exiting at the level of the facet joint as
well as at the next higher level, denervating a facet joint requires to be done
at two levels. The procedure may be performed with CT or fluoroscopic
guidance. The patient is prepared and positioned in a similar manner as
for facet injections. A 22 gauge spinal needle or RF needle is advanced in
a gun barrel fashion towards the transverse processes (eye of the ‘Scottie
dog’) above and below the target facet joint (Fig. 13.2). Once the position
is confirmed, 1 mL of nonionic contrast material is injected followed by RF
pulse at 80° for approximately 60 s.

FACET INJECTIONS VERSUS FACETAL DENERVATION

The choice between using intra-articular blocks or medial branch

blocks depends largely on the preference and training of the physician.
However, the following are some aspects that may influence the choice
of procedure:
  

1. I ntra-articular injections that require accurate placement of the needle

within the joint cavity are more difficult and time consuming than
nerve blocks. At times, joint entry may be impossible because of the
severe arthropathy. Care needs to be exercised not to overdistend the
joint.
2. Medial branch blocks are technically easier and carry no risk of
overdistention.
3. Possibility of leakage of intra-articular injected fluid into epidural
space and over to the nerve roots are more common with intra-
articular injections. This is minimal with medial branch blocks.
4. The requirements for steroids is much lower or none with medial
branch blocks compared to intra-articular injections.
5. Recent evidence has shown that medial branch blocks are
therapeutically more effective than intra-articular blocks.
6. If intra-articular inflammation is the proven and sole source of pain,
intra-articular injection with steroid may be the modality of choice.

II. CHRONIC PAIN SYNDROMES

 Current Status of Facetal Interventions 191

(a) (b)

FIGURE 13.2 Radio frequency ablation. (a) RF needle position in AP view. (b) Needle
position in Lateral view.

COMPLICATIONS OF FACETAL INTERVENTIONS

Major complications of facet joint infiltrations are fortunately uncom-

mon and can be avoided by meticulous attention to technique and steril-
ity. The complications are mainly related to improper needle placement,
bleeding or infection and effect of injected drugs. These include dural
puncture, haematoma formation, spinal cord or neural trauma, spinal
anaesthesia, septic arthritis/spondylitis, chemical meningitis and steroid
side effects. RF denervation may cause painful cutaneous dysesthesias,
transient increased pain due to neuritis or neurogenic inflammation,
anaesthesia dolorosa, cutaneous hyperaesthesia and deafferentation pain.
Also, post-RF denervation MRI studies have shown paraspinal enhance-
ment mimicking a paraspinal abscess with no apparent evidence of infec-
tion. This is attributed to a noninfectious postinflammatory process and
antibiotic therapy is not indicated on the basis of imaging findings alone.

CURRENT STATUS OF FACETAL INTERVENTIONS

For intra-articular injections of local anaesthetics and steroids, there is

moderate evidence for short- and long-term improvement in managing LBP.
Manchikanti et al. concluded that there was strong evidence for short-
term relief and moderate evidence for long-term relief of facet joint pain.
Further, they concluded that proper selection of patients with successful
diagnostic blocks and an optimal technique may be important to achieve
better results; they concluded that the evidence for pain relief with RF
neurotomy of medial branch nerves was moderate to strong in cervical
and lumbar spine.

II. CHRONIC PAIN SYNDROMES

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 C H A P T E R

14
Knee Pain

The knee, the largest joint in the body, is frequently involved in ath-
letic injuries and degenerative or inflammatory processes. Degenerative
disease of the knee joint is the most common reason for a patient's visit to
his family physician seeking relief from pain. This is closely followed by
sports injuries as the second leading cause for persistent and acute knee
pain. Erroneous notions about diagnosis and management, however, hin-
der the optimization of care.

CAUSES OF KNEE PAIN

The common causes of knee pain are

  

• Patellofemoral syndrome
• Patellar dislocation/subluxation
• Patellar tendinitis (‘jumper's knee’)
• Anterior/posterior cruciate ligament injuries
• Medial/lateral collateral ligament injuries
• OA
• Hamstring tendinitis
• Rheumatoid arthritis
• Popliteal tendonitis
• Infective conditions of knee (sepsis, tuberculosis)

EVALUATING THE PAINFUL KNEE

A correct diagnosis at the outset is crucial to effective management.

Comparison with the normal or uninjured knee is essential. Usually, find-
ings from the history and physical examination will establish the diagno-
sis. Observe the patient's walk and then perform the knee examination
when the patient is seated, supine and prone.

193
194 14. KNEE PAIN

DIAGNOSTIC CLUES IN PAINFUL KNEE

•  nset of pain is sudden or gradual

O
• Location and characteristics of pain
• Postinjury limitations on activity
• Note swelling, asymmetry and effusion
• Assess active and passive range of motion in both knees
• Palpate the medial, lateral borders of patellar tendon, anterior knee
and tibial tuberosity
• Perform specific tests to confirm suspicions
• Feel for crepitus, look for Baker cyst in prone position

WHAT THE SYMPTOMS INDICATE IN KNEE PAIN

Sign or symptom Most likely cause

Anterior knee pain Patellofemoral syndrome
Bursitis
Patellar tendinitis
Clicking or locking Meniscal injury
Joint mouse
Generalized pain Osteoarthritis
Septic arthritis
Tumour
Knee gives way or ‘goes out’ Meniscal injury
Anterior cruciate ligament insufficiency
Patellar subluxation
Quadriceps weakness
Medial or lateral knee pain Meniscal injury
Collateral ligament injury
Osteoarthritis
Fibular head dysfunction
Posterior knee pain Posterior horn meniscal damage
Baker cyst
Tendinitis
Snapping or popping at time of injury Meniscal injury
Ligament tear
Swelling Anterior cruciate ligament insufficiency
Acute over chronic osteoarthritis
Bursitis
Meniscal injury
Septic arthritis

IMAGING OF KNEE

Roentgenographic studies are frequently useful. Standing films

under weight-bearing conditions are usually the most informative
(Photograph 14.1).
II. CHRONIC PAIN SYNDROMES
 Imaging of knee 195

PHOTOGRAPH 14.1 X-ray knee in erect position showing osteoarthritic changes.

Following points are important in roentgenographic studies of knee pain:

  

• W ith anterior knee pain, obtain a Merchant view to check patellar tilt
in the femoral groove.
• With generalized knee pain in a young patient, tunnel-view X-ray
studies may reveal evidence of osteochondritis dessicans on the
femoral condyle.
• In OA of the knee joint, joint space narrowing seen in standardized
X-rays is also used as a measure of progression of OA. Osteophytes
are the hallmark of the disease and their presence is considered
important in diagnosis. However, their presence indicates advanced
stage of the disease. Other findings on X-ray are subchondral
bone sclerosis, subchondral cysts, deformity, loose bodies and
calcification.
  

MRI: Reserve MRI of knee for patients with uncertain diagnosis or

unresponsive conditions. It is useful in diagnosis of medial and lateral
collateral ligament injury. It is also useful in diagnosis of effusion, loose
bodies, cruciate ligament injury and tear.
Radioisotope bone scan provides a sensitive but nonspecific assess-
ment of the knee pathology. It is useful in identifying infective, degenera-
tive and metastatic lesions around the knee joint.
II. CHRONIC PAIN SYNDROMES
196 14. KNEE PAIN

LABORATORY INVESTIGATIONS

ESR, serum biochemistry and urine analysis are essentially normal in

OA, although age-related increase in ESR and positive rheumatoid factor
in low titer can occur in the normal population. Mild increase in C-reactive
protein has been demonstrated but is not clinically useful.
Diagnostic arthroscopy: Arthroscopy has developed into both an
adjunctive tool for diagnosis and an instrument for therapeutic interven-
tion. It is particularly useful in sports injuries such as cruciate ligament
tear, loose bodies as seen in degenerative arthritis, meniscal tears, etc.

MANAGEMENT OF KNEE PAIN

For an effective management of painful knee it should be the endeav-

our of the treating pain clinician to make a correct diagnosis, alleviate pain
quickly and provide a time frame for return to activity and sports.

OA OF KNEE JOINT

OA is by far the most prevalent joint disorder. It strongly associates

with ageing and is a major cause of pain and disability in the elderly.
The knee is the principal large joint to be targeted by OA, resulting
in disabling knee symptoms in 20% of the population over the age of
55 years, one-quarter of whom are severely disabled. The risk of dis-
ability attributable to knee OA alone is greater than that due to any
other medical condition. With the increasing proportion of elderly in
the population, OA will become an even more important health care
problem. Improved understanding and management of OA is therefore
clearly desirable.

THE NATURE OF OA

Pathologically OA may be defined as ‘a condition of synovial joints

characterized by focal hyaline cartilage loss together with subchondral
and marginal new bone formation’. The traditional view of OA is that it
is an age-related degenerative disease of cartilage that, once established,
inevitably progresses, and for which only surgical joint replacement can
make a real impact. This pessimistic view is widely held not only by the
general public but also by many health care professionals who manage
OA patients. It is increasingly apparent, however, that such a pessimistic
view is inappropriate.

II. CHRONIC PAIN SYNDROMES

 The Nature of OA 197

Several risk factors have been identified for development of OA. These
include
  

1. G eneral constitutional risk factors such as heredity, ageing, gender,

and obesity and local mechanical factors such as trauma, instability,
and occupational and recreational usage
2. Genetic factors are clearly important in the pathogenesis of OA. The
estimated variance attributed to heritability for hand, knee, or hip OA
is high at 40–60%

Clinical Features of Osteoarthritic Knee

There may be a delay of many years in the appearance of symptoms
of OA after cartilage degeneration has started. This is due in part to lack
of innervation of cartilage. The symptoms usually start insidiously in an
asymmetric fashion and then become symmetric.

Symptoms
  

1. P
 ain: Pain in or around the involved joints is the cardinal symptom
and usually starts as an intermittent localized deep ache, often
aggravated by use of the joint and relieved by rest. As the disease
progresses, the pain becomes persistent and in advanced cases, night
pain may be very disturbing and may suggest advanced stage.
  

Knee joint involvement is typically associated with pain on descend-

ing or ascending stairs, climbing into autorickshaws, rickshaws, buses,
etc. Patients invariably have problems in squatting for toilet. There
may sometimes be locking or buckling of knee joint. Hip involvement
causes problems of gait and pain in the groin or medial part of thigh.
  

2. S tiffness: Stiffness in joints on first awakening (morning stiffness) in OA

usually lasts 5–30 min (average 20 min). Stiffness occurring after periods
of rest or inactivity (gelling) is frequent and lasts for a few minutes.
3. Functional impairment: Functional impairment in OA is highly
variable. It depends on associated muscle wasting and weakness, and
on radiological severity of the disease.

Signs
The physical signs evident in OA of knee joint are variable but may
include the following:
  

1. B ony swelling (osteophyte) at the joint margins.

2. Restriction in range of movement.

II. CHRONIC PAIN SYNDROMES

198 14. KNEE PAIN

3. C oarse crepitus or crunching, initially reflecting the roughened

cartilage surfaces and later reflecting bone grating on bone.
4. Soft-tissue swelling and effusion, usually only modest.
5. Joint laxity, reflecting loss of cartilage and relative slackening of
ligament/capsule.
6. Joint deformity with malalignment across the joint, a late feature.
  
The physiological change that may accompany such structural OA
changes, at least at the knee is reduced quadriceps muscle strength. This
age-related feature is more marked in subjects with knee OA than in
matched non-OA controls.
The agreed objectives of management are to (1) educate the patient, (2)
control pain, (3) optimize function and (4) beneficially modify the OA process.
Nonpharmacological therapy in OA (ACR guidelines)
  

1. Patient education
a. Self-management programs (e.g. arthritis self-help course)
2. Health professional social support
3. Weight loss (if overweight)
4. Physical therapy
a. Range of motion exercises
b. Strengthening exercises (quadriceps exercises)
c. Assistive devices for ambulation
5. Occupational therapy
a. Joint protection and energy conservation
b. Assistive devices for activities of daily living and instrumental
activities of daily living
c. Aerobic exercise programs

EVIDENCE-BASED INTERVENTIONS

Evidence-based interventions that should be considered in all OA

patients include:
Education: Although the mechanisms are unclear, information access
and therapist contact both reduce the pain and disability of OA, improve
well-being, encourage restorative sleep and benefit comorbidity such as
obesity. Local strengthening exercise also reduces pain and disability, with
accompanying improvements in the reduced muscle strength, proprio-
ception, and balance that are associated with knee OA.
Reduction in adverse mechanical factors: Simple pacing of activities
throughout the day and use of shock-absorbing footwear and walking
aids can be beneficial.
Advice on weight loss for obese patients: Epidemiological data and
some recent trial data show that reduction in obesity improves symptoms
of OA and may retard further structural progression.

II. CHRONIC PAIN SYNDROMES

 Evidence-Based Interventions 199

Simple analgesia: Paracetamol is the accepted oral drug of first choice

and, if successful, is the preferred long-term analgesic. Paracetamol is
recommended because of its efficacy, lack of contraindications or drug
interactions, long-term safety, ready availability and low cost. It is admin-
istered in a dose range of 650–4000 mg/day. (Box 14.1)
Drugs used in the management of OA
  

1. Symptom-modifying agents
a. Fast acting – Paracetamol
NSAIDs
Narcotic analgesics
Nonopioid analgesics
b. Slow acting – Intra-articular hyaluronic acid
Oral chondrotin sulfate
Glucosamine sulfate
2. Disease-modifying agents
a. Drugs decreasing degeneration –
MMP inhibition – Doxycycline, chemically modified tetracyclins
Collagenase inhibitor – glycosaminoglycan polysulfuric acid
Elastase inhibitor – pentosan polysulfate

BOX 14.1

MEDICAL MANAGEMENT PROTOCOL

O F S Y M P T O M AT I C O S T E O A R T H R I T I S
OF THE KNEE
1. N onpharmacologic therapy
2. I f effusion is present, consider aspiration and injection of intra-articular
steroids (e.g. triamcinolone, methyl prednisolone)
3. Paracetamol (up to 1 g qid) for pain and symptom control
4. If necessary, add topical capsaicin cream
5. If response is inadequate, use alternative analgesic, low-dose ibupro-
fen (up to 400 mg/day), nimesulide (200 mg/day) or nonacetylated
salicylates
6. If response is inadequate, use full-dose NSAIDs (with omeprazole if
patient has risk factors for upper gastrointestinal bleeding or ulcer
disease)
7. If response is inadequate and surgery is contraindicated, consider
referral for joint lavage and/or arthroscopic debridement
8. If response is inadequate and surgery is indicated, consider referral
for joint surgery (osteotomy, total joint arthroplasty)

II. CHRONIC PAIN SYNDROMES

200 14. KNEE PAIN

Increasing tissue inhibitors of MMPs – glycosaminoglycan polysul-

furic acid
Antiplasmin activator – taxenamic acid
b. Drugs increasing regeneration – Growth factors
Chondrocyte transplant
Nutrient supplement for cartilage – chondrotin sulfate, glucos-
amine sulfate
c. Visco supplementation
3. Drugs used in patients with acute inflammation
NSAIDs
Intra-articular depot corticosteroids
In patients with crystals – colchicine
  

Various other interventions may be considered, as required, in addition

to the aforementioned core interventions. These include
  

1. O ther oral agents – combined analgesics, NSAIDs, opioid analgesics,

amitriptyline and ‘nutripharmaceuticals’ such as glucosamine and
chondroitin sulfate
2. Topical NSAIDs and capsaicin
3. Intra-articular injection of long-acting depot steroid or hyaluronan
and joint lavage
4. Environmental modifications such as a raised toilet seat and other
household aids
5. Other local physical treatments including heat, cold, acupuncture,
ultrasound, spa baths, patellar taping and knee braces
6. Surgical realignment (osteotomy) and joint replacement
  

Intra-articular steroids: Intra-articular steroids such as methyl pred-

nisolone 40–80 mg or triamcinolone 40 mg have been shown to decrease
cartilage degradation in animals. They produce marked improvement in
symptoms, usually lasting for weeks to months. But repetitive large-dose
injections are associated with decreased repair and may lead to more car-
tilage damage. It is recommended that their use should not exceed a maxi-
mum of three or four times a year.

Surgical Management of Osteoarthritic Knee

Various surgical therapies available for OA are loose body removal,
osteotomy, arthrodesis, athroplasty, synovectomy, debridement, tendon
repair and nerve decompression. Total knee joint replacements have
improved the quality of life and decreased the morbidity of OA. Most
studies report excellent long-term results in over 90% of patients undergo-
ing joint replacement. Joint replacement must be considered in any patient
presenting with end stage of joint disease.

II. CHRONIC PAIN SYNDROMES

 Meniscal Injuries of the Knee 201

LIGAMENTOUS INJURIES OF THE KNEE

Ligamentous injuries commonly occur after both contact and noncon-

tact injuries to the knee. Injuries include a sprain from tear of a few fibres to
complete tears of the ligament. Pain and instability of the knee are common
after ligament disruption. Tenderness over the medial or lateral aspect of
the knee suggests involvement of the medial or lateral collateral ligament.
MRI is helpful in diagnosis of the tear or laceration of the ligament.
Management includes use of NSAIDs, relative immobilization by bracing,
strengthening exercises and modification of activity. More severe injuries
will require arthroscopic evaluation and repair of the damaged ligament.

MENISCAL INJURIES OF THE KNEE

Meniscal injuries are frequently encountered in active adults or as

a result of sports injury. Pain localized to the joint line with or without
mechanical symptoms of locking suggests a meniscal tear. MRI is helpful
in diagnosing the nature of injury, although a diagnostic arthroscopy is
often required to directly visualize the injury. Rest, immobilization and
exercises are sufficient to treat pain because of small tears. Surgical recon-
struction is required only if the tear is large and is associated with anterior
cruciate deficiency.

II. CHRONIC PAIN SYNDROMES

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 C H A P T E R

15
Neuropathic Pain:
Mechanisms and
Management

The term neuropathic pain encompasses a wide spectrum of disease

states that present with a variety of signs and symptoms during the
natural course of disease. It occurs due to malfunction of the nocicep-
tive pathway anywhere along its length from peripheral to central
region.
Neuropathic pain is defined as ‘pain associated with injury, disease or
surgical section of the peripheral or central nervous system or alterna-
tively as pain initiated or caused by a primary lesion or dysfunction in the
nervous system’.

NEUROPATHIC PAIN STATES: AETIOLOGICAL

CLASSIFICATION

• T rauma/surgery: phantom limb, spinal cord injury, postmastectomy,

postcholecystectomy, postthoracotomy pain
• Ischaemic injury: central pain, diabetic neuropathy
• Infection/inflammatory: postherpetic neuralgia, human immunodefi-
ciency virus
• Cancer: invasion/compression of neural structures, chemotherapy-
induced polyneuropathy, postradiation plexopathy and myelopathy,
phantom breast pain
• Drugs: vinca alkaloids
• Compression: sciatica, carpal tunnel syndrome, radiculopathy
• Overactivity of SNS: complex regional pain syndrome
• Unknown: trigeminal neuralgia, meralgia paresthetica

203
204 15. NEUROPATHIC PAIN: MECHANISMS AND MANAGEMENT

CHARACTERISTICS OF NEUROPATHIC PAIN

Pain
• Different characteristics of pain like lancinating, burning, pin
pricking, stabbing
• Absence of ongoing tissue damage
• Delay in onset of pain after nerve injury
• Continuous, paroxysmal, electric shock-type sensation, spontaneous
• Unresponsiveness/poorly responsive to opioid treatment

Abnormal sensory signs

• Allodynia (pain due to a stimulus that does not normally provoke
pain)
• Hyperalgesia (an increased response to a stimulus that is normally
painful)
• Hyperaesthesia (increased sensitivity to stimulation, excluding the
special senses)
• Hyperpathia (abnormally painful reaction to a stimulus, especially a
repetitive stimulus, as well as an increased threshold)

Negative sensory signs

• Pain in the area of sensory loss
• Presence of a major neurological deficit

DIFFICULTIES IN DIAGNOSIS OF
NEUROPATHIC PAIN

•  o consensus on definition
N
• Rarely one diagnostic test
• Neuropathic pain perception is subjective
• Lack of specificity in diagnosis
• Pain system is dynamic and unpredictable
• Signs and symptoms change over time

MECHANISMS OF NEUROPATHIC PAIN

It is difficult to comprehend neuropathic pain states by any one path-

ological process. One can perceive that neural tissue injuries anywhere
along the nociceptive pathway may lead to further long-term changes in
the same nociceptive pathway at higher (spinal and central) levels and a
number of interlinked pathological processes may occur in unison at all

II. CHRONIC PAIN SYNDROMES

 Peripheral Mechanisms 205

Brain
Cerebral reorganisation
Molecular changes

Spinal cord

Spinal cord anatomical reorganisation

Dorsal horn denervation hypersensitivity
Molecular changes

Peripheral nerve fibers Sympathetic fibers

Ephaptic crosstalk
Ectopic discharges
Mechanosensitivity
Ephaptic crosstalk
Nociceptive sensitization

FIGURE 15.1 Postulated mechanisms of neuropathic pain.

levels, from peripheral to central, leading to complicated painful states

(Fig. 15.1).
Understanding these mechanisms is helping the pain clinicians to
develop treatment protocols specifically targeting those mechanisms
rather than controlling signs and symptoms.

PERIPHERAL MECHANISMS

They are particularly important for the development of allodynia,

hyperalgesia and ongoing pain associated with nerve injury.

Ectopic Discharge
A large increase in the level of spontaneous firing in the injured sensory
neurons as well as their uninjured neighbour neurons linked to the injury
site.
  

• E
 ctopic activity develops as a result of alterations in the expression of
sodium channels in the cell bodies and the terminal neuromas.

Ephatic Conduction
• C
 ross-excitation among afferent neurons having spontaneous fir-
ing capacity leading to amplification of depolarization of individual
neurons.

II. CHRONIC PAIN SYNDROMES

206 15. NEUROPATHIC PAIN: MECHANISMS AND MANAGEMENT

Collateral Sprouting
• P rimary afferent neuron injury leads to sprouting of collateral fibres
from sensory axons in their attempt to regenerate and reinnervate into
denervated areas.
• The sprouts of damaged afferents may become sensitive to low-threshold
mechanoreceptors or may become ectopic neural pacemaker nodules.

Coupling between SNS and the Sensory Nervous System

• A ctivity in the SNS initiates abnormal impulse traffic in sensory
neurons due to enhanced sensitivity to catecholamines leading to pain
perception.
• Coupling takes place at peripheral as well as spinal level in DRG.

Nociceptive Sensitization
• T
 here is an increase in bradykinin binding sites within DRG following
axotomy leading to hyperalgesia.

CENTRAL MECHANISMS

These mechanisms play an important role in variation in character,

severity, delay in onset of pain and patients behavioural response to pain.

Spinal Cord Anatomical Reorganization

Aδ and C fibres normally innervate lamina I and II of the dorsal horn
of the spinal cord and are responsible for nociceptive signalling while
Aβ fibres are large fast-conducting neurons that subserve lower thresh-
old nonnoxious inputs and innervate lamina III and IV (Fig. 15.2). How-
ever, after nerve injury, the central terminals of the large myelinated
primary afferent neurons sprout into lamina II establishing functional
synaptic contact with second-order neurons, resulting in interpretation
of low-threshold nonnoxious inputs from Aδ fibres as nociceptive in
origin.

Spinal Cord – Hyperexcitability (Central Sensitization)

• D
 evelopment of a sustained state of hyperexcitability of dorsal horn
neurons due to persistent afferent barrage associated with peripheral
nerve injury.

II. CHRONIC PAIN SYNDROMES

 Central Mechanisms 207

Normal terminations of primary afferents in the dorsal horn

A
C Superficial

Midline
Dorsal root ganglion

Deep
Dorsal horn

After nerve injury, C-fibre terminals atrophy and A-fibre

terminals sprout into the superficial dorsal horn

Superficial

Deep

FIGURE 15.2 Spinal cord anatomical reorganization.

• C ombination of increased activity in the excitatory (glutamate,

substance P, NMDA receptors, etc.) and a concomitant decrease
in activity in inhibitory (GABA, adenosine receptors, etc.)
systems within spinal cord contributes to the phenomenon of
central sensitization.
• Associated with windup phenomenon characterized by an increas-
ing response to repeated C-fibre volleys and contributing to
hyperalgesia.

Cerebral Reorganization
• F ollowing limb amputation and deafferentation, there is a reorganiza-
tion of the primary somatosensory cortex, subcortex and thalamus,
e.g. unusually large thalamic stump representation.
• There is a linear relationship between pain and degree of
reorganization.
• This phenomenon is mostly seen in patients with phantom pain
complex.

II. CHRONIC PAIN SYNDROMES

208 15. NEUROPATHIC PAIN: MECHANISMS AND MANAGEMENT

ASSESSMENT OF NEUROPATHIC PAIN

Unidimensional Scale
Visual Analogue Scale
• Measures intensity of pain
• Easy to administer
• No emphasis on sensory signs and symptoms and varying character
of pain

Multidimensional Scale
• N europathic pain scale
• Assesses 10 qualities: intensity, sharp, dull, hot, cold, sensitive, itch,
deep, surface, not unpleasant
• Monitor effects of therapy
• Not discriminative
• LANSS pain scale
• Five descriptor groups – skin sensations, skin colour, abnormal skin
sensitivity, paroxysmal pain, change in skin temperature
• Assessment of allodynia and altered pin-prick threshold
• Discriminative
• Sensitivity 83%, specificity 87%
• Neuropathic pain questionnaire
• 12 items (similar to LANSS)
• Discriminative
• Screen, diagnosis, assessment, monitoring, outcome
• Sensitivity 67%, specificity 74%
  

PainDETECT Questionnaire is another questionnaire that has been well

validated in studies, and has an advantage in that it is solely based on
answers that a patient can give for him/herself, with no requirement of his/
her clinical examination at the time of administration of the questionnaire.

Advantages of Multidimensional Scales

• Differentially measure different types of pain
• Improve specificity in diagnosis
• Provide mechanism-based understanding of neuropathic pain
• Target-specific monitoring of neuropathic pain treatments

PROTOCOL FOR TREATMENT

OF NEUROPATHIC PAIN

Flowchart showing treatment plan

II. CHRONIC PAIN SYNDROMES

 Guidelines for Neuropathic Pain Management 209

Neuropathic pain Sympathetic nervous

system contribution

Tricyclic antidepressants— Sympathetic plexus

nortriptyline/amitriptyline block

Gabapentin/anticonvulsants ± Topical medication

± TENS
± Psychological
management
Ketamine IV/subcutaneous infusion
± Botulinium toxin A
± local anaesthetic blocks/infusions

Trial opioids

Tramadol Strong opioids

Supportive care
Invasive therapy
• Spinal cord stimulation
• Spinal analgesia (methadone,
morphine, fentanyl ± clonidine,
midazolam, bupivacaine)

  

GUIDELINES FOR NEUROPATHIC

PAIN MANAGEMENT

The treating pain physician should consider the following before

deciding on the treatment modality.
  

• P atient's expectations are realistic.

• Partnership approach – goal is improvement in quality of life
(and not cure).
• Drug regimens are rationalized and prescribed in a time-contingent
manner.
• Manage comorbidities – sleep disturbance, depression, anxiety, decon-
ditioning, addiction.
• Follow-up, support and realistic optimism provided.
• Patient's participation in their own recovery process – lifestyle
changes, exercises, sleep and coping strategies.

II. CHRONIC PAIN SYNDROMES

210 15. NEUROPATHIC PAIN: MECHANISMS AND MANAGEMENT

MANAGEMENT OPTIONS BASED ON

PATHOPHYSIOLOGICAL MECHANISMS

Management of Ectopic Activity/Ephatic Conduction

• N a+ channel blockers – act as membrane stabilizers
• Phenytoin
• Lignocaine
• Carbamazepine
• Oxcarbazepine
• Gabapentin

Reducing Afferent Barrages from SNS and Nociceptor

Input
• S ympathetic plexus block
• Stellate ganglion block
• Lumbar sympathetic chain block
• Central neuraxial block
• Epidural infusions of adjuvants and local anaesthetics
• Intrathecal infusions
• Somatic/sensory nerve block
• Brachial plexus block
• Paravertebral block
• Lateral cutaneous nerve of thigh block
• Intercostal nerve block

Reducing Central Sensitization

• N MDA receptor – antagonists
• Ketamine
• Amitriptyline
• Methadone
• Gabapentin

Improving Descending Control

• L ocal inhibitory controls
• GABA-B agonist – baclofen
• Opioids – oxycodone, tramadol
• Descending inhibition from brain
• Clonidine – facilitates α 2 adrenergic inhibition
• Tricyclic antidepressants – blocks reuptake of noradrenaline and
serotonin

II. CHRONIC PAIN SYNDROMES

 Other Treatment Modalities for Managing Neuropathic Pain 211

PHARMACOTHERAPEUTICS IN
MANAGEMENT OF NEUROPATHIC PAIN

Drugs are recommended as first-line treatment of neuropathic pain

(Table 15.1).
• Drug subgroups used to treat neuropathic pain are
• Nonopioid analgesics
• Anticonvulsants
• Antidepressants
• Topical analgesics
• Opioid analgesics
• Membrane stabilizers
• NMDA receptor blocking agents

REASONS FOR OPIOIDS RELATIVE

NONRESPONSIVENESS IN NEUROPATHIC PAIN

• N o peripheral site of opioid analgesia as seen in inflammatory pain.

• Downregulation of opioid receptors in peripheral and spinal axons.
• Upregulation of cholecystokinin within DRG, which has opioid
antagonistic properties.
• Complex involvement of excitatory and inhibitory neurotransmit-
ter systems in the pathogenesis of neuropathic pain, which are not
responsive to opioids.

OTHER TREATMENT MODALITIES FOR

MANAGING NEUROPATHIC PAIN

• N eural blockade
• Sympathetic nerve block
• Somatic/sensory nerve block
• Physical therapies
• Relaxation therapies
• Cognitive behavioural therapy
• Neuromodulation
• TENS
• Spinal cord stimulation
• Neuroaxial analgesia
• Intrathecal drug delivery used for intrathecal infusion of methadone,
morphine ± clonidine, midazolam, bupivacaine
• Neurodestructive techniques
• Cordotomy

II. CHRONIC PAIN SYNDROMES

 TABLE 15.1 Recommended Medications for Neuropathic Pain

212
Medication Starting dose Maximum dose Titration Most common side effects Contraindications Remarks

Carbamazepine 100 mg bid Titrate to 100 mg every Sedation, dizziness, ataxia, Liver abnormalities, Side effects settle
intolerable side 3–7 days confusion, nausea, liver bone marrow with chronic
effects toxicity, blood dyscrasias, suppression, known treatment, used with

15. NEUROPATHIC PAIN: MECHANISMS AND MANAGEMENT

Stevens–Johnson syndrome sensitivity to tricyclic caution in elderly
compounds population
Capsaicin 0.025% 0.075% 4 times a day Burning sensation, redness Local infection, ulcer Initial burning and
(0.025–0.075%) pain may restrict
II. CHRONIC PAIN SYNDROMES

compliance. Advise
patient to persist
with treatment
EMLA (Eutectic 2.5% – 2–6 times a day – Local infection, ulcer Used with caution in
mixture of local children
anaesthetics)
Gabapentin 300 mg qid 3000 mg/day 300 mg every Sedation, dizziness, Demonstrated Improves in sleep,
(qid dosing) 3–7 days confusion, peripheral hypersensitivity social functioning,
oedema, weight pain to the drug or its vitality. Synergetic
ingredients action with
amitriptyline
Ketamine 250 mcg/kg IV 1000 mg/day Double the dose Sedation, confusion, Known Subcutaneous
infusion alternate day delirium, hallucinations, hypersensitivity, infusion can also be
nightmares psychiatric disorders used
Lidocaine patch Up to 3 Up to 3 patches None needed Localized skin irritation Known sensitivity to –
5% patches applied to local anaesthetics of
applied to painful skin area amide type
painful skin
area
 Lidocaine IV 5 mg/kg over – – Hypotension, sedation Moribund patients, Effective diagnostic
infusion 60 min heart block patients tool to identify if
a patient's pain

Other Treatment Modalities for Managing Neuropathic Pain

is responsive to
sodium channel
blockers
Opioids 2.5 mg bid Titrate to Nausea, sedation, Known Side effects settled
Methadone intolerable 2.5 mg every constipation, confusion, hypersensitivity down with chronic
side effects sweating, itching, in situations treatment except
II. CHRONIC PAIN SYNDROMES

week (qid)
depression where opioids are constipation and
Long-acting 10 mg every
contraindicated constriction of
oxycodone week
pupils
Long-acting 15 mg every
morphine week
Oxcarbazepine 300 mg qhs 1200 mg per day 300 mg every Sedation, dizziness, ataxia, Liver abnormalities, Side effect profile
week confusion, nausea, liver bone marrow is better than
toxicity, blood dyscrasia, suppression, known carbamazepine. Side
Stevens–Johnson syndrome sensitivity to tricyclic effects settle with
compounds chronic treatment
Phenytoin 100 mg bid Titrate to 100 mg every Sedation, dizziness, ataxia, Bradycardia, –
intolerable 3–7 days confusion, nausea, 2–3° heart block
side effects gingival hyperplasia, hypersensitivity
peripheral neuropathy,
Stevens–Johnson syndrome
Tizanidine 2 mg qhs 36 mg 2 mg every Sedation, dizziness, Liver abnormalities,
3–7 days (tid) hypotension, liver known
function abnormalities hypersensitivity

Continued

213
 214
TABLE 15.1 Recommended Medications for Neuropathic Pain—Cont’d

15. NEUROPATHIC PAIN: MECHANISMS AND MANAGEMENT

Most common side
Medication Starting dose Maximum dose Titration effects Contraindications Remarks

Tricyclic 10–25 mg qhs Titrate to toxic 10–25 mg every Dry mouth, sedation, Narrow-angle Pain relief
antidepressants serum level 5–7 days (entire dizziness, constipation, glaucoma, urinary independent of
II. CHRONIC PAIN SYNDROMES

nortriptyline, dose qhs) confusion, urinary retention, 2–3° heart antidepressant effect
amitriptyline hesitancy, orthostatic block, arrhythmia and is achieved at
hypotension hypersensitivity lower doses. Side
effects settle with
chronic treatment
except dryness of
mouth

Tramadol 50 mg bid 400 mg 50 mg every Nausea, sedation Previously Used with caution in
5–7 days (give demonstrated elderly population
tid or qid) sensitivity to the
drug or opioids

Pregabalin 75 mg bid 600 mg 75 mg every Sedation, confusion, Hypersensitivity Improves sleep,

3 days (bid) dizziness 70 days quicker acting well-
tolerated in elderly
population

EMLA, eutectic mixture of local anaesthetics; IV, intravenous.

 Conclusions 215

Future Therapeutic Agents

Cannabinoids
• No biologically relevant decrease in cannabinoid receptors following
nerve injury.
• There is therapeutic advantage of cannabinoids over opioids in man-
agement of neuropathic pain.

CONCLUSIONS

The past decade has witnessed tremendous gains in the basic science
of pain, particularly in neurophysiology, neuropharmacology and animal
models of disabling neuropathic pain states. The pace of clinical research
has also quickened and improved our understanding of the natural his-
tory of neuropathic pain. Knowledge of the mechanisms and treatment
of neuropathic pain has improved the lives of patients who until recently
had no alternative but to learn to live with their pain.

II. CHRONIC PAIN SYNDROMES

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 C H A P T E R

16
Herpetic Neuralgia

Herpes zoster produces two painful conditions: acute herpes zoster,

also known as shingles, and PHN.

ACUTE HERPES ZOSTER

Acute herpes zoster most commonly occurs in adults who have previ-
ously been infected with the chicken pox virus. An outbreak of the rash
may be due to an infection or a malignancy, especially lymphoma, or an
immunosuppressed state. Majority of cases occur without a known cause.
It is believed that the virus remains dormant in the dorsal root ganglion
and then later becomes reactivated. It multiplies in the dorsal root gan-
glion and is then transported down the sensory nerve to the nerve end-
ings, where the zoster lesions erupt on the skin, producing vesicular rash.
The lesions may be distributed in the region of the thoracic, cervical and/
or lumbar nerves and in the ophthalmic division of the trigeminal nerve.
The discomfort is generally described as a dull, burning, aching or shooting
pain. When the trigeminal ganglia is affected, there is pain in the affected dis-
tribution and headache. There may also be weakness of the eyelid muscles.

Management
The management of acute herpes zoster today consists primarily of
the use of acyclovir. Acyclovir is effective in reducing the time period of
the acute outbreak, in decreasing the pain and promoting healing of the
lesions. The medication is recommended in a dose of 10 mg/kg every 8 h.
The discomfort may also be treated with analgesic medications and anti-
inflammatory medications. The use of corticosteroids is unclear but may
help to reduce the risk of subsequent PHN. It is generally recommended
in a dose of 60 mg/day for 1 week and then tapered over the subsequent
2 weeks. Antidepressants and tranquilizers may relieve pain and associated
depression. A widely used combination is amitriptyline and fluphenazine.

217
218 16. HERPETIC NEURALGIA

Nerve blocks may also be effective. Local infiltration of triamcinolone as

a 0.2% solution in normal saline, in areas of eruption, provides excellent
relief from discomfort, reportedly approaching 100% efficacy.
Epidural blocks may also be effective in the treatment of acute herpes
zoster of the trunk and extremities. Blocks using local anaesthetics with-
out corticosteroids have been effective; some authors reported 70–100%
immediate relief, persisting for 1–5 months in follow-up. Local application
of calamine and capsiacin are also recommended.

POSTHERPETIC NEURALGIA

The pain of PHN follows an acute outbreak of herpes zoster. PHN is

defined as pain, paraesthesia, dysaesthesia, allodynia persisting for four
or more weeks after acute attack.
The characteristic pain of PHN usually includes both burning and aching
superimposed on paroxysms of shocks and jabs. It usually occurs in associa-
tion with dysesthesias, resulting in unpleasant sensation with the slightest
touch on the skin (allodynia). Thus, there are three primary components to
the discomfort:
1. Constant burning or gnawing pain
2. Paroxysmal shooting or shocking pain
3. Sharp, radiating pain that is elicited by very light stimulation

Aetiology
It follows a primary varicella infection. The varicella zoster virus, a
human DNA alpha herpes virus, establishes latency in the dorsal root
ganglia. In the majority of patients, a prodrome of dermatomal pain
(preherpetic neuralgia) precedes the appearance of the rash by several
days. Rare cases of prodromal pain lasting more than 100 days have
been described. The rash of herpes zoster is characterized by a unilateral
vesicular eruption in a dermatomal distribution, preceded by erythema-
tous maculopapular lesions. Crusting of the lesions follows and occurs in
7–15 days in the majority of the patients. There is predilection for involve-
ment of the thoracic dermatomes accounting for 50% of the cases, followed
by the ophthalmic division of the trigeminal nerve.

Distribution
In cranial nerve or in dermatomal distribution of somatic nerves. The
most common cranial nerve to be affected is the trigeminal nerve and its
branches. Decreasing order of frequency in the segmental distribution of
PHN: thoracic > cervical > lumbar.

II. CHRONIC PAIN SYNDROMES

 Postherpetic Neuralgia 219

Clinical Manifestations
Pain persisting for more than 3 months following the healing of skin
lesions has been described variously as burning deep, sharp stabbing, throb-
bing, lancinating, usually paroxysmal, and most commonly associated with
allodynia. Dynamic mechanical allodynia is a characteristic feature found in
58% of the patients. The area of positive sensory finding is far greater than
the area of scarring.

Management of PHN
Pharmacological Therapy
Pharmacological therapy is the mainstay of treatment in PHN. The
drugs commonly used in clinical practice are
1. G abapentin 300 mg HS on day 1, 300 mg BD on day 2 and 300 mg tds
on day 3. Dose may be doubled weekly up to a maximum dose of
2400 mg/day by week 3 or 3600 mg/day by week 4.
2. Pregabalin in a dose range of 75–300 mg/day. Start with a night
dose and then gradually escalate the dose to achieve the desirable
therapeutic effect
3. Carbamazepine – not very efficacious in PHN
4. Oral clonidine 0.2 mg/day may be useful
5. Amitriptyline 10–25 mg/day: use of amitriptyline at the time of herpes
zoster diagnosis showed a reduction in the prevalence of pain by
50% when compared to placebo at 6 months after the diagnosis of
zoster. Therefore, aggressive and/or pre-emptive treatment of pain to
lessen the chance of neuronal sensitization and maladaptive changes
in the peripheral and central nervous system is indicated.
6. It is believed that patients refractory to nonopioid antineuralgic agents
respond to opioid agents. Oxycodone (30 mg tid) and tramadol (50 mg
tid) were found to be efficacious.
7. Lidocaine – Infusing lidocaine has been reported to relieve pain of
PHN. A 5% lidocaine patch produces significant pain relief.

Interventional Therapy
1. Intercostal blocks – with local anaesthetic and steroids (Fig. 16.1). The
intercostal block can be performed at (1) the angle of rib posteriorly
and (2) the posterior axillary line anteriorly. After the usual skin
preparation, the needle entry is made over the rib selected for the
block. It should touch the lower half of the rib subcutaneously. At this
point, with one hand holding the needle and syringe, the other hand
moves caudally over the rib, in such a way that the needle point slips
off the rib. The needle is pushed about 3 mm deeper until a click is
felt. The hub is now turned downwards and the needle tip is directed

II. CHRONIC PAIN SYNDROMES

220 16. HERPETIC NEURALGIA

FIGURE 16.1 Intercostal nerve block. Note the position of the finger with the needle.

under the lower edge of the rib cephalad about 2–3 mm. Aspiration
for air or blood is performed. If aspiration is negative, 3 mL of local
anaesthetic is injected. For one intercostal space to be blocked, three
intercostal nerves of the corresponding dermatome and one above
and below have to be injected. We have found good results by adding
adjuvants like low-dose methyl prednisolone (10 mg/segment) and
ketamine 10 mg/segment. One can repeat up to a maximum of 10
blocks. Radiofrequency ablation of the intercostal nerves is also an
option available for these patients.
2. Sympathetic blocks such as stellate ganglion block and lumbar
sympathetic blocks for lesions in cervical and lumbar dermatomes
have shown varied responses.
3. Paravertebral blocks – with local anaesthetics and steroids. Once the
appropriate dermatomal involvement is determined, the procedure is
performed under monitored care.
  

The patient is placed either in sitting or supine position as per the con-
venience of the operator.
As with the intercostal block, one dermatome above and below the site
of pain are also blocked unless a continuous paravertebral infusion with a
catheter in situ is planned. The patient is seated with the neck flexed and
the shoulders drooping. The spinous process of the level to be injected is
marked and a point 2.5 cm lateral to it is selected. This point will overlie
the transverse process of the lower vertebra in the thoracic spine and the
corresponding vertebra in the lumbar region.
Under aseptic conditions, a 20 gauge 3.5 inch Touhy epidural needle
is inserted through a previously anaesthetized skin wheal, perpendicular
to all planes till contact is made with the transverse process. The distance

II. CHRONIC PAIN SYNDROMES

 Postherpetic Neuralgia 221

Dorsal root

Ventral ramus
Touhy needle Dorsal ramus
Spinal nerve
Sympathetic
Catheter rami communicantes
Sympathetic ganglion

Ventral root

FIGURE 16.2 Thoracic paravertebral block. Note the initial position of the needle with
reference to the transverse process and the later cephalad direction to walk into the paraver-
tebral space.

is noted. The needle is now withdrawn up to the skin and angled in a

manner so as to walk off the caudad edge of the transverse process only
0.5–1 cm beyond the predetermined distance or when a distinct pop is felt
in the thoracic region (Fig. 16.2). It is important to remember that a pop in
the lumbar region signifies a greater depth (psoas fascia) and the needle
should be withdrawn further.
Complications: Haematoma, inadvertent epidural or spinal injections,
pneumothorax and parenchymal lung injury.
Solution: 3–5 mL/segment of 0.125% bupivacaine results in good sym-
patholysis. We have used low-dose ketamine (0.25 mg/kg/segment) and
methyl prednisolone 10 mg/segment with moderate success. Continuous
paravertebral infusion can be used in patients presenting with severe
neuralgia.

II. CHRONIC PAIN SYNDROMES

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 C H A P T E R

17
Orofacial Pain

TRIGEMINAL NEURALGIA

Trigeminal neuralgia, also called tic douloureux, is one of the most severe
and distressing pain syndromes ever described. This condition is charac-
terized by excruciating, shooting, electric shock-like or stabbing pain in
the distribution of the trigeminal nerve.

Epidemiology
Trigeminal neuralgia is a disease of the elderly but it may occur in
young adults too. The peak incidence is between ages 50 and 70 years.

Aetiology
The region of impingement of the blood vessel on the trigeminal root
correlates with the region of face pain. When the pain is perceived in the
second or third trigeminal division, the usual finding is compression of
the rostral and anterior portion of the nerve by the superior cerebellar
artery. If first-division pain is present, the most frequent finding is cross-
compression of the trigeminal root in its caudal and posterior portion,
most often by the anterior inferior cerebellar artery (Box 17.1 and 17.2).

Pathophysiology
Both peripheral and central mechanisms are required for the produc-
tion of tic douloureux. Peripheral nerve lesion (in the trigeminal root or
distal) is the first event in a process that leads to central synaptic changes.
The response of the central synapses to altered peripheral events leads to
the development of tic douloureux. Such a complex theory is required to
explain many of the phenomena seen in Tic Douloureux: triggering by
nonnoxious stimuli, separation of the trigger area from the painful region,

223
224 17. OROFACIAL PAIN

BOX 17.1

P R I M A RY C AU S E S O F T R I G E M I N A L
NEURALGIA
1. M echanical compression of the trigeminal nerve as it leaves pons and
travels towards the Meckel cave (by a vein or arteriovenous malfor-
mation)
2. Herpes zoster
3. Multiple sclerosis
4. Abscess foci or areas of bone resorption in the maxilla or mandible
causing irritation to the trigeminal nerve

BOX 17.2

C AU S E S O F S E C O N D A RY T R I G E M I N A L
NEURALGIA
• Neoplasms
• Neurinoma of trigeminal nerve
• Meningioma
• Acoustic neurinoma
• Brain stem glioma
• Nasopharyngeal carcinoma
• Metastatic tumour
• Vascular lesions
• Aneurysm of circle of Willis
• Arteriovenous malformation
• Ectatic basilar artery of branches
• Arnold–Chiari malformation
• Syringobulbia pseudotumour cerebri
• Amyloidosis
• Sarcoidosis
• Syphillis
• Dejerine–Sottas disease
• Acromegaly
• Paget disease of skull
• Scleroderma

II. CHRONIC PAIN SYNDROMES

 Trigeminal Neuralgia 225

TABLE 17.1 Characteristic Features of Trigeminal Neuralgia

Feature Typical neuralgia (tic douloureux)

Frequency Intermittent: Every few moments to once a day or

even less

Pain-free intervals Always

Description Electric shock, stabbing, shooting

Location Unilateral; usually trigeminal; rarely nervus

intermedius, glossopharyngeal or vagal

Sensory changes None or mild hypaesthesia

Precipitating factor Triggered by nonnoxious stimulation, often in

interior face remote from pain

Autonomic changes None

Local tenderness None

Causative factors Vascular compression of nerve in subarachnoid

space; rarely multiple sclerosis

Common age at onset (year) >50

Gender 60% female

sudden onset and cessation of pain, and response to anticonvulsant

medications.

Symptoms and Signs

Tic is characterized by the following: electric or shock-like stabbing
pains; unilateral pain during any one episode; abrupt onset and termina-
tion of pain; pain-free intervals between attacks; nonnoxious stimulation
triggering the pain, which is often in a different area of the face; minimal or
no sensory loss in the region of pain; and pain restricted to the trigeminal
nerve (Table 17.1).
The history of bilateral tic pain can be elicited in approximately 3% of
patients. Rarely does a patient have bilateral tic pain during one episode;
usually an interval of years separates the occurrence of pain on the two sides.

Triggering
Specific triggering stimuli like touching the face or chewing, talking
or swallowing are common. Many patients report that exposure of the
face to cold triggers their pain. The cutaneous trigger is always a non-
noxious stimulus and is usually located in the anterior face.
The trigger area is always ipsilateral to the pain but can be in the same
or a different division of the trigeminal nerve.

II. CHRONIC PAIN SYNDROMES

226 17. OROFACIAL PAIN

C2

V1

V1

V2

V2

V3
C3 V3
C4

PHOTOGRAPH 17.1 Area of sensory distribution of the three divisions of trigeminal

nerve.

V1 (20%)
V3 (36%)

V2 (44%)

FIGURE 17.1 Distribution of pain among divisions of the trigeminal nerve. V1 –

ophthalamic division; V2 – maxillary division; V3 – mandibular division.

Distribution of the Pain

In majority of patients with Tic Douloureux, the pain is restricted to the
trigeminal dermatomes. The most common site of tic pain is the combina-
tion of the second and third divisions; the rarest site is the combination of
the first and third divisions (Photograph 17.1).

Diagnosis
The disease must be distinguished from atypical pain of the unilateral
variety. Atypical fascial pains are characterized by continuous burning

II. CHRONIC PAIN SYNDROMES

 Trigeminal Neuralgia 227

pain and not electric-like shock. They do not have specific triggers and are
often not located in the trigeminal territory. Atypical face pains are most
common in young women.
Local pathologic processes in the paranasal sinuses, jaws, teeth, phar-
ynx, or base of the skull can lead to severe pain. This type of facial pain
is usually constant and is described as aching, throbbing or burning but
rarely shock-like. The pain is not triggered by nonnoxious stimuli remote
from the painful area and if a branch of the nerve is involved in the dis-
ease, sensory loss can occur.
X-ray of the skull, computed tomography scan head, or magnetic res-
onance imaging should be done where indicated to rule out secondary
pathology.

Pharmacological Treatment
The mainstays of the pharmacological management of trigeminal neu-
ralgia are the anticonvulsant medications such as carbamazepine and
phenytoin.

Carbamazepine
Carbamazepine (Tegretol) is the most likely drug to control tic doulou-
reux. This drug should be started on a daily dosage of 100 mg; the dose
is increased by increments of 100 mg every 2 days until a daily dosage of
600 mg is reached. After 1 week at 600 mg/day if no pain relief is seen, the
daily dosage should be increased to 800 mg for 1 week. This process can be
repeated until a total daily dosage of 1800 mg is reached.

Phenytoin
Second choice of medication. Dosage for reaching the optimal serum
level is 300–400 mg/day given in two divided doses.

Other Drugs
Baclofen (Lioresal) is a drug that was developed for the treatment of
spasticity but Fromm, Terrence, and Chattha (1984) found it effective in
some patients with tic douloureux. It must be started gradually – 5 mg is
given per day, and the dose is increased by 5 mg every 2 days until either
pain relief or toxicity occurs.
Gabapentin and pregabalin are anticonvulsants that may be effec-
tive for tic douloureux. The initial dose of gabapentin should be 300 mg
for 3 days; if this is tolerated, the dose can be immediately increased to
300 mg three or four times a day. If this is tolerated after 1 week, the dose
can be increased gradually to a maximum of 4800 mg/day. Pregabalin
also has to be initiated at a dose of 75 mg/day and gradually increased to
300 mg/day.

II. CHRONIC PAIN SYNDROMES

228 17. OROFACIAL PAIN

Interventional Procedures
Local Anaesthetic Blocks
A local anaesthetic injected either into the trigger area or painful site
temporarily stops the pain of tic douloureux. Nerve blocks can also be
used to show the patients the effects of a planned neurectomy or total
rhizotomy.

Neurolytic Blocks
Alcohol or phenol blocks of the peripheral branches of the trigeminal
nerve or of the gasserian ganglion can be used in the management of tic
douloureux.
Blocks of the branches of the trigeminal nerve are often necessary in
patients who are refractory to oral medication. There are several reasons
for using this form of treatment:
1. I t may allow the patient to experience the kind of numbness obtained
after a destructive procedure on the nerve ganglion.
2. The debilitated patients may be allowed a period of oral intake and
better nutrition.
3. It may have a diagnostic significance by differentiating some forms of
atypical facial pain.
4. It may help to relieve severe debilitating acute pain until medication
can be started and become effective.
5. Some patients obtain prolonged or permanent relief. The procedure
may be repeated when necessary.

Gasserian Gangliolysis
A needle is placed through the cheek into the foramen ovale under flu-
oroscopic guidance. The presence of free CSF confirms needle position.
Further confirmation can be achieved by injecting 1–2 mL of water-soluble
contrast. Gangliolysis can be achieved by injecting 0.5 mL of anhydrous
glycerol or 6% phenol.
Pulsed radiofrequency ablation is presently the technique of choice for
gangliolysis.

Procedure for Maxillary Nerve Block

Patient is placed supine with the head straight, the mandibular notch is
identified, which is most easily done by having the patient open and close
the mouth. A 22 gauge 8 cm needle is then placed perpendicular to the skin
at the posterior and inferior aspects of the notch, which should be close to
the middle of the zygoma. The needle is advanced until it comes in contact
with the lateral pterygoid plate (4–5 cm). The needle is then withdrawn
and redirected anteriorly and superiorly at about a 45° angle towards the

II. CHRONIC PAIN SYNDROMES

 Trigeminal Neuralgia 229

PHOTOGRAPH 17.2 Maxillary nerve block. Note the direction of the needle.

upper root of the nose. The needle is again advanced into the pterygopala-
tine fossa until a paraesthesia is obtained or else the block will have a high
rate of failure (Photograph 17.2). To minimize a CSF injection, the needle
should not be advanced farther than 1.5 cm past the lateral pterygoid plate.
A total volume of 3–5 mL of local anaesthetic is injected, although some
authors advocate the use of as much as 10 mL. Neurolysis can be achieved
with 6% phenol or absolute alcohol. A maximum volume of 1–1.5 mL is
delivered in 0.1 mL divided doses.
Pulsed radiofrequency can also be used for nerve ablation. Needle
placement is confirmed radiologically. After appropriate sensory stimu-
lation and motor stimulation (as detailed in appropriate section) pulsed
radiofrequency is given for 120–180 s at 60°C.

Complications of Maxillary Nerve Block

1. Accidental anaesthetic injection into the pterygomaxillary fissure
(when the needle is advanced too cephalad or too deep) causes
temporary blindness with reversible agents and permanent blindness
with neurolytic agents.
2. Due to the extremely vascular nature of this region, any accidental
intravascular injection will lead to local anaesthetic toxicity.
3. Haematoma formation can be avoided by careful negative aspiration.

II. CHRONIC PAIN SYNDROMES

230 17. OROFACIAL PAIN

PHOTOGRAPH 17.3 Infraorbital block. Note the position of the needle in the infraor-
bital foramen.

4. O rbital swelling, anaesthesia of the orbital tissues ophthalmoplegia,

loss of visual acuity, or diplopia can occur if the local anaesthetic or
neurolytic solution enters the infraorbital fissure.
5. Accidental injury to the pharynx can occur. Aspiration of air usually
indicates that the needle has been placed too far posteriorly and the
pharynx has been entered. It is important to then change the position
of the needle before proceeding.

Infraorbital Nerve Block

This is one of the terminal branches of the maxillary division of the
trigeminal nerve innervating the area of the lower eyelid, upper eyelid
and its mucosa, infrolateral portion of the nose and the vestibule.
Procedure: Infraorbital ridge of the maxilla is identified and the infra-
orbital foramen is palpated about 2 cm lateral to the nose in line with the
pupil in neutral gaze. The infraorbital canal lies at 45° angle backwards
and upwards to its exit from the maxilla. Using a 24 gauge half inch
needle, locate a point just below and medial to the infraorbital foramen
and enter the canal maintaining a 45° angle to the skin (Photograph 17.3).
Do not advance the needle more than 0.5 cm and deposit the desired
solution.
Solution: 3 mL of 0.25% bupivacaine with 10 mg of methylprednisolone
or 1 mL of 6% phenol or 1 mL of absolute alcohol.
Radiofrequency lesioning can also be performed.
Complications: (1) Damage to orbital contents if the needle is advanced
too far or if large volumes of neurolytic agents are used. (2) Haematoma of
the cheek. (3) Anaesthesia dolorosa following neurolytic blocks.

II. CHRONIC PAIN SYNDROMES

 Glossopharyngeal Neuralgia 231

Mandibular Nerve Block

Procedure: Position of the patient is same as for the maxillary nerve
block. The landmarks are also the same. The needle is introduced through
the mandibular notch of the mandible and advanced through the infra-
temporal fossa, with the lateral pterygoid plate serving as a bony end
point. The needle is walked backwards off the lateral pterygoid plate
maintaining the same depth as the plate until paraesthesia of the lower
lip, lower jaw, or ipsilateral tongue or ear is obtained.
Pulsed radiofrequency ablation can be performed after the position of
the needle has been confirmed and appropriate sensory and motor stimu-
lation done.
Solution: 5 mL of 0.5% bupivacaine for diagnosis, 2 mL of 6% phenol or
absolute alcohol for therapeutic block.
Complications: Injury to the pharynx as aforementioned can occur here
too. Accidental injections into the middle meningeal artery can take place
if careful aspiration is not done. Haematomas of the cheek can occur.

Blocks of the Terminal Branches of the Mandibular Nerve

• Inferior alveolar nerve: In the anterior border of the ramus of the
mandible the needle is inserted at a point medial to and approxi-
mately 1 cm above the occlusal surface of the third molar. The needle
is advanced along the medial side of the ramus to a depth of 2–3 cm
till paraesthesia is elicited or periosteum is contacted (withdraw
needle by 0.5 cm) and deposit the drug (0.5–1 mL).
• Mental nerve: An area approximately 2 cm from the midline in a plane
parallel to the supraorbital and infraorbital foramina is identified.
A 25 gauge 1.5 inch needle is advanced towards the foramen. After
eliciting paraesthesias, 0.5 mL of alcohol or 8% phenol is injected to
produce complete neurolysis.

Blocks of the Terminal Branches of the Ophthalmic Division

• Supraorbital and supratrochlear nerves: The supraorbital notch in
the supraorbital ridge of the frontal bone is identified. The needle is
advanced perpendicular to the skin towards the subraorbital notch for
the supraorbital block and medial to the notch for the supratrochlear
block.
• Solution: 1 mL of 0.5% bupivacaine for diagnosis and 0.5 mL phenol or
alcohol for therapeutic.

GLOSSOPHARYNGEAL NEURALGIA

GN is a type of orofacial neurogenic pain characterized by shock-like

pain in the territory of the glossopharyngeal nerve. It is in every way

II. CHRONIC PAIN SYNDROMES

232 17. OROFACIAL PAIN

similar to tic douloureux except for the distribution of the pain and the
customary site of the triggering stimulus. It is less common than trigemi-
nal neuralgia. The incidence ratio is about 1:100. The International Asso-
ciation for the Study of Pain defined this neuralgia as a sudden, severe,
brief, stabbing, recurrent pain in the distribution of the glossopharyngeal
nerve.

Aetiology
The aetiology of primary GN is unknown. It can be secondary due to
vascular component compressing the nerve as it exits from the cranium
through the jugular foramen; it is also seen in patients with multiple scle-
rosis or neck malignancies.

Symptoms and Signs

GN is characterized by excruciating shock-like pain in the region of the
tonsillar fossa, pharynx or base of the tongue. It can radiate to the ear or
the angle of the jaw or into the upper lateral neck. The trigger zone is often
in the same area, and patients frequently report that swallowing, yawn-
ing, clearing the throat, or talking is the precipitating stimulus. Chewing
or touching the face does not precipitate an attack.

Diagnosis
The nature of the pain, its description by the patient and chronology of
the attacks are typical. Blocking the trigger area with local anaesthetic can
confirm the site of the trigger and nerve involvement. The diagnosis can
be confirmed by cessation of pain when this nerve is blocked at the jugular
foramen or when topical anaesthesia of the pharynx stops the pain.

Treatment
Medical
Pain due to GN is quite troublesome and distressing to the patients.
These patients are often referred to pain clinics from other specialities
such as otorhinolaryngology, dental surgery, neurology, or neurosurgery,
with or without therapeutic trials. The first drug of choice for GN is car-
bamazepine starting from a low dose of 100–200 mg/day to a maximum
of 1000–1200 mg/day. Some patients may become refractory to treatment
with time. The other anticonvulsants that are recommended for this neu-
ropathic pain are phenytoin, sodium valproate, clonazepam and gaba-
pentin. These drugs block the sodium channel and are able to suppress
spontaneous discharge in A-delta and C-fibres. Gabapentin (Neurontin)

II. CHRONIC PAIN SYNDROMES

 Glossopharyngeal Neuralgia 233

has been found to be an effective therapeutic option in patients refractory

to carbamazepine treatment. The most common adverse effects of gaba-
pentin are somnolence, dizziness, ataxia and fatigue, and they are usually
mild to moderate in severity.
Successful treatment with baclofen has been reported in patients with
GN who were receiving carbamazepine monotherapy. The disadvantages
are excessive weakness, sedation and ataxia with higher doses and its pro-
longed use.
As an adjuvant drug therapy, tricyclic antidepressants are used in the
treatment of GN. The commonly used drug is amitriptyline, which causes
an inhibitory effect on the nociceptive pathway via descending pathways
on the dorsal horn region of the spinal cord by increasing the levels of
serotonin and noradrenaline in the brain stem by blocking neural uptake.

INTERVENTIONAL PROCEDURES
The glossopharyngeal nerve can be blocked using a series of blocks
with dilute local anaesthetic with or without steroids. Neurolytic blocks
can be performed using alcohol or phenol. Care must be taken while per-
forming these procedures due to the proximity of internal carotid artery.

TECHNIQUE OF GLOSSOPHARYNGEAL NERVE BLOCK

Position of patient is supine with the head turned to the opposite side.
Landmarks: Line joining the mastoid process and angle of the mandible
is visualized. The entry point is marked as the midpoint of this line. The
fluoroscope is then placed in an oblique position such that the styloid pro-
cess corresponds to the midpoint marked above.
Procedure: Under aseptic conditions a 22 gauge 1.5 inch needle is
attached to a syringe with desired solution, the needle is advanced at
this midpoint in a plane perpendicular to the skin. The styloid process
is encountered within 3 cm. Now the needle is withdrawn slightly and is
walked off the styloid process posteriorly. As soon as bony contact is lost
and aspiration is negative for blood or CSF, 5 mL of the desired solution
is deposited.
If radiofrequency is planned, after walking off the styloid process sen-
sory and motor stimulation is done as per routine. Pulsed radiofrequency
waves are delivered at 42°C for 120 s.
Solutions: 5 mL of 0.25% bupivacaine or 5 mL of 0.5% lignocaine. When
steroid injections are desired (when the patient does not respond to phar-
macotherapy and repeated local anaesthetic blocks), 80 mg methylpred-
nisolone is added to the first dose followed by 40 mg in the subsequent
injections. For neurolytic blocks, 1 mL of phenol or absolute alcohol is
used.
Number of blocks: Minimum 5 and up to a maximum of 10 for one
cycle. The blocks can be repeated daily or on alternate days.

II. CHRONIC PAIN SYNDROMES

234 17. OROFACIAL PAIN

Radiofrequency thermocoagulation of the ninth cranial nerve and epi-

dural electrical stimulation of the motor cortex have all been tried in an
attempt to relieve pain with limited success.
Surgical treatment is recommended in GN secondary to local infections,
elongated styloid process, neurovascular abnormalities, ossified elongated
styloid ligament, and intra- or extracranial tumours. Surgery should be
undertaken only when the advantages outweigh the complications.

COMPLICATIONS
1. D ue to the proximity of the glossopharyngeal nerve to the vagus and
accessory nerves, any spillover can produce anaesthesia of the larynx,
weakness of trapezius muscle, and sternocleidomastoid paralysis on
the ipsilateral side.
2. Dysphagia due to paralysis of the stylopharyngeus muscle.
3. Dysphonia due to ipsilateral vocal cord palsy.
4. Reflex tachycardia because of vagal blockade.
5. Accidental intravascular (internal jugular vein and carotid artery)
injection and haematoma formation.
6. Anaesthesia dolorosa postprocedure dysaesthesias following neurolytic
blocks. Sloughing of skin and subcutaneous tissue may occur.
7. Aspiration due to anaesthesia of larynx and pharynx. It is advisable to
limit oral intake for a few hours after the block.

II. CHRONIC PAIN SYNDROMES

 C H A P T E R

18
Scar Neuralgia/Painful
Scars

Surgical incisions and trauma inevitably damage cutaneous and

subcutaneous nerves. Damage to these nerves lead to sprouting of the
injured nerve and this produces neuroma formation and resultant scar
pain. The incidence of persistent scar pain following surgery or trauma
is not yet known. However, painful scars and persistent pain follow-
ing surgical incisions and trauma do occur after at least 10% of surgical
operations.
Neuromas formed as a result of damage to cutaneous nerves develop
spontaneous electrical discharges. Changes also occur in the central ner-
vous system where deafferentation occurs, especially when there is dam-
age to a large sensory nerve. The deafferented neurons on the dorsal horns
become hypersensitive, responding to neuronal circuits to which they do
not normally respond. Animal studies have suggested a genetic predis-
position in patients who develop scar neuromata and persistent pain.
Observation in humans suggests that patients who develop neuromas
and incisional pain frequently have recurrences if an attempt is made to
remove the neuroma surgically.

CLINICAL PRESENTATION

Patients complain of persistent pain in the operative/trauma scars

2 weeks following surgery or injury. Pain is generally a continuous one
and is aggravated on palpation and exertion. It is unusual for a whole
scar to be painful but ‘trigger points’ may be found in a scar. These can be
associated with hyperaesthesia and radiation of pain along dermatomes
from the scar. Hyperaesthesia is a common feature with over 90% of scar
demonstrating this sign. Approximately 10% patients have allodynia. The
incidence of type of operation or trauma that had caused the painful scar

235
236 18. SCAR NEURALGIA/PAINFUL SCARS

TABLE 18.1 Incidence of Type of Surgical Operation Causing Painful Scar

Procedure Incidence (%)

Inguinal hernia repair 22–40

Thoracotomy 14–22

Pyelolithotomy 3–8

Breast surgery 13–17

Appendectomy 4–9

Cholecystectomy 3–20

Dental surgery 3–5

Caesarean section 3–7

Amputation 50–80

is shown in Table 18.1. On examination, majority of patients have a dis-

crete palpable tender nodule related to the scar. Hyperaesthesia and allo-
dynia can also be easily elicited.

COMMON OPERATIVE PROCEDURES PREDISPOSING

A PAINFUL SCAR

• I nguinal hernia repair

• Thoracotomy
• Pyelolithotomy
• Breast surgery
• Appendectomy
• Cholecystectomy

TREATMENT PROTOCOL

In patients with persistent scar pain of less than 6 weeks duration, an

initial trial with the use of drugs is often the first line of treatment. Some
of the most common drugs used in combination are
  

•  aracetamol (up to 1000 mg/day)

P
• Serratiopeptidase
• Piroxicam 10–20 mg/day
• Amitriptyline 25 mg/day single dose
• Anticonvulsants such as carbamazepine (up to 600 mg/day) and
gabapentin (up to 600–900 mg/day) in patients with allodynia and
hyperalgesia

II. CHRONIC PAIN SYNDROMES

 Treatment Protocol 237

• T ramadol 100–150 mg/day by oral route

• Local capsaicin
  

A 2- to 3-week trial of a combination of nonsteroidal anti-inflammatory

drugs such as paracetamol, piroxicam along with serratiopeptidase,
amitriptyline, local capsaicin and gabapentin can produce good pain
relief in over 35% patients. These drugs are then gradually tapered off.
If the scar pain is of more than 6 weeks duration or has not responded
to the pharmacological approach, interventional therapy is opted for.
The normal treatment plan in the pain clinic depends on the clinical
findings. Patients with a palpable discrete tender nodule in the sub-
cutaneous tissue within the area of surgical tissue dissection are given
an injection into the tender nodule as well as the painful scar of 20 mg
methyl prednisolone acetate (Depomedrol) in 3–5 mL of 0.25% bupiva-
caine. The infiltration of scar done every alternate day on 6–10 occasions
produces persistent pain relief in majority of patients. It is important to
remember that the total dose of methyl prednisolone during the course
of these injections should not exceed 120 mg. If pain relief lasts for less
than 2 weeks, but the initial injection had removed the pain for the
expected duration effect of the local anaesthetic, or had recurred after
several such injections, then neurolytic injections of aqueous phenol 8%
or phenol 10% in 50% glycerine and 50% water are done in the same
way. Patients with hyperaesthetic scars are also administered low doses
of amitriptyline (25–50 mg), carbamazepine (up to 600 mg daily) or gab-
apentin (up to 900 mg daily) in divided doses. Patients with hyperalge-
sic scars also show good relief with TENS.

Treatment Modalities for Relief from Scar Pain

•  ocal anaesthetics and steroid injections in the scar
L
• Neurolytic injections in scar neuromas
• TENS in the hyperalgesic areas of scar
• Nerve blocks repeatedly with bupivacaine 0.25% and low doses of
methyl prednisolone
  

It is difficult to explain how local anaesthetic and steroid injections can

produce long-lasting pain relief. It has been suggested that an afferent
efferent neuronal loop at spinal segmental level is broken by injecting
local anaesthetic to the neuroma. It is also possible that methyl pred-
nisolone acetate has a neurolytic effect, as steroids are known to have a
myotoxic effect. The datacard on methyl prednisolone acetate states that
it inhibits fibroplasia. This disturbance of normal healing might prevent
the spontaneous activity of the neuroma and steroids have been shown to
prevent the development of spontaneous firing within experimental neu-
romata. Certainly, steroids have a membrane-stabilizing effect, and block

II. CHRONIC PAIN SYNDROMES

238 18. SCAR NEURALGIA/PAINFUL SCARS

C-fibre and A-fibre transmission. The longevity of action of methyl pred-

nisolone acetate might help to produce a permanent desensitization of
the neuroma. The reassurance and demonstration by temporary analgesia
that their pain was not due to a serious internal derangement, consequen-
tial upon or coincidental to the operation undoubtedly allays the fear of
many patients and is sufficient therapy for some. The effect of phenol on
the neuroma is probably quite simply neurolytic.
It is generally held that surgical explorations have no place in the treat-
ment of scar neuromata and that the new neuroma produced by surgical
excision is just as likely to be painful. However, operations in selected
patients can be invaluable, and the overall results of treatment can be bet-
ter than is generally believed.
The usefulness of sympathetic blocks for hyperpathic scars is theoreti-
cally justified, although in our clinical practice we have not administered
such blocks in scar neuralgias very often.

II. CHRONIC PAIN SYNDROMES

 C H A P T E R

19
Complex Regional Pain
Syndrome

CRPS is a challenging neuropathic pain states quite difficult to com-

prehend and treat. Although not yet fully understood, advances are being
made in the knowledge of the mechanisms and treatment involved with
CRPS. CRPS was earlier known as causalgia, RSD, shoulder-hand syn-
drome, Sudeck dystrophy and a variety of other terminologies. The term
RSD was introduced by Evans in as early as 1946. Some of the earliest and
most interesting descriptions of causalgia came from the American Civil
War by Silas Weir Mitchell (1916).
CRPS is the term introduced in 1994 by International Association for
the Study of Pain and is defined as a ‘painful syndrome that develops after
an initiating noxious event such as trauma’. Ongoing pain is often associ-
ated with hyperalgesia to cutaneous stimuli.

TYPES OF CRPS

CRPS type 1 (formerly RSD): A syndrome that usually develops after

an initiating noxious event, is not limited to the distribution of a single
peripheral nerve, and is apparently disproportionate to the inciting event.
It is associated at some point with evidence of oedema, changes in skin
blood flow, abnormal sudomotor activity in the region of the pain, and
allodynia or hyperalgesia.
CRPS type 2 (formerly causalgia): A syndrome of sustained burning
pain, allodynia and hyperpathia after a traumatic nerve lesion, often con-
tinued with vasomotor dysfunction and later trophic changes.

239
240 19. COMPLEX REGIONAL PAIN SYNDROME

DIAGNOSTIC FEATURES OF CRPS

1. C ontinuing pain that is disproportionate to any inciting agent.

2. Must report at least one symptom in each of the following four
categories:
a. Sensory: Reports of hyperaesthesia.
b. Vasomotor: Reports of temperature asymmetry and/or skin colour
changes and/or skin colour asymmetry.
c. Sudomotor/oedema: Reports of oedema and/or changes and/or
sweating asymmetry.
d. Motor/trophic: Reports of decreased range of motion and/or motor
dysfunction (weakness, tremor, and dystonia) and/or trophic
changes (hair, nail, and skin).
3. M
 ust display at least one sign in two or more of the following categories:
a. Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia
(to light touch).
b. Vasomotor: Evidence of temperature asymmetry and/or skin
colour changes and/or asymmetry.
c. Sudomotor/oedema: Evidence of oedema and/or sweating
changes and/or sweating asymmetry.
d. Motor/trophic: Evidence of decreased range of motion and/
or motor dysfunction (weakness, tremor, and dystonia) and/or
trophic changes (hair, nail, and skin).
  

Diagnosis of CRPS would be precluded by the existence of any known

pathology that would otherwise account for symptoms and signs present
in the distal parts of an extremity but outside the territory of an injured
nerve.
The term CRPS was chosen for the following reasons:
  

• C omplex signifies the varied clinical features found in these conditions.

• Regional emphasizes that in the majority of cases it involves a region
of the body, usually an extremity, but may occur on another part of
the body or spread to different areas of the body.
• Pain is considered essential to the diagnosis of CRPS and includes pain
that is spontaneous or evoked such as allodynia or hyperalgesia. In
rare cases otherwise resembling CRPS, pain may be minimal or absent.
  

The cardinal symptoms and signs that constitute CRPS are as follows:
  

1. Pain
a. Follows a known initiating noxious event, seems to be physically
quite minor.
b. Disproportionate in duration, severity and distribution.
c. Noxious event may occur peripherally, in the CNS, or in the viscera.

II. CHRONIC PAIN SYNDROMES

 Diagnostic Features of CRPS 241

d. M ay be spontaneous, deep and aching in quality aggravated by

orthostasis and touch.
e. May be associated with allodynia or hyperalgesia.
2. V
 asomotor and sudomotor abnormalities
Tend to be more obvious early in the course of the disorder.
a. Swelling of affected joints and other soft tissues.
b. Temperature differences that may be either colder or warmer than
the contralateral extremity.
c. Associated with changes in skin colour – red, dusky, and blue.
3. Trophic changes
These are generally described as occurring late in the disorder.
a. Skin, nail and hair growth changes.
4. Motor changes
a. Weakness
b. Tremor
c. Reduced movement
d. Dystonia.
  

Three clinical stages of CRPS type 1 are classified as follows:

  

1. A cute stage (hyperaemic)

2. Dystrophic stage (ischaemic)
3. Atrophic stage.

Acute stage
•  ommences at the time of injury.
C
• Characterized by constant moderate burning pain.
• Localized to the area of injury.
• Associated with hyperpathia, allodynia and hyperalgesia.
• Skin – red and warm.
• Evidence of localized oedema, muscle spasm and tenderness.
• Stage can be completely reversed by sympathetic blockade.
• If untreated, can progress to the second dystrophic stage.

Dystrophic Stage
The dystrophic stage is characterized by
  

• s preading of oedema;
• increasing stiffness of the joints and muscular wasting;
• pain which is usually spontaneous and burning in nature and may
radiate proximally or distally from the site of injury;
• pronounced hyperpathia and allodynia;
• moist, cyanotic and cold skin;

II. CHRONIC PAIN SYNDROMES

242 19. COMPLEX REGIONAL PAIN SYNDROME

• c oarse hair.
• s ympathetic blocks may still be effective in reversing the process
though a larger series of blocks or a prolonged sympathetic blockade
may be necessary to afford permanent relief;
• if not treated, it progresses to the third atrophic stage.

Atrophic Stage
The atrophic stage is characterized by
  

• s mooth, glossy, tight, pale or cyanotic skin;

• loss of hair;
• lowering of local temperature;
• extreme weakness and limitation of motion at virtually all of the
involved joints;
• contracture of flexor tendons;
• advanced osteoporosis;
• aggravated by weight bearing, movement and frequently by exposure
to cold;
• in the atrophic stage, syndrome becomes irreversible. Although
sympathetic blockade may still provide the temporary relief, it is no
longer effective in terminating the process permanently.

AETIOLOGY AND PATHOPHYSIOLOGY

Understanding of pathophysiology of CRPS has significantly improved

over 2001–10. It has been established that in certain patients with CRPS,
pain depends on continued sympathetic activity in affected areas. Roberts
introduced the term ‘SMP’ to describe the aspect of pain which is relieved
by blockade of efferent sympathetic nervous system.
Certain models have been proposed to explain how CRPS produces
disproportionate pain in duration as well as in severity, in response to
noxious stimuli. The model (Fig. 19.1) which could help in understanding
the role of SMP in CRPS is as follows:
  

1. A fferent sensitization, in which afferent nociceptive fibres are

sensitized by chemical compounds – i.e. prostaglandins – released
from sympathetic terminals, resulting in aberrant activity in response
to mechanical, thermal and chemical stimulation.
2. Ephaptic activity of abnormal synaptic connections between efferent
sympathetic and afferent sensory nerves resulting in aberrant
impulses.
3. Increased density of adrenergic receptors on the plasma membrane
of nociceptive afferents leads to chemical coupling of sympathetic
sensory system, leading to excessive painful signal transmission.
  

II. CHRONIC PAIN SYNDROMES

 Noxious stimulus PNS CNS

Somatic pain SMP

Aetiology and Pathophysiology

II. CHRONIC PAIN SYNDROMES

Nociceptors CNS
modulation
Afferent sensitization Synaptic Increased adrenergic
by chemical compounds connections receptor density

PG NE

Sympathetic nervous
system

FIGURE 19.1 Model representing the role of sympathetic nervous system in complex regional pain syndrome. CNS, central nervous system; NE,
norepinephrine; PG, prostaglandin; PNS, peripheral nervous system; SMP, sympathetically maintained pain.

243
244 19. COMPLEX REGIONAL PAIN SYNDROME

This altered physiological state keeps the CNS in a sensitized state and
any minor noxious stimulus in the affected area is interpreted as severe
pain, in terms of intensity as well as duration, by CNS.

MANAGEMENT OF CRPS

Management of CRPS involves multidisciplinary co-ordinated approach

to function restoration built around a treatment algorithm, and attempts
to normalize functions should guide therapy, keeping in mind that each
patient needs to have treatment plans tailored to his individual problems.
Comprehensive diagnostic evaluation and early and aggressive ther-
apeutic interventions are imperative to prevent onset of the irreversible
stage III. While progress is being made in treating patients with CRPS, it is
important to remember that the goals of care in CRPS are to
  

1.  erform a comprehensive diagnostic evaluation;

p
2. be prompt and aggressive in treatment interventions;
3. assess and reassess the patient's clinical and psychological status;
4. be consistently supportive;
5. strive for the maximal pain relief and functional improvement.
  

The therapeutic approach often calls for a combination of treatments.

Antiepileptics, opioids, antidepressants, vasodilators and topical agents
along with regional sympathetic blocks and a rehabilitation program can
help several patients suffering from these disorders. However, the main-
stay for therapy of CRPS is sympathetic efferent blockade, primarily by
sympathetic chain/ganglion blockade at various anatomical sites by
injecting local anaesthetic or neurolytic agent or RF ablation depending
upon the region affected.

TREATMENT PROTOCOL OF CRPS

When a patient with CRPS reports in a pain clinic, a detailed history

and a comprehensive physical examination are undertaken and are docu-
mented. The patient is assessed for the following clinical parameters and
the same parameters are assessed for clinical evidence of recovery during
treatment period.
  

•  ain (on visual analogue scale 1–10)

P
• Neuropathic pain scale
• Hyperalgesia/allodynia/hyperaesthesia
• Skin colour/temperature
• Oedemas
• Range of motion

II. CHRONIC PAIN SYNDROMES

 Treatment Protocol of CRPS 245

CRPS of Upper Extremity: Mild to Moderate Pain

• I ntermittent SGB at C6 level by classical anterior paratracheal
approach.
• Injection of bupivacaine 0.25% (10 mL) at each sitting.
• A series of 10–15 blocks is administered on alternate days to each
patient.
  

Effectiveness of block at each sitting is assessed by the following

methods:
  

1.  resence of Horner syndrome

P
2. Feeling of warmth in limb
3. Rise in temperature of limb (by telethermometry)
4. Improvement in pulse oximeter graph/saturation (by pulse oximeter).

CRPS of Upper Extremity: Moderate to Severe Pain

Continuous SGB
Continuous SGB through ambulatory infusion pump using mixture of
bupivacaine and morphine was first described in a case report by Owen
Flakenberg et al. (1992) and they concluded that continuous infusion with
a mixture of bupivacaine and morphine provided prolonged relief from
symptoms in RSD compared to single-shot injections. Continuous SGB
has been found useful when (1) conservative treatment with physical ther-
apy, mild analgesics and other drugs has failed; (2) conservative therapy
and intermittent SGB have failed; and (3) patients show limited and short-
lived response to intermittent SGB.
  

Advantages of continuous SGB

1. P rolonged sympathetic block provides faster relief from
sympathetically mediated pain.
2. Multiple injections are avoided.
3. Incidence of accidental vascular injection is significantly reduced.
4. Provides continuous relief from associated symptoms.
  

Contraindications: In spite of SGB being very effective and treatment of

choice in CRPS of upper extremity, there are certain circumstances where
this
  
block is contraindicated, which are as follows:
1. Absolute contraindication
a. Patient on anticoagulant therapy
b. Patient having pneumothorax or pneumonectomy on the
contralateral side
c. Recent cardiac infarction.
2. Relative contraindications

II. CHRONIC PAIN SYNDROMES

246 19. COMPLEX REGIONAL PAIN SYNDROME

a. G
 laucoma
b. M  arked impairment of cardiac conduction system
  
(e.g. atrioventricular heart block).
Technique: After careful and detailed evacuation, the patient is selected
for block. Informed consent must be obtained. Potential risks, complica-
tions, and possible side effects should be explained in detail. The patient
should share the responsibility for decision making and must understand
the risks and the fact that complications do occur. All standard resuscita-
tive gadgets need to be readily accessible.
The patient is made to lie supine with the head resting flat on the table
without a pillow; the C6 tubercle (Chassaignac's) is usually located 2.5 cm
lateral and cephaloid to midsternal notch at the cricoid level. At the point
of entry, the index finger of left hand is insinuated in the groove between
the trachea and medial border of the sternocleidomastoid muscle and the
common carotid artery is well felt and retraced laterally. A 20 gauge IV
cannula is then attached to a 10 mL saline-filled syringe, which is inserted
perpendicular to the skin medial to index finger till it hits the C6 tuber-
cle (Photograph 19.1). Aspiration test is done to rule out the presence of
blood and cerebrospinal fluid. The stylet is then taken out and cannula is
firmly secured to skin with sutures and connected to the ambulatory elas-
tomeric infusion pump filled with the local anaesthetic agent bupivacaine
0.125% to deliver a fixed flow of 2 mL/h for 7–10 days; during the infusion

(a) (b)

(c) (d)

PHOTOGRAPH 19.1 Continuous stellate ganglion block. (a) Identifying the land-
marks. (b) Insertion of cannula. (c) Injection of drug. (d) Cannula in place.

II. CHRONIC PAIN SYNDROMES

 Treatment Protocol of CRPS 247

period, patient is assessed continuously for clinical evidence of recovery

(Photograph 19.2).
Complications and side effects: A proper technique is used and due
attention is given to safety measures while giving SGB although it is a sim-
ple, safe, minimally invasive and an effective procedure. Most unpleasant
side effects result from Horner syndrome, e.g. ptosis, miosis and nasal
congestion. Common complications result from diffusion of local anaes-
thetic into nearby nervous structures. These include the recurrent laryn-
geal nerve with complaints of hoarseness, feeling of a lump in the throat,
and sometimes a subjective shortness of breath. Partial brachial plexus
block can also occur. The two most feared complications are intraspinal
and intravascular injections of local anaesthetic. Respiratory embarrass-
ment and need for mechanical ventilation can result from injection into

(a)

(b)

PHOTOGRAPH 19.2 (a) Fixation of cannula. (b) Ambulatory patient with continuous
stellate ganglion block.

II. CHRONIC PAIN SYNDROMES

248 19. COMPLEX REGIONAL PAIN SYNDROME

intrathecal space. Sinus arrest syndrome, haematoma formation, severe

hypotension, migraine headache, delayed subdural block and pneumo-
thorax have been reported following SGB.

CRPS of Lower Extremity: Mild Disease

Medications and adjuvants.

CRPS of Lower Extremity: Moderate to Severe Disease

Percutaneous lumbar sympathectomy by either RF ablation or chemi-
cal neurolysis by phenol or alcohol.

Lumbar Sympathectomy by RF Ablation

The procedure is performed under mild sedation in prone position.
The RF cannula is introduced 5 cm lateral to spinous process of L2, L3,
L4, and vertebral bodies (L3, L4 and L5 if the foot is involved). The area
is made aseptic and a disposable, sterile top-pole needle (23 gauge,
150 mm long) is inserted through the wheal under the guidance of
C-arm with image intensifier. The needle is directed to the junction of
the middle and lower thirds of vertebral body at L2 and at the junction of
the middle and upper thirds at L3 according to lateral fluoroscopy. The
midvertebral body is targeted at L4. If the foot is involved, L5 vertebral
body is targeted as well. The position of needle tip is checked by X-ray
in PA and lateral views. In lateral view, the needle tip should barely
reach anterior border of vertebral body. The sympathetic chain was then
identified by administering injection of 0.5–1 mL of omnipaque, which
is checked in lateral and PA views. After noting the spread of contrast
material behind facet joint line on PA view and after negative aspiration
for blood, 1–2 mL of 1.0% lignocaine solution is injected through the
needle. This is taken as the test block. The test block is done at L2, L3,
and L4 levels if the foot is not involved or at L3, L4 and L5 levels if the
foot is involved. After 2 min, skin temperature at great toe, heel and foot
is checked. If skin temperature change of at least 1°C is obtained, it is
taken as a positive sympathetic block. If any sensory or motor dysfunc-
tion is noted after test block, the results are considered invalid and the
test block is repeated.
After 5 min, the RF electrode is introduced inside the RF cannula and
is kept in position for a total of 90 s at a temperature of 80°C. The can-
nula is then advanced anteriorly by 5 mm and a second lesioning is made.
Lesioning sites are at L2, L3, and L4 levels or L3, L4, and L5 levels (if the
foot is involved). Each time, the temperature as well as colour change of
the foot is observed. When a satisfactory effect is achieved, the RF cannula
is removed.

II. CHRONIC PAIN SYNDROMES

 Treatment Protocol of CRPS 249

Patients are continuously followed up in the pain clinic for clinical evi-
dence of recovery. Patients who have inadequate recovery or who need
frequent repeated sympatholysis are also prescribed medication.
  

Advantages of RF ablation in CRPS

• Low morbidity and no mortality
• Least possibility of neuroma formation
• No radiculopathy
• Minimally invasive
• Outpatient procedure.
  

Chemical neurolysis by injecting 2–3 mL of 6% phenol at each site is

also used for sympathetic neurolysis.

Drug Therapy in CRPS

Two basic classes of drugs are used:
Class A: drugs used for prophylaxis to manage pain in CRPS and other
symptoms (daily drugs).
Class B: abortive drugs for crisis management (rescue agents).

Class A
TRICYCLIC ANTIDEPRESSANTS
Patients with CRPS have usually visited multiple physicians and have
continuously suffered for prolonged period and are therefore very a­ nxious,
depressed and suspicious about the outcome of t­reatment ­modalities. In
these patients, TCA are very effective. ­Amitriptyline is the most com-
monly used drug with a d ­ osage of 12.5–50 mg hs; nortriptyline is given at
a dosage of 10–20 mg hs.
Side effects: Dryness of mouth, constipation, epigastric distress, urinary
retention, blurred vision, palpitation, sedation, and fine tremors.
Cautions: Used with caution in patients of hyperthyroidism, ischaemic
heart disease, renal and hepatic diseases.

ANTIEPILEPTIC DRUGS
Gabapentin works primarily by enhancing natural GABA systems in
pain modulation but may also have some impact in suppressing excit-
atory amino acids such as glutamate. Gabapentin is frequently adminis-
tered to CRPS patients at a dosage to start with 300 mg once a day and
gradually increased to 300 mg thrice a day to four times a day. Dizziness
and fatigue are the major side effects frequently encountered and can be
taken care of by increasing the dosage gradually. Oxcarbazepine and car-
bamazepine are another group of drugs frequently administered; sedation
with oxcarbazepine is much less than carbamazepine. Oxcarbazepine is

II. CHRONIC PAIN SYNDROMES

250 19. COMPLEX REGIONAL PAIN SYNDROME

started with a dosage of 300 mg once a day and is gradually increased to

900–1200 mg daily.
NONSTEROIDAL ANTI-INFLAMMATORY DRUGS
They are particularly useful in cases where there is considerable inflam-
mation. Aspirin and ibuprofen are frequently prescribed. However, gas-
tric irritation remains a main concern, and so these drugs are usually
combined with drugs like ranitidine and pantoprazole. They are used
with caution in patients having coexisting renal disease. Cox-2 inhibitors
like etoricoxib and valdecoxib are not found to be very effective though
supposed to have minimal gastric irritation properties and should be used
with caution in patients with cardiovascular diseases.

PERIPHERAL VASODILATORS
Patients having intense vasoconstriction, supposedly due to overactiv-
ity of sympathetic nervous system, are frequently administered drugs like
nifedipine 5–20 mg twice or thrice a day, pentoxifylline 400 mg thrice a
day, and xanthinol nicotinate 500 mg twice a day. Flushing of skin can be
troublesome in some patients. Oral nifedipine has been found to show
persistent and promising results.
Patients with severe burning sensation, allodynia, hyperalgesia or
hyperaesthesia are advised to apply lidocaine jelly 2% or eutectic mixture
of local anaesthetics cream. It is effective in some patients for short dura-
tion and repeated application is required.
Class B
STEROIDS
Steroids are used for a short period (5–7 days) only when severe inflam-
mation resulting in intractable pain is present. Prednisolone 20 mg twice a
day to thrice a day is usually prescribed. Dexamethasone 2–4 mg twice a
day is another alternative steroid used frequently.
OPIOIDS
Patients complaining of severe pain and who have already received
NSAIDs are administered opioids for a short duration in early phase. Usu-
ally tramadol at a dosage of 50–100 mg three times a day is prescribed,
which is withdrawn gradually as other treatment modalities become
effective.
When all the above modalities fail, the following are considered:
  

• IVRA
In patient's refractory to conventional treatment modalities, intravenous
regional sympathetic blockade is achieved by using bretylium 0.5 mg/kg
body weight with lidocaine 0.5%, 40 mL for upper extremity and 60 mL
for lower extremity. The results are equivocal.

II. CHRONIC PAIN SYNDROMES

 Treatment Protocol of CRPS 251

• Programmable implantable devices

Spinal cord stimulation: spinal cord stimulator is effective and relieves
pain by modulating spinal pain signalling neurons and resetting altered
spinal physiological state.
Continuous intrathecal morphine with clonidine and/or midazolam
infusion by programmable implantable drug delivery system may also be
used as a last resort in patients where both pharmacological and interven-
tional therapies fail.
• Physiotherapy
• The principle of functional restoration is based on a steady pro-
gression from very gentle movements on an active basis to gentle
weight bearing.
• Manage oedema, optimize range of motion and encourage general
aerobic activity throughout.
• Gradual desensitization to increasing sensory stimulus goes along
with increased function. Desensitization techniques are rubbing
with silk, cotton and then towelling or contrast baths.
• Gradually increasing the strength and flexibility with ultimate
return to normal use is the goal, and this is accomplished by a
series of exercises and devices (e.g. foam rubber balls progressing
to spring grip strengtheners) and mat exercises.
• The physiotherapist is also actively involved in gait training and
postural correction.
• CRPS of upper extremity: weight-loading part of the treatment
starts with small objects carried in the hand, and soon progresses to
a handled bag, which can later be loaded with heavier weights.
• CRPS of lower extremity: partial weight-bearing with gait training.
• Vocational rehabilitation
• Patients are advised to continue in their job or go back to job as
early as possible.
• Employers are advised to make required adjustments in nature of
work as and when necessary.
• Recreational therapy
• Recreational therapy helps in rebuilding their confidence in
themselves and in developing positive outlook towards life.
• Patients are encouraged to take part in recreational activities, retain/
revive their hobbies, and participate in dance, drama and music.
• Cognitive behavioural therapy
• Patients who continue to have depression and/or anxiety, avoiding
gainful employment or taking undue advantage of the disease are
managed with the help of clinical psychologists.
Cognitive behavioural psychotherapy is the mainstay of treatment in
the atrophic stage of CRPS and those with intractable pain.

II. CHRONIC PAIN SYNDROMES

252 19. COMPLEX REGIONAL PAIN SYNDROME

CONCLUSION

CRPS presents with varied clinical features, pain being the most domi-
nant one. Better understanding of pathophysiological mechanisms of
CRPS and/with role of overactivity of sympathetic nervous system and
technological advancement in treatment modalities has helped pain cli-
nicians to diagnose the entity more accurately, controlling signs and
symptoms in majority of patients and preventing them progressing to
irreversible atrophic stage. However, continued research is needed to con-
vert the symptom-oriented treatment approach into mechanism-­targeted
treatment approach to tailor treatment plan according to individual
patient's requirement.

II. CHRONIC PAIN SYNDROMES

 C H A P T E R

20
Pelvic Pain

Pelvic pain that persists for more than 6 months duration is a clini-
cal entity often presenting to a pain clinician. The incidence of CPP is
not fully known although it is known to affect an estimated 12–15%
woman in the United States. The aetiology often remains obscure in spite
of extensive workup. In many patients who have no obvious pathology,
pelvic structures may inadvertently be removed for their physiological
variations. For example, approximately 12% of all hysterectomies are
performed for pelvic pain. Unfortunately, there are no data regarding the
prevalence of CPP in India.

CAUSES OF CPP
CPP occurs because of the following causes
  

Gynaecological
• C yclic
• Primary dysmenorrhoea
• Secondary dysmenorrhoea
• Noncyclic
• Endometriosis/adenomyosis
• Chronic PIDs, adhesions
• Ovarian remnant syndrome/retention syndrome
• Adnexal cysts
• Chronic ectopic pregnancy
• Pelvic congestion syndrome
• Ovarian neoplasm
• Pelvic relaxation
• Cervical stenosis
• Imperforate hymen

253
254 20. PELVIC PAIN

• I ntrauterine contraceptive device

• Uterine anomalies
• Leiomyomata
• Endometrial/cervical polyps
  

Genitourinary
• Bladder neoplasm
• Chronic urinary tract infection and interstitial cystitis
• Urethral syndrome
• Ureteral diverticuli or polyps
• Ureterolithiasis
• Detrusor dyssynergia
• Urethral caruncle and diverticulum
  

Gastrointestinal
• Inflammatory bowel disease
• IBS
• Carcinoma colon and diverticulitis
• Recurrent partial small bowel obstruction
• Infectious diarrhoea
• Hernias
• Recurrent appendicitis
• Abdominal angina
• Abdominal epilepsy/abdominal migraine
  

Musculoskeletal
• Chronic low-back pain and its causes
• Myofascial pain syndrome/fibromyalgia
• Pelvic floor myalgia
• Piriformis syndrome
• Chronic coccygeal pain
• Rectus tendon strain
  

Neurological
• N erve entrapment syndrome
• Neoplasia of spinal cord or sacral nerve neuromas
  

Systemic
• Porphyria
• Systemic lupus erythematosus
• Lymphoma
• Neurofibromatosis
  

Others
• B ipolar personality disorder/depression
• Familial Mediterranean fever
• Somatic referral

II. CHRONIC PAIN SYNDROMES

 Diagnosis and Management of CPP 255

NEUROANATOMY OF PELVIC PAIN

The lower abdominal wall and anterior vulva, urethra and clitoris are
innervated by mixed (motor and sensory) somatic nerves derived from L1
and L2. The anus, perineum and lower vagina are innervated by somatic
branches of the pudendal nerve, which is derived from S2 to S4 ganglia.
Pain impulses from pelvis are transmitted as shown in the following
flowchart:
Upper vagina, cervix, uterine corpus, inner one-third of fallopian tube,
broad ligament, upper bladder, terminal ileum and terminal large bowel
↓
Vaginal, uterine and hypogastric plexus
↓
Superior hypogastric plexus (presacral nerve)
↓
Lower thoracic/lumbar sympathetic chain
↓
Through dorsal roots of T11, T12, and L1 enter the spinal cord
Some pain impulses from the upper vagina cervix and lower uterine
segment travel in the nervi erigentes via pelvic parasympathetics to S2–S4
segments.
Urogenital sinus structures such as lower vagina, rectum and lower
bladder are innervated by both thoracolumbar and sacral afferents.
Afferents from ovary, outer two-thirds of the fallopian tube and upper
ureter
↓
Travel along ovarian artery
Enter the lumbar sympathetic chain at L4
↓
Ascend with the chain to enter the spinal cord at T9 and T10

DIAGNOSIS AND MANAGEMENT OF CPP

A detailed history and physical examination along with appropriate

diagnostic test when indicated by history and physical examination are
essential prerequisites for appropriate management of CPP. Clinical aspects
and management strategies in some important clinical pathological condi-
tions causing CPP are presented here.

Adhesions
Adhesions are well accepted as causes of intestinal obstruction and
infertility. However, their role as a cause of CPP is controversial. Adhesions

II. CHRONIC PAIN SYNDROMES

256 20. PELVIC PAIN

are present in 16–44% of CPP patients. CPP due to adhesions is known

to be exacerbated by sudden movements, intercourse or certain physical
activities. Pain is usually consistent in its location although over time, the
area of involvement may expand.
Laparoscopy is not only the gold standard for the diagnosis of adhe-
sion but also the preferred method of treatment. However, the outcome
after laparoscopic adhesionolysis is not consistent, possibly because
not all adhesions produce pain all the time. This is an area where CLPM
may prove to be especially valuable. During CLPM, patients under
local anaesthesia and conscious sedation guide in determining which
adhesions are associated with pain.

Endometriosis
The incidence of endometriosis in patients undergoing laparoscopy
for CPP is anywhere from 5 to 37%. The most common symptoms of
endometriosis are dysmenorrhoea, dyspareunia, infertility and abnor-
mal uterine bleeding. Symptoms may vary depending on involvement
of vagina, rectum, ureter, bowel wall, etc.
Examination may reveal tenderness and nodularity on the rectovaginal
examination of the uterosacral ligament and posterior cul-de-sac.
Laparoscopy is necessary for definitive diagnosis. Endometriosis can
be treated hormonally using danazol, progestins and GnRH analogues to
create pseudomenopause and to atrophy ectopic endometrial implants.
Laparoscopic electro- or laser surgery is reserved for severe endometrio-
sis. Patients who do not desire fertility may opt for total abdominal hys-
terectomy with bilateral salpingo-oophorectomy.
Superior hypogastric plexus blocks are most effective for conservative
management of endometriosis causing midline dysmenorrhoea.

Pelvic Congestion
Taylor (1954) suggested that emotional stress could lead to autonomic
dysfunction causing smooth muscle spasm and congestion of the veins
draining ovaries, uterus and vulva. Patients complain of secondary dys-
menorrhoea, low-back pain, dyspareunia, infertility and menorrhagia.
The pain is usually bilateral, moving, lower pelvic in distribution and
exacerbates with menstrual period. On examination, patients may have
tenderness over the uterus. The fundus of the uterus and cervix are often
bulky. The parametria are tender and indurated.
Pelvic venography is the only reliable way to diagnose this syndrome.
Selective ovarian venography has also been used. Appropriate therapy for
pelvic congestion is uncertain. Medroxyprogesterone has been shown to
be effective along with psychotherapy.

II. CHRONIC PAIN SYNDROMES

 Diagnosis and Management of CPP 257

The combinations of GnRH agonist with add-back estradiol and

medroxyprogesterone can also be used. Surgical approaches such as lapa-
roscopic ovarian vein ligation and hysterectomy with bilateral salpingo-
oophorectomy have shown efficacy in recalcitrant cases. Radiologic
transcatheter embolization of ovarian veins has been suggested as an
alternative to surgical ligation. The long-term efficacy of all these tech-
niques remains to be evaluated.

Salpingo-oophoritis
Patients usually have symptoms and signs of acute or subacute infec-
tion before the pain becomes chronic. Commonly, patients have frequent
recurrent infections.

Sweet and Gibbs Clinical Criteria for Diagnosis of Salpingo-

oophoritis
  

1. H istory of lower abdominal pain, lower abdominal tenderness, and

cervical motion tenderness
2. Adnexal tenderness
3. Temperature >38°C
4. Leukocytosis (TLC > 10,500/mm3), culdocentesis fluid containing
white cells and bacteria on Gram staining
5. Presence of an inflammatory mass
6. Elevated erythrocyte sedimentation rate
7. Gram stain from endocervix revealing Gram-negative intracellular
diplococci or a monoclonal smear from the endocervical secretions
revealing chlamydia
8. Laparoscopy with peritoneal fluid cultures is diagnostic
  

Broad-spectrum antibiotics with anaerobic coverage are the standard

treatment. Rarely, hysterectomy and salpingo-oophorectomy are required.

Ovarian Remnant Syndrome

CPP in a patient who has undergone hysterectomy and bilateral
s­ alpingo-oophorectomy may be due to residual ovarian cortical tissue
that is left in situ after a difficult dissection. Often the patient has had mul-
tiple pelvic operations with the uterus and adnexa removed sequentially.
The patient may complain of cyclic pelvic pain accompanied by perito-
neal signs. The patient may have a history of flank pain and frequent uri-
nary tract infection; there may be intermittent, partial bowel obstruction.
The painful symptoms usually arise 2–5 years after surgery. It usually
occurs in reproductive years. The diagnosis of ovarian remnant should
be considered in any woman with lower abdominal pain or an ipsilateral

II. CHRONIC PAIN SYNDROMES

258 20. PELVIC PAIN

pelvic mass several months or more after an oophorectomy. The absence

of hot flashes in a woman not receiving hormonal r­ eplacement follow-
ing bilateral oophorectomy should be a signal to carefully investigate for
ovarian remnant. Pelvic examination may reveal a tender mass in the lat-
eral region of the pelvis. Transvaginal ultrasound shows a pelvic mass in
50–85% cases. The diagnostic accuracy of ultrasound may be improved
by pretreatment with clomiphene citrate. Follicle stimulating hormone
assays are useful in suspected cases. Measurement of estradiol levels fol-
lowing GnRH agonist administration is one of the sensitive methods for
diagnosis.
Laparotomy and removal of residual ovarian tissue is the optimum
treatment.
Medical therapy consists of hormonal suppression with depot medroxy-
progesterone acetate, danazol or GnRH agonist.

Cyclic Pelvic Pain

Primary dysmenorrhoea refers to the pain with menses when there
is no pelvic pathology. It usually appears within 1–2 years after men-
arche, with the establishment of ovulatory cycles. Secondary dysmenor-
rhoea has painful menses with underlying pelvic pathology. It usually
occurs years after menarche and may occur with anovulatory cycles.
The aetiology of primary dysmenorrhoea is increased uterine prosta-
glandin production. Prostaglandin synthetase inhibitors such as mef-
enamic acid are effective in 70–80% cases. For a patient who has no
contraindications to oral contraceptive agents and desires contracep-
tion, the oral contraceptive pill is the treatment of choice. If the patient
does not respond to prostaglandin synthetase inhibitors or does not
desire contraception, narcotic analgesics should be administered for
2–3 days per month. Patients resistant to the above-mentioned treat-
ment may respond to acupuncture, TENS or superior hypogastric
plexus blocks.
Surgical approaches include laparoscopic uterine nerve ablation and, in
selected cases of secondary dysmenorrhoea - hysterectomy.
Long-term or controlled studies of the neurodestructive procedures are
lacking. The management of secondary dysmenorrhoea involves treat-
ment of the underlying pathology.

Gastroenterological Causes of Pelvic Pain

IBS is one of the common causes of lower abdominal pain accounting
for 7–60% referrals for CPP. The predominant symptoms include abdomi-
nal pain, flatulence, alternating diarrhoea and constipation. The pain is

II. CHRONIC PAIN SYNDROMES

 Diagnosis and Management of CPP 259

intermittent or constant, colicky and predominantly left lower quadrant

in location. Pain often improves with bowel movement. Symptoms are
usually worse during periods of stress, anxiety, depression and premen-
strual/menstrual phases of the cycle. IBS is a waxing and waning disorder,
the diagnosis of which is usually made on the basis of history. The treat-
ment consists of reassurance, education, stress reduction, anticholinergic
or other antispasmodic agents, bulk-forming agents or high-fibre diet and
low-dose tricyclic antidepressants. Patients with chronic diarrhoea must
be evaluated by a gastroenterologist.
Tumours of gastrointestinal tract can cause CPP. The most frequent
and early symptoms of bowel carcinomas are change in bowel habits and
abdominal pain. Rectal bleeding and weight loss are signs of advanced dis-
ease per rectal examination, sigmoidoscopy and biopsy as well as barium
enema may reveal the diagnosis. Cancer pain management is discussed
elsewhere in this book.
Abdominal wall hernias, cystocele, rectocele or enterocele may cause
CPP. This type of pain usually responds to surgery.

Urologic Causes of CPP

Patients with cystitis complain of suprapubic pain, dysuria, fre-
quency, and urgency, and have pyuria on urine analysis and a positive
urine culture. The symptoms usually respond to antibiotic therapy. In
cases of recurrent infections, antibiotics may have to be administered
postcoitally, possibly for a prolonged period of time. When a patient
complains of frequency, urgency, and suprapubic pain and lab stud-
ies are negative, the patient may actually have interstitial cystitis. The
consensus criteria for diagnosis of interstitial cystitis include at least
two of the following:
  

1.  ain on bladder filling relieved by emptying

P
2. Pain in suprapubic, pelvic, urethral, vaginal or perineal region
3. Glomerulations on endoscopy
4. Decreased compliance on cystometrogram
  

Treatment includes intravesical instillation of dimethylsulfoxide, ana-

logues of glycosaminoglycan, TENS and biofeedback, oral anticholiner-
gics, antihistamines, antispasmodics, nonsteroidal anti-inflammatory
drugs, tricyclic antidepressants and pentosan polysulfate sodium have all
been utilized with some success.
Very severe chronic suprapubic pain may be caused by infiltrating car-
cinoma of bladder, cervix, uterus or rectum. These conditions should be
apparent after performing the history, pelvic exam, urinalysis, cystoscopy,
intravenous pyelography and/or CT urogram.

II. CHRONIC PAIN SYNDROMES

260 20. PELVIC PAIN

Nerve Entrapment Syndromes

The syndromes most commonly occur months to years after Pfannen-
stiel skin or other lower abdominal and even laparoscopic incisions. It
can also follow trauma. Commonly involved nerves include ilioinguinal
(T12 and L1), iliohypogastric (T12 and L1) and genitofemoral (L1 and L2).
Symptoms include pain that is elicited by exercise and relieved by bed
rest. The pain is described as stabbing, colicky and sudden. Pain is usu-
ally judged as coming from the abdomen and not from the skin. Nausea,
bloating, menstruation and full bladder may exacerbate the pain of nerve
entrapment.
On examination, pain can usually be localized with the finger tip. The
maximal point of tenderness is the neuromuscular foramen at the rectus
margin medial and inferior to the anterior superior iliac spine or in the case
of spontaneous nerve entrapment of other abdominal cutaneous nerves,
at the site of exit from the aponeurosis. On tensing the abdominal wall in
a straight leg raising manoeuvre, the pain is exacerbated if nerve entrap-
ment syndrome is present. When the abdominal wall is relaxed, the pain
is relieved and becomes more diffuse. The diagnosis is confirmed by injec-
tion of 2–4 mL 0.25% bupivacaine, which produces immediate pain relief.
Some patients may require 2–3 weekly injections. If visceral pathology
and psychological factors are ruled out, surgical removal of the involved
nerves may be considered as a last resort. Low-dose tricyclic antidepres-
sants (amitriptyline 10–50 mg/day) and anticonvulsants (carbamazepine
100–300 mg/day) are also useful for pain control.

Musculoskeletal Causes of CPP

Women complaining of low-back ache without complaints of pelvic
pain rarely have gynaecological pathology as the case of their pain. How-
ever, low-back pain may accompany pelvic pathology. The management
of low-back ache is complex and is discussed elsewhere.

Myofascial Pain
Myofascial pain is defined as ‘pain and/or autonomic phenomena
referred from active myofascial trigger points, with associated dysfunc-
tion’. Some researchers have noted incidence of myofascial syndrome in
patients with somatic pathology. Trigger points have been noted in most
women presenting to pain clinic with complaints of CPP. Clinically, myo-
fascial pain is exacerbated by activity within muscle or muscle groups. In
the case of abdominal wall and pelvic floor trigger points, pain is exac-
erbated by aetiology in deeper visceral structures (bladder/rectal full-
ness, menstruation, sexual intercourse, etc.). On examination, pressure on

II. CHRONIC PAIN SYNDROMES

 Diagnosis and Management of CPP 261

the trigger points evokes local and referred pain. Pain is exacerbated by
straight leg raising manoeuvre. Treatment includes injecting the trigger
points with local anaesthetics, treating depression, anxiety and learned
behaviour patterns that may exacerbate the conditions. Tricyclic antide-
pressants and anticonvulsants or physical therapy may also be useful.

Pelvic Floor Pain Syndrome

PFPS is caused by or associated with pain and tenderness of levator
ani, coccygeus or piriformis muscles or their associated fascia or inser-
tions. It may be a form of tension myalgia similar to tension headache. It
occurs predominantly in women in their 40s and 50s. Abnormalities of
posture are important. Most women are ‘slumpers’ or ‘slouchers’ who sit
with pressure on the upper buttocks, coccyx and base of spine rather than
on ischial tuberosities. PFPS may also result from trigger points of one or
more of the muscles of the pelvis. Symptoms are vague and poorly local-
ized. Low-back pain and radiation to the sacrum at the area of insertion of
the levator ani is common. Radiation to the hip and down the back of the
thigh like sciatica is particularly characteristic of piriformis spasm. Pain
is often described as aching, throbbing or heaviness. Pain may be quite
severe and in some patients, the patient awakens from sleep because of
rectal pain (proctalgia fugax) or vaginal pain (colpalgia fugax). Character-
istically, pain from levator ani spasm starts in the afternoon and becomes
progressively worse as the day passes. Pain is increased by long sitting
or prolonged standing in one position. Dyspareunia is a common symp-
tom. It is not worsened by bowel movements. On examination, tender-
ness and spasm of levator muscles may be elicited. The tenderness may
be unilateral.
The classic treatment for PFPS is Thiele massage, done with the rec-
tal finger massaging the involved, tender muscles with a firm sweeping
motion. Fifteen to twenty strokes, taking about 5 min are done at each
treatment. This is repeated daily for 4–5 days, and then every other day
until improvement. Hot sitz baths, ultrasound, bed rest, relaxation exer-
cises, biofeedback training, analgesics, Kegel exercises, TENS, acupunc-
ture and infiltration with steroid and/or local anaesthetics (especially if
trigger points are present) are all treatments for PFPS. Treatment with
diazepam may be helpful for acute control of spasm and pain. Currently,
there are no well-performed studies to make any specific recommenda-
tions about the treatment of this condition.

Central Factors in CPP

Descending pain modulating mechanisms originating in brain or spinal
cord involve various endogenous endorphins, enkephalins and excitatory

II. CHRONIC PAIN SYNDROMES

262 20. PELVIC PAIN

amino acids. Anxiety, depression and other psychological factors may

be facilitators or inhibitors of neurological transmission. According to a
­‘diathesis-stress’ model of pain, a woman is more susceptible in certain
social contexts to develop chronic pain based on her preexisting vulnera-
bilities including those related to cognitive, affective, biological and behav-
ioural factors. Functioning studies on women with CPP have documented
a high level of psychological disturbance as well as past exposure to child-
hood sexual abuse. Interestingly, treatment resulting in subjective improve-
ment in pain severity and increased activity level produces a significant
improvement in personality profiles. Few studies have found a higher like-
lihood of depressive disorders in the family histories of women whose pain
could not be attributed to organic pathology. It has been suggested that
pain may reflect a masked depression, in view of the common neurotrans-
mitter pathways mediating pain and mood. Several studies have found a
higher prevalence of sexual abuse, substance abuse, functional dyspareu-
nia and inhibited sexual desire. By drawing on the learned helplessness
model for depression, abuse may predispose to chronicity of pain because
it increases the vulnerability to depression and helplessness in the face of
adversity. In view of these findings, the importance of obtaining sexual and
physical abuse history cannot be overemphasized. It is not unreasonable to
state that CPP with or without pathology is likely to involve all levels of the
neuraxis and to direct management approaches accordingly.

ROLE OF SURGICAL MANAGEMENT IN CPP

Diagnostic Laparoscopy
Between 10 and 70% of patients have no obvious pathology and two-
thirds of patients have findings of adhesions that may or may not play
a role in their pain. Multidisciplinary approach to CPP management is
successful in 65–90% of patients regardless of the presence of minimal
pathology. Therefore, laparoscopy should be reserved for patients with
signs and/or symptoms of endometriosis, cyclic pelvic pain or infertility,
and for patients in whom other pathology has been ruled out.

Hysterectomy
Up to 19% of hysterectomies are performed for the sole indication of
CPP, and 30% of patients presenting to pain clinic have already undergone
hysterectomy without experiencing relief from pain. Reiter and associates
(1991) noted a decline in the incidence of hysterectomy for the indica-
tion of CPP from 16.3 to 5.8% after the initiation of a multidisciplinary
approach to the management of CPP. Nevertheless, hysterectomy remains
an option for appropriately selected patients with pain of uterine origin.

II. CHRONIC PAIN SYNDROMES

 Role of Superior Hypogastric Plexus Block in CPP 263

ROLE OF SUPERIOR HYPOGASTRIC PLEXUS BLOCK

IN CPP

Superior hypogastric plexus block receives the major afferent supply

from the cervix, uterus and proximal fallopian tubes. Afferents travel-
ling with the sympathetic supply from the bladder and rectum also pass
through the superior hypogastric plexus. The nerve supply to the adnexal
structures bypasses the hypogastric plexus as the afferents from the ovary
travel with sympathetic fibres accompanying the ovarian artery to the supe-
rior mesenteric plexus to enter the spinal cord at T9 and T10. These auto-
nomic relationships constitute the rationale for emphasis on differentiating
dysmenorrhoea with maximum intensity of the pain localized to the uterus
with radiation to the sacrum from lateralizing pain radiating to the lumbar
region. Superior hypogastric plexus block is beneficial in the management
of central pelvic pain in the setting of both cyclic and noncyclic pain, moder-
ate to severe endometriosis and CPP of malignant origin.

Superior Hypogastric Plexus Block

Described by Plancarte in 1990, superior hypogastric plexus block has
been found very effective in pelvic cancer pain. It is a bilateral retroperi-
toneal structure situated at the level of lower third of L5 and upper third
of S1 at the sacral promontory close to the bifurcation of common iliac
vessels.

Indications
Superior hypogastric plexus neurolytic block is used to treat intractable
pelvic pain secondary to neoplastic disease like cancer cervix and uterus,
prostate cancer, testicular cancer and radiation enteritis. It may also be
used for treating benign CPP due to endometriosis and PID adhesions.
Success may be improved further if neurolysis is performed before
extensive tumour infiltration shelters the targeted structures. Physicians
performing the blockade should be aware of the facts that injuries to com-
mon iliac vessels leading to haematoma formation and shock as well as
hollow viscera injuries like bladder and rectum have been described.

Procedures
The patient assumes prone position and L4–L5 intervertebral space is
identified under fluoroscopy. A 22 gauge spinal needle is inserted 5–7 cm
from midline 30° caudally and 45° medially. The tip of the needle is
directed towards the anterolateral aspect of the lower border of L5 verte-
bra (Fig. 20.1). Needle is advanced 1 cm past L5 vertebral body to the ret-
roperitoneal space, which is identified by a give way ‘pop’. The spread of
radiocontrast dye should show smooth posterior contour corresponding
to anterior psoas fascia (Fig. 20.2).

II. CHRONIC PAIN SYNDROMES

264 20. PELVIC PAIN

Psoas m.
Common iliac a.

Superior hypogastric plexus

Sympathetic trunk 7 cm

(a)

L5–S1

(b)
FIGURE 20.1 Superior hypogastric plexus block. (a) Anatomical location of the Superior
Hypogastric Plexus. (b) Block Technique showing the tip of the needle directed towards
anterlolateral aspect of the lower border of L5.

FIGURE 20.2 Spread of radiocontrast dye confirming the right position of the needle.

II. CHRONIC PAIN SYNDROMES

 Multidisciplinary Approach to CPP Management 265

CT-guided placement of needle is also recommended by Waldman

and his colleagues. De Leon Casasola et al. suggested avoiding unilateral
approach in patients with cancer because spread of neurolytic agent could
be impeded by retroperitoneal infiltration by tumour. After confirming
the accurate placement of the needle tip, neurolysis is achieved by inject-
ing 8 mL of 8% aqueous phenol on each side.

MULTIDISCIPLINARY APPROACH TO CPP

MANAGEMENT

Multidisciplinary pain management seems to be the best approach to

CPP. Our multidisciplinary pain management program was successful in
reducing pain by at least 50% in 85% of the subjects. At our pain clinic,
peripheral factors are managed by the pain specialist. Spinal cord and cen-
tral factors related to pain modulation are addressed with trigger point
injections, centrally acting medications, acupuncture or TENS. Cognitive
behavioural and other psychological factors are addressed by the psy-
chologist. Gynaecological, urological and gastroenterological causes are
managed in consultation with the concerned specialty.

II. CHRONIC PAIN SYNDROMES

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 C H A P T E R

21
Perineal Pain

Chronic perineal pain is a poorly defined entity. There is no standard

definition of what constitutes chronic perineal pain. It has been vari-
ously described as a component of urogenital and rectal pain syndromes
or chronic pelvic pain syndromes. Anatomically, perineum is ‘a space
bounded anteriorly by scrotum in males, and the mons pubis in females,
posteriorly by the buttocks, and on each side by the upper part of the
medial side of the thigh’. It is divided into urogenital region anteriorly
and anal region posteriorly. Urogenital region comprises external genital
organs and anal region comprises the termination of the anal canal in the
median plane and an ischiorectal fossa on each side.

NEUROANATOMY OF PERINEUM

The perineum comprises diverse anatomical structures with mixed

sympathetic, parasympathetic, somatic and sensory innervations. In
a broad anatomical view, dual projections from the thoracolumbar and
sacral segments of the spinal cord carry out this innervation, converging
primarily into discrete peripheral neuronal plexuses before distributing
nerve fibres throughout the pelvis including perineum. Interactive neuro-
nal pathways routing from higher origins in the brain through the spinal
cord add to the complexity of neuronal regulation.
The role of the sympathetic nervous system in causing disease genera-
tion and maintenance of pain is not clear. It might be due to invasion of
the perineural sheath of the pelvic sympathetic and somatic nerves as also
of the blood vessels, producing sympathetic pain in the pelvis and lower
extremity. Perhaps sympathetic nervous system is involved in at least
the minority of patients whose pain diminishes after diagnostic ganglion
impar blocks with 4–6 mL of 0.25% bupivacaine.
The differential diagnosis of chronic perineal pain is wide and complex
as depicted in Box 21.1.

267
268 21. PERINEAL PAIN

BOX 21.1

DIFFERENTIAL DIAGNOSIS OF
C H R O N I C P E R I N E A L PA I N
• As a part of specific genitourinary syndromes
• Interstitial cystitis
• Urethral syndrome
• Clitoral/penile pain
• Testicular pain
• Vulvodynia
• Prostatodynia
• Coccygodynia
• Gastroenterological pathology
• Proctological pathology
• Urological pathology
• Gynaecological pathology
• Neurological pathology
• Peripheral neuropathies
• Diabetes mellitus
• Acquired immunodeficiency syndrome (AIDS)
• Pudendal nerve entrapment
• Sacral meningeal cysts
• Plexiform neurofibromas (involving nerves of the perineum)
• Painful tardive perineal pain syndrome due to neuroleptic drug
exposure
• Rarely, as a very prominent feature of Parkinson disease

Clinical Presentation
Patients usually present with a vague, poorly localized, burning
and/or sharp, stinging pain in the perineum radiating to either vagina
or rectum. It is generally a continuous pain with periods of aggravation.
There may be associated psychological depression and anxiety in these
patients. Clinical examination does not reveal any neurological finding
or any other positive sign.

Management of Chronic Perineal Pain

Various interventions have been proposed for the management of
chronic perineal pain. These include oral medications such as gabapen-
tin, carbamazepine, amitriptyline and various antidepressants. Local

II. CHRONIC PAIN SYNDROMES

 Ganglion Impar Block 269

anaesthetic blocks of pudendal nerve or surgical neurolysis, transposi-

tion of pudendal nerve and surgical resection of sacral meningeal cysts or
meningiomas have also been reported. But lack of evidence regarding their
efficacy and application complicates the management of perineal pain.

Therapeutic Modalities for Managing Perineal Pain

• P
 harmacological approach  
• Oral anticonvulsant drugs such as gabapentin and carbamazepine
and tricyclic antidepressant such as amitriptyline in low doses
(25–50 mg hs single dose)
• Fluoxetine (10–20 mg/day)
• NSAIDs such as Etoricoxib 90 mg daily
  

• Nonpharmacological and interventional approach  

• Pudendal nerve block with 0.5% bupivacaine and later with 8%
phenol
• Surgical transposition of pudendal nerve and sympathetic plexus
(ganglion impar) block

GANGLION IMPAR BLOCK

Pain arising from disorders of the visceral and somatic structures in

the pelvis and perineum is a common cause of discomfort and disabil-
ity, especially among women. The most characteristic feature of sym-
pathetic mediated pain in perineal region is a poorly localized vague
pain accompanied by sensations of burning and urgency. Ganglion
impar (ganglion of Walther) is the retroperitoneal structure at the level
of sacrococcygeal junction that marks the termination of paired para-
vertebral sympathetic chains. The role of ganglion impar in the gen-
eration and maintenance of chronic perineal pain is not clear. Although
anatomically the interconnections of the ganglion impar are rarely
described in any detail, even in the anatomic literature, it is likely that
the sympathetic component of these pain syndromes derives, at least in
part, from this structure.

Indications
Interruption of ganglion impar, first described by Plancarte et al., has been
an approved treatment for managing intractable, sympathetically mediated
perineal pain resulting from advanced carcinoma cervix, carcinoma endo-
metrium, colon and bladder. Visceral phantom pain of the rectum and anus
after surgical palliative intervention may also benefit from this block. Few

II. CHRONIC PAIN SYNDROMES

270 21. PERINEAL PAIN

Retroperitoneal
Space

Needle-Inside-Needle
Ganglion Impar

Sacrococcygeal
Rectum Junction
Anococcygeal
Ligament

Anus

FIGURE 21.1 Ganglion impar block.

complications like epidural injection of neurolytic agent, rectal and subperi-

osteal injection have been reported to be due to wrong needle placement.

Procedure
Chemical neurolysis has been the technique of choice for therapeutic
neurolytic blockade of the ganglion impar, although viable alternative
techniques such as cryoablation have been suggested. The therapeutic/
neurolytic ganglion impar block is now commonly performed by the
transcoccygeal approach. The patient is placed in the prone position with
a pillow beneath the lower abdomen. The site of the needle insertion is
located by palpating the sacral cornu and by using a fluoroscope after
aseptic preparation. A wheal of local anaesthesia is raised at the site of the
needle insertion. Under the guidance of a fluoroscope C-arm in a lateral
position, a 22-gauge type-B beveled, 5-cm needle is inserted through the
skin piercing the dorsal sacrococcygeal ligament at the midline. The needle
is then advanced through the vertebral disc until the tip is placed anterior
to the ventral sacrococcygeal ligament, felt as a loss of resistance. The posi-
tion of the needle tip is confirmed by injecting 1 mL of radio opaque dye
into the retroperitoneal space. The spread of dye gives a “reverse comma”

II. CHRONIC PAIN SYNDROMES

 Ganglion Impar Block 271

(a) (b)

FIGURE 21.2 Fluoroscopic confirmation of needle position by injecting the contrast dye.
(a) AP view and, (b) Lateral view.

appearance when seen in a lateral view (Fig 21.1 and 21.2). Once the posi-
tion of the needle tip is confirmed the desired drug is injected. The thera-
peutic block is performed by injecting 0.25% bupivacaine and 40 mg of
methylprednisolone acetate (10 mL), and the neurolytic block is performed
with 4–6 mL of 8% aqueous phenol.This procedure is an important tool in
the interdisciplinary approach to management of chronic perineal pain. In
view of the diverse factors involved in the causation of chronic perineal
pain, the role of an effective multidisciplinary approach to managing this
condition cannot be overemphasized.

II. CHRONIC PAIN SYNDROMES

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 C H A P T E R

22
Peripheral Vascular
Diseases

Chronic pain remains a frequent diagnostic feature of many vascular

diseases. The control of pain in these disorders is an integral part of man-
aging these patients because it not only mitigates human suffering but also
allows aggressive physical and occupational rehabilitation to be carried
out. The aetiology of these vascular diseases is multifactorial (Box 22.1)
and, therefore the importance of multidisciplinary approach to pain man-
agement is appropriate. The exact incidence and prevalence of peripheral
vascular diseases have not been studied. Nevertheless, it remains a signifi-
cant problem among Indian population. In this chapter, the management
of pain in common peripheral vascular diseases is discussed briefly.

NEUROANATOMY AND NEUROPHYSIOLOGY OF

PERIPHERAL VASCULATURE

The innervations of blood vessels include afferent fibres, some of which

transmit nociceptive impulses. These are components of either spinal
nerves or cranial nerves depending on the region. The efferent fibres are
sympathetic nerves with a predominance of vasoconstrictors and also
some vasodilator fibres. When sympathetic hyperactivity occurs, pro-
voked by anxiety, fear, apprehension or exposure to cold, vasoconstrictor
fibre activity predominates. Block of vasoconstrictor fibres causes dilation
of blood vessels to the extremity because tonic impulses that normally are
connected to the vessels in a more or less constant stream to maintain the
musculature in a state of tonus are removed. The dilation of the arterioles,
smaller arteries and veins is not complete because the muscles of these
vessels have an intrinsic tone. The intrinsic vasomotor tone can be com-
pletely eliminated by direct vasomotor paralysis induced by histamine,
local anaesthetics applied to the blood vessels or administration of sys-
temic agents that directly paralyse the muscles of these vessels.

273
274 22. PERIPHERAL VASCULAR DISEASES

BOX 22.1

C A U S E S O F P E R I P H E R A L VA S C U L A R
DISEASE

Diseases of Medium-Sized Arteries

• Thromboangiitis obliterans
• Arteriosclerosis obliterans
• Acute arterial occlusion
• Aneurysms

Diseases of Small Arteries

• Embolism
• Collagen vascular diseases – systemic lupus erythematosus,
­scleroderma, systemic sclerosis rheumatoid arthritis
• Congenital arteriovenous malformation

Diseases of Microcirculation
• Raynaud phenomenon
• Raynaud disease
• Acrocyanosis
• Livedo reticularis
• Erythromelalgia

Diseases of Peripheral Veins and Lymphatics

• Thrombophlebitis
• Phlegmasia alba and cerulea dolens
• Deep venous thrombosis
• Varicose veins
• Postthrombotic syndrome

Mechanisms of Pain in Peripheral Vascular Disease

1. I nadequate perfusion of tissues
2. Sudden changes in dimension of vessels – aneurysm and vessel spasm
3. Secondary changes – ulceration and gangrene
4. Rupture of the vessels
5. Impaired venous return

II. CHRONIC PAIN SYNDROMES

 Neuroanatomy and Neurophysiology of Peripheral Vasculature 275

Clinical Features of Peripheral Vascular Disease

• Pain
• Decreased or absent pulses
• Abnormal skin colour
• Diminished/elevated skin temperature
• Swelling (oedema)
• Trophic changes of skin and its appendages
  

Pain: Intermittent pain (claudication) is precipitated by exercise and

relieved by rest. This type of pain occurs in TAO, ASO, vasculitis and
entrapment syndromes. Continuous pain is produced by sudden arterial
occlusion, ulceration, gangrene, ischaemic neuropathy, inflammation of
arteries, veins or lymphatics and by venous or lymphatic congestion.
The intensity of pain varies according to the aetiology, degree and
acuteness of circulatory imbalance. The quality of pain also varies with the
disease process and mechanism of the pain. The pain of intermittent clau-
dication is usually sharp and often burning in character and is promptly
relieved by cessation of the activity that precipitates the pain. The pain of
ischaemic neuropathy is aching in character, associated with paraesthesia.
The pain of sudden arterial occlusion is usually sharp when the lesion
involves somatic structures and is dull and aching when the occlusion
involves viscera. The pain of erythromelalgia is usually burning and is
aggravated by heat and relieved by cold.

Diagnostic Investigations
Doppler Flowmetry
It is done to note the quality of the arterial pulsations and to compare
the blood pressure at ankle with that in the arm (ABI). Normally, the ankle
systolic pressure should be equal to or greater than the brachial systolic
pressure (ABI > 0.9). With arterial insufficiency in the lower limb, how-
ever, the ABI is <0.9, depending on the degree of insufficiency. With mild
insufficiency, the ABI is between 0.7 and 0.9; with moderate disease, it is
between 0.5 and 0.7; and with severe disease, it is <0.5. Ischaemic skin
lesions would not be expected to heal with an ABI of <0.4. The sensitivity
of these tests can be increased by exercise on a treadmill or on a bicycle to
the point of claudication. Postexercise ankle blood pressure falls often to
unrecognizable levels requiring several minutes to return to the pre-exer-
cise level. This test is most useful in following the progress of the disease
with or without therapy.

Duplex Ultrasound
This technique involves the use of high-resolution B-mode ­ultrasound
imaging and Doppler ultrasound to obtain images of arteries and

II. CHRONIC PAIN SYNDROMES

276 22. PERIPHERAL VASCULAR DISEASES

veins, to localize arterial and venous occlusions, and to make detailed

­haemodynamic assessments of flow within normal and affected vessels.

Angiography
An angiogram is done only after a decision has been taken that inter-
vention is appropriate. It involves the injection of a radiopaque solution
into the arterial tree, generally by a retrograde percutaneous Seldinger
method, usually involving the femoral (occasionally the brachial or axil-
lary) artery.
In TAO, the arteriographic findings are typical enough to be a confir-
mative evidence of diagnosis (Fig. 22.1).
Collateral arteries, when present, are usually tortuous and have a ‘cork
screw appearance’. TAO must be differentiated from other occlusive dis-
eases, including ASO, scleroderma associated with secondary Raynaud
phenomenon, and occlusive arterial disease due to chronic occupational
trauma.

Digital Subtraction Angiography

This technique employs a computer system to digitize the angiographic
information. The image before contrast injection is subtracted from the
contrast image, yielding greater clarity. DSA may be carried out by arte-
rial or venous injection of contrast. The arterial injection allows the use of

(a) (b)

FIGURE 22.1 Angiogram showing an a. arterial occlusive disease with stenosis of

­profunda femoral artery and b. Diffuse Arteriosclerosis in both legs.

II. CHRONIC PAIN SYNDROMES

 Diseases of Medium-Sized Arteries 277

finer catheters and less contrast agent than the conventional angiography.
The venous injection avoids the need for arterial puncture completely,
although rather high volumes of contrast agent must be injected into a
large vein.

DISEASES OF MEDIUM-SIZED ARTERIES

Thromboangiitis Obliterans
Also called ‘Buerger disease’, it is a disease entity that causes a specific
nonatherosclerotic lesion involving arteries, veins and nerves of the extrem-
ity that frequently lead to the development of gangrene (Buerger, 1908). TAO
is an occlusive disease of medium-sized and small arteries and veins affect-
ing chiefly the distal parts of the lower and upper limbs of young adult male
smokers. The arterial lesions are often associated with recurrent episodes
of segmental superficial thrombophlebitis. The vessels commonly involved
are tibial, radial, ulnar, plantar, palmar and digital arteries. Larger arteries
such as the femoral and brachial are affected later when the disease is severe
and progressive. There is usually a bilateral, symmetrical involvement.
Patients usually present with intermittent claudication in the legs and
hands. Cold sensitivity may be present. As the disease progresses, patients
develop ischaemic rest pain which is often very severe, burning in nature
and is aggravated by elevation of the extremity. Pain may or may not be
relieved by dependency. If ulceration and gangrene develop, the pain is
localized to the regions adjacent to the ulcers or gangrenous tissue and
has the characteristics of rest pain. The diagnosis is usually confirmed by
Doppler flowmetry studies of suspected vessels.

Management
1. Cessation of smoking is important.
2. Sympathetic blocks: For many of these patients, sympathetic blocks
with local anaesthetics (lumbar sympathetic block and stellate
ganglion block) may give temporary relief of vasospasm and pain, but
it is of little value in relieving claudication. Chemical, radiofrequency
or surgical sympathectomy may be effective in relieving the rest
pain and, for a small percentage of patients, the claudication. If
sympathectomy is contemplated, several prognostic sympathetic
blocks (stellate ganglion or lumbar sympathetic) with 10 mL of 0.25%
bupivacaine should be used to predict the effects of the prolonged
interruption. In the past, skin temperature, plethysmographic,
and sympatho galvanic responses were used to select patients for
sympathectomy. Recently, walking tolerance test is being used to
establish the degree of increase in peripheral blood flow, consequent
to sympatholysis.

II. CHRONIC PAIN SYNDROMES

278 22. PERIPHERAL VASCULAR DISEASES

3. A nalgesics: Mild to moderate pain may be controlled with systemic

nonnarcotic analgesics (ibuprofen 600–1200 mg/day in three divided
doses and/or tramadol 150–300 mg/day in three divided doses) used
alone or combined with codeine titrated up to 120 mg four hourly.
Potent narcotics such as oral morphine sulfate titrated to obtain
adequate pain relief may be used for short periods of time to control
severe pain.
4. Epidural infusions: Epidural local anaesthetics ± opioid infusions
(bupivacaine 0.0625–0.125% ± fentanyl 2–5 mcg/mL at the rate of
5–10 mL/h) may be used to control acute attacks of severe pain.
5. Surgical procedures: Amputation, as a last resort, is generally curative
and wound healing problems are rare because arterial inflow is good.
Surgical sympathectomy is rarely performed nowadays because of the
advent of chemical/radiofrequency ablation of sympathetic plexus.

Arteriosclerosis Obliterans
The most commonly involved arteries are lower abdominal aorta, iliac
arteries, femoral, popliteal and tibial. It is a slow, insidious, degenerative
disease occurring in persons older than 50 years. In approximately one-
third of the patients, ASO is associated with coronary artery disease.
The severity of ischaemia depends on the site and extent of the ­arterial
lesion and on the adequacy of the collateral circulation. When the ­collateral
circulation is adequate, the patient experiences intermittent ­claudication
especially during exercise. Later, when the flow through c­ollaterals
becomes inadequate, the patient experiences rest pain. Further progres-
sion can result in skin ulceration and gangrene.

Management
1. Vascular grafts that can bypass the obstruction of large or medium-
sized vessels in the limb remain the mainstay of treatment.
2. However, in patients for whom bypass graft surgery cannot be used
because the obliterative disease is too extensive and sympathectomy is
effective in relieving pain and postponing amputation. Percutaneous
chemical or radiofrequency sympathectomy is preferred over surgical
sympathectomy because they are least invasive, can be performed
on an outpatient basis and have low postoperative morbidity and
mortality. Best results are obtained in patients with rest pain not
amenable to arterial reconstruction. Studies have showed relief
from rest pain in 30–40% of patients who underwent percutaneous
sympathectomy. The mean duration of pain relief obtained with these
procedures is about 6 months. About 10% of the patients might require
repeat block on the same side within 3–12 months; little credible
evidence supports the use of sympathectomy for ASO.

II. CHRONIC PAIN SYNDROMES

 Diseases of the Microcirculation 279

Other Measures
• Adequate control of diabetes mellitus
• Cessation of smoking
• Weight reduction in obese patients
• Supervised exercise programs
• Foot care
• Avoidance of exposure to cold
• Adjunctive medications, e.g. aspirin
• Vasodilators, e.g. xanthinol nicotinate
• α-blockers, prazosin 1–5 mg bid or tid

Haemorheologic Agents
• Pentoxifylline 600–1200 mg/day in three divided doses
• Cilostazol
• Praxilene (naftidrofuryl oxalate)
  

Among the adjunctive medications, only haemorheologic agents have

been shown to improve walking distance in patients with intermittent
claudication.

Pain Control
Nonsteroidal anti-inflammatory drugs with or without codeine as men-
tioned earlier can be used for long periods of time with insignificant risk
of physical dependence and little risk of addiction or tolerance. For severe
rest pain, potent narcotics can be used for several weeks, but such patients
usually require either revascularization or amputation.

DISEASES OF THE MICROCIRCULATION

Raynaud Disease
It is a benign, episodic digital vasospasm in response to cold or emo-
tional stimuli.
Allen and Brown Criteria (1932) for diagnosis of Raynaud disease:
  

1. A ttacks can be precipitated either by exposure to cold or emotional

stimuli.
2. Involvement is bilateral and symmetric.
3. No evidence of occlusive disease involving digital arteries.
4. Trophic or gangrenous change is rare.
5. The disease duration of >2 years.
6. There must be no evidence of an underlying disease that could cause
the symptoms.
  

II. CHRONIC PAIN SYNDROMES

280 22. PERIPHERAL VASCULAR DISEASES

This disease commonly affects young women. Patients note that on

exposure to cold, the fingers turn white, then blue, and finally red dur-
ing the attack; patients also notice numb fingers (rarely toes) during the
attack.

Management
1. Reassurance about the benign nature of the condition
2. Avoidance of cold exposure
3. Adjuvant medication
  

Calcium-channel blockers – nifedipine 10–30 mg/day; α-blockers –

prazosin 1–5 mg bid or tid and phenoxybenzamine 10–60 mg orally bid.
In patients who are disabled by severe disease, regional sympathetic
denervation can be used as diagnostic and prognostic procedures, espe-
cially if sympathectomy is being considered. In recalcitrant cases, chemical
sympathectomy with phenol or radiofrequency sympathectomy provides
good results for several months.

Raynaud Phenomenon
It is characterized by the same symptomatology as Raynaud disease
but is caused by different underlying disorders. The condition is usually
unilateral. The treatment should be directed towards the elimination of
underlying cause. In cases of digital ulceration, local therapy with protec-
tion of the limb, antibiotics and occasionally topical nitroglycerin admin-
istration may be successful. Surgical debridement may be necessary, but
healing is usually slow.
Regional sympathetic blocks (stellate ganglion or lumbar sympathetic
blocks) are considered in intractable cases. Before considering chemical/
radiofrequency or surgical sympathectomy, at least 10 diagnostic and ther-
apeutic sympathetic blocks (stellate ganglion or lumbar sympathetic) are
done with 10 mL of 0.25% bupivacaine. If these blocks produce adequate
vasodilation and decrease existing pain, then chemical or radiofrequency
sympathectomy may be considered.

Acute Arterial Occlusion

It may be caused by thrombosis, embolism or direct injury due to intra-
arterial injection of drugs such as thiopentone sodium. Pain develops
rapidly as a result of tissue ischaemia, which may be the product of the
primary obstruction and reflex collateral vasospasm.

Management
1. Surgical embolectomy/transcatheter thrombolysis within 4–6 h after
the embolic episode is the treatment of choice in almost all early cases
of emboli in extremities.

II. CHRONIC PAIN SYNDROMES

 Diseases of the Microcirculation 281

2. T hrombolytic therapy with intra-arterial streptokinase (loading dose

25,000–250,000 IU followed by an infusion of 5000–15,000 IU/h) or
tissue plasminogen activator.
3. Anticoagulant therapy with intravenous heparin (loading dose
7500–10,000 IU followed by infusion of 1000–1500 IU/h) to maintain
APTT at twice the control value. Warfarin is administered during the
first week of treatment with heparin. The dose of warfarin should be
adjusted to maintain INR of 2.0–3.0.
  

Before the advent of anticoagulant therapy, continuous epidural anal-

gesia with low concentration of local anaesthetics with or without opi-
oids (bupivacaine 0.0625–0.125% ± fentanyl 2–5 mcg/mL at the rate of
5–10 mL/h) was administered to relieve pain and to anaesthetize the
patient for surgical intervention. The increased risk of epidural haema-
toma precludes the use of epidural analgesia during thrombolytic/antico-
agulant therapy. However, in cases of arterial occlusion involving vessels
of the upper limb, brachial plexus block with 20–40 mL of 0.25% bupiva-
caine can provide preoperative and postoperative pain relief. Postopera-
tive pain relief can be prolonged using continuous brachial plexus block
techniques. Stellate ganglion block, either intermittent or continuous, per-
formed with 0.25% bupivacaine may relieve reflex spasm, but it does not
provide pain relief and anaesthesia for surgery. Continuous stellate gan-
glion block is superior to intermittent stellate ganglion block as it provides
superior quality of analgesia with lesser incidence of adverse effects.

Role of SCS in Peripheral Vascular Diseases

Peripheral vascular disease is one of the most common indications
for SCS. In peripheral vascular disease, SCS increases blood flow with or
without modulation of the sympathetic outflow, whereas in coronary isch-
aemia, it also reduces tissue oxygen demand, thereby increasing anginal
threshold. Researchers have shown that this is the result of vasodilation
produced by an antidromic activation of dorsal root structures as well
as an inhibitory effect on sympathetic function. SCS can be successfully
used in the management of peripheral vascular diseases including recal-
citrant Raynaud phenomenon. Patients with unreconstructable chronic
critical limb ischaemia are candidates for this procedure. Pain relief can
be achieved in 60–90% of patients, whereas limb salvage rate is about
60–80%. SCS also improves healing of ischaemic foot ulcers. SCS has been
discussed in detail elsewhere in this book.

II. CHRONIC PAIN SYNDROMES

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 S E C T I O N III

Pain Management:
New Perspectives
23 Pain Management in Rheumatological Diseases 285
24 Pain Management in the Elderly 305
25 Osteoporosis 319
26 Pain Management by Rehabilitative Approaches 329
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 C H A P T E R

23
Pain Management
in Rheumatological
Diseases
Pain, which is often chronic and unremitting, is the leading concern of
patients with rheumatic diseases. Moreover, relief of pain is often the main
reason why these patients seek medical attention. Despite this, the major
focus of rheumatologists has not been pain relief, but rather control of
inflammation, prevention of structural damage, and preservation of phys-
ical function. Although pharmacologic therapies are available that can
effectively treat other aspects of rheumatic diseases, such as inflammation
and bone erosion, patients are often left with unrelieved pain. This repre-
sents a major, unmet medical need that has a considerable impact not only
on a patient's quality of life and physical function but also on healthcare
resources. This chapter on pain management highlights the latest devel-
opments in pain-relief approaches for chronic musculoskeletal pain and
discusses strategies that can be used to tackle the numerous management
challenges in this field.
Even though it is well documented that in early rheumatoid arthri-
tis, the principal cause of loss of physical function is pain, focussing on
achieving effective pain relief is difficult; in general, rheumatologists tend
to believe that control of inflammation will alleviate pain and, therefore,
devote little attention to understanding and controlling chronic pain
per se. In this regard, it is noteworthy that specific outcome measures in
clinical trials of antirheumatic therapies, including the number of painful
joints and levels of generalized pain, are standard even when the agent
tested has no intrinsic analgesic properties. Indeed, patients with mus-
culoskeletal pain syndromes are often referred elsewhere by rheumatolo-
gists even though these syndromes are common and often debilitating.
Why is this the case, and how can rheumatologists improve the manage-
ment of pain in patients with musculoskeletal disorders? These questions
are not just academic and ethical ones, but are also highly practical in an

285
286 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

age when multiple consultations are often precluded. Pain management

specialists can best fill in the gap and effectively address issues of pain
management in a large number of patients. However, the pain specialist
has to acquire an in-depth knowledge of various rheumatological disor-
ders in order to control pain in various spondyloarthropathies and other
rheumatic disorders.

TYPES OF PAIN AND PATHOPHYSIOLOGY OF PAIN IN

RHEUMATIC DISEASES

Pain perception and the development of chronic pain is a complex pro-

cess of neural integration implying response of peripheral tissue damage
and transduction of information in peripheral and central nervous systems.
Adequate pain management requires subtle differentiation of rheumatic
pain. Pain can be divided into various classes depending on anatomical
origin in the musculoskeletal system or special aspects in pathophysiol-
ogy. Articular pain is distinguished from extra-articular pain which can be
subdivided into muscular/musculotendinous or neurogenic pain. Mus-
cular pain is caused by muscle stress due to protective posture, impaired
joint function or malposition, myositis or cortisone-induced myopathy.
Neurogenic compression syndromes or entrapment syndromes induce
neurogenic pain. Tissue damage and chronic inflammation are not solely
responsible for pain perception in rheumatic diseases. Chronic rheumatic
pain can also be categorized into nociceptive/inflammatory, peripheral
neuropathic and central neuropathic/functional.
Owing to complex pathophysiology, rheumatic pain is often of mixed
type and the concept of central neuropathic pain is currently the focus of
research, in particular, in chronic pain syndromes such as fibromyalgia and
chronic low-back pain. Classical nociceptive pain pathway/sensation starts
with depolarization of A delta and C fibres acting as primary afferent neu-
rons. Tissue damage occurring in systemic inflammatory or degenerative
rheumatic diseases as well as localized tenosynovitis, bursitis or arthritis can
induce firing of peripheral neurons. Nociceptors activate ascending dorsal
horn neurons (lateral and medial spinothalamic tract) which transfer the sig-
nal to brainstem and thalamus, thereby projecting to the somatosensory cor-
tex, hypothalamus and limbic system. Afferent sensory neurons induce the
release of neurotransmitters such as glutamate, substance P and GABA in
the dorsal horn influencing pain transmission. Interneurons and descending
spinal pathways such as periaqueductal grey, serotonergic as well as norad-
renergic systems modulate the pain pathway. Cannabinoid receptors and
opioid receptors have inhibitory effects. Despite dense sensory and sympa-
thetic innervation of joint capsules, ligaments, menisci, periosteum, syno-
vial blood vessels and subchondral bone, normal joints are not innervated.

III. PAIN MANAGEMENT: NEW PERSPECTIVES

 Types of Pain and Pathophysiology of Pain in Rheumatic Diseases 287

During inflammation, primary afferent neurons are sensitized and silent

nociceptor start firing. Their activation threshold decreases and they are
activated even by gentle and nonpainful stimuli. This process is called
peripheral sensitization. Inflammatory molecules such as prostanoids, TNF,
chemokines, kinins and growth factors are produced in damaged tissue and
stimulate primary afferent neurons. Vice versa activated peripheral neurons
release inflammatory mediators. This neurogenic inflammation maintains
a ‘vicious circle’ of persistent activation of nociceptive and immune system
causing chronic rheumatic pain. TNF has neurostimulatory properties by
inducing upregulation of expression of substance P in the central nervous
system. Persistent activation of nociceptors and increasing production of
neurotransmitters and prostanoids result in central sensitization, especially
in sensory neurons of the dorsal horn.
Sustained local inflammation induces peripheral and central sensi-
tization as well as pathological nerve growth with innervation of carti-
lage contributing to development of chronic pain in rheumatic diseases.
Furthermore, tissue damage or entrapment can affect nociceptors and
peripheral neuropathic pain can develop. Patients complain of electrical
sensations, burning pain, coldness, numbness or itching. In rheumatoid
arthritis, chronic inflammation denervates the synovium and may cause
neuropathic pain or sensations of joint swelling. Central neuropathic pain,
formerly known as functional pain, is characterized by chronic widespread
pain in different regions of the body as observed in fibromyalgia. Usually
no structural abnormalities can be identified. This type of pain is often
accompanied by symptoms such as fatigue, depression, sleep disturbance
and memory difficulties. Dysfunction in central nervous system and
imbalance of neurotransmitters such as norepinephrine, GABA, serotonin,
glutamate, and substance P can cause augmented central pain process-
ing. Functional neuroimaging studies could reveal that patients with cen-
tral pain exhibit increased activity in the brain regions that are involved
in pain processing when compared with that of the healthy individuals.
The stress-induced increase of cytokines such as TNF could account for
higher pain levels in patients with depression and anxiety. Genetic and
environmental factors like early-life trauma, physical trauma, infections
or emotional stress can contribute to the development of central neuro-
pathic pain. Central neuropathic pain is not only observed in patients with
chronic pain syndromes like fibromyalgia but also seen in patients with
OA and rheumatoid arthritis.
Patients with ankylosing spondylitis, psoriatic arthritis or OA have a
higher pain threshold compared with those of rheumatoid arthritis under-
lining the concept of sustained inflammation and pain perception in rheu-
matoid arthritis. Allodynia or hyperalgesia are common sensations in
patients with rheumatic diseases. Hypersensitivity to stimuli like gentle
touching which are usually nonpainful is called allodynia. Pain perception

III. PAIN MANAGEMENT: NEW PERSPECTIVES

288 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

differs between rheumatic diseases and also between individuals suffering

from equal diseases making it difficult and challenging to distinguish the
types of pain and to treat patients properly. The current concept of chronic
rheumatic pain implies a complex, multifactorial pathophysiological
model with nociceptive and neuropathic pain components (Fig. 23.1).

Sources of Rheumatic Pain

Arthritic – Joint damage due to any cause includes a combination of
inflammatory and mechanical processes that can cause chronic pain.
Neuropathic – Neuropathic pain serves no adaptive purpose. It arises
directly from central and peripheral damages caused by injury, disease, or
medical treatment.
Myofascial – Myofascial pain syndrome occurs in areas of muscles,
usually in just one quadrant, often in the back, neck, and shoulders. It is
associated with trigger points.
Mechanical – Mechanical disorders include muscle or ligament injuries
of upper or lower back (sprain), disc disease, facet OA, spondylolisthesis,
and spinal stenosis. Mechanical pain is greater with movement or physical
loading.
Muscularity – Sometimes, muscles learn to transmit pain signals even
after the underlying injury to the bone or joint heals. It is because they
undergo tightening to protect the injured area as soon as it occurs.

Systemic
opioids, CNS NSAIDs, antihistamines,
anxiolytics antiserotoninergics
Site of
Anticonvulsants injury
Spinal opioids,
alpha agonists
Tricyclics
Nociceptive
afferent
Alpha & beta adrenergic
Conduction blockade
blockade
Spinal Blood vessels
cord Sympathetic
efferent

Systemic suppression Motor Skeletal

Beta adrenergic blockade efferent muscle
Insulin glucose? Antispasmodics
‘High dose’ glucocorticoids?
Branch-chain amino acids?

FIGURE 23.1 Postulated sites of action of pain and the medications used to treat pain at
these sites.

III. PAIN MANAGEMENT: NEW PERSPECTIVES

 Types of Pain and Pathophysiology of Pain in Rheumatic Diseases 289

Emotional status – People, in general, suffering from depression and

anxiety are prone to experience more pain.
Smoking – Smoking individuals experience more pain and obtain
less relief with medications. It is because nicotine reduces body stores
of vitamin C, adversely affects the pain processing mechanisms of the
brain and interacts with opioid pain medications.
Trauma – People who have experienced childhood injuries and trauma
show more pain sensitivity when they experience pain in adulthood.
Weather – People experience arthritic more pain during winter season.
Sleep – Sleep deprivation increases pain perception.

Assessment of Pain
Self-report is the primary source of assessment for a verbal, cognitively
intact person.
Family/care provider reports of pain are included for children and
adults who are unable to give self-report. A systematic, validated pain
assessment tool is selected to assess the parameters of pain, which include
the following:
• Location of pain
• Effect of pain on function and ADLs
• Level of pain at rest and during activity
• Medication usage
• P – provoking or precipitating factors
• Q – quality of pain (patients' pain description – aching and
throbbing)
• R – radiation of pain (Does the pain extend from the site?)
• S – severity of pain (intensity, 0–10 scale)
• T – timing (occasional, intermittent, and constant).
  

A standardized tool with established validity is used to assess the

intensity of pain.
Rating scales – A number of rating scales have been used in clinical
research.
• Visual analogue scale
• Numeric rating scale
• Verbal scale
• Faces scale
• Behavioural scale.
  

The main problem is that rating scales are unidimensional, measuring

the intensity of pain and fail to reflect many qualities of the pain with its
sensory, emotional and evaluative components. However, despite these
shortcomings, in clinical practice where time is at a premium, simple rating
scales are more practical than questionnaires.

III. PAIN MANAGEMENT: NEW PERSPECTIVES

290 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

Pain assessment also includes physiological and behavioural indicators

of pain, and should be included in populations such as infants, children,
cognitively impaired and in persons with acute pain. The following param-
eters are part of a comprehensive pain assessment:
• Physical examination, relevant laboratory and diagnostic tests
• Effect and understanding of current illness
• Meaning of pain and distress caused by the pain
• Coping responses to stress and pain
• Effects on ADLs (especially in the frail elderly and noncognizant person)
• Psychosocial and spiritual effects
• Psychological – social variables (anxiety and depression)
• Situational factors – culture, language, ethnic factors, economic effects
of pain and treatment
• Person's preferences and expectations/beliefs/myths about pain
management methods.
  

Pain is reassessed on a regular basis according to the type and intensity

of pain and the treatment plan. The following parameters are included in
the regular reassessment of pain:
• Current pain intensity, quality and location
• Intensity of pain at its worst in past 24 h, at rest and on movement
• Extent of pain relief achieved – response (reduction on pain intensity
scale)
• Barriers to implementing the treatment plan
• Effects of pain on ADLs, sleep and mood
• Side effects of medications for pain treatment (nausea and
constipation)
• Level of sedation
• Strategies used to relieve pain (pharmacological and
nonpharmacological).
  

Advocate changes to the treatment plan if pain is not being relieved.

One should not forget to refer patients, whose pain is not relieved after
following standard principles of pain management, to a specialist skilled
in dealing with the particular type of pain and use a multidisciplinary
team to address the complex emotional, psychosocial, spiritual and con-
comitant medical factors involved.

Pain Questionnaires
The MPQ is multidimensional, measuring many qualities of pain more
than its quantity. It asks about the sensation of pain, how frequently it
occurs, how much it hurts, and what it feels like to be in pain. The ques-
tionnaire is valid, reliable and consistent. Most important of all, perhaps,
it is useful and sensitive to change. It uses descriptors which fall into four
major groups.

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 Pain Management in Rheumatological Disorders 291

Sensory (1–10)
Affective (11–15)
Evaluative (16)
Miscellaneous (17–20)

There is some consistency in the choice of words used by patients

suffering from the same or similar pain syndromes. The MPQ is used
to produce a total score, the pain rating index, which provides an index
of overall pain intensity. It also gives a rating for present pain intensity.

PAIN MANAGEMENT IN RHEUMATOLOGICAL

DISORDERS

A comprehensive approach involving pharmacological, nonpharmaco-

logical, intervention and complementary methods may be used to achieve
pain relief in rheumatic diseases. OA is the most common type of arthritis
requiring pain management. Disease-modifying medication and biologic
response modifiers can improve disease states in patients with inflamma-
tory musculoskeletal diseases. After the inflammatory component is con-
trolled, treatment goals shift to those similar to secondary OA and other
degenerative joint diseases. Relief of pain and improvement in functional
status are essential components of effective therapy.
Pain may be treated with pure analgesic such as acetaminophen,
NSAIDs, and opioids in various combinations and doses for effective and
sustained benefits. Adjunctive therapy with agents such as topical anal-
gesics, intra-articular viscoelastic supplements, tricyclic antidepressants,
anticonvulsants, muscle relaxants, and anxiolytics may also be helpful.
Nonpharmacologic therapies such as exercise, physical therapy, and psy-
chologic counselling may also diminish pain and improve outcome in
patients with rheumatic diseases. One may also consider yoga, acupunc-
ture, biofeedback, massage, relaxation techniques, and other alternative
therapies.

Stratified Care
A stratified-care approach to pain treatment permits patient-specific
tailoring of analgesia and accomplishes the goal of pain-free relief with a
rapid return to normal activities. It differs from traditional care in which
pain is initially treated with a nonspecific medication, such as a simple
analgesic or NSAID, regardless of pain severity. Using a stratified-care
approach, initial treatment is typically based on pain severity, as reflected
by measures of clinical disability and function (Table 23.1).

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292 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

TABLE 23.1 Stratified-Care Approach to the Management of Pain

HISTORY
Medical and pain history
Cognitive-behavioural evaluation
Review medical records
Generate and test hypothesis
EXAMINATION
Physical examination
Neurological examination
Order and evaluate investigations
DIAGNOSIS
Physical examination
Neurological: Make diagnosis and define underlying pain pathology
(nociceptive/neuropathic/mixed)
MANAGEMENT
Manage primary pathology – medical/surgical
Provide symptomatic therapy
Physical therapy
Cognitive-behavioural therapy
Pain medication
Mild pain – nonopioids ± adjuvant
Moderate pain – atypical/weak/mild opioids ± adjuvant
Severe pain – strong opioids ± nonopioids ± adjuvant
REASSESS PAIN
Evaluate Pain Relief
Physical Examination to assess the Progress of Medication
Change Medical treatment if less relief

The World Health Organization Analgesic Ladder

In 1990, the World Health Organization formed an international panel
of pain management authorities to define best practice standards for use
of pharmacologic treatments of pain. Although originally developed for
treatment of cancer pain, the Canadian three-step ladder approach has been
used for other types of pain as well. When initiating analgesia, it is impor-
tant that the patient starts at the appropriate step along the ladder. For mild
pain, start at step one; for moderate pain, at step two; and for severe pain,
at step three. As the severity of pain increases, maximize the dosing at the
current step and then, if this is insufficient, move up the ladder (Fig. 23.2).
Step 1 – For mild to moderate pain, use (unless contraindicated) aspi-
rin, acetaminophen, or other NSAID. These drugs obey first-order kinet-
ics and may be dosed up to recommended maximums. Adjuvant drugs
to enhance analgesic efficacy, treat concurrent symptoms that exacerbate

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 Pharmacological Options in Pain Management 293

STEP 4: Indication: Failed step 3

Intervention/invasive approach

STEP 3:
Opioids for moderate to severe pain
± Nonopioids, ± adjuvants

STEP 2:
Opioids for mild to moderate pain
+ Nonopioids, ± adjuvant

STEP 1:
Nonopioids
± adjuvant

FIGURE 23.2 Modified four-step ladder approach.

pain, and provide independent analgesic activity for specific types of pain
may be used at any step.
Step 2 – When pain persists or increases (moderate to moderately severe
pain), add (do not substitute) a weak opioid such as codeine, hydroco-
done, or tramadol to the NSAID. The opioids in this class are close in
potency to morphine (mg for mg). However, they have been termed ‘weak’
opioids because, in combination, they have a ceiling to their analgesic
potential due to the maximum amounts of acetaminophen or ASA that
can be administered per 24 h (i.e. 4 g acetaminophen per 24 h). Adjuvant
analgesics are also used as appropriate.
Step 3 – If pain continues or becomes moderate to severe, increase the
opioid potency or dose. Replace weaker opioids with more potent opioids
(morphine, hydromorphone, oxycodone, methadone, fentanyl, or levorph-
anol). Nonopioid analgesics and adjuvant analgesics are also appropriate.
In contrast with the step-one and step-two analgesics, there is no ceiling
effect or upper limit to the dose of opioids when titrating to relieve pain.
Step 4 – Several authors have informally invoked ‘step four’ to indicate
approaches that should be reserved for patients whose pain is not controlled
by competent use of the analgesic approaches outlined in the first three
steps. In general, ‘step four’ involves invasive approaches for pain relief
such as parenteral infusion of opioids, intrathecal administration of opioids
and neuroablative techniques such as cordotomy and ganglion blockade.

PHARMACOLOGICAL OPTIONS IN PAIN

MANAGEMENT

Pharmacological management of pain should have the following aims:

• E ffectively control pain
• Easily self-administered

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294 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

•  inimal side effects

M
• Minimal risk associated with long-term use
• Rapid onset and long acting
• Safely combined with other therapies
  

A pharmacotherapeutic plan begins with a thorough pain and anal-

gesic medication history to identify the nature of the pain. The history
taking should cover the description of pain (e.g. exacerbation, modula-
tion of pain; pain quality and intensity; pain sites as local, disseminated
or regional; characteristics and temporal relationships of pain), cur-
rent medications (prescription, over-the-counter, others), recreational
agents, past treatments and their success or failure, adverse effects and
allergic reactions. Complete blood chemistry should be considered.
We should have the knowledge of the pharmacodynamics, pharmaco-
kinetics, and potential drug interactions and contraindications of the
planned therapy. Further the pain should be routinely assessed at each
patient visit, allowing us to judge the patient’s compliance and effects
of the therapy.
Pharmacological management may involve the use of the following
types of medicines along with other medicines that do not have a direct
effect but an adjuvant effect in order to relieve pain. Table 23.2 shows the
various agents used for pain management, their mechanism of action, use
and limitations with example of each class.
• Analgesics and NSAIDs
• Opioids
• Corticosteroids
• Adjuvants

Analgesics and NSAIDs

Acetaminophen – It is an analgesic and antipyretic without anti-
inflammatory effects. Its central mechanism of action may be mediated
through a COX-2 mechanism. The daily dose of acetaminophen should
not exceed 4 g.
Traditional NSAIDs – They block the formation of prostaglandins
through the two COX namely COX-l and COX-2 enzyme inhibition. The
physiological COX-l catalyzes the production of several cytoprotective
prostaglandins that coat the stomach lining with mucus and aid platelet
aggregation. COX-2 catalyzes the conversion of arachidonic acid to the
inflammatory prostaglandins that are involved in the three key biologic
functions: sensitizing skin pain receptors, elevating body temperature
through the hypothalamus, and recruiting inflammatory cells towards
injured body parts. GI bleeding is a worrisome complication in those at
risk. Risk factors include age over 65 years, co-morbid medical conditions,
use of glucocorticoids, a history of peptic ulcer disease, a history of upper

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 Pharmacological Options in Pain Management 295

TABLE 23.2 Various Agents Used for Pain Management, Their Mechanism of
Action, Use and Limitations with Example of Each Class
Potential
Agent Mechanisms Use Limitations Example

Acetaminophen Probable Mild acute/ Potential Acetaminophen

central chronic pain hepatotoxicity;
mechanism; avoid in hepatic
blocks pain and renal
impulse insufficiency
generation
Nonselective Inhibit COX-2 Mild to GI distress, Ibuprofen,
NSAIDs to reduce moderate bleeding, naproxen,
prostaglandin acute/ ulcer; renal diclofenac,
synthesis chronic pain and hepatic nabumetone,
dysfunction; aceclofenac
possible
inhibition of
bone healing;
and oedema,
hypertension,
drug
interactions,
and allergic
reactions
COX-2-selective Selectively Mild to Possible Celecoxib
inhibitor NSAIDs inhibit COX-2 moderate, inhibition of
to reduce acute/ bone healing;
prostaglandin chronic oedema,
synthesis pain, or hypertension,
with risk drug
factors like interactions,
GI ulcers allergic
and other reactions;
tolerability cardiovascular
issues events
Opioids (analgesic) CNS effects Moderate to Constipation, Codeine,
at opioid severe pain, nausea, hydrocodone,
receptors better for respiratory oxycodone,
(pure micro; short-term depression; morphine,
agonist/ use. Not potential for fentanyl,
antagonist) usually first habituation hydromorphone,
line (overmedication butorphanol
may encourage
overuse of
arthritic joints,
which can
aggravate the
condition)

(Continued)

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296 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

TABLE 23.2 Various Agents Used for Pain Management, Their Mechanism of
Action, Use and Limitations with Example of Each Class

Potential
Agent Mechanisms Use Limitations Example

Atypical opioid CNS effects Moderate to Nausea, Tramadol

(analgesic) by binding moderately constipation,
to micro severe dizziness. Avoid
receptors; pain as an in patients
blocking alternative with seizure
select 5HT to NSAIDs disorders
and NE or first line
reuptake
Corticosteroids Initial Symptomatic Risk of Prednisone,
(anti-inflammatory, production of relief in (pain osteoporosis, prednisolone,
immunosuppressive) leukotrienes, and swelling) Cushinoid methylprednisolone
prostaglandin, in rheumatic symptoms,
histamines; disease hypertension,
reduce and other potential drug
activity of autoimmune interactions,
inflammatory conditions; risk of infection,
cells; increase may slow diabetes mellitus,
β-cell disease fluid retention,
production progression weight gain

CNS, central nervous system; COX-2, cyclooxygenase-2; 5-HT, serotonin; GI, gastrointestinal; IL,
interleukin; NE, norepinephrine; NSAID, nonsteroidal anti-inflammatory drug.

GI bleeding, and use of anticoagulants. The renal and cardiovascular sys-

tems are also affected because prostaglandins are necessary for renal
blood flow and the secretion of sodium and chloride. Prostaglandin inhi-
bition has been shown to raise mean arterial blood pressure. Acute renal
failure has been implicated in dehydrated or other volume-depleted
patients taking NSAIDs.
COX-2-specific inhibitors – They are options for patients who are at
increased risk for a serious GI adverse event. These agents preferentially
block the COX-2 enzyme while allowing the pathways catalyzed by
COX-l to proceed. Theoretically, this inhibits the formation of the inflam-
matory prostaglandins while allowing the production of the homeostatic
prostaglandins. A concern is that selective inhibition of antithrombotic
prostaglandins might increase cardiovascular events. Patients receiving
rofecoxib during the Vioxx GI Outcomes Research Study suffered cardio-
vascular events at a higher rate than those in the naproxen group.

Opioids
Typical opioids – They act by binding to opioid receptors, which
are of three subtypes (mu, kappa, and delta). The binding with the mu

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 Pharmacological Options in Pain Management 297

receptor besides resulting in morphine like analgesia is also associated

with euphoria, decreased GI motility and miosis. The opioid analgesics
in common usage may be divided into those which are full mu agonists,
partial agonists and mixed agonist–antagonists. The pure agonist drugs
are most useful in chronic intractable pain. The mixed agonist–antagonist
opioids (such as pentazocine, butorphanol and nalbuphine) and the par-
tial agonist opioids (such as buprenorphine) have a ceiling effect to the
analgesia they produce, and may precipitate acute pain and opioid with-
drawal symptoms if combined with a pure opioid agonist. Many of the
problematic side effects associated with opioid use, such as respiratory
depression, sedation, and constipation, are mediated through receptors
different from those that result in pain relief. Further opioid analgesics
may carry the risk of abuse, although this abuse is most common when
the patient is taking a variety of agents. Doubts or concerns about opioid
efficacy, tolerance, and abuse or addiction should no longer be used to
justify withholding opioids from patients with well-defined rheumatic
disease pain.
The uncommon side effects of the opioids are manageable. The dys-
phoria and confusion that occasionally occur may be managed by ensur-
ing adequate hydration and renal clearance, lowering the opioid dose,
changing the opioid analgesic or by adding low doses of a neuroleptic
drug such as haloperidol, chlorpromazine or risperidone. The pruritus
and urticaria that occur with opioids is not immune mediated, but a
nonspecific release of histamine from mast cells in the skin. This may be
managed with antihistamines or changing to an alternative opioid anal-
gesic. In the patient taking opioid analgesics for any significant length of
time, it is difficult to demonstrate significant respiratory depression even
with large doses of opioids.
Opioid overdose presents first as mild drowsiness, proceeds to persis-
tent somnolence, then to a poorly arousable state and finally to respira-
tory depression. These changes may be associated with increasing restless,
agitation, confusion, dreams, hallucinations, myoclonic jerks or even sud-
den onset of seizures. If the patient is not arousable, has a respiratory rate
<6–8/min or there is significant hypoxemia or hypotension present, opioid
reversal with naloxone may be warranted.
Atypical opioids – Tramadol has a binary mechanism of action which
combines the centrally acting opioid mu activity with a secondary spinal
mechanism of monoamine reuptake inhibition. It has a weak affinity
for mu-opioid receptors, in conjunction with serotonin and norepineph-
rine reuptake blockade. The analgesic efficacy of tramadol is similar to
that of weak opioids such as codeine and dextropropoxyphene, but it
causes fewer opioid-type adverse effects such as nausea, drowsiness,
vomiting, and dry mouth. Side effects include nausea, constipation, and
drowsiness.

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298 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

Corticosteroids
They reduce pain both by their anti-inflammatory effect of reducing
arachidonic acid release to form prostaglandins and by decreasing swell-
ing and pressure on nerve endings. They may also provide mood eleva-
tion, antiemetic activity and appetite stimulation. In pain management,
they are most commonly taken by mouth to relieve the pain of arthritis
and by injection along with local anaesthetics in arthritic joints and in the
spinal canal to relive back pain. Undesirable effects such as hyperglycae-
mia, weight gain, myopathy, osteoporosis and dysphoria or psychosis
may complicate prolonged therapy. In high doses given for more than a
few days, they can cause avascular necrosis to the femoral head.

Adjuvant Agents
Some medicines, besides being used for hypertension, depression, con-
vulsions or osteoporosis, have primary analgesic activity themselves and
may be used alone or as co-analgesics.
Alpha-2 adrenergic drugs – They are used as sedative and anxiolytics in
the management of pain. Some of the drugs of this class are clonidine and
tizanidine. They can cause fatigue and dry mouth.
Anticonvulsants (such as carbamazepine, valproate, clonazepam, phe-
nytoin, gabapentin and pregabalin) are used either alone or in addition to
opioids or other co-analgesics to manage neuropathic pain.
Tricyclic antidepressants (such as amitriptyline, desipramine, imipra-
mine, and nortriptyline) are useful in pain management in general, and
neuropathic pain in particular. They have innate analgesic properties
and are effective through mechanisms that include enhanced inhibitory
modulation of nociceptive impulses at the level of the dorsal horn. If the
anticholinergic side effects (amitriptyline and imipramine) are undesirable
or troublesome, the secondary amine tricyclics (nortriptyline and desip-
ramine) may be effective analgesics and produce fewer side effects. The
selective serotonin reuptake inhibitor class of antidepressants has not been
shown to be useful in similar ways to the tricyclic antidepressants.
Bisphosphonates (such as pamidronate) and calcitonin have been used
as adjuvant analgesics in the management of bone pain. They inhibit
osteoclast activity on bone and have been reported to reduce pain signifi-
cantly in at least some patients.

DEVELOPMENT OF NEW MEDICATIONS

Pharmacological pain management is restricted because of signifi-

cant side effects or contraindications of NSAIDs and opioids. Develop-
ment of new medication is in the focus of current research. Tapentadol

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 Nonpharmacological Pain Treatment 299

hydrochloride is a micro-opioid-receptor agonist and norepinephrine

reuptake inhibitor for the treatment of moderate and severe pain exhibit-
ing less GI side effects compared to traditional opioids and is effective
in neuropathic and/or inflammatory pain. Cardiovascular and GI side
effects limit pain control with NSAIDs.
Naproxcinod is a newly developed COX-inhibiting nitric oxide donator
which shows an improved safety profile due to release of NO. NO acts in
the vasculature inducing positive effects on blood pressure and mucosal
integrity in the GI tract.
Further studies are needed to evaluate the role of dopaminergic
agents, N-methyl-d-aspartate receptor antagonists, GABA agonists, and
5-hydroxytryptamine 3 receptor antagonist in complex pain syndromes
with central pain components.

NONPHARMACOLOGICAL PAIN TREATMENT

Education has a tremendous effect on sufficient pain control in patients

with rheumatic diseases. Information about the disease and therapeutic
options can reduce the fear of long-term consequences, such as loss of
function, joint damage, chronic pain, and implications on social and family
life. Self-management strategies provide patients with a wide range of
possibilities to influence their course of the disease. Exercise, joint pro-
tection techniques and appropriate use of pharmacological pain therapy
encourage patients to cooperate with their attending physician.
For sufficient pain control, the psychological status of the patient
has to be evaluated. Depression can worsen the perceived pain. There-
fore, rheumatoid arthritis patients describing severe pain without active
disease could benefit from psychological therapy. Additional CBT, bio-
feedback, relaxation training and self-care education can improve the
patient's well being.
Patients with rheumatic diseases are often physically inactive. Physio-
therapy and exercise programs support mental and physical patients with
rheumatic diseases should always be encouraged to get exercise. Owing
to chronic pain, they often feel weak and fatigue causes impaired activity.
On one hand, patients fear exacerbation of musculoskeletal pain when
moving. Consequently, avoidance of exercise deteriorates muscle strength
and physical condition. On the other hand, excessive exercise aggravates
fatigue and flares can occur. Mild exercise like walking, water aerobics,
and bicycling, being appropriate for age and condition, can support phys-
ical fitness and comfort. Physical therapy with heat or cold can reinforce
therapeutic effects. In particular in nociceptive pain, application of moder-
ate heat (e.g. paraffin, packs, and hydrotherapy) can improve pain control.
In generalized pain syndromes, sauna, baths, showers or hot mud can be

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300 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

effective. Cold therapy (e.g. packs, sprays or immersion) is recommended

in acute pain states as seen in flares of rheumatic diseases.
Transcutaneous electrical nerve stimulation is an independent option of
physical therapy at home. Synovectomy and arthroplasty are therapeutic
options in patients with continuous pain, joint deformity and functional
loss. The role of complementary therapies in pain management needs to
be further examined. For optimal pain management, a combination of
different medications is often necessary.

Interventions in Rheumatic Pain Management

Injection therapy with local anaesthetics and steroids is the mainstay in
managing chronic back pain due to a variety of causes. Some of the newer
interventions in this area are as follows:
Facet joint injections and denervation: Facet joint injections and facet
joint denervation continue in the repertoire of many pain practitioners.
Our experience has shown the effectiveness of facet blocks and radio
frequency medial branch denervation in managing low-back pain.
Root sleeve/transforaminal injections: Selective nerve root injections of
corticosteroids are significantly more effective than interlaminar approach
of epidural steroids. The use of fluoroscopy for perineural or transforaminal
injection is essential to ensure that the needle is as close to the affected nerve
root as possible.
Ozone discectomy (nucleolysis): Chemiodiscolysis or discectomy with
an intradiscal injection of oxygen–ozone mixture has added a new dimen-
sion to the percutaneous interventional procedures for disk herniation and
protrusion. These techniques have minimized the invasive nature of sur-
gery and avoid or decrease complications like infection linked to surgery.
Sympathetic blockade: Sympathetic nerve blocks are used for pain
due to vascular insufficiency, visceral pain, and pain that is thought to
have a sympathetic component. Neurolytic and radio frequency lumbar
sympathetic plexus ablation relieve pain at rest and improve healing of
skin ulcers in patients with atherosclerosis, diabetes, and Burgers disease
although the procedure is of much less benefit for claudication.

Common Pain Disorders in Rheumatology

Pain disorders of the musculoskeletal system require systematic
approach that should be based on the knowledge of the aetiopathogenesis
of the disease.
Neck pain: Neck pain or cervical pain is due to the involvement of the
cervical vertebrae or nerves of the cervical spine or the muscles of the neck.
There are a number of causes of neck pain. Some of the important causes
of neck pain are injuries and accidents, OA in the neck, spinal stenosis,

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 Nonpharmacological Pain Treatment 301

degenerative disc disease, poor posture, obesity and cervical spondylosis.

Cervical spondylosis is one of the important causes of neck, shoulder and
upper arm pain. It can present with neck muscle pain alone in the ini-
tial phase of the disease process. In this condition, the cervical vertebrae
undergo wear and tear and the nerves get caught between them. This
pinched nerve causes pain. Management involves mainly proper exercise,
sleep and work posture modification and medication aimed at pain relief
and treatment of cause.
Rheumatoid arthritis: A swollen, hot, discoloured and painful joint
with reduction of range of movements is a common presentation of all
inflammatory arthritidies. Besides management of the cause by disease
modification, the primary management of the joint is advocating RICE
regime. Pain is managed by stratified-care approach. Intra-articular aspi-
ration and glucocorticoid injection provide good pain relief and stop the
inflammatory process, thereby preventing joint damage.
Gouty arthritis: Gouty arthritis results from accumulation of crystals of
monosodium urate in the joints and in the tendons. This leads to inflam-
mation of that tissue causing pain. The pain is treated by analgesics and
NSAIDs. RICE regime and intra-articular aspiration and glucocorticoid
injections are used as for any other inflammatory arthritis. Uricosuric
drugs should not be started in acute painful attack.
OA: It is the most common joint disease in the world. It is primarily a
disease of the cartilage of the weight-bearing joints, commonly the knee
and hip. The other joints involved are bases of thumb, neck and lower back.
The bone pain results from the juxta-articular destruction of the joint sur-
face. The muscle pain is due to the spasm of the muscles and other soft
tissues around the joint. The management involves proper grading (clini-
cally mild, moderate and severe) and radiologically grade (1–4) of the level
of damage followed by cause and biomechanics assessment. Correction of
cause and appropriate pharmacological and nonpharmacological therapies
as per the grade is advocated. Acute flair of pains could be caused due
to ligamentous strain, meniscal tear, haemarthrosis, shedding of calcium
pyrophosphate or hydroxyapatite crystals or cartilage debris into the joint
space, effusion, or subchondral microfractures. These have to be managed
accordingly.
Fibromyalgia: As per the EULAR guidelines, nine recommendations
for management of fibromyalgia have been put forward based on the
strength of evidence and they are graded A, B, C, and D (Table 23.3).
Shoulder pain: It could be due to involvement of either the shoulder
bones and joints or the muscles and soft tissues around it. Most of the
cases of shoulder pain are muscle pains due to the involvement of peri-
arthritic muscles. The problems could be any out of the three categories,
i.e. tendonitis/bursitis pain, injury/instability of the shoulder joint or
arthritis. Frozen shoulder or adhesive capsulitis is one of the important

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302 23. PAIN MANAGEMENT IN RHEUMATOLOGICAL DISEASES

TABLE 23.3 EULAR Guidelines for the Management of Fibromyalgia

No Recommendation Evidence Strength

GENERAL RECOMMENDATIONS
1 Recognize that fibromyalgia is a complex and heterogeneous D
condition; it involves ‘abnormal pain processing and other
secondary features’; full understanding must be based on a
comprehensive assessment of the patient's pain, function,
and ‘psychosocial context’.

2 A multidisciplinary treatment approach with a combination D

of nonpharmacological and pharmacological modalities is
optimal. (D reflects expert opinion and general practice.)
NONPHARMACOLOGICAL MANAGEMENT
3 Heated pool treatment (or balneotherapy) is effective B
in improving pain and function, both with and without
exercise.

4 Exercise programs tailored to the individual including C

strength training and aerobic exercise.

5 Cognitive-behavioural therapy (CBT) may be helpful for D

some patients.

6 Other therapies include relaxation, rehabilitation, C

physiotherapy, and psychological support.
PHARMACOLOGICAL MANAGEMENT
7 Analgesics

a Tramadol is recommended for pain management. A

b Simple analgesics such as ‘paracetamol and other weak D

opioids’ can be considered while strong opioids and
corticosteroids are not recommended.

8 Antidepressants – amitriptyline, fluoxetine, duloxetine, A

milnacipran, moclobemide, and pirlindole – often improve
fibromyalgia patient function and reduce pain, and are
therefore recommended.

9 Tropisetron, pramipexole, and pregabalin reduce pain and are A

recommended.

Strength of evidence: A, evidence includes a large, high-quality study; B, small number of studies; fairly
high quality; C, based on expert opinion, some experimental evidence; D, based on expert opinion.

causes of shoulder pain, in which the movements at the shoulder joint

are restricted and painful. Treatment involves the use of appropriate pain
medicine depending on the severity, adjunct medicines like muscle relax-
ants for the periarticular spasm and physiotherapy. Local steroid, botuli-
num toxin, and viscoelastic supplement injections have been advocated in
those refractory to primary pharmacological intervention.

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 Conclusion 303

Bursitis/tendonitis: Bursitis/tendonitis are another common presenta-

tion of inflammatory musculoskeletal diseases. They should primarily be
treated with rest, ice fermentation, compression support and limb elevation
followed by splints and pads. If they do not respond, then glucocorticoid
injections and even surgery is indicated.

CONCLUSION

Pain is a cardinal symptom in patients with rheumatic disease. It

impacts functioning, quality of life and causes disability. The pain is fre-
quently multifactorial in origin and has both central and peripheral com-
ponents. Disease activity is only marginally related to the extent of pain
severity, and pain-related presentation can differ widely between individ-
uals. Cognitions and emotions contribute to different perception of pain.
Although remission of rheumatic diseases can be achieved with use of
oral disease-modifying antirheumatic drugs or biological therapies, treat-
ment of pain can be a challenge in every day practice. Assessment of pain
is pivotal for monitoring therapy response and must take into account
various factors. Nonpharmacologic interventions such as exercise and
CBT as well as the use of analgesics such as COX inhibitors or opioids
should aim to achieve at better quality of life for patients with rheumatic
diseases and should help to maintain.

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 C H A P T E R

24
Pain Management in the
Elderly

The elderly population comprises the fastest growing segment of the

world's population. As patients age, the incidence and prevalence of cer-
tain pain syndromes increase. Pain may be underreported as some elderly
patients incorrectly believe that pain is a normal process of aging. Pain
is ubiquitous among older persons. An estimated 80–85% of all persons
experience a significant health problem that predisposes them to pain at
some time after 65 years of age. Of these, 25–50% will experience signifi-
cant pain, and the percentage increases to more than 60% in hospitalized
patients. Age-specific morbidity rates for persistent pain increase with
age for most conditions. The limited data available suggest that 36–83%
of the older population reports some degree of pain that may interfere
with daily activities and the quality of life. Although pain is common in
older patients, pain relief is not. A study from the Eastern Co-operative
Oncology Group showed that 41% of 3000 cancer patients suffered with
­inadequate pain management, and being older than 70 years of age was
the most common risk factor identified for poor pain control.
Chronic geriatric pain may be defined as ‘an unpleasant sensory and
emotional experience associated with actual or potential tissue damage,
or described in terms of such damage, for persons who are either aged
(65–79 years old) or very aged (80 and over) and who have had pain for
greater than 3 months’. The consequences of this pain include impaired
ADLs and ambulation, depression, and strain on the healthcare economy.
Pain may also be related to complications associated with deconditioning,
gait abnormalities, accidents, polypharmacy, and cognitive decline.
Why do physicians fail when it comes to relieving pain, especially
in older adults? Insufficient education in pain management must take
much of the blame, along with a lack of instruments to measure pain
and physician attitudes towards pain. Ignorance of recommendations
and guidelines for pain control, and concern among physicians about

305
306 24. PAIN MANAGEMENT IN THE ELDERLY

prescribing appropriate analgesics for elderly patients directly or indi-

rectly affect pain and its management.
Recently, there has been a major push to develop age-appropriate
pain assessment tools, including several observer-rated scales of behav-
ioural pain indicators for use in those with dementia. There has also
been the release of several comprehensive guidelines for the assess-
ment and management of pain in older persons, although the c­ urrent
evidence base used to guide clinical practice is extremely limited.
Unfortunately, despite these advances, pain remains grossly under-
treated in older persons, regardless of the healthcare setting. With the
demographic imperative of a rapidly aging society, much greater atten-
tion is now being devoted to the problem of geriatric pain, with new
initiatives in healthcare planning, calls for better professional educa-
tion in geriatrics and pain management as well as new directions and
funding resources for research into this important problem. Of course,
this increased awareness must still be translated into action, not just
because better pain relief for older adults is an ethically desirable
­outcome, but out of the sheer necessity of dealing with the millions
of older persons who will suffer from persistent and bothersome pain
in the years to come. A multidisciplinary approach is recommended
to investigate all possible options for optimal management, including
pharmacotherapy, interventional procedures, physical rehabilitation,
and psychological support.

AETIOPATHOGENESIS OF PAIN IN THE ELDERLY

Common clinical syndromes causing pain in older persons include osteo-

arthritis, rheumatoid arthritis, temporal arthritis, polymyalgia ­rheumatica,
osteomalacia, osteoporosis, cervical spondylosis, angina, herpes zoster,
postherpetic neuralgia, trigeminal neuralgia, sympathetic d ­ystrophies
and neuropathies (diabetic, alcoholic, and malnutrition) (Table 24.1). The
site of reported pain varies widely in prevalence figures among different
studies.
The prevalence of articular pain and hand and foot pain is double in
adults aged 65 years and older when compared with that of the younger
adults. Conversely, the prevalence of headache shows a progressive
decrease after its peak prevalence at the age 45–50 years. Chest pain also
peaks in middle age but declines thereafter, despite the high mortality
from ischaemic heart disease. The trend for abdominal pain is similar,
whereas back pain does not vary with age. In summary, it appears that the
frequency of head, abdominal and chest pain is reduced in older people
and joint pain is increased.

III. PAIN MANAGEMENT: NEW PERSPECTIVES

 Aetiopathogenesis of Pain in the Elderly 307

TABLE 24.1 Pathophysiologic Classification of Chronic Pain in Elderly Patients

NOCICEPTIVE PAIN
Arthropathies (e.g. rheumatoid arthritis, osteoarthritis, gout, posttraumatic arthropathies,
mechanical neck and back syndromes)
Myalgia (e.g. myofascial pain syndromes)
Skin and mucosal ulcerations
Nonarticular inflammatory disorders (e.g. polymyalgia rheumatica)
Ischaemic disorders
Visceral pain (pain of internal organs and viscera)
NEUROPATHIC PAIN
Postherpetic neuralgia
Trigeminal neuralgia
Painful diabetic polyneuropathy
Poststroke pain (central pain)
Postamputation pain
Myelopathic or radiculopathic pain (e.g. spinal stenosis, arachnoiditis, and root sleeve
fibrosis)
Atypical facial pain
Causalgia-like syndromes (complex regional pain syndromes)
MIXED OR UNDETERMINED PATHOPHYSIOLOGY
Chronic recurrent headaches (e.g. tension headaches, migraine headaches, and mixed
headaches)
Vasculopathic pain syndromes (e.g. painful vasculitis)
PSYCHOLOGICALLY BASED PAIN SYNDROMES
Somatization disorders
Hysterical reactions

Pain in elderly persons is associated with much impairment in the qual-

ity of life. So far, clinical research has focussed little attention on pain in old
age. Pain is often classified as inevitable epiphenomena in the elderly. But
present studies show that difference between older and younger patients
appears less important than similarities. There is some evidence to suggest
that the raised pain threshold in elderly is because of altered physiology
of peripheral and central pain mechanisms combined with psychologi-
cal attitudes, such as stoicism and reluctance to confirm the presence of
pain. However, once pain is experienced, older persons describe the same
severity, quality and psychological disturbance as younger persons. Cog-
nitive factors play an important mediational role between pain and conse-
quent levels of suffering.

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308 24. PAIN MANAGEMENT IN THE ELDERLY

PAIN ASSESSMENT IN ELDERLY

Assessment of pain severity in elderly requires specialized pain

scales which have been developed with seniors in mind and greater
testing of older pain scales in elderly populations have helped to iden-
tify ­measures of pain more suited to geriatric age group. Few clinicians
would ­ consider prescribing an antihypertensive medication without
monitoring the patient's blood pressure. Yet prescribing an analgesic
without ­monitoring the benefit through an accepted pain scale seems
to be relatively common. Validated pain instruments are rarely used to
monitor pain.
One reason is that finding appropriate tools for the evaluation of pain,
especially in older patients, can be difficult. Few instruments that assess
pain have been standardized in an older population. Visual analogue
scales and those that use descriptive terms such as ‘lancinating’ may be of
limited use in patients with compromised cognition, low visual acuity, or
a low education level.
One pain instrument that has been validated and shown to be respon-
sive to changes in pain status in older persons is the Functional Pain
Scale. This scale (Table 24.2) incorporates three levels of assessment.
Pain is rated as ‘tolerable’ or ‘intolerable’. If the patient reports pain
as ­intolerable, further evaluation and intervention should be rendered
immediately, with frequent follow-up to ensure rapid improvement into
the tolerable range.
An objective functional component makes the instrument more sensi-
tive to changes in pain level than numbers alone. Patients may rank pain
at the highest level; if they are afraid, they will not receive adequate pain
medication. If a patient always reports pain at 5, even when there has
been improvement clearly, this instrument allows the clinician to adjust
the score based on the patient's function.
The 0–5 scale presents a means of monitoring change in function
(i.e. response to therapy). Ideally, all patients should reach a functional
level of 0–2, and preferably 0–1.

TABLE 24.2 Functional Pain Scale for Elderly Population

Score Description of pain by patient function

0 No pain
1 Tolerable (and does not prevent any activities)
2 Tolerable (but does prevent some activities)
3 Intolerable (but can use telephone, watch TV, or read)
4 Intolerable (cannot use telephone, watch TV, or read)
5 Intolerable (and unable to verbally communicate because of pain)

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 Management of Pain in the Elderly 309

After assessing the intensity of pain, one should perform a thorough

examination. An overview is discussed here:
  

• C omplete history and physical examination, with focus on most

pressing pain issues
• Review of location of pain, intensity, exacerbating and/or alleviating
factors, and impact on mood and sleep
• Screening for cognitive impairment such as the Folstein mini mental
examination
• Screening for depression
• A review of the patient's ADLs (bathing, dressing, toileting, transfers,
feeding, and continence) and instrumental ADLs (use of phone, travel,
shopping, food preparation, housework, laundry, taking medicine,
and handling finances)
• Assessment of gait and balance
• Examining basic visual and auditory function.

MANAGEMENT OF PAIN IN THE ELDERLY

The management of chronic pain should be a priority in geriatric care since

the emotional component of the pain and suffering may be considerable.
Alleviation of pain in the elderly requires meticulous diagnosis of the causal
pain mechanisms as well as a holistic approach, which gives due regard to
psychological and social consequences of pain. Management of chronic pain
in older patients differs from that in younger patients because of age-related
changes in metabolism and an increased likelihood of multiple medication
use. The release of guidelines in 2009 by the American Geriatrics Society on
The Management of Chronic Pain in older Persons is a breakthrough in helping
to manage pain in this population. These guidelines focus on pharmacologi-
cal and nonpharmacological approaches used in pain control and help to
provide a framework for rational nosology and therapeutic strategy.
Treatment modalities for pain in the elderly may be categorized into the
following areas. A multidisciplinary approach is recommended to investi-
gate all possible options for optimal management:
  

1.  harmacotherapy (most commonly employed)

P
2. Psychological support
3. Physical rehabilitation
4. Interventional procedures.

Pharmacological Interventions in Pain Management

Drug treatment is generally the first and most widely used treatment
modality to control geriatric pain. It is relatively simple to implement

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310 24. PAIN MANAGEMENT IN THE ELDERLY

and consists of NSAIDs, muscle relaxants, opioids, and other adjuvant

therapy. Prescribing these medications is not without risks, however. The
patient's cognitive, p
­ hysiological, and functional status may be affected.
The American Geriatric Society and the WHO have put together counsel
to arrive at some form of consensus as to the best approach in this patient
population.
When prescribing analgesics for elderly patients, it is best to
  

1.  se drugs that have a short half life;

u
2. prescribe one drug at a time;
3. begin with low doses;
4. be aware of additive effects; and
5. follow them closely for any adverse effect.

Summary of 2009 American Geriatric Society Recommendations

NONOPIOIDS
Nonopioid analgesics fall into two categories: acetaminophen and
NSAIDs. Included are salicylates such as aspirin, various classes of
NSAIDs, and the new COX-2-specific inhibitors.
Acetaminophen should be considered as initial and ongoing pharmaco-
therapy in the treatment of persistent pain, particularly musculoskeletal
pain, owing to its demonstrated effectiveness and good safety profile
(high quality of evidence and strong recommendation).
Absolute contraindication of acetaminophen is liver failure. Relative
contraindication and caution should be used in hepatic insufficiency,
chronic alcohol abuse or dependence. Maximum daily recommended
­dosages of 4 g/24 h should not be exceeded and must include ‘hidden
sources’ such as from combination pills.
Nonselective NSAIDs and COX-2 selective inhibitors may be considered
rarely, and with extreme caution, in highly selected individuals (high
quality of evidence and strong recommendation). These agents should be
used when all other (safer) therapies have failed and there is evidence of
continuing therapeutic goals not met and ongoing assessment of risks and
complications outweighed by therapeutic benefits.
Absolute contraindications of COX-2 inhibitors are current active
­peptic ulcer disease, chronic kidney disease and heart failure. Relative
contraindications are hypertension, Helicobacter pylori, history of peptic
ulcer disease, and concomitant use of corticosteroids or selective serotonin
reuptake inhibitors.
Older persons taking nonselective NSAIDs should use a proton pump
inhibitor or misoprostol for gastrointestinal protection. Patients taking a
COX-2-selective inhibitor with aspirin should use a proton pump inhibi-
tor or misoprostol for gastrointestinal protection. Patients should not
take more than one nonselective NSAID or COX-2 selective inhibitor for
pain control. Patients taking aspirin for cardioprophylaxis should not

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 Management of Pain in the Elderly 311

use ibuprofen. Patients taking nonselective NSAIDs and COX-2-selective

inhibitors should be routinely assessed for gastrointestinal and renal tox-
icity, hypertension, heart failure, and other drug–drug and drug–disease
interactions.

OPIOIDS
  

• P atients with moderate to severe pain, pain-related functional

impairment, or diminished quality of life because of pain should be
­considered for opioid therapy.
• Patients with frequent or continuous pain on a daily basis may be
treated with around-the-clock time-contingent dosing aimed at
achieving steady-state opioid therapy.
• Clinicians should anticipate, assess for, and identify potential opioid-
associated adverse effects.
• Maximal safe doses of acetaminophen or NSAIDs should not be
exceeded when using fixed-dose opioid combination agents as part of
an analgesic regimen.
• When long-acting opioid preparations are prescribed, breakthrough
pain should be anticipated, assessed, and prevented or treated using
short-acting immediate-release opioid medications.
• Patients taking opioid analgesics should be reassessed for ongoing
attainment of therapeutic goals, adverse effects, and safe and respon-
sible medication use.
  

Overview of the WHO Recommendations: Analgesic Ladder – Significant

overlap occurs between chronic geriatric pain and cancer pain. For this
reason, following the WHO recommendations for pain management is
appropriate. In order to maintain freedom from pain, WHO recommends
(1) administration of drugs ‘by the clock’ (e.g. every 3–6 h), (2) medica-
tion by mouth individualized for the patient, and finally (3) following the
‘analgesic ladder’ (which was modified for elderly population). The basic
principles of analgesic ladder are as follows:
  

• F or mild pain, the most appropriate first choice for relatively safe
analgesia is acetaminophen.
• For mild to moderate pain or pain uncontrolled with acetaminophen,
the use of NSAIDs is appropriate.
• For pain refractory to NSAIDs, or pain rated as moderate initially,
a weaker opioid (e.g. codeine) is the appropriate first choice. Other
weak opioids that may be used include hydrocodone, propoxyphene,
and oxycodone in combination with acetaminophen.
• For pain refractory to the previous plan, or pain rated as severe, a
pure opioid agonist (e.g. morphine) is selected. Other pure opioids
to consider include hydromorphone, fentanyl, levorphanol, and
oxycodone.

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312 24. PAIN MANAGEMENT IN THE ELDERLY

• A
 djuvant medication may be used to relieve fear and anxiety in
the patient as well as for synergism with the previously named
medications.
Newer Opiates and the Elderly
As new guidelines are released discussing the adverse reactions of
NSAIDs and the elderly and there is a move towards opiate ­conversion,
the search for new and safer opiates is inevitable. Most of the older opi-
ates have a known efficacy and safety profile when used in an older
population. One of the newer opiates, oxymorphone, has recently been
studied as it is metabolized in a non-cytochrome P-450 pathway and,
therefore, bypasses many of the drug–drug interactions common to the
elderly. Moreover, the drug is still renally excreted, so it should be used
with ­caution in elderly patients who already have a decreased glomerular
­filtration rate. The problem arises as it is not as familiar as many of the
other opiates typically used; however, indications suggest that it is safe in
the elderly and should be used in the same way as the other opiates, start-
ing with a low dose and increasing it slowly. Synthetic opioid analgesics
such as tramadol and tapentadol may be useful in the treatment of older
patients, although adverse effects are more common and potentially more
serious in this population.
Advances in analgesics’ selectivity, alternative medicine, and progress
in the identification of nonopioid pain receptors and the development of
pharmacological products to target them are just a few of the changes that
have altered the clinician's thinking about treating pain. The management
of pain in the older population is complicated by the adverse effects that can
occur with pain medications, as well as age-related alterations in physio-
logic factors, pharmacodynamics of drug distribution and metabolism, and
pain perception. Adverse drug reactions occur in older patients at greater
than twice the frequency of younger subjects, and the risk rises as the num-
ber of medications increases. An older person taking six ­medications is
14 times more likely to have an adverse reaction than a younger person
taking the same number of medications. Based on these statistics, any new
medication should be added to the drug regimen with care.

Adjuvant Drug Therapy in Elderly Population

Adjuvant drug therapy should be considered at all times to enhance
the analgesic effects of other medications. It is often necessary to try dif-
ferent drugs to determine the best regimen for a particular patient. Some
of the adjuvant drugs used to treat pain include but are not limited to the
following:
  

1. A
 ntidepressants
2. A nticonvulsants

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 Management of Pain in the Elderly 313

3.  lpha-2 adrenergic agonists

A
4. Local anaesthetics
5. Corticosteroids
6. Baclofen
7. N-methyl-d-aspartate receptor agonists
8. Muscle relaxants
9. Topical creams and gels
10. Neuroleptics
11. Antihistamines
12. Psychostimulants
13. Calcitonin
  

Older patients who do not experience adequate pain control with

traditional analgesics may benefit from a variety of adjuvant medica-
tions. These drugs have no analgesic properties as such, but may be
helpful in maximizing pain control while allowing low doses of opi-
oids to be used.

Adjuvant Analgesic Drugs

  

• A ll patients with neuropathic pain are candidates for adjuvant

analgesics. A number of anticonvulsant medications, including car-
bamazepine, clonazepam, valproic acid, phenobarbital, phenytoin,
gabapentin and pregabalin, have been shown to provide partial relief
of pain, primarily for patients with neuropathic conditions. The mech-
anism of action for pain reduction is not well understood, and each
medication has its own unique set of possible significant side effects.
Over-dosage can be fatal, although clonazepam and gabapentin have
wide therapeutic ranges. Anticonvulsants also can interact with and
reduce or increase the potency of other medications the patient is
taking.
• Patients with fibromyalgia are candidates for a trial of approved
­adjuvant analgesics.
• Patients with other types of refractory persistent pain may be candi-
dates for certain adjuvant analgesics (e.g. back pain, headache, diffuse
bone pain, and temporomandibular disorder).
• Tertiary tricyclic antidepressants (amitriptyline, imipramine, and
doxepin) should be avoided because of higher risk for adverse effects
such as anticholinergic effects and cognitive impairment.
• Agents may be used alone, but often the effects are enhanced
when used in combination with other pain analgesics and nondrug
strategies.
• Therapy should begin with the lowest possible dose and increase
slowly based on response and side effects, with the caveat that some
agents have a delayed onset of action and therapeutic benefits are

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314 24. PAIN MANAGEMENT IN THE ELDERLY

slow to develop. For example, gabapentin and pregabalin may require

2–3 weeks for onset of efficacy.
• An adequate therapeutic trial should be conducted before discontinu-
ation of a seemingly ineffective treatment.

Other Adjuvant Drugs

  

• L ong-term systemic corticosteroids should be reserved for patients

with pain-associated inflammatory disorders or metastatic bone
pain. Osteoarthritis should not be considered an inflammatory
disorder.
• Patients with localized neuropathic pain are candidates for topical
lidocaine.
• Patients with other localized nonneuropathic persistent pain may be
candidates for topical NSAIDs.
• Topical agents such as doxepin, capsaicin and lignocaine have
gained popularity for use in certain neuropathic pain conditions
such as diabetic neuropathy, postherpetic neuralgia, or neuroma
pain.
Capsaicin: Capsaicin decreases pain transmission by depleting
peptides (such as substance P) that are released at nerve terminals
and mediate pain transmission. Several studies have suggested that
capsaicin cream can be an effective analgesic in at least some types of
neuropathic pain.
An adequate trial of capsaicin generally requires four applications
daily for at least 3–4 weeks. Some patients may experience a burning
sensation, which usually diminishes over time. Special care should be
taken to avoid contact with the eyes or mucous membranes.
EMLA: EMLA cream is used prior to painful procedures such as
venipuncture, lumbar puncture, and wart removal. EMLA cream may
also be helpful in the treatment of postherpetic neuralgia, ischaemic
neuropathy, and a variety of neuropathic conditions.
• Many other agents for specific pain syndromes may require caution
in older persons and merit further research (e.g. glucosamine, chon-
droitin, cannabinoids, botulinum toxin, alpha-2 adrenergic agonists,
calcitonin, vitamin D, bisphosphonates, and ketamine) (low quality of
evidence and weak recommendation).

Physical Rehabilitation
The rehabilitative aspect of pain management may help the patient
live a more independent and functional life. Rehabilitation may involve
adapting to loss of physical, psychological, or social skills. The assessment
of ADLs can help assess the level of function and direct treatment. The

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 Management of Pain in the Elderly 315

objectives of rehabilitation include stabilizing the primary disorder, pre-

venting secondary injuries, decreasing pain perception via a multidisci-
plinary approach, treating functional deficits, and promoting adaptations
to current disabilities.
TENS in elderly patients: In elderly patients with acute and chronic pain,
TENS is an important modality for relief of pain, particularly in patients
with intolerance to oral and systemic analgesics. TENS is particularly
suited for treatment of pain in neurogenic origin such as postherpetic
neuralgia, intercostals neuritis, and so on. Chronic back pain and arthritic
pain are also amenable to treatment with TENS. Rarely central pain states
such as brachial avulsion injury and the pain of spinal injury can also be
treated by TENS. However, visceral and psychogenic pain is not suit-
able for treatment with TENS. The only absolute contradiction for using
TENS is in elderly patients with pacemakers or other implanted electrical
devices, which may be affected by the field generated by the stimulator.
The use of TENS in elderly patients is remarkably free from any adverse
effect. However, 10% of the patients may experience an aggravation of
pain in the initial days of stating pain therapy.

Psychological Support
Because pain is a complex sensory and emotional experience, psycho-
logical modalities should be employed in the pain management model.
The psychological branch of pain also explains why some patients with
minimal disease may have excruciating pain, whereas others with severe
disease may have minimal complaints. Pain-coping strategies may include
relaxation, prayer, and attention-diversion techniques. Depression and
anxiety in the geriatric patient must be addressed with psychotherapy,
meditation, and medication. Furthermore, the socio-environmental vari-
ables of each patient should be adjusted to help the patient cope with
pain. A solid support system including relatives and caregivers should be
established.

Interventions for Pain Management in the Elderly

Interventional pain modalities may help to determine the underlying
cause of pain and also help to arrive at a precise diagnosis. It often allevi-
ates the need for heavy medication use, thereby sparing the patient from
unwanted side effects associated with larger doses of drugs. Nerve blocks
are some of the most commonly used interventional procedures employed
by pain physicians; these help not only with diagnosis but also prognosis,
pre-emptive analgesia, and sometimes definitive therapy. Other interven-
tions that may be used include chemical neurolysis, radiofrequency lesion-
ing, cryoneurolysis neuroaugmentation, and neuraxial drug delivery.

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316 24. PAIN MANAGEMENT IN THE ELDERLY

Nerve entrapment syndromes: Entrapment syndromes commonly involve

the following nerves: intercostals nerve (after thoractomy), ilioinguinal
nerve (after hernia repair), lateral cutaneous nerve of the thigh, median
nerve (carpal tunnel syndrome) and intercostobrachial nerve (after ­axillary
surgery). There is evidence of beneficial clinical effect and s­ cientific jus-
tification for the use of injected steroids in these painful entrapment
syndromes.
Cranial nerve blocks: The cranial nerves are frequent targets for nerve
blocking techniques. Blocks for glossopharyngeal neuralgia, occipital
­neuralgia and sphenopalatine neuralgia, glycerol and alcohol injections
of the Gasserian ganglion and radiofrequency lesioning have been used
successfully by us for trigeminal neuralgia and cluster headaches.

Interventions for Spinal Pain

Injection therapy with local anaesthetics and steroids is the mainstay in
managing chronic back pain due to a variety of causes. Neurogenic clau-
dication due to lumbar canal stenosis, radicular pain due to a prolapsed
intervertebral disc, and facet arthropathy are some of the common causes
of back and leg pain in the elderly population. Root sleeve/transforaminal
epidural injections of corticosteroids are significantly effective in relieving
chronic back and leg pain in this age group (Fig. 24.1). The use of fluoros-
copy for perineural or transforaminal injection is essential to ensure that
the needle is as close to the affected nerve root as possible.
Sympathetic blockade: Sympathetic nerve blocks are used for pain
due to vascular insufficiency, visceral pain, and pain that is thought to
have a sympathetic component. Neurolytic and radiofrequency lumbar

FIGURE 24.1 Transforaminal (root sleeve) epidural injection in an elderly patient with
lumbar canal stenosis and radiculopathy.

III. PAIN MANAGEMENT: NEW PERSPECTIVES

 Management of Pain in the Elderly 317

sympathetic plexus ablation relieve pain at rest and improve healing of

skin ulcers in patients with atherosclerosis, diabetes, Buerger's disease
although the procedure is of much less benefit for claudication.

Cancer Pain Management in the Elderly

Pain due to advanced cancer is often seen in elderly age group and pal-
liation of pain and other symptoms is important in patients who are near
the end of life. An integration of knowledge from the fields of geriatrics,
pain management and palliative care is needed to ensure adequate pain
control for the older patient who is dying. Availability of oral (morphine
tablets) and transdermal opioids (transdermal fentanyl and transdermal
buprenorphine) has considerably helped in control of terminal cancer
pain. Use of other modalities such as neurolytics blocks psychological
strategies and rarely advanced interventional pain management methods
such as intrathecal pump implantation for continuous opioid infusion
have also helped in an effective control of pain in older persons.
Effective management of chronic pain in older persons is attainable,
although unnecessarily elusive. Health professional have a moral impera-
tive to help elderly people in pain. A host of factors can impede a­ ssessment
and drug management, including impaired cognitive function, ­multiple
potential causes of pain, pharmacokinetics and pharmacodynamics unique
to the geriatric population, and clinician anxiety regarding a­ nalgesic addic-
tion. In the geriatric population, some of the most prevalent chronic pain
management cases involve osteoarthritis, low-back pain, and neuropathy.
Effective pain management is achieved with analgesics (acetaminophen
and NSAIDs), opioids, nonopioid agents (e.g. anticonvulsants) and inva-
sive techniques (epidural steroid injections/nerve blocks). Persistent pain
is not an inevitable part of aging but is fairly common among the elderly.
The treatment of pain may be complicated by multiple problems that are
far less likely to occur in younger adults. Barriers to effective manage-
ment include challenges to proper pain assessment, underreporting of
pain by patients, atypical manifestations of pain in the elderly, and a need
for increased appreciation of the pharmacokinetic and pharmacodynamic
changes of aging. Physicians can provide appropriate analgesia in geriat-
ric patients through proper assessment, a multidisciplinary approach, and
appropriate use of treatment modalities.

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 C H A P T E R

25
Osteoporosis

Osteoporosis is a systemic skeletal disorder that results from an imbal-

ance in bone remodelling, leading to a reduction in bone strength, with
microarchitectural disruption and skeletal fragility, increasing fracture
susceptibility. Osteoporosis is among the most common bone diseases.
Multiple definitions exist, for example, osteoporosis is defined by the NOF
as ‘porous bone’, by the WHO based on diagnostic test results, and by the
National Institutes of Health as ‘a skeletal disorder characterized by com-
promised bone strength predisposing to an increased risk of fracture’. The
disease often develops unnoticed over many years, with no symptoms
or discomfort until a fracture occurs. Brittle-bone disease or osteoporosis
causes more fractures of the hip, wrists and spine than hard falls or acci-
dents. According to WHO estimates, one in two Indian women and one
in three men over the age of 50 years have weak bones. Among the young,
osteoporosis is the leading cause of wrist fractures.
Osteoporosis is a widespread disorder with a significant worldwide
health and economic impact. Each year in India, there are an estimated
500,000 spinal fractures, 300,000 hip bone fractures and 500,000 fractures
of other bones of the body attributed to osteoporosis alone. About 80%
of these fractures occur from relatively minor falls or accidents. In many
affected people, bone loss is gradual and without warning signs until
the disease is advanced. Osteoporosis is also known as ‘the silent killer’
because a person usually does not know they have it until is too late.

FACTS OF OSTEOPOROSIS

• A bout 80% of those affected by osteoporosis are women.

• One in three women and one in eight men over age 50 years will have
an osteoporosis-related fracture in their lifetime.
• Significant risk has been reported in people of all ethnic backgrounds.
• Osteoporosis can strike at any age.

319
320 25. OSTEOPOROSIS

• I n most Western countries, while the peak incidence of osteoporosis

occurs at about 70–80 years of age, in India it may afflict those
10–20 years younger, at age 50–60 years.
• In addition to being a common disease, osteoporosis significantly
increases health care costs.

PATHOPHYSIOLOGY OF OSTEOPOROSIS

Human bone undergoes a continuous remodelling process mediated

by osteoblasts and osteoclasts. Osteoblasts generate new bone tissue,
and osteoclasts break down bone tissue. Throughout normal growth in
childhood and adolescence, the activity of osteoblasts surpasses that
of osteoclasts, allowing bone density to increase. Bone remodelling is
affected by various hormones, including parathyroid hormone, cal-
citriol, calcitonin, oestrogen, testosterone, growth hormone, insulin-like
growth factor, thyroid hormone, and cortisol. Dietary calcium and vita-
min D are also critical for bone health. Calcium serves as an essential
component of bone tissue, and vitamin D facilitates adequate calcium
absorption from the gut. Bone mass is at its greatest between the ages
of 20 and 30 years. At this age, osteoclast activity and osteoblast activity
are equivalent for some time, allowing bone density to be maintained.
Then the activity of osteoclasts begins to surpass that of osteoblasts,
and bone mass declines. This decline in bone density may progress to
osteoporosis.

Risk Factors
Risk factors for osteoporosis include
  

• Female sex
• Age > 70 years
• Caucasian or Asian race
• Early onset of menopause
• Longer postmenopausal interval
• Inactivity, especially lack of weight-bearing exercise
  

Osteoporosis can be classified as primary or secondary. Primary osteo-

porosis is simply the form seen in older persons and women past meno-
pause in which bone loss is accelerated over that predicted for age and
sex. Secondary osteoporosis results from a variety of identifiable condi-
tions that may include the following:
  

• M etabolic bone disease, such as hyperparathyroidism

• Neoplasia, as with multiple myeloma or metastatic carcinoma

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 Diagnosis of Osteoporosis 321

• Malnutrition
• Drug therapy, as with corticosteroids
• Prolonged immobilization
• Weightlessness with space travel
  

Modifiable risk factors that may potentiate osteoporosis include

  

1. Smoking
2. Alcohol abuse
3. Excessive caffeine consumption
4. Excessive dietary protein consumption
5. Lack of dietary calcium
6. Lack of sunlight exposure (to generate endogenous vitamin D)

SIGNS AND SYMPTOMS OF OSTEOPOROSIS

Osteoporosis can be present without any symptoms for decades because

osteoporosis does not cause symptoms until bone fractures. Moreover,
some osteoporotic fractures may escape detection for years when they do
not cause symptoms. Therefore, patients may not be aware of their osteo-
porosis until they suffer a painful fracture. The symptom associated with
osteoporotic fractures usually is pain; the location of the pain depends
on the location of the fracture. The symptoms of osteoporosis in men are
similar to the symptoms of osteoporosis in women.
Fractures of the spine (vertebra) can cause severe ‘band-like’ pain that
radiates from the back to the sides of the body. Over the years, repeated
spinal fractures can lead to chronic lower back pain as well as loss of height
and/or curving of the spine due to collapse of the vertebrae. The collapse
gives individuals a hunched-back appearance of the upper back, often
called a ‘dowager hump’ because it commonly is seen in elderly women.
Muscle spasms are also known to cause pain in people with osteoporo-
sis. They are the result of nerves being pinched as one's muscles tense to
protect the joints, and in turn the bones.
In some individuals, the microscopic fractures that can occur as bone
thins can be experienced as painful. One patient described the sensation
as ‘having a toothache deep in the bone’.

DIAGNOSIS OF OSTEOPOROSIS

Diagnosis of osteoporosis is made by three methods:

  

1. R adiographic measurement of bone density

2. Laboratory biochemical markers
3. Bone with pathologic assessment
  

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322 25. OSTEOPOROSIS

BMD measurement is necessary for the diagnosis of osteoporo-

sis. DEXA scans are widely available and are recommended by mul-
tiple guidelines as the best way to measure BMD. This is in contrast
to portable ultrasound machines that are frequently used in commu-
nity screenings. Correlation between ultrasound-measured BMD and
DEXA-measured BMD is poor. A DEXA scan reports several numbers,
including an actual measurement of BMD in grams per square centime-
tre, a T score, and a Z score. The T score is the most clinically relevant
number and the basis for classifying deficient BMD. The T score is a
comparison of the results with BMD in a gender-matched young adult
(∼25–30 years of age, when BMD is estimated to be at its peak). T scores
are reported as standard deviations from the expected BMD of a gen-
der-matched young adult. A T score of equal to or less than −2.5 (or 2.5
standard deviations below the norm) is osteoporosis. A T score between
−1.0 and −2.5 is osteopenia. The Z score is an age- and gender-matched
result. Z scores are not currently used in the diagnosis and management
of osteoporosis.

Laboratory Evaluation for Secondary Causes

of Osteoporosis
• Renal profile (urea and creatinine)
• Calcium, phosphorus, and magnesium
• Liver function tests
• Full blood count
• 25-Hydroxyvitamin D (25OHD)
• Thyroid stimulating hormone
• Parathyroid hormone

Additional Laboratory Tests if Indicated

• Sex hormones (testosterone, oestradiol, luteinizing hormone,
and follicular stimulating hormone)
• Coeliac serology
• Serum/urine protein electrophoresis
• Erythrocyte sedimentation rate
• 24 h Urine calcium/creatinine
• Bone-turnover markers
• 24 h Urine free cortisol
• Prolactin
• Iron studies
• Serum tryptase and histamine levels
• Homocysteine
• Rheumatoid factor
• Skin biopsy for connective tissue disorders

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 Clinical Management and Therapeutic Interventions in Osteoporosis 323

GUIDELINES FOR PREVENTION OF OSTEOPOROSIS

Several clinical guidelines provide recommendations for prevention,

screening, and treatment of osteoporosis. The guidelines put forth by the
NOF are the most general and widely applicable, because these address
osteoporosis resulting from any aetiology. Several key features regard-
ing osteoporosis treatment are noteworthy in the NOF guidelines. Treat-
ment should be initiated in patients with hip or vertebral fractures as
well as in patients with a T score of equal to or less than −2.5. In addi-
tion, treatment should be started in postmenopausal women and men
aged 50 years and older with osteopenia at the femoral neck or spine and
an elevated fracture risk as calculated by the WHO FRAX. Treatment
options discussed in various guidelines consist of bisphosphonates, oes-
trogen, calcitonin, teriparatide, and raloxifene.

CLINICAL MANAGEMENT AND THERAPEUTIC

INTERVENTIONS IN OSTEOPOROSIS

Treatment is aimed at reducing future fracture risk and should be tai-

lored to the individual patient. The emphasis should be on early recogni-
tion and effective management of patients at high fracture risk.
Persons with osteoporosis may benefit from an improved diet, including
supplementation with vitamin D and calcium, and moderate exercise to help
slow further bone loss. Most drug therapies work by decreasing bone resorp-
tion. At any given time, there is bone that has been resorbed but not replaced,
and this accounts for about 5–10% of bone mass. By decreasing resorption
of bone, a gain in bone density of 5–10% is possible, taking about 2–3 years.
However, no drug therapy will restore bone mass to normal. Women past
menopause with accelerated bone loss may benefit from hormonal therapy
using oestrogen with progesterone. The oestrogen retards bone resorption
and thus diminishes bone loss. This effect is most prominent in the first years
after menopause, while risks from hormone replacement therapy increase.

Pharmacological Interventions
One of the more common nonestrogen therapies is the use of bisphos-
phonates such as alendronate or risedronate that act as an inhibitor of
osteoclastic activity.
Bisphosphonates are the mainstay of therapy for osteoporosis.
Four are currently approved by the Food and Drug Administration
for the treatment of osteoporosis: alendronate, risedronate, ibandronate,
and zoledronic acid (Table 25.1). Bisphosphonates bind to hydroxyapatite
and block the enzyme farnesyl pyrophosphate synthase in bone tissue

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324 25. OSTEOPOROSIS

TABLE 25.1 FDA Approved Bisphosphonates for Treatment of Osteoporosis

Bisphosphonates Dose

Alendronate 10 mg daily or 70 mg weekly

Risedronate 5 mg daily or 35 mg weekly

Ibandronate 150 mg monthly

Zoledronic acid 5 mg/100 mL, once yearly

Raloxifene 60 mg daily

Salmon calcitonin nasal spray 200 IU daily

Teriparatide 20 mcg subcutaneously once a day

and inhibit osteoclast-mediated bone resorption. Alendronate, risedro-

nate, and ibandronate are all available as both daily and intermittent
(weekly or monthly) dosage forms. Zoledronic acid is administered as
an annual intravenous infusion. The most common side effects with oral
bisphosphonates are GI side effects, generally oesophageal irritation or
heartburn. These effects, along with the very low bioavailability, contrib-
ute to the specific and detailed patient administration instructions. Zole-
dronic acid has GI side effects similar to placebo, but is associated with
myalgias, fever, and headache. Serum creatinine should be assessed before
and after use of zoledronic acid due to reports of renal failure after treat-
ment. All bisphosphonates are not recommended for use with renal dys-
function. Intermittent dosing of bisphosphonates (weekly and monthly)
may decrease risk of administration-related adverse effects. The bisphos-
phonates both improve BMD and also reduce the incidence of hip and
nonvertebral fractures.
Calcitonin-salmon is also an antiresorptive therapy for osteoporosis, and
affects BMD by inhibiting the activity of osteoclasts. It is available in a non-
oral (nasal spray) formulation for the treatment of osteoporosis. It should
be administered daily in alternating nostrils. Common side effects are local,
and include nasal irritation and occasionally epistaxis. Calcitonin has dem-
onstrated positive effects on spinal BMD, but has not been shown to sig-
nificantly affect hip. In addition to its effects on spinal BMD, calcitonin has
been shown to alleviate pain from vertebral osteoporotic compression frac-
tures. The mechanism of calcitonin-produced analgesia remains unclear,
but it has been proposed to include beta endorphins and prostaglandins.
Raloxifene is a selective oestrogen receptor modulator. It antagonizes
oestrogen receptors in some tissues and it is an agonist of oestrogen recep-
tors in other tissues, such as bone tissue. Oestrogen affects the balance of
osteoclast and osteoblast activities, and its deficiency is associated with an
increase in osteoclastic activity. Raloxifene is administered as a once-daily
oral formulation. Side effects include hot flashes, especially during the

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 Clinical Management and Therapeutic Interventions in Osteoporosis 325

first 6 months of therapy. Raloxifene has been associated with an increase

in thromboembolic events and carries a black box warning about this risk.
Teriparatide is parathyroid hormone produced using recombinant
DNA technology. Teriparatide has anabolic effects on bone, stimulating
the activity of osteoblasts. It is administered as a once-daily subcutane-
ous injection. Side effects include orthostatic hypotension, nausea, myal-
gia, and arthralgia. Teriparatide has a black box warning regarding risk of
osteosarcoma. Osteosarcoma was observed in rats exposed to teriparatide
at doses much higher than the currently approved dose. Teriparatide is
not recommended for use beyond 2 years due to lack of safety and efficacy
data. After 2 years, some studies suggest that the addition of bisphospho-
nates helps continue increase in BMD or helps maintain BMD gained dur-
ing teriparatide treatment.
Denosumab, an antiresorptive therapy, prevents the activation of
receptor activator of nuclear factor kappa B (RANK) ligand receptors
on the surface of osteoclasts. The RANK receptor plays a role in forma-
tion, function, and survival of osteoclasts. Denosumab is administered
by a health care professional as a twice-yearly subcutaneous injection.
The most commonly reported side effects include back and musculoskel-
etal pain, pain in extremity, cystitis, and hypercholesterolaemia. Serious
reported side effects include serious infections and osteonecrosis of the
jaw. Patients at risk of infection (including patients on immunosuppres-
sive therapy) should have a risk–benefit evaluation prior to considering
denosumab therapy. Denosumab improves BMD and decreases fractures.
No head-to-head comparative trials exist to guide selection of osteoporo-
sis therapy for a specific patient. Of the guidelines, there is discordance
on which therapies are used as first-line treatment. The NAMS and ACR
guidelines recommend use of bisphosphonates as first-line therapy, but
offer no suggestion on choosing a specific bisphosphonate. Practitioners
must rely on their own analysis of efficacy, safety, and cost when deciding
between currently available therapies.

Nonpharmacological Intervention
This includes modification of general lifestyle factors, such as a bal-
anced diet containing calcium and vitamin D, smoking cessation and
avoidance of heavy alcohol use. A regular exercise routine should be
encouraged, including weight-bearing and muscle-strengthening exer-
cises. In a Cochrane analysis of 18 randomized-controlled trials examining
the effectiveness of exercise therapy in preventing bone loss in postmeno-
pausal women, aerobics, weight-bearing and resistance exercises were all
effective on the BMD of the spine. Walking was effective on both BMD of
the spine and the hip and should be recommended as it is the easiest and
simplest program to implement.

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326 25. OSTEOPOROSIS

The role of calcium and vitamin D supplementation in reducing falls

and fractures is not clear. A reduction in calcium intake or absorption
and/or vitamin D deficiency/insufficiency leads to secondary hyperpara-
thyroidism, which contributes to accelerated bone loss in the elderly. The
antifracture effect of vitamin D is more pronounced in the vitamin D-defi-
cient institutionalized elderly and involves, in part, its effect on muscle
strength and therefore in falls prevention. Vitamin D deficiency impairs
neuromuscular function, increasing falls risk (Fig. 25.1). As calcium was
given along with vitamin D in many of the positive trials, it has become
routine clinical practice to replete both calcium and vitamin D. Indeed, all
trials of antifracture therapies have been carried out in subjects given both
calcium and vitamin D as adjunct. It can be concluded therefore that the
antifracture abilities of these drugs apply to calcium-replete and vitamin
D-replete individuals.
The reduction in intestinal calcium absorption associated with vitamin D
inadequacy triggers the release of parathyroid hormone, which mediates
the mobilization of calcium from bone, resulting in a reduction in BMD.
This homoeostatic response to vitamin D inadequacy may increase the risk
of fractures. Another important consequence of vitamin D inadequacy is a
decrease in neuromuscular function.
What constitutes optimum vitamin D status is still a subject of debate
and is defined in some studies as a serum 25OHD concentration of >50
or 75 nmol/L. Based on available evidence, it has been suggested that,
although estimates of serum 25OHD level needed for optimal sup-
pression of PTH varied widely, optimal vitamin D status clusters in the
75–80 nmol/L range with a lower risk of fracture at serum levels >75 nmol/L.
Calcium absorption is considered to be impaired under conditions of vita-
min D deficiency, although it is uncertain at what vitamin D status calcium
absorption is fully normalized. Patients with very low vitamin D levels
showed a surprisingly high incidence of osteomalacia but there was no

Calcium absorption – ↓
Vitamin D insufficiency

Bone mineral density – ↓

Neuromuscular function – ↓

Parathyroid hormone – ↑

Fracture risk – ↑

FIGURE 25.1 Consequences of vitamin D deficiency/insufficiency.

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 Conclusions 327

evidence of osteomalacia with 25OHD concentrations >75 nmol/L, sug-

gesting this may be an appropriate cut-off for optimal bone health.
Supplementation with calcium in osteoporosis prevention is currently in
question following a recent meta-analysis that showed calcium supplements
to be associated with about a 30% increased risk of myocardial infarction.

SURGERY FOR OSTEOPOROSIS

Kyphoplasty, or balloon kyphoplasty, is performed to stabilize vertebral

compression fractures, restore lost vertebral body height, and alleviate
pain. Vertebroplasty is performed to treat some patients with osteoporo-
sis. Cement is injected into the affected vertebrae to stabilize the fracture.
A pain physician is able to determine if kyphoplasty or vertebroplasty is
the best treatment for the patient.

SUMMARY

In summary, osteoporosis is a multifactorial disease that is an impor-

tant public health and financial problem, associated with increased mor-
tality and morbidity. Recently released fracture risk prognostic tools
incorporate BMD and other independent clinical risk factors to estimate
an individual's absolute fracture risk, thus aiding treatment decisions.
Management should address investigation for secondary causes of osteo-
porosis and correction of this where possible. Treatment should focus on
both nonpharmacological and pharmacological measures. Bisphospho-
nates are currently recommended as first choice treatment to postmeno-
pausal women and men aged more than 50 years, in accordance with the
NICE guidelines, due to its cost-effectiveness and broad spectrum fracture
efficacy data. To date, there is no consensus on best practice when it comes
to treatment monitoring. Both BMD and BTMs, when used appropriately,
are clinically useful surrogates of antifracture effectiveness; however, limi-
tations and benefits of both should be taken into account.

CONCLUSIONS

• O steoporosis and osteoporosis-related fractures are a common disor-

der that affects one in two women and one in five men. It is a systemic
skeletal disorder that occurs as a result of an imbalance between bone
formation and bone resorption.
• FRAX calculates the 10-year probability of an osteoporotic fracture.
This is computed from multiple extraskeletal clinical risk factors with

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328 25. OSTEOPOROSIS

and without BMD at the femoral neck. It provides an aid in the assess-
ment of an individual's fracture risk and in determining whether
therapeutic intervention is required.
• Osteoporosis is preventable and treatable. Treatment includes non-
pharmacological as well as pharmacological interventions.
• Nonpharmacological intervention includes modification of general
lifestyle factors such as smoking cessation, avoidance of heavy alcohol
use, ensuring regular weight-bearing exercise and optimum calcium/
vitamin D intake.

Future Therapies
Several therapies for osteoporosis are currently being investigated.
These include oral calcitonin, odanacatib, and oral parathyroid hormone.
Oral calcitonin is being studied in postmenopausal women for both pre-
vention and treatment of osteoporosis. End points do not include frac-
tures, but are limited to BMD and urinary bone-turnover markers as a
surrogate indicator of effects on BMD. Odanacatib is a cathepsin K inhibi-
tor. Cathepsin K is an enzyme that affects the function of osteoclasts,
meaning that odanacatib will also be an antiresorptive agent. Odanacatib
is being evaluated as an oral weekly formulation in both men and women
with osteoporosis. End points include both BMD and fractures. Oral para-
thyroid hormone is currently undergoing safety and efficacy studies for
osteoporosis treatment. End points include urinary bone-turnover mark-
ers as a surrogate indicator of effects on BMD. If approved, these therapies
offer both new mechanisms of treating low BMD as well as new formula-
tions that may be more palatable.

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 C H A P T E R

26
Pain Management
by Rehabilitative
Approaches

A physical medicine and rehabilitation approach to acute and chronic

pain syndromes includes a wide spectrum of treatment focus. Whether
assessing or treating acute or chronic pain syndromes, management
should include a biopsychosocial approach. Assessment may include a
focused joint and functional examination including more global areas
of impairment (i.e. gait, balance, and endurance) and disability. More
complicated multidimensional chronic pain conditions may require the
use of a more collaborative continuum of multidisciplinary and inter-
disciplinary treatment approaches. Regardless of the scope of care that
each individual patient requires, treatment options may include active
PT, rational polypharmacy, CBT, and the use of passive modalities.
Treatment goals generally emphasize achieving analgesia, improving
psychosocial functioning, and reintegration of recreational or leisure
pursuits (i.e. community activities and sports). Progress in all therapies
necessitates close monitoring by the pain physician and other health
care providers and necessitates ongoing communication between
members of the treatment team.

PHYSICAL THERAPY

PT can be an important part of the treatment strategy. PT techniques

are useful in teaching patients to control pain, move in safe and struc-
turally correct ways, improve ROM, and increase flexibility, strength and
endurance. ‘Active’ and ‘passive’ modalities can both be used, but active
modalities, such as therapeutic exercise, are particularly important when
the goal is to improve both comfort and function.

329
330 26. PAIN MANAGEMENT BY REHABILITATIVE APPROACHES

TABLE 26.1 Physical Rehabilitation Interventions

•  revent reinjury/provide support: orthotics (braces, corsets, splints)
P
•  hysical modalities: heat, cold and electricity
P
• Traction
• M anual techniques: mobilization, massage, manipulation
• E xercise: aerobic conditioning, specific exercises

Physical rehabilitation emphasizes the use of modalities such as heat,

cold, and electricity and hands-on techniques such as manipulation,
mobilization, massage, and traction. It also involves planning so as to
balance rest for the injured part, prevention of reinjury through use of
orthotic devices (braces, corsets, and splints), and strengthening by spe-
cific exercise programs (Table 26.1). Physical methods of pain control can
aid in aggressive mobilization and nonsurgical rehabilitative treatment of
patients with acute as well as chronic pain.

Bed Rest
The use of prolonged bed rest in the treatment of patients with neck and
low back pain and associated disorders is without any significant scien-
tific merit. Bed rest supports immobilization with its deleterious effects on
bone, connective tissue, muscle, and psychosocial well-being. For severe
radicular symptoms, limited bed rest of less than 48 h may be beneficial to
allow for reduction of significant muscle spasm brought on with upright
activity. Patients should be instructed to avoid resting with the head in a
hyperflexed or extended position. Two days of bed rest is commonly cited
as the appropriate duration for the individual with low back pain, and
although no literature exists to support the use of bed rest in neck pain
disorders, 48 h would be considered the window for bed rest in individu-
als with these conditions, as well.

Thermal Modalities
Thermal modalities include a variety of methods that produce heating
and cooling of the tissues to manage acute and chronic musculoskeletal
pain. Superficial heat, such as moist hot packs, increases skin and joint
temperatures and blood flow, and may decrease joint stiffness and muscle
spasms.
Heat, one of the oldest modalities to relieve pain, can also decrease
muscle spasm and improve function (Table 26.2). Superficial heat can be
provided by means of hot packs, hot water bottles, hot moist compresses,
electrical heating pads, or chemical or gel packs. It can also be provided
through immersion in water (hydrotherapy) such as through whirlpool,

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 Physical Therapy 331

TABLE 26.2 Therapeutic Heat

• S uperficial
• Hot pack, hot water bottle, moist compress
• Heating pad: electric, chemical or gel pack
• Hydrotherapy: whirlpool, heated pool
• Fluidotherapy
• Deep
• Diathermy: shortwave, microwave
• Ultrasound

Hubbard tank, or heated pools. All these modalities convey heat by con-
duction or convection. Superficial heat elevates the temperature of tissues
and provides the greatest effect at 0.5 cm or less from the surface of the
skin.
Deep heating (diathermy) is achieved by converting another form of
energy to heat. In shortwave diathermy, high-frequency electrical currents
are converted to heat, while microwave diathermy uses electromagnetic
radiation as the source. Ultrasound, first introduced for medical use in the
late 1940s, uses high-frequency acoustic vibration that is converted into
heat. Deep-heating modalities increase temperature to depths of 3–5 cm.
Ultrasound is the preferred treatment in most painful disorders, especially
those arising from soft tissues and ligaments, as it has greater penetration
and also nonthermal effects, such as increasing extensibility of tissues. All
these modalities require specialized equipment and trained professionals.
It is not indicated in acute inflammatory conditions where it may serve to
exacerbate the inflammatory response and typically provides only short-
term benefit when used in isolation. It is perhaps best used in the region
of the upper trapezius or lumbar paraspinals to facilitate active stretching
and strengthening.
Physiological effects of heat include analgesia, increased flexibility of
collagenous tissues, and reduction of muscle spasm through selective
decrease in excitation of nociceptive nerve endings. Increased muscle tem-
perature also decreases spindle sensitivity and reduces ‘muscle spasm’.
Heat increases blood flow to the warmed area, which also may accelerate
healing. Because heat increases extensibility of collagen tissues, it may be
helpful to do stretching exercises of shortened muscles after heat therapy.
For example, in patients with adhesive capsulitis (‘frozen shoulder’) or
postsurgical scarring, ultrasound followed by deep massage and stretch-
ing is effective in rehabilitation treatment. The analgesic effects of heat
may be explained by the gate control theory of pain modulation.
Superficial heating modalities have advantages over diathermy as they
can easily be used at home and provide independence and self-control to
patients. Heating pads, hydrotherapy, infrared lamps (sunlamps), hydro-
collator packs, and paraffin wax can readily be used at home.

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332 26. PAIN MANAGEMENT BY REHABILITATIVE APPROACHES

A recent addition to superficial heating modalities is fluidotherapy.

This device circulates warm air through small cellulose granules under
thermostatic control. The advantage of this modality is its ability to pro-
vide superficial heating to an extremity without placing it in a dependent
position (as would be required in hydrotherapy) and thus to reduce the
potential for development of oedema.
Microwave and shortwave diathermy techniques are contraindicated
in the presence of metal because metals selectively absorb energy and
generate heat that can damage surrounding tissues. Microwave dia-
thermy also selectively heats tissue with high water content and thus
is contraindicated over joints with effusions or cavities with fluids. Dia-
thermy is generally contraindicated in areas of active malignancy. Both
shortwave and microwave diathermy are contraindicated for patients
with pacemakers. Ultrasound has the unique advantage of being safe
around metal and useful over small areas. It increases extensibility of
tissue and thus is helpful in treating trigger points, tight tendons, and
capsular structures.

Cryotherapy
Cryotherapy works by decreasing nerve conduction velocity, termed
cold-induced neuropraxia, along pain fibres with a reduction of the muscle
spindle activity responsible for mediating local muscle tone. Application
of cold is a common and practical treatment for pain. Ice packs, commer-
cially prepared chemical gel packs, and cold packs (Table 26.3) are easily
available and can be used at home. Cold packs are usually applied for
15 min and are helpful because they conform to body contours and pro-
duce comfortable and safe pain relief. Ice massage, a specific technique
in which the skin is rubbed with a block of ice, produces three stages of
sensation. The patient first experiences coolness lasting a few minutes, fol-
lowed by a burning sensation for a few minutes, and then numbness and
pain relief. Ice massage is particularly useful in treating small areas such
a trigger points, tendons, and bursae, and should precede massage and
stretching programs.
The use of ethyl chloride and fluoromethane, both vapocoolant sprays,
has been popularized in the treatment of myofascial trigger points. While
the involved muscle is at passive stretch, the trigger point and referred

TABLE 26.3 Cryotherapy

•  old packs
C
• Ice massage
• Ethyl chloride (vapocoolant spray)
• Fluoromethane (vapocoolant spray)

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 Physical Therapy 333

area of pain are sprayed in unidirectional parallel sweeps. This applica-

tion is usually followed by slow steady stretch of the muscle.
Cold is the immediate treatment of choice after acute injuries and is also
used to inactivate trigger points after a muscle is injected. Cold relieves pain
and decreases the inflammatory response and associated swelling. It also
reduces local metabolic activity of underlying tissues, slows nerve conduc-
tion and, by its direct effect on muscle spindle activity, reduces muscle spasm
and guarding. Cold therapy is contraindicated for any medical condition
in which vasoconstriction will increase symptoms, such as certain connec-
tive tissue disorders and Raynaud phenomenon, and in some patients with
hypersensitivity to cold that manifests as a histamine-like response.

Bracing
Immobilization has been used for thousands of years to treat injuries to
the human body. Unfortunately, immobilization may lead to deleterious
effects that may compromise treatment outcome, such as muscle fibre atro-
phy, decreased proprioception, and loss of cervical and lumbar ROM. This
loss may be a clinically significant problem in an individual who already has
compromised muscle function. In acute neck pain secondary to whiplash
injury, there is no advantage of a cervical collar in the treatment of patients
with soft-tissue injury with respect to the duration or degree of persistent
pain as compared with matched control subjects treated without use of a
cervical collar. The existing literature has failed to demonstrate the efficacy
of lumbar bracing as a means to prevent low back injury in the workplace.

Traction
Cervical traction is a therapeutic modality that can be administered
with the patient in the supine or seated position. Traction may reduce
neck pain and works through a number of mechanisms including pas-
sive stretching of myofascial elements, gapping of facet joints, improving
neural foraminal opening, and reducing cervical disc herniation. It has
been found to reduce radicular symptoms in individuals with confirmed
radiculopathy and localized neck pain in individuals with cervicogenic
pain and spondylosis. Cervical traction may be initiated during PT with
the patient properly instructed in home use. It is not a stand-alone treat-
ment modality and should be done in conjunction with ROM exercises,
appropriate strengthening, and correction of postural issues.

Transcutaneous Electrical Nerve Stimulation

TENS has been used to treat patients with various pain conditions,
including neck and low back pain. Success may be dictated by many factors,

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334 26. PAIN MANAGEMENT BY REHABILITATIVE APPROACHES

including electrode placement, chronicity of the problem, and previous

modes of treatment. TENS is generally used in chronic pain conditions and
not indicated in the initial management of acute cervical or lumbar spine
pain. Overall, research is limited in regard to the isolated use of TENS in
the treatment of patients with acute cervical and lumbar spine disorders,
although it has been used in combination with ROM exercises, spray and
stretch, and myofascial release.

Manipulation and Mobilization

Manipulative treatment is commonly used in the treatment of patients
with neck pain and associated disorders. Many different types of man-
ual treatment exist, including soft-tissue myofascial release, muscle
energy/contract-relax, and high-velocity low-amplitude manipulation.
Soft-tissue myofascial release may include various techniques, includ-
ing effleurage, pétrissage, friction, and tapotement. It has been shown
to improve flexibility, decrease the perception of pain, and decrease the
levels of stress hormones.
Manipulation and mobilization have gained support in the treatment
of patients with acute low back pain. Although several studies have dem-
onstrated the efficacy of manipulation and soft-tissue mobilization in the
treatment of patients with acute low back pain, some have not been found
to be effective. The current literature is confounded by poor study design,
execution, and poorly quantifiable objective measures. The consensus of
the Agency for Health Care Policy and Research guidelines was that man-
ual medicine techniques can relieve acute pain and reduce symptoms in
the initial 1–4 weeks of treatment.
Manual therapy includes techniques that use a ‘hands-on’ approach
such as massage (stroking, friction, kneading), manipulation, and
mobilization.
Massage includes stroking, friction, and kneading of muscles and soft
tissues. Stroking massage decreases oedema and produces relaxation of
muscle, while friction and kneading massage break down intramuscular
adhesions and prepare the muscles and soft tissues for stretching. They
are effective in reducing oedema, stiffness, and pain, especially in myofas-
cial trigger points. Massage can be taught to patients and family members
for home use.
Mobilization includes techniques in which a trained physical or occupa-
tional therapist uses a manual approach to handle tissues including mus-
cles and fascia. Myofascial release is a method of soft-tissue mobilization
that focuses on the fascial component, which is believed to cause pain and
dysfunction.
Manipulation is a skilled, passive movement of a spinal segment, usu-
ally within and occasionally beyond its active ROM. Various medical

III. PAIN MANAGEMENT: NEW PERSPECTIVES

 Physical Therapy 335

professionals, including osteopathic physicians, chiropractors, and pri-

mary care physicians, use spinal manipulation but differ in rationale and
techniques used.

Therapeutic Exercise
The most important element of physical rehabilitation addresses
improvement in function through therapeutic exercises designed to
increase functional activity. Exercises include ROM, stretching, strength-
ening, general cardiovascular conditioning, specific exercises, and relax-
ation exercises. ROM exercises increase and preserve joint ROM. They
can be done passively by a physical therapist or family member, actively
by the patient, or can be active–assistive, when the patient performs the
ROM while assisted by another person who increases the ROM with
gentle stretch. ROM exercises increase elasticity of soft tissue, especially
when accompanied by gentle stretch. Muscles that cross two joints such
as the hamstrings, gastrosoleus group, hip flexors, pectorals, finger flex-
ors and extensors, and paraspinal muscles frequently become tight and
shortened, causing poor posture and pain. Stretching these muscles with
ROM exercises improves body mechanics, posture, and function. ROM
and stretching exercises should be preceded by application of heat and are
transferable to a home program.

Strengthening Exercises
These exercises can be done isometrically, in which muscle length is
unchanged but tension is increased, or isotonically, by active contraction
of the muscle with ROM against resistance. Isometric exercises incorpo-
rate gradual increases in resistive force and repetitions. Most strength-
ening exercise programs can be taught to patients for continued use at
home.
General cardiovascular conditioning exercises involve the whole body and
increase aerobic capacity. They increase physical capabilities, reduce pain,
and increase endurance. A combination of ROM, stretching, flexibility,
strengthening, and aerobic exercise is an essential part of physical reha-
bilitation to significantly improve function of patients deconditioned by
effects of chronic pain.
Specific exercise protocols have been proposed for different clinical con-
ditions. The Williams flexion exercises recommended in the 1950s were
replaced by McKenzie extension exercises in the 1980s and by combined
lumbar stabilization exercises in the 1990s. Controversy remains, but most
authors agree on the benefits of combined aerobic conditioning, stretch-
ing, and fitness exercises to increase flexibility, posture, and endurance.
Aerobic exercises such as walking on a treadmill, riding a stationary

III. PAIN MANAGEMENT: NEW PERSPECTIVES

336 26. PAIN MANAGEMENT BY REHABILITATIVE APPROACHES

bicycle, or swimming are rhythmic, repetitive, dynamic activities that use

large muscle groups.
A program that combines ROM, stretching, flexibility, strengthening,
general aerobic exercise, and relaxation is necessary to improve function
of patients deconditioned by effects of chronic pain.
Relaxation exercises are beneficial to reduce anxiety, autonomic hyper-
activity, and muscle tension, all seen in chronic pain states. Techniques
such as imagery, progressive muscle relaxation, controlled breathing, or
listening to relaxation tapes are commonly used in programs designed
to manage chronic pain. Their adaptability for use at home and in other
environments is another advantage.
Pain rehabilitation is an integrated process that addresses medical man-
agement and treats the physical, psychological, social, vocational, emo-
tional, and legal aspects of persons with acute and chronic pain. The
physical rehabilitation techniques described, in addition to appropriate
pharmacological, anaesthesiological, surgical, and psychological/behav-
ioural approaches, will enhance independence and functional ability
in persons with pain-related disability. Every clinician treating patients
with pain should have a good understanding of physical rehabilita-
tion approaches in the comprehensive management of pain and related
disability.

PSYCHOLOGICAL/MIND–BODY THERAPIES FOR

CHRONIC PAIN MANAGEMENT

Psychological factors are important contributors to the intensity of pain

and to the disability associated with chronic pain. Pain and stress are inti-
mately related. There may be a vicious cycle in which pain causes stress,
and stress, in turn, causes more pain. Mind/body approaches address
these issues and provide a variety of benefits, including a greater sense
of control, improved coping skills, decreased pain intensity and distress,
changes in the way pain is perceived and understood, and increased sense
of well-being and relaxation. These approaches may be very valuable for
adults and children with pain.

Cognitive-Behavioural Therapy
CBT has proved to be effective in reducing pain and disability when it is
used as part of a therapeutic strategy for chronic pain. CBT addresses the
psychological component of pain, including attitudes and feelings, coping
skills, and a sense of control over one's condition. It can provide educa-
tional information and diffuse feelings of fear and helplessness. CBT may
include training in various types of relaxation approaches, which can help

III. PAIN MANAGEMENT: NEW PERSPECTIVES

 Psychological/Mind–Body Therapies for Chronic Pain Management 337

people in chronic pain lower their overall level of arousal, decrease muscle
tension, control distress, and decrease pain, depression and disability.
CBT has been found to be effective as part of a treatment regimen for a
variety of pain conditions including episodic migraine and chronic daily
headache, chronic musculoskeletal pain, pain in the well elderly, chronic
cancer pain, rheumatoid arthritis and osteoarthritis, fibromyalgia, myofas-
cial temporomandibular disorders, chronic low back pain, carpal tunnel
syndrome pain, and chronic pelvic pain. It has been suggested to benefit
patients with chronic fatigue syndrome, irritable bowel syndrome, and
anxiety. Although research into the use of CBT in children is in the early
stages, it holds promise for reducing pain-related distress in children.

Biofeedback
Biofeedback is the use of electronic monitoring instruments to provide
patients with immediate feedback on heart rate, blood pressure, muscle
tension, or brain wave activity. This allows the patient to learn how to
influence these bodily responses through conscious control and regula-
tion. Electromyographic biofeedback, for example, can teach patients how
to relax a particular muscle or how to achieve more generalized relax-
ation for stress reduction. Biofeedback has been shown to be effective in
the management of migraine headaches, fibromyalgia, temporomandibu-
lar disorders, rheumatoid arthritis, Raynaud disease, tension headaches,
headaches in children and the pain associated with irritable bowel.

III. PAIN MANAGEMENT: NEW PERSPECTIVES

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S E C T I O N IV

CANCER PAIN
27 Cancer Pain 341
28 Cancer Pain Management 345
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 C H A P T E R

27
Cancer Pain

CANCER PAIN: PREVALENCE AND IMPACT

Pain is among the most common symptom in cancer patients (Table 27.1).
It is estimated that 4 million cancer patients suffer pain globally and for
most of these patients, pain is not satisfactorily relieved. Of the 1 million
people who get cancer in India every year, the vast majority is incurable
at the time of diagnosis and is in need of pain and palliative care only. It
is estimated that by the year 2020 there will be 2–2.5 million new cases
in India every year. 80% of these patients will require Pain Management/
Palliative care as the only treatment. Numerous surveys performed in the
United States and Europe during the past 2 decades indicate that chronic
pain is experienced by 30–50% of patients who are undergoing active treat-
ment for a solid tumour. The prevalence rate in children with cancer is
lower because of the higher proportion of haematologic malignancy; those
with solid tumours, however, often have the same kinds of chronic pain as
their adult counterparts. Surveys of adult cancer patients with advanced
disease, which are often performed in a hospice or palliative care setting,
indicate that the prevalence of pain increases to 90% towards the end of life.
Although developed countries have established government policies
on pain, cancer pain and terminal care, developing countries such as India
and other Asian and African countries still have no national policy on the
care of terminal cancer patients or palliative care. There is an urgent need
for fresh initiatives in this direction and we should now take a lead in for-
mulating a National Cancer Pain Relief programme. Freedom from pain,
suffering and access to palliative care should be seen as a right of every
cancer patient (Table 27.2).
In the cancer population, pain is associated with both psychological
distress and functional impairment. The impact on mood, function, and

341
342 27. CANCER PAIN

TABLE 27.1 Cancer Pain

Pain is one of the most prevalent symptoms related to cancer

Pain is one of the most feared and burdensome problem in cancer patients

Cancer Pain is muti-focal, multi-causal and dynamic

Most patients will have more than one type of pain: Neuropathic, Nociceptive
Visceral, Mixed

TABLE 27.2 Reasons for Inadequate Cancer Pain Control

Failure to appreciate intensity of pain and reluctance to evaluate etiology of pain

Lack of training in Basic and Interventional pain management

Fear of prescribing opioids (Opiophobia)

Governmental restriction on sale of opioids

quality of life may be related to many facets of pain, including its severity,
temporal relations and meaning. The relationship between severity and
impact has been well characterized by a recent survey. It demonstrated
that pain rated from 1 to 4 on a 10 point scale had a generally mild impact
on function; pain of this severity adversely affected overall enjoyment of
life. Pain rated 5 and 6 on a 10 point scale had a moderate impact on func-
tion, and pain rated 7 or greater had a severe impact.
For over two decades, WHO has taken a lead in establishing a consen-
sus for a scientifically valid method of relieving cancer pain that is rela-
tively simple, inexpensive and easy to apply at community level, known
as the WHO's ‘three step analgesic ladder’ method. Data from prospec-
tive surveys suggest that 70% of patients with cancer pain could attain
adequate relief from the systematic administration of the drug therapies
endorsed by the WHO. Unfortunately, this potential success rate is not
achieved in routine practice settings. In a recent survey of ambulatory can-
cer patients, a pain management index was devised to assess the degree to
which analgesic therapy is consistent with WHO guidelines; according to
this measure, more than 40% of patients were undertreated. Among other
factors, undertreatment was associated with minority status, female sex
and history of substance abuse.
The continuing undertreatment of cancer pain can be traced to prob-
lems at multiple levels: clinician's knowledge and attitude, patient
underreporting and noncompliance and system-wide impediments to
optimal analgesic therapy. Practitioners can improve this situation by
ensuring that their medical information is current and that patients
receive appropriate education. Recent studies have reinforced the need

IV. CANCER PAIN

 Cancer Pain: Prevalence and Impact 343

TABLE 27.3 Causes of Pain in Cancer

Tumour infiltration
Involvement of nerves/plexus
Bony metastasis in spine, pelvic bones, ribs
Massive ascites/pleural effusion
Infiltration of peritoneum and viscera
Related to therapy

TABLE 27.4 Classification of Cancer Pain

Types Examples

Somatic Bone metastasis

Visceral Pancreatic cancer

Neuropathic Plexopathy or neuralgia

Sympathetically maintained pain Reflex sympathetic dystrophy

to continually reassure patients about the safety of analgesic therapy

and to encourage pain reporting by those who may minimize symptoms
because of stoicism, a desire to be liked, or a concern about distracting
the physician from the disease.

Cancer Pain: Management Strategies

Relief of cancer pain is possible. The protocols for pain treatment have
to be laid down keeping in view the Indian perspective. The key points
are simplicity and low cost of the technology used to manage pain and
other symptoms. A judicious use of available NSAIDs, opioids, chemo-
therapy, radiotherapy and neurolytic blocks can be adopted to minimize
the pain and improve the quality of life of terminally ill patients. Sys-
temic opioid therapy is widely accepted as a first-line approach to man-
agement of moderate or severe chronic cancer pain. WHO advocates
the use of the analgesic step ladder and predicts a favourable outcome
in about 70% of patients. In clinical practice, this rate of success is not
realized, largely because of undertreatment and multifactorial aetiology
of pain syndromes in advanced cancer patients (Tables 27.3 and 27.4).
Some patients would also have intolerable side effects of oral opioids
forcing them to abandon the use of these drugs. These patients are
poorly responsive to opioid therapy and must be considered for alter-
native analgesic strategies. Pain clinicians should be able to identify
poor opioid responsiveness and pursue clinical approaches that may
improve outcome.

IV. CANCER PAIN

344 27. CANCER PAIN

Neurolytic sympathetic procedures for pain conditions due to pan-

creatic and pelvic cancers should be intended as adjuvant techniques to
reduce analgesic consumption and not as a panacea, given that multiple
pain mechanisms are involved. Neurolytic blocks such as coeliac plexus
blockade is the preferred method for managing pain caused by neo-
plastic infiltration of upper abdominal viscera, including pancreas, liver
and stomach. These blocks relieve pain by 50–90% in such patients with
relief lasting from 1 to 12 months. Pancreatic pain is more amendable to
sympathetic blocks than pain due to pelvic cancers.
The role of neuroablative techniques for somatic and neuropathic pain
of cancer is often debatable. However, chemical neurolysis and pituitary
ablations have been reported to relieve diffuse and multifocal pain syn-
dromes. Transdermal fentanyl citrate also provides a new option for pain
management and as an adjuvant for managing severe cancer pain.
Intrathecal drug delivery implantable systems play a major role in
managing cancer pain in patients with a long life expectancy. Intrathe-
cally administered opioids such as morphine and alpha adrenergic ago-
nist such as clonidine provide a comprehensive and complete relief from
pain and suffering in select group of patients. The quality of life achieved
after such interventions is far superior to other methods and patient can
achieve complete independence in a very short span of time. However,
the only drawback of this technique is its cost, which is prohibitive and
beyond the reach of a common individual.
Our experience of many years in a large referral institution indicates
that cancer pain treatment is a continuum starting with physical therapy
and neuropsychology techniques escalating to NSAIDs, weak narcotics,
strong opioids and finally advanced interventional techniques and opera-
tive interventions. After diagnosis and evaluating the level of pain, selec-
tion of method with the best chance for optimal reduction of pain with the
least occurrence of side effects, is indicated. Numerous nonpharmacologi-
cal approaches such as chemical neurolysis, neurostimulatory methods,
intrathecal opioid delivery systems, rehabilitative (e.g. an arthrosis in a
patient with painful limb) and psychological (e.g. cognitive) interventions
may be considered for control of pain. Although linked conceptually, the
scope of these therapies is obviously very broad and there are substantive
differences in their indications and implementation. The choice of therapy
must integrate the type of pain, its function, the overall disease burden on
the patient and psychological aspects of cancer. As a general rule, if opioid
analgesics are not sufficient, interventional therapies and other surgical
management should be considered. The WHO guidelines for cancer pain
reduction procedures ignores physical medicine, neuropsychology, neu-
rolytic interventions and advanced interventions, and completely favours
exclusive reliance on pharmacological modalities. This critical omission is
due to the lack of equipment and personnels trained in such disciplines in
underdeveloped and developing countries.

IV. CANCER PAIN

 C H A P T E R

28
Cancer Pain
Management

Pain control remains a significant problem despite recent advances in

the understanding of pain mechanisms and pain management in cancer
patients. Patients with cancer often have multiple pain problems and most
of them can be effectively controlled.
Epidemiological studies have shown that pain occurs more often in
advanced or terminal stage of cancer. The pain experienced in a cancer
patient is highly dependent on psychosocial circumstances. Pain in cancer
patients is often multiaetiological and there is no simple relation between
the location of the lesion and severity of pain.

CANCER PAIN: MAGNITUDE OF PROBLEM

• A bout 10 lakh new cancer patients every year in India
• About 60–80% of patients present in advanced stage, hence incurable
• About 60% cancer patients require only pain management and
­palliative care
• About 40% receive inadequate treatment for pain management with
poor QOL in terminal stages
• Only 28% cancer patients receive palliative care

WHY CANCER PAIN SHOULD BE CONTROLLED?

• I t is an avoidable suffering
• To avoid the psychological effects of continuous cancer pain such
as anxiety, depression, worthlessness, lack of sleep, anger, loss of
­­appetite and suicidal tendencies
• Pain leads to a poor QOL – nonproductive, no recreational activity

345
346 28. CANCER PAIN MANAGEMENT

• F amily and social withdrawal – no meaningful social and family

contributions
• Patient remains in a vegetative state – feeling of worthlessness
  

Pain in cancer is multiaetiological, related to malignancy itself or due to

unrelated causes. Thus pain in cancer could be due to
  

1. M alignancy itself: bone metastases, soft tissue, muscle, skin infiltration

2. Malignancy treatment:
a. Surgery – phantom limb syndrome, postsurgical neuropathic pain
like carcinoma breast, scar neuralgia
b. Chemotherapy – induced apthous ulcers, acute gastritis
c. Radiotherapy – induced fibrosis, contracture
3. Related to malignancy – compression or infiltration of nervous
structures, infiltration or occlusion of blood vessels, obstruction of
hollow viscous, obstruction of the ductal system of a solid viscous,
distension of an encapsulated viscous, increased intracranial pressure,
myopathy and muscle spasm
4. Coexisting diseases – diabetic neuropathy, complex regional pain
syndrome, postherpetic neuralgia

Reasons for Inadequate Cancer Pain Control

• L ack of awareness among health care workers, policy makers and
public that methods for cancer pain management are available.
• Lack of financial resources, health care delivery systems and trained
personnel.
• Fear among treating physicians of psychological dependence and
drug abuse of opioids.
• Strict legal provisions for accessibility to opioids.
• Lack of will to formulate national policy for cancer pain relief and
­palliative care.

ASSESSMENT OF CANCER PAIN

AND RELATED PROBLEMS

A detailed history and thorough general physical examination is

undertaken when the patient is enrolled in the pain clinic. The inten-
sity of pain is measured on the VAS and other components of pain like
somatic, neuropathic, visceral or sympathetically maintained pain are
measured by different scales such as the impact of pain on the QOL score
of patient, and the treatment patient has already received is also noted. It
is also necessary to evaluate the affective, behavioural and social distur-
bances. Severity of pain determines the strength of analgesics required.

IV. CANCER PAIN

 Assessment of Cancer Pain and Related Problems 347

The type and cause of pain will influence the choice of adjuvant analge-
sic and interventional modalities to be chosen.
During the period of treatment all the patients are continuously mon-
itored for the efficacy of treatment and for the need of modification of
­treatment. The parameters used are
  

• V
 AS (1–10)
• P erformance scale
• ADL score – the domains covered are
- Eating
- Dressing
- Writing
- Use of household items
• QOL scores (SF 36) – the domains covered are
- Physical
- Bodily pain
- General health
- Vitality
- Social functioning
- Emotional
- Mental health
  

For the purposes of research and documentation, Eastern Cooperative

Oncology Group performance scale and Karnofsky rating (Table 28.1) and
WHO QOL score are used.

TABLE 28.1 Eastern Cooperative Oncology Group Performance Scale and Karnofsky
Rating
ECOG PS
grade rating Description Karnofsky

0 Fully active, able to carry out all ­pre-disease activity 100

without restriction
1 Restricted physical strenuous activity, but ambulatory and 80–90
able to carry out work of a light or sedentary nature (light
house work and office work)
2 Ambulatory and capable of all self-care but unable to 60–70
carry out any work activities: up to about >50% of waking
hours
3 Capable to limited self-care, confined to bed or chair >50% 40–50
of waking hours
4 Completely disabled, cannot carry on any self-care, totally ≥30
confined to bed or chair

ECOG PS, Eastern Cooperative Oncology Group performance scale.

IV. CANCER PAIN

348 28. CANCER PAIN MANAGEMENT

BASIC PRINCIPLES AND APPROACHES

TO CANCER PAIN MANAGEMENT

There are certain basic principles and approaches that have been
described to pain management in cancer patient, although each patient
needs to have treatment plans tailored to his or her individual problems.
The basic principles to cancer pain management are
  

• T reatment of cancer – surgery, radiation and/or chemotherapy

• Modulation of central perception of pain – analgesics, antidepres-
sants, anxiolytics, disruption of nociceptive transmission within the
central nervous system: neuroaxial analgesia, neuroablation
• Palliative care
• Immobilization – rest, cervical collar, etc.
  

Better understanding of pathophysiological mechanisms of cancer

pain and development of newer modalities for diagnosis and treatment
of cancer pain has helped tremendously in developing pain medicine as
a subspeciality. Expertise in regional nerve blocks and skills of dealing
with highly potent drugs have put anaesthesiologists in the driver's seat
of this subspeciality. Anaesthesiologists thus play a key role in cancer pain
­management presently and in future too.

Guidelines for Cancer Pain Management

Presently, two main models of guidelines for cancer pain management
are described: (1) WHO analgesic ladder (Fig. 28.1) and (2) pain treatment
continuum (Fig. 28.2).

Advantages
• Effective pain relief can be achieved in 75–80% of cancer patients.
• It is simple to use.
• Assessment of cancer pain and related problems.

Disadvantages
• It gives minimal emphasis on regional nerve blocks, which is very
suitable for patients who are travelling long distances in search of
treatment and regular follow-up is difficult.
• Puts a lot of emphasis on opioid treatment in spite of the known fact that
opioids are not widely and easily available, particularly oral morphine.
  

Pain treatment continuum need not be followed as strictly as depicted

in Figure 28.2. More than one treatment modality can be employed at
one time and one modality can supersede another modality according to
­individual needs.

IV. CANCER PAIN

 Basic Principles and Approaches to Cancer Pain Management 349

IV Intrathecal Strong Intrathecal

Epidural Mor- opiates and Bupre- Epidural
phine opioids norphine Oral
III Oral

II Oral Oral
Weak Tramadol, (rectal)
(rectal)
Codeine opiates and tilidine
opioids and others


I Oral Antirheumatics, Oral
(rectal) Nonnarcotic e.g. acetylsali- (rectal)
Paracetamol, analgesics cylic acid, diclo-
dipyrone fenac, ibupro-
fen and others

FIGURE 28.1 WHO analgesic ladder.

Pain control
Neuroablation
The cancer Neuroablation
pain treatment Intraspinal drug infusion
Spinal analgesia
continuum Nerve blocks
Interventions (nerve blocks)
Progressively Strong opioids
Strong opioids (morphine)
more intensive Weak opioids
Weak opioids (tramadol,
treatment from
Nonopioids
codeine)
bottom to top
Antitumour therapy Adjuvant medications
(radiation, chemo,
NSAIDs
surgery, etc.)
Over the counter medications
Pain

FIGURE 28.2 Pain treatment continuum.

IV. CANCER PAIN

350 28. CANCER PAIN MANAGEMENT

Various steps involved in the management of cancer pain are summa-

rized in the following flowchart:

Treatment protocol for cancer pain management

Assessment

Pain unrelated Cancer pain No pain

to cancer

Treat according to Initiate

source of pain analgesic ladder

Add as indicated:
Palliative therapies Reassessment Pain relief
Continue treatment
Radiation therapy as needed
Nerve blocks
Pain persists
Surgery
Antineoplastic therapy
Adjuvant drugs
Psychosocial interventions Consider other
Physical modalities aetiologies and
treatments

Unacceptable Diffuse Neuropathic pain Movement- Mucositis

side effects bone pain (Peripheral related pain Oral mouth-
Use different Optimize neuropathies, Surgical or washes and
drugs or NSAID and plexopathies, physical local
change route opioid doses spinal cord stabilization of anaesthetic
of Radio- compression) affected part rinses
administration pharma- Adjuvant drugs Nerve blocks Opioids
Manage side ceuticals Opioids titrated to Neuroablative Transdermal
effects Bisphos- effect surgery and Patient
Adjuvant phonates Radiation therapy neurolytic controlled
drugs Hemibody Spinal opioids procedures analgesia,
Cognitive therapy with local intravenous,
behavioral Hypophy- anaesthetics for and sub-
modalities sectomy intractable lower cutaneous
body pain Antibiotics
Neurolytic
procedures

Reassessment

  

IV. CANCER PAIN

 Pharmacological Approach to Cancer Pain Management 351

PHARMACOLOGICAL APPROACH TO CANCER

PAIN MANAGEMENT

Drug therapy is the cornerstone of cancer pain management. It is effec-

tive, relatively low risk, inexpensive, and usually works quickly. Even
within the same family of analgesic drugs, individual variations in effect
and side effects are well recognized.

Paracetamol and NSAIDs

This fairly large class of drugs has a significant part to play in the
management of cancer pain. By virtue of their action on blocking syn-
thesis of prostaglandins (which activate nociceptive fibres) they can be
of ­particular value in managing pain emanating from skin, muscle and
bone.
NSAIDs are effective in mild pain and have an opioid dose-spar-
ing effect that helps reduce side effects when given with opioids for
moderate to severe pain. Paracetamol is included with aspirin and
other NSAIDs because it has similar analgesic potency, although it
lacks peripheral a­ nti-inflammatory activity. Side effects can occur any
time and patients who take paracetamol or NSAIDs, especially elderly
patients, are followed carefully.
Commonly used drugs and oral dosages are as follows:

Paracetamol 650 mg 4 hrly.

Aspirin 650 mg 4 hrly.
Ibuprofen 400–600 mg 6 hrly.
Ketoprofen 25–60 mg 6-8 hrly.
Mefenamic acid 250 mg 6 hrly.
Naproxen sodium 275 mg 6-8 hrly.

Cyclooxygenase-2 Inhibitors
Although cyclooxygenase-2 inhibitors like celecoxib and etoricoxib
have gastric irritation sparing properties, their analgesic potency is
far lower than stronger NSAIDs. These drugs are to be used with cau-
tion in patients having cardiovascular morbidity and coexisting renal
disease.

Doses
Celecoxib 100–200 mg once or twice daily.
Etoricoxib 90–120 mg/day.

IV. CANCER PAIN

352 28. CANCER PAIN MANAGEMENT

Opioids
Systemic opioid therapy is widely accepted as the first-line approach to
the management of moderate or severe chronic cancer pain. It results in
effective pain control in as many as 85% of patients. Oral opioids are effec-
tive, easily titrable, and have a favourable benefit-to-risk ratio. In clinical
practice, this rate of success is not realized, largely because u
­ ndertreatment
continues to be a significant problem.
Even if undertreatment were eliminated, some cancer patients would
nonetheless continue to experience an unsatisfactory balance between
analgesia and side effects, despite efforts to optimize the dose. These
patients are poorly responsive to opioid therapy and must be considered
for alternative analgesic strategies.

Opioid Responsiveness
Opioid responsiveness may be explained in terms of probability of
adequate analgesia (satisfactory relief without intolerable and unmanage-
able side effects) that can be attained during gradual dose titration. This
might be viewed as maximal efficacy from a clinically relevant perspective
­without or with minimal side effect.
The mechanisms that underlie this variability in opioid responsive-
ness are
  

• P ain syndrome – neuropathic pain

• Severe breakthrough pains
• Patient-related factors – psychological distress, advanced age, major
organ failure

Analgesic Strategies for Poorly Responsive Patients

Four distinct strategies should be considered when a patient is rec-
ognized as responding poorly during a trial of systemic opioid therapy
(Table 28.2).

OPIOID ROTATION

Sequential trials, or so-called opioid rotation, are now considered a

standard clinical approach, which is designed to convert a poorly respon-
sive patient to a responsive one by identifying an opioid with a more
favourable balance between analgesic and side effects.
Guidelines for opioid rotation (Box 28.1) are intended to reduce the risk
of relative overdosing or underdosing as one opioid is discontinued and
another is administered. These guidelines require a working knowledge
of the equianalgesic dosage.

IV. CANCER PAIN

 Opioid Rotation 353

TABLE 28.2 Alternative Strategies for Patients with Poorly Responsive Pain
Approach Therapeutic options

Opening the ‘therapeutic window’ More aggressive side effects treatment, e.g. a
psychostimulant for sedation
Identifying an opioid with a more Opioid rotation
favourable balance between analgesia
and side effects
Pharmacological techniques that reduce Coadministration of a nonopioid analgesic or
the systemic opioid requirement an adjuvant analgesic. Neuraxial drug infusion
Nonpharmacological techniques to Anaesthesiologic approaches, e.g. neurolysis
reduce systemic opioid requirement Surgical approaches, e.g. bracing
Psychological approaches, e.g. cognitive therapy

BOX 28.1

EMPIRICAL GUIDELINES FOR OPIOID

R O T AT I O N
• Use the equianalgesic table to calculate a dose of the new opioid
roughly equivalent to the dose of the current opioid.
• Determine the clinically relevant starting point.
• If switching to any opioid other than methadone or fentanyl,
decrease the equianalgesic dose by 25–50%.
• If switching to methadone, reduce the dose by 75–90%.
• If switching to transdermal fentanyl, do not reduce the
­equianalgesic dose.
• Consider further dose adjustments based on medical condition and
pain.
• If the patient is elderly or has significant organ failure, consider
further dose reduction.
• If the patient has severe pain, consider a lesser dose reduction.
• Calculate a rescue dose as 5–15% of the total daily opioid dose and
administer at an appropriate interval.
• Reassess and titrate the new opioids.

Weak Opioids
Codeine is metabolized to morphine in the body. Many codeine
preparations are available commercially containing combinations
of codeine, paracetamol and ibuprofen. It can be of value in mild to
­moderate pain.
Tramadol is another drug frequently used in mild to moderate pain
with caution in patient having seizure disorders.

IV. CANCER PAIN

354 28. CANCER PAIN MANAGEMENT

The dosages of opioids are as follows:

Morphine 10 mg q 3–4 h maximum up to 400 mg/day (after titration shift to

morphine controlled release tablets)
Codeine 120–360 mg q 3–4 h
Tramadol 50–100 mg q 8–12 h maximum up to 400 mg/day

Tapentadol is a new synthetic opioid frequently used for severe

c­ ancer-related pain. It is administered in divided doses of 100–400 mg/day.
Tapentadol has the advantage of lesser incidence of nausea, vomiting and
constipation as compared to other opioids.

Strong Opioids
Morphine remains the ‘gold standard’ analgesic for treatment of moder-
ate to severe cancer pain. However, multiple side effects like constipation,
nausea, vomiting, sedation, pruritus and urinary retention are frequently
seen, although they are self-limiting. Patients should always be prescribed
laxatives, antiemetics, H2 blockers and antihistaminics to counteract the
side effects of oral morphine.

Transdermal Fentanyl
Transdermal fentanyl patches are also effective in treating moderate to
severe cancer pain and they provide analgesia up to 72 h. The limiting
­factor is their high cost.

Transdermal Buprenorphine
Transdermal buprenorphine patches are also very effective in mild to
moderate cancer pain. They provide analgesia up to 7 days and are avail-
able in strengths of 5, 10 and 20 mcg.

Adjuvant Drugs
Adjuvant drugs are very useful in treating pain syndromes that are rel-
atively poorly responsive to opioid therapy. Besides, they have important
role in palliative care.
Anticonvulsants: It is well established that the GABA receptors at spi-
nal cord level have an influence on pain transmission. Agents active at
the GABA receptors such as the anticonvulsants can often be beneficial in
reducing pain. They are particularly effective in pain syndrome otherwise
thought of as being opiate partially or opiate nonsensitive such as neuro-
pathic pains.
Commonly used anticonvulsant drugs are (initial dose – maximum dose):

IV. CANCER PAIN

 Opioid Rotation 355

Initial dose Maximum dose

Gabapentin 300 mg hs 300 mg qid
Oxcarbazepine 300 mg hs 600 mg bd
Carbamazepine 200 mg bd 400–1000 mg/day
Phenytoin 200 hs 400 hs/day

Antidepressants are also useful in the pharmacological management of

neuropathic pain. These drugs have innate analgesic properties and may
potentiate the analgesic effects of opioids. The most widely used drugs
and their dosages are the following:
Amitriptyline (tricyclic antidepressant) 12.5–50 mg hs
Nortriptyline (tricyclic antidepressant) 10–20 mg hs
Fluoxetine (selective serotonin reuptake 20–40 mg/day (divided doses)
inhibitor)

Corticosteroids provide a range of effects including mood elevation, anti-

inflammatory activity, antiemetic activity, induce a degree of euphoria,
appetite stimulation and may be beneficial in the management of cachexia
and anorexia. They reduce cerebral and spinal cord oedema and are essen-
tial in the emergency management of elevated intracranial pressure and
epidural spinal cord compression. Five possible mechanisms exist for this.
First, there is a reduction in inflammation and hence less stimulation of
the pain fibres. Second, steroids have a blocking effect on C-fibre trans-
mission (these fibres are important in the transmission of pain). Third,
steroids have a weak local anaesthetic effect, and if a long-acting steroid is
used, presumably this weak local anaesthetic effect is prolonged. Fourth,
steroids reduce the ectopic discharge from neuromas, and such neuromas
may arise in the area of nerve damage. Finally, steroids have an effect on
dorsal horn cells, which are important in pain transmission. Commonly
used steroids are
Prednisolone 20–40 mg tds
Dexamethasone 8 mg tds intravenous/intramuscular
Betamethasone 2–4 mg bd
Methyl prednisolone 4–8 mg tds

Neuron revitalizer such as methoxycobalamine is the drug supposed to

be possessing properties of neuron regeneration and revitalization. It is
prescribed in doses of 500 mcg thrice a day in patients with nerve damage
or infiltration of nerves.
Muscle relaxants are often used as adjuvants with NSAIDs and opi-
oids for muscle spasm. Tizanidine is a centrally acting muscle relaxant
used in doses of 2 mg tds to start with titrating to up to 6 mg tds. Chlor-
zoxone is another muscle relaxant commonly used in doses of 375 mg
bd twice a day.

IV. CANCER PAIN

356 28. CANCER PAIN MANAGEMENT

Bisphosphonates are commonly used in patients of multimyeloma and

bone metastases of carcinoma breast for relief of bone pain.
Osteoclast inhibitors such as salmon calcitonin are used in neuropathic
pain and bone pain.

NEUROLYTIC BLOCKS IN CANCER PAIN

MANAGEMENT

Somatic and sensory nerve blocks are used in the treatment of any pain
produced by nerve involvement by tumour or in a pain localized to an area
served by a particular nerve. Nerve blockade is initially performed with
local anaesthetics, which confirms that prolonged relief can be achieved
by blockade and this is then followed up by a more ‘permanent’ technique
such as neurolytic block using phenol, alcohol, a cryoprobe or radiofre-
quency ablation. The list of nerves that can be blocked is extensive and a
majority of nerves are easily accessible to blockade, provided knowledge
of their anatomical relationship is known.

Somatic and Sensory Block

• P aravertebral block: carcinoma lung, rib secondaries
• Intercostal nerve block: carcinoma breast, rib secondaries
• Mandibular and maxillary nerve block: carcinoma of cheek, mandible,
salivary gland tumours
• Deep and superficial cervical block: nerve tumours, thyroid cancer

Sympathetic Plexus Block

Sympathetically maintained pain can be an important cause of cancer
pain especially since it does not necessarily respond particularly well to
opiates. It is characterized by a fairly diffuse burning type of pain (not in a
nerve root distribution) and may be accompanied by an increase in sweat-
ing and oedema. It may involve limbs, head or trunk.
Sympathetic plexus blocks are commonly used in the following conditions:
  

• S tellate ganglion block: ophthalmic tumours, upper limb

malignancies
• Coeliac plexus block: carcinomas of liver, pancreas and stomach
• Lumbar plexus block: pelvic and lower limb malignancies
• Superior hypogastric plexus block: pelvic carcinomas (carcinoma
cervix, body of uterus)
• Ganglion of impar block: perineal pain (carcinoma rectum)
  

IV. CANCER PAIN

 Spinal Analgesia 357

The limitation of these blocks are

  

•  ain relief up to 60–70%

P
• New pathways develop due to rapid spread of malignancy
• Development of the deafferentation pain syndromes
• Morbidity of the procedure: paraplegia, hypotension as seen follow-
ing coeliac plexus block
• No significant improvement in QOL or ADL
• Pain relief for 3–4 months only

SPINAL ANALGESIA

Implantable Externally Programmable Systems for Spinal

Analgesia
After the discovery of opiate receptors in substantia gelatinosa of dor-
sal horn of spinal cord, spinal analgesia with morphine has come up in a
big way for the control of intractable cancer pains.
Spinal opioid analgesia is used when
  

• T reatment with systemic strong opioids provides effective pain relief

but with unacceptable side effects
• Unsuccessful treatment with sequentially strong opioid trials despite
escalating doses
• Life expectancy > 3–6 months
  

The drugs/medications used for intraspinal administration are mor-

phine, fentanyl, sufentanil, clonidine, bupivacaine and midazolam.
Intraspinal morphine remains the ‘gold standard’ therapy because of
long duration of action, high affinity for receptors, high cerebrospinal
fluid solubility and spread and 5–10 times more potency than intra-
venous dose. The doses of intraspinal opioids are highly individual-
ized and depend on pain intensity, age of the patient and the extent of
disease.
In our clinical experience, we have used continuous intrathecal mor-
phine infusion ranging from 0.5 mg/day to 12.5 mg/day with programma-
ble implantable pump. Patients having components of neuropathic pain,
combined intrathecal infusion of morphine and clonidine (30–120 mcg/
day) or morphine and midazolam (1.2 mg/day) is used.
Central analgesia: Intravenous lignocaine infusion has been found to be
effective in treating the neuropathic pain component in cancer patients.
The dose is 5 mg/kg over 60 min and duration of analgesia is up to
3 weeks.

IV. CANCER PAIN

358 28. CANCER PAIN MANAGEMENT

ADJUVANTS FOR CANCER PAIN MANAGEMENT

Transcutaneous Electrical Nerve Stimulation

Controlled, low-voltage electrical stimulation is applied to the large
myelinated peripheral nerve fibres via cutaneous electrodes to inhibit
pain transmission. Although part of the efficacy of TENS can be attrib-
uted to a placebo effect, patients with mild pain may benefit from a trial
of TENS.

Cognitive Behavioural Interventions

Cognitive behavioural interventions are an important part of a mul-
timodal approach to pain management. They help to give the patient a
sense of control and to develop coping skills to deal with the pain.
Interventions introduced early in the course of illness are more likely to
succeed because they can be learnt and practiced by patients while they
have sufficient strength and energy. Patients and their families should be
given information about and encouraged to try several strategies, and
to select one or more of these cognitive behavioural techniques to use
regularly.

Relaxation
Simple relaxation techniques like slow rhythmic breathing and simple
touch, massage or warmth are used for brief pain control.

Yoga, Meditation, Spirituality

Patients are encouraged to take part in yoga and meditation and
indulge in spiritual exercises.

DIFFICULT PAIN SYNDROMES AND POOR

PROGNOSTIC FACTORS

Specific pain syndromes and individual patient factors can indicate

poor prognosis for analgesic response. Patients with these poor prognostic
factors are significantly less likely to achieve good pain control.
Risk factors for poor pain control in cancer patients are
  

• N  europathic pain
• I ncidental/breakthrough pain
• T  olerance to opioids

IV. CANCER PAIN

 Palliative Care 359

• S evere psychological stress with severe depression

• Alcohol or drug abuse
  

It is important to identify patients with poor prognostic pain syn-

dromes in order to optimize their pain management by addressing their
specific needs. Patients with these risk factors usually need more complex
approaches to pain management.

PALLIATIVE CARE

The definition of palliative care encompasses the following:

  

•  ffirms life and regards dying as a normal process

A
• Neither hastens nor postpones death
• Provides relief from pain and distressing symptoms
• Integrates psychological and spiritual aspect of pain care
• Help patients live as actively as possible
• Provides support system to patient's family

Methods of Palliative Care

General
• Good oral hygiene
• Pain control
• Antibiotics
• Swallowing exercises
• Bed sore/ulcer care
• Tracheostomy/colostomy stoma care
• Ventilatory care
• Symptomatic care

Nutrition
• Calorie-rich and high-protein diet
• Vitamins and mineral supplementation
• Semisolid, liquid diet
• Enteral/parenteral diet
• Nasogastric tube feeding/feeding jejunostomy

Therapeutic Options
• Radiotherapy
• Neck, retro-orbital, gonadal, and salivary gland tumours
• Laser therapy
• Cutaneous and mucosal lesions
• Useful endoscopically

IV. CANCER PAIN

360 28. CANCER PAIN MANAGEMENT

• P hotodynamic therapy
• Obstructive lesions of lower trachea and main bronchus
• Cryotherapy
• Oral cavity tumours and intercostal nerve blocks
• Chemotherapy
• Carcinoma breast, carcinoma lung, gonadal and genitourinary
tumours

Surgical Procedures
• Head and neck reconstruction – continuous flap/free flap
• Mandibular reconstruction – pedicle graft
• Debulking surgery – radical neck dissection
• Bypass surgery – gastrointestinal tract and urinary tract
• Feeding surgery – gastrostomy and feeding jejunostomy
• Amputations – limb tumours
• Pain conducting tract interruptions

Rehabilitation
• Rehabilitation
• Orthopaedic appliances
• External laryngeal vibrator
• Artificial eye, dentures, and hair
• Psychological support
• Counselling, yoga, meditation, and spirituality
• Family support system
• Counselling, financial assistance, and re-employment

CONCLUSION

Patients with cancer experience numerous symptoms, impairments

in physical and psychosocial functioning, and other problems that can
undermine QOL. For more than two decades, pain has been recognized
as a major QOL concern in the cancer population. The need for improved
cancer pain management has been forcefully advanced by various world
bodies. Physicians have compelling reasons to focus attention on the prob-
lem of pain in cancer. The recognition of pain should be viewed as a fun-
damental objective of the medical care offered to these patients, and all
clinicians who treat patients with cancer should become familiar with the
principles of pain assessment and management.

IV. CANCER PAIN

 S E C T I O N V

ADVANCED
INTERVENTIONAL
PAIN MANAGEMENT
29 Advanced Interventional Pain Management
Modalities 363
30 Spinal Cord Stimulation for Management of Chronic
Intractable Pain 367
31 Continuous Intrathecal Drug Delivery Systems
for Management of Cancer and Nonmalignant
Pain 375
32 Radio Frequency Ablation in Pain Management 383
33 Vertebroplasty and Kyphoplasty 391
34 Management of Spasticity 397
This page intentionally left blank
     
 C H A P T E R

29
Advanced Interventional
Pain Management
Modalities

In last two decades, there has been a tremendous advance in our under-
standing of mechanisms that underlie causes of pain and the treatment of
patients with acute and chronic pain. This has resulted chiefly due to an
extensive experimental and clinical research being undertaken to under-
stand the pathophysiology of pain. In the 1960s, pain was considered just
an inevitable sensory response to tissue damage and no considerations
were given to the affective dimension of this miserable experience and
none whatsoever to the accompanying anxiety and stress. However, it was
only as late as 1994 that a proper definition of pain was brought forward
as ‘Pain is an unpleasant sensory and emotional experience associated
with actual or potential tissue damage, or described in terms of such a
damage.’ This description of pain was even endorsed by the International
Association for the Study of Pain – the world body monitoring various
researches on experimental and clinical pain.
Pain clinic, an idea advocated by Bonica in the 1950s and further
enriched by inputs from Fordyce and Sternbach in the 1970s, is cropping
up globally. Pain clinics have an important role to play in the health care
systems of the developing countries and cater to a very large number of
chronic pain patients including those with intractable cancer pain. The
pain clinicians in these countries have the dilemma of providing the best
pain treatment but within the available resources. Keeping pace with the
technological advances in pain management worldwide, pain clinics in
developing countries are also employing newer methods of pain assess-
ment, pain imaging and advanced interventional strategies for managing
patients with chronic pain. The multidisciplinary approach to the man-
agement of pain at these centres include the effective use of both the tra-
ditional modalities such as yoga and acupuncture as well as the advanced

363
364 29. ADVANCED INTERVENTIONAL PAIN MANAGEMENT MODALITIES

interventional pain management techniques such as dorsal column stim-

ulation, radio frequency lesioning and intrathecal pump implantation.
Although majority of patients with chronic intractable pain are treated
with the conventional methods, interventions such as dorsal column stim-
ulation have definitely benefited a large subset of patients such as those
with failed back and refractory neuropathic pain.
Continuous delivery of opioids by an implanted intrathecal pump pro-
vides excellent pain relief even in refractory cancer pain. Radio frequency
lesioning of sympathetic plexus in patients with peripheral vascular dis-
ease and those with sympathetically maintained pain has simplified the
management of these disorders to a great extent. Intradiscal electrother-
mal therapy is a new, minimally invasive approach for the treatment of
discogenic low back pain. Initial results with this treatment are encourag-
ing, but more clinical studies are needed to prove its efficacy. It involves
percutaneously threading a flexible catheter (SpineCath, Neurotherm Inc.,
USA) into the disc tissue with fluoroscopic guidance. The catheter is com-
posed of a thermal resistive coil, which enables its distal part to heat to the
desired temperature.
Percutaneous discectomy has been performed over the past few years.
Innovative percutaneous techniques utilizing devices for both manual and
automated removal of nucleus pulposus have been developed. Percuta-
neous discectomy using both mechanical and laser-based instrumentation
has opened up many options and warranted more studies in the clinical
setting. The chief benefits of such minimally invasive techniques include
good success rates, reduced trauma, lower costs and less time lost from
work. Hydrocision discectomy and ozone discectomy are few procedures
that are very commonly used by pain clinicians for a definitive treatment
of contained disc protrusions.
Botulinum toxin type A has been used clinically to provide relief from
pain in a number of disorders believed to be due to overactive striated
or smooth muscles, such as cervical dystonia, spasticity, rectal sphinc-
ter spasm with fissure, achalasia and myofacial pain syndrome. Pain
relief is achieved by reducing muscle hyperactivity and spasm. Prelimi-
nary evidence suggests that it may also be beneficial in the treatment of
tension-type headache and migraine associated with muscle spasm. Thus,
based on the needs of the community, these advanced interventional pain
modalities are now integral part of management options offered in the
pain clinics across the world.
With the aging population in our country, symptomatic osteoporotic
compression fractures are increasingly common. Osteolytic compression
fractures from spinal metastasis are also becoming more frequently seen
because of the longer life expectancy from improvements in chemother-
apy. Percutaneous vertebroplasty and Kyphoplasty have been shown to
be efficient procedures to treat pain due to these fractures. It is a minimally

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 29. ADVANCED INTERVENTIONAL PAIN MANAGEMENT MODALITIES 365

invasive procedure performed under local anesthesia and sedation.

Injection of PMMA (bone cement) provides immediate stability when it
hardens, and permits the patient to ambulate without pain. Appropriate
patient selection is the key to clinical success. However, this procedure
must be treated with respect, and has to be performed by physicians with
the necessary training.
A lot has been achieved to conquer the chronic intractable pain with the
help of interventional pain management techniques. However, challeng-
ing conditions do keep on appearing and to meet them further advanced
interventional techniques are being developed, of which deep brain stim-
ulation and brain mapping are in experimental stages. We hope that in
future, patients who are not treatable by the existing techniques will be
benefited by further inventions in the field of interventional pain manage-
ment techniques. The future definitely belongs to us and humankind will
suffer less and less with time.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

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 C H A P T E R

30
Spinal Cord Stimulation
for Management of
Chronic Intractable Pain

Electrical stimulation for treatment of pain was first documented in

600 B.C., utilizing electrical power from the torpedo fish. In 1967, SCS
was introduced by Shealy and associates. Their work was based on the
‘gate control’ theory of pain proposed by Melzack and Wall. With recent
advances in technology, SCS has become a part of minimally invasive
treatment for controlling intractable chronic pain syndromes. The stim-
ulating electrodes are placed in the epidural space percutaneously in a
manner similar to the placement of an epidural catheter. Improvements in
hardware design and selection criteria have enhanced the efficacy of SCS,
and success rates of 50–70% have been reported in different series.

MECHANISM OF ACTION OF SCS

The Melzack and Wall (1965) ‘gate control’ theory of pain was the foun-
dation for the first SCS trials. It was based on the idea that stimulation
of A-beta fibres closes the dorsal horn ‘gate’ and reduces the nocicep-
tive input from the periphery. However, it seems that other mechanisms,
like increased dorsal horn inhibitory action of neurotransmitters such as
gamma-amino butyric acid and adenosine A-1 and the potential activa-
tion of descending analgesia pathways by serotonin and norepinephrine
are other explanations for SCS action (Box 30.1).
The probable mechanism for pain relief in ischaemic heart disease is
redistribution of the coronary blood flow from regions with normal perfu-
sion to regions with impaired perfusion.

367
368 30. SPINAL CORD STIMULATION

BOX 30.1

MECHANISM OF ACTION OF SCS

• Mechanism of action
• Segmental, antidromic activation of A-beta afferents (gate control
theory)
• Blocking of transmission in the spinothalamic tract
• Supraspinal pain inhibition
• Activation of central inhibitory mechanisms influencing sympa-
thetic efferent neurons
• Activation of putative neurotransmitters or neuromodulators

BOX 30.2

P AT I E N T S E L E C T I O N C R I T E R I A F O R
S P I N A L C O R D S T I M U L AT O R I M P L A N T
• More conservative therapies have failed
• An observable pathology exists that is concordant with the pain
complaint
• Further surgical intervention is not indicated
• No serious untreated drug habituation exists
• Psychological evaluation and clearance for implantation has been
obtained
• No contraindications to implantation exist. These include sepsis,
coagulopathy, etc
• Trial screening has been successful

PATIENT SELECTION, INDICATIONS AND

CONTRAINDICATIONS OF SCS

When patient symptoms and sequelae of pain cannot be controlled sat-

isfactorily with conventional modes of treatment like nonsteroidal anti-
inflammatory drugs, weak and strong opioids, physical and occupational
therapies and cognitive and behavioural therapies or side effects of high
doses of opioid are intolerable, then the patient should be given a trial of
SCS (Box 30.2). Before SCS implantation, a psychological evaluation of the
patient is recommended.
Thus, the indications of SCS implant are (Box 30.3)
  

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Patient Selection, Indications and Contraindications of SCS 369

BOX 30.3

I N D I C AT I O N S O F S C S
• Indications
• Failed back surgery syndrome (FBSS)
• Complex regional pain syndrome of lower extremity and upper
extremity
• Nerve injuries causing causalgia
• Peripheral vascular diseases
• Phantom limb syndrome
• Chronic intractable angina

1. P atients with CRPS or with neuropathic pain symptoms of upper or

lower extremities are the best candidates for SCS trial.
2. Patients with FBSS may respond well to SCS. It has been documented
that patients with FBSS respond better to SCS than to reoperation. This
applies in particular to LBP with a radiating component to the leg. In
these patients, the chance of long-term success with SCS varies from
12 to 88%, with an average efficacy of 59% as indicated by a systematic
review of the literature. In addition, 25% of patients may return to
work, 61% show an improvement in activities of daily living, and
40–84% decrease their consumption of analgesics.
3. Diabetic neuropathy may respond well to SCS, but the infection risks
in these patients are higher than in the nondiabetic population.
4. The use of SCS in postherpetic neuralgia is controversial.
5. Phantom limb pain is another indication of SCS.
6. Severe peripheral vascular disease is also an indication for SCS.
Patients with advanced peripheral vascular disease who are not fit
for surgical management respond well to SCS, with reported efficacy
rates ranging from 60 to 100%. Besides providing pain relief, SCS
promotes ulcer healing and potentially contributes to limb salvage.
7. Ischaemic heart disease refractory to pharmacological and surgical
treatment may respond well to SCS, with reported efficacy rates
of 60–80% several years after implantation. These patients have
demonstrated a reduction in anginal pain, decreased use of short-
acting nitrates, and increased exercise capacity.

Contraindications
Infection, drug abuse, and severe psychiatric disease are major contra-
indications for SCS implantation.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

370 30. SPINAL CORD STIMULATION

SCS TRIAL

Before proceeding with permanent SCS implantation, a stimulation

trial is warranted. The trial allows patients to evaluate the SCS analgesic
activity in their everyday surroundings. The criteria for a successful trial
include at least 50% pain reduction, a decrease in analgesic intake, and
significant functional improvement. The SCS trial is a minimally invasive
procedure (similar to placing an epidural catheter), and it can positively
predict a long-term outcome in 50–70% of cases.
Minimal trial time should be 24 h, although many centres perform
3–7 day trials. The trial begins in the hospital with proper SCS adjustment,
after which the patient is discharged for several days of home trial. In
cases of equivocal results, the trial time can be extended.

CHOICE OF SCS HARDWARE

The permanent SCS hardware consists of the SCS lead, an extension

cable, a power source, and a pulse generator. The number of electrodes in
the lead varies from four (Medtronic and St. Jude’s) to eight (St. Jude’s). The
distance between the electrodes and the length of the leads can also differ.
It is not clear whether an increased number of electrodes provides better
coverage, but it might be beneficial in case of lead migration. The leads with
minimal space between electrodes (such as the Medtronic Quad compact
lead) are better suited for localized pain (such as foot pain) or isolated axial
LBP cases. Many leads contain a removable stylet, which eases lead steering
during implantation.
There are two types of pulse generators:
  

1. T he completely IPG containing a battery.

2. An IPG supplied by external power through the radiofrequency
antenna applied to the skin.
  

The implanted pulse generator is more convenient to use and can be

easily adjusted by the patient using a small telemetry device. Patients can
turn the stimulator on and off, and they can control the stimulation ampli-
tude, frequency, and pulse width. A separate external programmer allows
more complex IPG reprogramming by the physician. In case of inadequate
stimulation, the physician can change the polarity and the number of func-
tioning electrodes to provide better stimulation coverage. The batteries
have to be changed every 3–6 years, which requires a brief visit to the oper-
ating room. The battery life depends on the duration of stimulation and
the stimulation amplitude. The externally powered IPG, therefore, has an
advantage over the implanted one in patients requiring higher amplitudes
of stimulation, which deplete implanted batteries in a short time.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Implantation Technique 371

IMPLANTATION TECHNIQUE

Strict aseptic conditions are paramount for implantation procedure.

For lumbar lead placement, the patient is placed in the prone position,
and for cervical placement both prone and lateral decubitus positions
are used. The patient is prepared and draped in the usual fashion. Both
trial and permanent implantations are performed under local anaesthe-
sia with light IV sedation. The most common entry sites are the T12–
L1 and L1–L2 spinal interspaces for the lumbar area and C7 –T1 for the
cervical area.
For the percutaneous SCS trial, the Tuohy needle entry site is at the
level of the spinous process below the desired interspace. It is important
to achieve a shallow entry angle or to use the alternate Piles needle. The
needle tip should stay close to midline during insertion. As the needle
is advanced, loss-of-resistance technique is used to identify the epidural
space. At this point, the SCS lead is inserted into the epidural space under
continuous fluoroscopic guidance. The curved stylet, or curved lead tip,
allows lead steering. The lead tip, during insertion and at the final posi-
tion, should lie at the lateral border of the spinous process on the ipsilat-
eral side of the pain (Fig. 30.1).
Once an adequate lead position is obtained, the trial stimulation is
performed. It is important that stimulation paresthesias provide 70–
80% overlap with the patient's pain location. Adequate patient feed-
back during this stage is important. Maximal effort should be used to
provide adequate pain coverage, since this optimizes the trial. Frequent
lead repositioning might be needed during this stage. Once adequate
coverage is achieved, the needle is removed under continuous fluo-
roscopy, ensuring no change in lead position. The lead is then taped to
the skin.
Permanent stimulator placement technique is similar to the trial. The
SCS trial as well as the permanent SCS placement is performed in the
operating room. Under local anaesthesia and IV sedation, a skin incision
is made along the cervical or lumbar insertion site. Tissue dissection is
performed until lumbar fascia is encountered. At that point, the Tuohy
needle and the stimulator lead are inserted. Once adequate coverage is
obtained, the Tuohy needle is removed under continuous fluoroscopic
guidance and the SCS lead is anchored with sutures to the fascia and
supraspinous ligament. The pocket for the IPG is made in the gluteal or
abdominal area. The SCS lead is then connected to the IPG through an
extension cable tunnelled through the skin. The skin and subcutaneous
tissues are closed in layers.
Patients should avoid any extreme activity for the first 6–8 weeks fol-
lowing permanent SCS implantation to prevent lead migration and allow
for epidural scar tissue formation.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

372 30. SPINAL CORD STIMULATION

Electrodes

Lead wire

Extension

SCS lead trial placed in the

epidural thoracic space

(a) (b) Pulse generator

FIGURE 30.1 (a) Placement of SCS trial lead. (b) Pulse generator is implanted.

LEAD POSITIONING

The SCS topographic coverage depends on the spinal level at which the
SCS lead tip is positioned. The following landmarks are for orientation
only; the variance can be very high in individual patients. Careful intraop-
erative mapping is needed for optimal coverage (‘sweet spot placement’).
The SCS electrode placement for various sites of pain is as follows:
Upper extremity: Between C2 and C5. The shoulder area can be dif-
ficult to cover.
Foot: between T11 and L1.
Lower extremity: At the T9–10 level.
Low back: A level between T8 and T10; parallel leads can be used.
Chest: At the T1–2 level.
Occipital neuralgia: At C1–C2 levels.
Pelvic pain: At S2 to S4, leads may be placed retrogradely.

COMPLICATIONS OF SCS IMPLANTATION

The most commonly encountered complications of SCS are hardware

failure, lead migration, infection, skin irritation at the IPG site and failure
to provide pain relief.
Bleeding at the IPG site (subcutaneous haematoma) is usually self-­
limiting and gradually reabsorbs in a few weeks. If infection occurs at the
IPG insertion site, make sure to aspirate the site before initiating antibiotic
coverage and removing the hardware.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Conclusion 373

CONCLUSION

There is a general agreement that SCS is an indispensable treatment

modality for many patients with chronic neuropathic pain, particularly
after lesions of peripheral nerves or spinal roots. There is no evidence that
SCS influences nociceptive type of pain and its effect on pain in periph-
eral vascular disease and intractable angina is secondary to stimulation-
induced vasodilatation. SCS is a minimally invasive procedure that is well
tolerated by patients and associated with very low risk of serious compli-
cations. SCS is presently underused probably because of its prohibitively
high cost. However, our experience indicates that SCS treatment in refrac-
tory pain syndromes is cost-effective.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

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 C H A P T E R

31
Continuous Intrathecal
Drug Delivery Systems
for Management
of Cancer and
Nonmalignant Pain

Intrathecal drug delivery has gained its popularity since the discov-
ery of opioid receptors in the spinal cord. It provides targeted delivery
of medications and avoids side effects encountered by systemic admin-
istration of drugs. Opioids are delivered to the intrathecal space via a
surgically implanted subcutaneous pump containing a reservoir for the
medication. The pump is easily refilled with medication every 2–4 months
depending on the infusion rate.
Medications other than opioids have been used recently for intrathe-
cal delivery. This includes local anaesthetics, clonidine, midazolam and
baclofen, given alone or in combination with opioids. Because numerous
receptors involved in nociceptive transmission are located in the spinal
cord, this approach seems to be very promising. The efficacy of intrathecal
drug delivery has been shown in patients with malignant and nonmalig-
nant pain.
The completely implanted intrathecal system has many advantages
over the epidural drug delivery via an external catheter. The epidural
route is more costly because of the maintenance needed for the external
system, and it is frequently more inconvenient for the patient; therefore,
it should be reserved for short-term use only (less than 3 months). The
completely implanted intrathecal delivery is preferred when treatment is
expected to last longer than 3–6 months. Patients with implanted intrathe-
cal pumps may safely undergo a MRI procedure for other purposes.

375
 PATIENT SELECTION
  

1. C ancer pain patients respond well to intrathecal therapy in carefully

selected patients. The following cancer patients might be considered
for intrathecal trial:
a. Patients who develop intolerable side effects to opioids given by
oral or parenteral route (nausea, vomiting, sedation, constipation)
b. Patients who have a life expectancy of more than 3 months
c. Patients who have no obstruction in CSF flow
d. Patients who have neuropathic cancer pain that does not respond to
oral regimen and nerve blocks.
2. Nonmalignant pain may respond to intrathecal therapy but it should
be considered as a last resort. In general, patients with cancer pain
tend to respond better to intrathecal therapy than patients with
nonmalignant pain. Therefore, the selection criteria for intrathecal
therapy for nonmalignant pain should be very strict (Table 31.1). Only
patients who have failed nerve blocks, oral medications, physical
therapy, and cognitive–behavioural programs and who have passed
psychological evaluation should be considered for intrathecal trial.

Screening
Before considering implantation of intrathecal hardware, patients
should undergo a trial procedure to better assess the odds of a favourable
outcome. The actual trial procedure varies, and no consensus has been
made on the best procedure. Preceding the trial, oral opioids are either
discontinued or decreased substantially. It is important to monitor the
patient for signs of respiratory depression during the trial. The most com-
mon screening methods are the following (Flowchart):

Sequential trial of
intraspinal/epidural opioids
(screening)

Responder Nonresponder

Admixture of
Permanent opioid/LA/
system clonidine

Nonresponder

Midazolam and
other
experimental
drugs

  
V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT
 Patient Selection 377

An intrathecal trial is performed by implanting the temporary intra-

thecal catheter. Paediatric or standard epidural catheters can be used for
this purpose. After intrathecal placement, the catheter is taped to the
skin. The medication bolus is given first, followed by continuous infu-
sion via an external infusion pump. The intrathecal opioid dose starts at
1/300th of the usual oral daily dose. The patient is kept in a hospital, for
several days up to 3 weeks, during which time the infusion rate is gradu-
ally increased. The longer the trial time is, the smaller the likelihood of a
placebo response. The patient pain intensity score, functional status, and
use of medications for breakthrough pain are monitored during the trial
period (Fig. 31.1).
An epidural trial is performed in the same way as the intrathecal trial,
except that the catheter is placed in the epidural space. The administered
epidural opioid daily dose is higher than the intrathecal one, representing
1/30th of the usual daily oral dose.
A one-time bolus is the simplest screening method. The intrathecal
bolus of medication is given and the patient is monitored for 24 h. The
pain intensity score, functional status, and use of medications for break-
through pain are monitored. This method does not allow dose titration, as
the other methods do, but it can provide information on patient response
to intrathecal opioids.

TABLE 31.1 Pain Syndromes Responsive to Intraspinal Drugs

• N ociceptive pain (opioid responsive)
• Neuropathic pain (may require higher doses of opioids than nociceptive pain)

FIGURE 31.1 Externally programmable intrathecal pump.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

378 31. CONTINUOUS INTRATHECAL DRUG DELIVERY SYSTEMS

HARDWARE SELECTION

Two kinds of pumps exist:

  

1. B attery-powered externally programmable pumps (Fig. 31.1)

2. Nonprogrammable pumps, many of them gas driven
  

The amount of medication delivered by nonprogrammable pumps

is dependent on drug concentration as infusion rate is fixed. Although
externally programmable pumps offer the great advantage of adjustable
infusion rates of different combinations, fixed-rate pumps can be used in
patients requiring less frequent rate adjustments.

MEDICATION SELECTION AND DOSAGE

All intrathecally administered medications should be preservative free.

The most commonly administered intrathecal medication is morphine.
Other opioids include fentanyl, sufentanil, hydromorphone and meperi-
dine (Table 31.2).
To convert intrathecal doses to other routes of administration, the fol-
lowing ratios are used: (1) intrathecal to epidural, 1:10; (2) intrathecal to
IV, 1:100; (3) intrathecal to oral, 1:300. In opioid-naive patients, morphine
should be started at 0.2 mg/day and gradually increased (Table 31.3). In
opioid-tolerant patients, the initial intrathecal dose should be less than the
conversion dose, and oral opioids should be used for breakthrough pain.
Gradually, the intrathecal dose should be increased and breakthrough
pain medications discontinued.

TABLE 31.2 Drugs for Intraspinal Administration

FDA approved Drugs Preservative-free morphine

Preservative-free baclofen

Preservative-free clonidine

Ziconitide

Other Drugs used for Intraspinal Fentanyl

Administration
Sufentanil

Midazolam

Meperidine

Methadone

Neostigmine

FDA, US Food and Drug Administration.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Complications and Side Effects 379

TABLE 31.3 Dose of Intraspinal Opioid

• H ighly individualized and depends on pain intensity, age, disease
• 300 mg oral morphine = 100 mg parenteral morphine = 10 mg epidural morphine = 1 mg
intrathecal morphine
• Dose range 0.5–20 mg morphine/day

The addition of local anaesthetics to intrathecal opioids may be used for

cancer and nonmalignant pain, with particular benefit to patients with a
neuropathic component of pain. A typical bupivacaine dose range is from
2 to 30 mg/day, although dosages of over 100 mg/day have been reported.
Alphadrenergic agonists (clonidine, epinephrine) can be used in conjunc-
tion with opioids. Clonidine is now approved by the US Food and Drug
Administration for epidural administration, and its intrathecal-equivalent
dosage is 50–900 mg/day. It should be carefully titrated since it can cause
significant hypotension (most severe in dosage range of 400–570 mg/day).

COMPLICATIONS AND SIDE EFFECTS

Medication-related complications: Medication-related side effects and

complications of neuraxial opiates include respiratory depression, pru-
ritus, nausea, vomiting, urinary retention, reduced libido, oedema with
weight gain, and constipation.
Respiratory depression can occur immediately after opioid administra-
tion or with several hours' delay. It is much more frequent in opioid-naive
patients. The factors increasing the risk for respiratory depression are
advanced age, high opioid dose, and concomitant use of baclofen, benzo-
diazepines, and sedatives. Monitoring the vital signs and pulse oximetry
is mandatory following initiation of an intrathecal opioid infusion.
The treatment of respiratory depression depends on its severity. The
intrathecal infusion should be discontinued or reduced. If the patient
cannot be aroused, IV naloxone should be administered. In severe cases,
intrathecal naloxone can be administered in conjunction with airway pro-
tection and assisted ventilation.
Pruritus, nausea, and vomiting usually occur with initiation of intrathe-
cal opioid bolus administration and can precede the onset of pain relief.
These side effects can be prevented by more gradual opioid dose increase.
The incidence of urinary retention ranges from 40 to 80% and is not
dose dependent.
Hormonal abnormalities are reported with intrathecal opioid admin-
istration. Serum lipids, oestrogens, androgens, insulin-like growth factor
1, and 24 h urinary cortisol should be monitored in these patients. There
is a 3–5% incidence of decreased libido in patients receiving intrathecal
opioid therapy because of hormonal abnormalities. Persistent decreased

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

380 31. CONTINUOUS INTRATHECAL DRUG DELIVERY SYSTEMS

libido may require hormonal replacement. Approximately 5–10% of

patients may experience weight gain and oedema, which is not dose
dependent.
Surgical complications: Infection at the pump insertion site may
require complete hardware removal. Symptoms of infection are fever and
pain at the insertion site, local increase in temperature, and oedema. Anti-
biotics should be started after wound cultures (by aspiration) are obtained.
Seroma at the insertion site is usually benign and does not require revi-
sion. Necrosis and skin perforations can also occur and should be surgi-
cally treated.
Meningitis presents with stiff neck, fever, and meningeal signs. The
CSF can be obtained from the pump for cultures and cell count.
Granuloma formation at the catheter tip is a very rare complica-
tion, potentially leading to cord compression. MRI of the spinal cord is
indicated if neurologic symptoms occur in these patients. Bleeding at
the pump site usually spontaneously resolves, although it can increase
the incidence of infection. Epidural haematoma can lead to spinal cord
compression.
A CSF leak occurs after almost every intrathecal pump placement and
if significant can lead to severe postdural puncture headache. If conserva-
tive therapy fails, headache can be treated with an epidural blood patch.
However, the patch should be performed under fluoroscopic guidance to
avoid risk of intrathecal catheter damage.
Hardware complications: Hardware complications usually involve
the catheter and rarely the pump. Catheter kinking, disconnection, dis-
lodgement, breaks, and migration can occur. Withdrawal symptoms and
loss of analgesia are signs of inadequate drug delivery and warrant fur-
ther investigation. Although the catheter is radiopaque and can be seen
on fluoroscopy, it should be tested with a nonionic-contrast bolus. Before
administering the bolus, medication should be aspirated from the cath-
eter dead space to avoid overdose. This can be accomplished through the
pump side port. If the pump does not have a side port, it should be emp-
tied, filled with radiolabelled tracer and imaged.
Pump failures can also occur. Torsion of the pump within the pocket
and subsequent catheter kinking can be prevented by adequate pump
anchoring. The most serious technique-related complication is drug over-
dose caused by filling the pump through the side port. If this occurs, the
CSF should be partially replaced with saline and the patient immediately
transferred to the intensive care unit. Intrathecal naloxone should be
administered.
Other mechanical pump failures include battery depletion and inter-
nal pump failure. The manufacturer's recommendations and testing
protocols should be followed meticulously to rule out internal pump
failure.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Conclusion 381

CONCLUSION

A lot has been achieved to conquer the chronic intractable pain with
the help of interventional pain management techniques and other sup-
port adjunctive modalities. However, challenging conditions do keep on
appearing and to meet them further advanced interventional techniques
are being developed, of which deep brain stimulation and brain mapping
are in experimental stages. We hope that in future patients who are not
treatable by the existing techniques will be benefited by further inven-
tions in the field of interventional and noninterventional pain manage-
ment techniques.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

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 C H A P T E R

32
Radio Frequency Ablation
in Pain Management

Over the years, many techniques have been used to selectively destroy
nervous tissue in the spinal axis, brain and other locations in the body.
Of the various techniques that have been used, the RF technique has
proved itself to be the most effective and is certainly the most widely
used (Box 32.1).

PRINCIPLE OF RF

RF is an alternating electric field with oscillating frequency of

500,000 Hz. RF is a widely used method for ablating nervous tissue.
The basic principle of RF lesions involves the placement of an insulated
electrode shaft with an uninsulated tip into nervous tissue. If an electri-
cal generator source is connected to this shaft, the electrical impedance
of the surrounding tissue will allow a current to flow from the genera-
tor source into the tissue itself. Regardless of current frequency, when
that current flows through a source of resistance, heat is generated in
the tissue. Since the current spreads into the tissue as it leaves the tip
of the electrode, the greater density of treatment, as well as the hottest
part of the lesion, will be in the tissue directly adjacent to the tip of the
electrode. With this technique, a very high-frequency current is passed
down a thermocouple probe that is inserted through special cannula,
fully insulated except for its tip. When the current is passed down the
thermocouple probe, it heats the surrounding tissues to a temperature
that can be totally controlled by the operator. Thus, the nerve can first
be located by passing stimulating current down the thermocouple probe
and then a well circumscribed lesion can be produced (Fig. 32.1). Since
myelinated fibres are more resistant to heat than unmyelinated fibres,
differential effects can be produced.

383
384 32. RADIO FREQUENCY ABLATION IN PAIN MANAGEMENT

BOX 32.1

R A D I O F R E Q U E N C Y A B L AT I O N
• A new perspective in the management of acute and chronic pain
• Great advantage over conventional neurodestructive procedures
• Provides prolonged and complete pain relief
• Significantly better outcome as compared to neurolysis with alcohol

Guide tube

Electrode Active (lesion)

Electrical (RF) current electrode
generator meter

Electrode
RF output voltage Indifferent
terminals meter (dispersive)
electrode

Basic RF lesioning circuit

Exposed tip Insulated shaft

s
line
ld
E fie

E+
44°C +E
isotherm

A typical electrical field around the

exposed tip of RF electrode

FIGURE 32.1 Principle of radio frequency lesioning.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Indications of RF Neuroablation 385

INDICATIONS OF RF NEUROABLATION

RF neuroablation is frequently carried out for the following:

  

• L umbar sympathectomy for peripheral vascular disorders and CRPS

of lower extremity.
• Ablation of gasserian ganglion or of individual branches for trigemi-
nal neuralgia.
• Cervical, thoracic, lumbar facet joint denervation.
• Stellate ganglion lesioning for CRPS of upper extremity.
• Cervical, thoracic, lumbar and sacral rhizolysis.
• Sacroiliac joint denervation.
• Intervertebral disc annuloplasty in intervertebral disc prolapse.

Advantages
Major advantages are the least possibility of neuroma formation, no
radiculopathy, low morbidity, zero mortality, cost-effectivity and mini-
mally invasive. Over the years, the technique of RF lesioning has been
refined so as to avoid problems such as tissue charring, boiling and uncon-
trolled tissue lesions.

Procedure
RF ablation is carried out in an operation theatre setup under strict
aseptic conditions and in the presence of all resuscitation facilities.
The cannula (Photograph 32.1) is placed in close proximity to the
nerve in question under fluoroscopic control. The stylet is removed from

PHOTOGRAPH 32.1 Radio frequency ablation in progress.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

386 32. RADIO FREQUENCY ABLATION IN PAIN MANAGEMENT

PHOTOGRAPH 32.2 Radio frequency needles/kits for ablation.

the cannula and replaced by a thermocouple probe. The operator then

attempts to find the nerve by low-voltage stimulation at a frequency
50–100 Hz, the strongest possible sensory stimulation at the lowest pos-
sible voltage. If the cannula is actually resting on the nerve, the minimum
stimulation required to produce a discharge is 0.5 mA or approximately
0.25 V for a standard 500 Ω tissue impedance. Cannula should be within
3 mm of the nerve in order to create adequate lesion indicated by maxi-
mum stimulation level around 0.6 V. To ensure that the cannula is not dan-
gerously close to any motor nerve, low-frequency stimulation of 2 Hz is
given and muscle twitching is noted. When the operator is satisfied that
the needle is safely in position, a RF current is passed through the thermo-
couple probe. The current heats up the surrounding tissues and produces
a lesion in the nerve that has been targeted. The lesion will grow until a
steady state is reached. To ensure adequate lesioning, a desired tempera-
ture of 80–90°C is required for 60–120 s.
The modern thermocouple electrodes are small, quite accurate at mea-
suring temperature and impedance as well as in generating the RF lesion
(Photograph 32.2). Newer lesion generators such as RFG-3C allow accu-
rate measurement of impedance, a broad range of electrical stimulation,
highly accurate temperature monitoring and control of lesion duration.
Thus, it is an excellent method for controlling the size of the coagulative
lesion. Since the size of the lesion depends upon the temperature of the
lesion itself, modern cannula tips are equipped with electrodes that accu-
rately measure temperature.
In modern RF lesion equipment, it is absolutely mandatory that any
system utilized allows measurement of impedance and has the ability to
  

• s timulate at a wider range of frequencies

• accurately time the duration of the lesion

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 RF Ablation versus Chemical Neurolysis 387

PHOTOGRAPH 32.3 Radio frequency lesion generator (Cosman).

• a ccurately measure the lesion temperature

• accurately measure amperage and voltage
• slowly increase temperature with time
  

We are currently using the COSMAN RF lesion generator (pulsed and

standard RF) at our centre (Photograph 32.3). This RF lesion generator
allows all the above-mentioned functions to be performed in real time.
The RF lesion generator utilizes frequencies of approximately 500 kilo-
cycles per second. Utilizing frequencies in this range is advantageous
because they allow for more uniform and better circumscribed lesions.
At any given electrical current, thermal equilibrium is established in
approximately 60 s. This can vary, however, in areas of highly vascular
tissue. It has been shown that the most satisfactory method to control
lesion size is that of maintaining a constant electrode tip temperature for
a period of 1 or 2 min. When utilizing this method, lesion size will depend
directly on the temperature measured (temperature dependent lesions).

RF ABLATION VERSUS CHEMICAL NEUROLYSIS

The advantages of RF techniques over other neurodestructive methods

are as follows:
  

• T he lesion size can be adequately controlled

• Good monitoring of the lesion temperature can be performed with a
thermal coupled electrode

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

388 32. RADIO FREQUENCY ABLATION IN PAIN MANAGEMENT

• A ccurate placement of electrode is facilitated with electrical stimula-

tion and impedance monitoring
• Ability to utilize the same RF cannula for different types of 3.8 spinal
axis lesions
• Can be performed under local anaesthesia or sedation
• Rapid recovery
• Low morbidity and mortality
• Ability to repeat RF lesions if the neural pathway regenerates
  

RF lesioning has been established as an accepted modality of treatment

in lumbar facet joint pain, sacroiliac joint pain, plantar fasciitis, upper tho-
racic sympathectomy, stellate ganglion block, cardiac conduction abnor-
malities, etc.
The commonly performed RF procedures at our centre include
  

• Lumbar sympathectomy
• Medial branch neurotomy (facet denervation) (Photograph 32.4)
• Dorsal root ganglionotomy
• Coeliac plexus block
• Upper thoracic sympathectomy
• Stellate ganglion block
• Mandibular/maxillary nerve block

PULSED RF

Pulsed RF has been recently described as a technique to apply a rela-

tively high voltage near a nerve but without the usual effects of a rise
in temperature or subsequent nerve injury. Sluijter (1998) presented the
technique of pulsed RF where only short bursts of RF are applied to the
nerve by the use of a modified RF machine, where it was claimed the tip
temperature of the probe was only 42°C (Sluijter, et al 1998). It was stated

(a) (b)

PHOTOGRAPH 32.4 Medial Lumbar branch RF Ablation (facet denervation) in progress

showing needle in position (a) Oblique view and (b) Lateral view.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Conclusions 389

there was no clinical evidence of neural damage and little postoperative

soreness such as is experienced often after conventional high-temperature
RF lesioning. The RF machine would deliver a pulse of RF (of 300 kHz)
for 30 ms out of a cycle. The voltage reached with this machine was in the
region of 25–35 V and the output was adjusted so that the temperature
reached was no more than 42°C.
The mechanism by which pulsed RF treatment works is unclear. One
possibility is that it works in a manner similar to transcutaneous elec-
trical nerve stimulation, activating both spinal and supraspinal mecha-
nisms, which may reduce pain perception. Interestingly, there has been
recent interest in the mechanisms by which long-term depression may be
induced within the spinal cord. Pulsed RF is delivered at between 1 and
2 Hz, a frequency which is identical to that shown to induce long-term
depression in the spinal cord.
Pulsed RF has the following advantages over the RF heat lesion:
  

• I t is a virtually painless procedure

• As far as the observations go there is no sign of neurodestruction
• The method might therefore be suitable for use in patients with neuro-
pathic pain
• The method seems suitable for use in conditions where one would
hesitate to generate heat, such as in a very narrow intervertebral fora-
men or in very critical segments, such as C8 and T1 and the lower
sacral segments
  

However, further double-blind studies are required to establish the effi-

cacy of pulsed RF on a long-term basis.

CONCLUSIONS

The applications of RF lesion generated in the nervous system for a

variety of therapeutic purposes have had excellent success. The modern
RF lesion generator assists the clinicians to improve target determination
and accurately place the electrode close to the targeted nerve. In compari-
son to other selective neuroablation techniques, RF offers several clinical
and practical advantages, including safety and ease of operation.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

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 C H A P T E R

33
Vertebroplasty and
Kyphoplasty

One of the most painful conditions of the spine is a vertebral body col-
lapse. Although it is quite common among women of older age, men are
not quite exempt. Osteoporosis is one of the leading causes of disability
in the old population. Not only does it lead to vertebral compression frac-
tures, but can also cause some of the serious hip fractures. Older patients
with multiple systemic diseases like cardiac, pulmonary and endocrine
may not be good candidates for a more invasive neurosurgical repair of
these fractures.
Over the past 10–15 years, percutaneous procedures like vertebroplasty
and balloon kyphoplasty have gained significant popularity, and have
been shown to be extremely effective tools in the treatment of the defor-
mities and pain arising from the vertebral compression fractures. Some
studies have shown a better outcome with kyphoplasty than with ver-
tebroplasty. It has been shown that the increase in vertebral height was
greater with kyphoplasty than with vertebroplasty, the original vertebral
height was restored in 93% of vertebrae with kyphoplasty and in 82%
with vertebroplasty and there was a greater decrease in wedge angle with
kyphoplasty than with vertebroplasty. When compared with conservative
therapy, percutaneous vertebroplasty results in prompt pain relief and
rapid rehabilitation.
Most common levels of vertebral compression fractures happen to
be in the thoracic spine. However, other levels in the lumbar spine can
also be affected. Plain X-rays of the spine are most helpful in revealing
the compression deformity especially in a lateral view; however, mag-
netic resonance imaging or contrast enhanced computed tomography of
spine may be necessary to evaluate neurological compromise. A posi-
tron emission tomography scan can be helpful in evaluating metastatic
disease.

391
392 33. VERTEBROPLASTY AND KYPHOPLASTY

VERTEBROPLASTY

Vertebroplasty is a procedure whereby a cement-like substance PMMA

is injected percutaneously into the collapsed vertebral body, helping it
regain some of its height and shape.

Two Objectives of Vertebroplasty

• P
 ain management
• S tabilization

Indications of Vertebroplasty
•  ainful osteoporotic fractures refractory to medical therapy
P
• Unstable painful metastasis and multiple myelomas
• Painful vertebral haemangioma
• Painful fracture associated with osteonecrosis
• Reinforcement of weakened vertebra prior to surgical stabilization

Contraindications to Vertebroplasty
•  esponsive or healed osteoporotic fracture
R
• Presence of untreated coagulopathy
• Prophylaxis for osteopenic patients
• Discitis/osteomyelitis or sepsis
  

Newer filling materials like bone substitutes, e.g. composite resin mate-
rials, calcium phosphate or calcium sulfate cements are also available. The
vertebroplasty kits consist of all the necessary paraphernalia including the
syringes, trocars, cement and other compounds, mixing chambers, and
sometimes even a hammer to drive the trocar into the vertebral body and
a long holder to stabilize the trocar to keep the physician's hands out of
the X-ray field (Fig. 33.1).
The procedure is carried out in a sterile operating room environment
usually in an outpatient surgery centre. Patient is placed prone on the
operating room table. Strict aseptic precautions are carried out throughout
the procedure and a surgical prep and drape are utilized. Mild intrave-
nous analgesia is provided for comfort and a qualified individual moni-
tors all the vital signs of the patient.
Approach to the patient's collapsed vertebral body is posterolateral
or posterior through the pedicle of the vertebra. Although some physi-
cians practice a bipedicular approach, a unipedicular approach may be
sufficient in many patients. Under an oblique or anteroposterior (depend-
ing on the level of the vertebra) fluoroscopic view, the pedicle of the ver-
tebra to be treated is optimized for placement of the trocar (Fig. 33.2).

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Vertebroplasty 393

FIGURE 33.1 Trocar in the vertebral body.

FIGURE 33.2 Fluoroscopic confirmation of trocar.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

394 33. VERTEBROPLASTY AND KYPHOPLASTY

After infiltrating the skin and deeper tissues, the trocar is advanced so
that it contacts the pedicle at its outer edge, and is then driven by screw-
ing motion of the hand or by a gentle tap with a surgical hammer into the
vertebral body. Repeated anteroposterior and lateral views are obtained to
ascertain the direction of approach and the final position. Advancement
of the trocar is very frequently carried out under live fluoroscopic view.
Once the position of the tip is confirmed to be within the centre of the
vertebral body, the trocar is readied for injection of the filler material. The
filler is mixed in an enclosed chamber by mixing the monomer and the
polymer. It usually contains radiopaque barium sulfate. It is extremely
important to monitor the cement delivery under a live fluoroscopic view.
Any leakage within the epidural space can have disastrous results. For
this reason, it is also very important to have the trocar follow the outer
wall of the pedicle rather than the inner wall, to avoid any damage to the
pedicle leading to epidural exposure. Venous embolization has also been
reported. Anaphylactic reaction to the PMMA is also one of the risk factors
that can even cause death, especially when multiple levels of collapsed
vertebrae are treated at once. Other complications are similar to other
invasive spine therapeutics. The incidence of complications is very low
in experienced hands, once again emphasizing the importance of proper
training and experience. Once injected, the cement would usually harden
within 10 min.

Complications of Vertebroplasty
• Fractured pedicle
• Fracture of transverse process
• Migration of PMMA into epidural venous plexus
• Paralysis (rarely)
• Cement leakage into spinal canal, veins, disc space and
soft tissues

KYPHOPLASTY

Kyphoplasty is another procedure, which is effective in the treatment

of vertebral body compression fractures. It too utilizes bone cement; how-
ever, the delivery method is different.
The advantages of kyphoplasty are
  

• I t is a balloon-assisted vertebroplasty
• It restores the vertebral heights
• It allows the use of viscous cement
• It reduces cement leakage

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Kyphoplasty 395

Indications of Kyphoplasty
•  ain score of >4
P
• Progressive vertebral collapse
• Pain of more than 6 weeks duration
• Complete collapse of vertebral body

Contraindications to Kyphoplasty
• L oss of more than 80% of vertebral height
• Infection
• Bone retropulsion with neurological compromise
  

The procedure is usually performed in the operating room, but not

very commonly as an outpatient procedure. Placement of the ‘tube’ into
the collapsed vertebral body requires a small incision in the back and the
tube is then guided through posterior or posterolateral approach (once
again depending on the level being treated), via the pedicle into the ver-
tebral body. Once in place, a balloon (similar to an angioplasty balloon) is
inserted via the tube and inflated with a liquid to create a cavity within
the collapsed vertebra (Fig. 33.3). It is then removed and the cavity is filled
with the bone cement PMMA similar to vertebroplasty. The vertebro-
plasty method uses the pressure of injection to ‘inflate’ the vertebral body,
whereas kyphoplasty uses a balloon to create such inflation. The rate of
pedicular fracture is slightly higher with kyphoplasty.

FIGURE 33.3 Balloon kyphoplasty.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

396 33. VERTEBROPLASTY AND KYPHOPLASTY

In summary, vertebroplasty and kyphoplasty are highly effective treat-

ment methods for vertebral body compression fractures caused by several
ailments. As compared to the treatments in the past, which included rest,
analgesics and, sometimes, even surgery, these minimally invasive percu-
taneous procedures certainly are very promising and effective modalities
for a patient in severe pain.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 C H A P T E R

34
Management of
Spasticity

Spasticity is a widespread and debilitating condition. While its inci-

dence is not known with certainty, it is likely that spasticity affects over
12 million people worldwide. As one part of UMN syndrome, spasticity
can affect the entire range of patients' function. It may lead to musculo-
skeletal complications including contracture, pain and dislocations.
‘Spasticity is a motor disorder characterized by velocity dependent
increase in tonic stretch reflexes (“muscle tone”) with exaggerated ten-
don jerks, resulting from hyperexcitability of the stretch reflex, as are
component of UMN syndrome. (There are) other features of the UMN
syndrome resulting from the release of flexor reflexes, such as flexor
spasms (and) the negative symptoms such as the pattern of weakness
and loss of dexterity caused by withdrawal of the influence of descend-
ing motor pathways’.
Spasticity is often painful. It can make simple activities of daily liv-
ing time consuming, difficult or impossible for an individual to do alone,
placing greater demands on the caregiver and the individual. Spasticity
can increase medical complications such as pressure sores, pneumonia
and painful deformities (contractures). An individual's ability to socialize
and enjoy hobbies and recreational activities get limited. Treating spastic-
ity can decrease health care costs, increase functional ability and reduce
the care required. The overall quality of life of the individual and the fam-
ily gets greatly improved because of the treatment.
Evaluating and treating a person with spasticity is not easy. The patient
wants things that current treatment cannot provide such as more inde-
pendence, more strength and more coordination. Certain aspects, such as
control of painful spasms and decrease in resistance to passive movement
can now be reliably treated.

397
398 34. MANAGEMENT OF SPASTICITY

The clinician should weigh the benefits of treatment against possible

risks before setting the goals of treatment. In this chapter, we have given a
general overview of spasticity in neurological disease and provided some
guidelines for its rational treatment based on our experience in Pain Clinic
at the All India Institute of Medical Sciences.

AETIOLOGY OF SPASTICITY

Spasticity results from disorder or injury to central nervous system,

either brain or spinal cord. The common aetiologies include brain injury,
cerebral palsy, stroke, multiple sclerosis and spinal cord injury.

Natural Progression of Spasticity

Tonic activation

Contractions under ischemic conditions

Activate group 4 muscle nociceptors

Reflex spasm

Muscle shortening

Bony torsion

Joint instability

Degenerative arthritis
  
Symptoms and Signs of UMN Syndrome
Positive symptoms may include
  

• Hypertonicity
• Clonus
• Exaggerated deep tendon reflexes
• Muscle spasms
• Scissoring
• Fixed joints
  

There may be negative symptoms such as

  

• W  eakness
• I ncoordination
• F  atiguability
  

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Goal Setting in Spasticity Control 399

PHOTOGRAPH 34.1 A spastic child with hypertonicity of hip adductors and gastrosoleus
muscles.

Weakness of muscles is resistant to treatment with the sole exception

that when the opposing muscle groups are unequally affected by spastic-
ity (imbalance), selective weakening of that group of muscles improves
the overall function (Photograph 34.1).

GOAL SETTING IN SPASTICITY CONTROL

There are a number of treatment options available for spasticity con-

trol. The treatment should be ‘individualized’. It is important for the
individual, family and health care team to agree upon realistic treatment
goals. This process can help in avoiding disappointment that might occur
if the treatments do not produce the results the individual and/or family
hoped for.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

400 34. MANAGEMENT OF SPASTICITY

Goals of spasticity management are

  

•  ecrease in pain
D
• Decrease in contractures
• Improved mobility
• Facilitate activities of daily living
• Save caregiver's time

MEASUREMENT OF SPASTICITY

Some components of the spasticity syndrome are also useful diagnos-

tically during a general physical examination. The presence of clonus,
hyperreflexia, mass spasms and alterations of muscle tone are helpful in
localizing the lesion of the central nervous system.
The other reason is to assess the effectiveness of a therapeutic interven-
tion. Evaluation consists of the following:
  

• Gait
• Range of motion
• Balance skills
• Sleeping patterns
• Endurance – spasticity can wear one out but so can medications used
to control spasticity
  

Tests used for evaluation of spasticity:

  

1. M uscle strength – Medical Research Council grading – grade 5

(normal) to grade 0 (total paralysis)
2. Deep tendon reflexes – grade 0 (absent) to grade 4 (clonus)
3. Ashworth scale (Table 34.1). Ashworth scale is the ‘gold standard’ for
semiquantitative clinical assessment of spasticity
4. Global pain scale
5. Spasm frequency scale (Table 34.2): Spasm frequency score is obtained
visually or electronically. It records the number of spasms observed

TABLE 34.1 Ashworth Scale for Measurement of Spasticity

Grade Description

0 No increase

1 Slight increase producing a catch when joint is moved in flexion or extension

2 More marked, but joint easily flexed

3 Considerable increase, and passive movement difficult

4 Affected part rigid in flexion or extension

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Spasticity Treatment Protocols 401

during a given period of time, usually 1 h. The spasm score can be

quite variable because the number of spasms is affected by position,
activity and many other factors
6. Bilateral adductor tone scoring system (Table 34.3)

SPASTICITY TREATMENT PROTOCOLS

Knowing the diagnosis is good,

Knowing the course is better,
Knowing the cure is best.

None of the above treatment options is best for all individuals. All
treatment modalities have the potential for side effects that should
be weighed against their benefits. The most effective treatment plan
aims to strike a balance between the positive and negative effects of
the treatment. The best treatment option is the one that is most likely
to achieve the goals agreed upon by the individual, family and health
care team.

TABLE 34.2 Spasm Frequency Scale for Measurement of Spasticity

Grade Description

0 No spasms

1 No spontaneous spasms (except with vigorous motor stimulation)

2 Occasional spontaneous spasms and easily induced spasms

3 More than 1 but less than 10 spontaneous spasms per hour

4 More than 10 spontaneous spasms per hour

TABLE 34.3 Bilateral Adductor Tone Scoring System

Grade Description

0 No increase in tone

1 Increased tone, hips easily abducted to 45° by one person

2 Hips abducted to 45° by one person with mild effort

3 Hips abducted to 45° by one person with moderate effort

4 Two people required to abduct hips to 45°

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

402 34. MANAGEMENT OF SPASTICITY

PRINCIPLES OF SPASTICITY MANAGEMENT

  

1. Systemic versus local treatment

  

Local treatments are those that are directed at a specific muscle or nerve.
These local treatments include BTx A, phenol and alcohol neurolysis. They
avoid systemic side effects such as sedation, confusion, hepatotoxicity and
diffuse weakness. Local treatment is also preferred when there is focal
imbalance of agonist and antagonist muscle tone or the intervention is
desired on only a few muscles. Systemic medications have the advantage
of affecting large areas and are therefore useful in treating widespread
conditions such as paraplegia or hemiplegia.
  

2. Timing of treatment
  

Choice of treatment will often depend on the length of time the spas-
ticity has been present. Orthotic braces in first few weeks after a stroke
or spinal cord injury may not be the best use of resources. Similarly, the
use of invasive treatments, including intrathecal implantation of baclofen
pump or other surgical procedures, is rarely warranted in the first few
months.
  

3. Complications
  

Sedation is the most common side effect of oral medications for

spasticity. Many patients find sedation adversely affecting their abil-
ity to function. Cerebral injury patients are particularly prone to seda-
tion. Dosages in medications must be quite low initially, often below
the therapeutic threshold, and can only be increased slowly. Dantrolene
is less sedating than the centrally acting benzodiazepines or gamma-
aminobutyric acid agonist.
Weakness is another common adverse event. Weakness is usually dose-
dependent and is particularly prone to occur with dantrolene.
Hepatotoxicity is particularly associated with tizanidine and dan-
trolene. Particularly as doses escalate, liver functions should be monitored
regularly.
  

4. Cost of the treatment

  

It depends upon the treatment option selected. It can range from the
rather inexpensive dantrolene or diazepam to the extremely expensive
BTx A.
  

5. Nonneurological exacerbators in spastic hypertonia

  

Pain, fatigue, anxiety, wounds, fractures, systemic infection, ingrown

toe nail, heterotropic ossification, urinary retention, constipation, intra-
abdominal infections can all exacerbate hypertonicity and thus spasticity.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Principles of Spasticity Management 403

Algorithmic Approach to Spasticity Management

Spasticity

Evaluation
Etiology
Effectiveness of intervention
Goal setting
Clinician + patient + family
Treatment
Team approach
Timing of treatment
Systemic / local treatment
Watch for complications
Treat exacerbating conditions

Physical therapy Medications Local chemodenervation Surgery

Stretching Systemic Spinal Phenol/ Botulinum Orthopaedic Neurosurgery

Strengthening alcohol toxin Contracture Selective
Oral Intrathecal motor nerve release dorsal
Orthoses and
Baclofen baclofen block rhizotomy
serial casts Tendon
Positioning Benzodiazepines transfer
Cold Dantrolene Neurectomy
application sodium osteotomy
Electrical Tizanidine Arthrodesis
stimulation
Biofeedback

  
Treatment Modalities
1. Physical therapy
  

These treatments are designed to reduce the muscle tone, maintain

or improve range of motion and mobility, increase strength and coor-
dination and improve comfort. They include stretching, strengthening,
orthoses and casts, positioning, cold packs, electrical stimulation and
biofeedback.

Aims of Physical Therapy

• Enhance ease of care giving
• Improve hygiene
• Preserve skin integrity
• Allow active assisted movement
• Eliminate and prevent pain

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

404 34. MANAGEMENT OF SPASTICITY

• M aintain normal tone durably and comfortably

• Allow maximum functional interaction of the patient with the
environment

Principles of Physical Therapy

• Midline orientation and symmetry
• Segmental rotation
• Prevention and correction of mass reflexes and postures
• Movement out of traditional plane and on the diagonal
• Positioning of proximal segments first so that the distal segments will
follow
• Avoidance of excessive support to the patient
• Tone changes with position, time of the day and activity
• Spasticity can be reduced by sustained stretch

Physiotherapeutic Modalities Used in Spasticity Treatment

• Facilitation/inhibition involves the following:
• Neurodevelopmental technique to analyse the postural reflex activ-
ity and to normalize it to the extent possible
• Proprioceptive neuromuscular facilitation. Total movement pattern
is facilitated to promote motor learning
• Patterning motor learning
• Sensory integration
• Reflex inhibitory postures
• Deep pressure
• Successive induction
• Rhythmic stabilization
• Conventional therapies include the following:
• Reduce irritative phenomenon/aversive stimuli
• Functional approach
• Positioning
• Neuromuscular re-education
• Contract – relax–contract technique
• Treatment of secondary orthopaedic deformities
• Biofeedback techniques train the patient to reproduce with
their paretic arm the EMG patterns produced by the normal arm
during functional tasks. It is also used to quieten the EMG activity
of the spastic agonist during functional tasks.
• Physical modalities used to modulate or inhibit spasticity are
• Cooling/heat
• Vibration
• Hydrotherapy
• Acupuncture
• Casting and orthotic devices

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Principles of Spasticity Management 405

• E  lectrical stimulation: beneficial in neuromuscular re-education.

Antagonist to the spastic muscle is stimulated to achieve reciprocal
inhibition of agonist
2. Oral medications (Table 34.4)
  

Oral medications may be used to reduce the spasticity and perhaps

lessen some of the associated movements such as dystonia.
  

3. C
 hemodenervation (neurolytic motor nerve blocks and BTx
injection)
  

Chemodenervation is the use of chemicals to interrupt the flow of nerve

impulses to spastic muscles. Chemodenervation reduces spastic muscu-
lar contraction to allow normal position or function of the involved limb.
Three chemicals are widely used for chemodenervation: absolute alcohol
and 6–8% phenol are directly injected onto the nerve or muscles to destroy
them; 6–8% phenol is preferred over alcohol because of its lesser incidence
of dysesthesia. BTx A is often used for smaller distal muscles, although it
can also be used in larger muscles. BTx may be used in combination with
either of the two. Alcohol and 6–8% phenol are effective for spasticity in
large, proximal muscle.
These agents should be considered when there are specific goals that
can be met within a finite time, such as during a period where more
intense physical and occupational therapy are performed.
The most commonly used agents for temporary treatment are phenol,
motor nerve blocks and BTx A injection. The treatment converts paresis
with muscular hyperactivity to paresis with muscular hypoactivity.
Application in cerebral palsy includes the management of toe walking
(dynamic equinus), scissoring (hip adductor spasticity), crouching gait
(hamstring spasticity) in the lower limb and adducted shoulder, flexed
elbow, pronated forearm, flexed wrist, thumb-in-palm, clenched fist,
intrinsic plus hand in the upper limb.
Phenol at 6–8% concentration affects nerve fibres of all sizes and they
undergo Wallerian degeneration with destruction of axons and myelin.
The destroyed axons do regenerate in time duration of 3–6 months. This
accounts for temporary effect of phenol. There may be reinnervation of
denervated muscle by motor neurons other than those that originally
innervated them.

Technique of Neurolytic Blocks

In children with spasticity of obturator muscle and gastrosoleus
muscle, spasm causes scissoring gait and toe walking. Obturator nerve
block and posterior tibial nerve block are given to relieve the spasm of
these muscles.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 406
TABLE 34.4 Drugs Used for Reduction of Spasticity
Drug Mechanism of action Pharmacological actions Adverse effects Dose

Baclofen Agonist for GABA B Reduce both active and Sedation, truncal, hypotonia, Adult – Start 40–80 mg/day
V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

receptors in spinal passive tone change in bladder habits 3 divided doses

cord, and cortical Children – 5–10 mg/day
effect (maximum 30–40 mg/day)

Benzodiazepines – Increase GABAergic Relief of the painful Habituation, sedation, increased Adult – Diazepam start

34. MANAGEMENT OF SPASTICITY

diazepam, lorazepam, transmission spasm increase in sleep, secretions, rebound seizure with 2–5 mg at night slowly titrate
clonazepam decrease in muscle tone, abrupt withdrawal, preferred for upwards to a maximum of
anticonvulsant effect use at night 60 mg/day
Children – 0.8–0.12 mg/
kg/day

Dantrolene Directly on the Decreased muscle Muscle weakness, gastrointestinal Adult – Start 25 mg/day to a
sarcoplasmic tone upset, hepatotoxicity fatigue maximum of 400 mg/day in
reticulum divided doses
Children – 0.5–0.2 mg/kg/day
in divided doses

Clonidine and Alpha2 adrenergic Decreased muscle Fatigue, disturbed sleep, risk of Adult – Tizanidine. Start
tizanidine agonist tone rebound hypertension if stopped 4 mg bedtime to maximum of
suddenly 36 mg/day in divided doses
Dantrolene and tizanidine are Children – 0.5 mg/kg/day to a
usually not prescribed together maximum of 3 mg/kg (10 kg)
because of increased risk of liver to 12 mg/kg (40 kg)
toxicity

GABA, gamma-aminobutyric acid.

 Principles of Spasticity Management 407

(a)

(b)

PHOTOGRAPH 34.2 Neurolytic blocks using nerve stimulator of (a) obturator and
(b) posterior tibial nerves.

Obturator Nerve Block

Patient is placed in supine position and legs slightly abducted. The
pubic tubercle on the involved side is identified by palpation. A point
1 cm lateral and 1 cm inferior to the public tubercle is identified. A regional
anaesthesia needle is slowly advanced perpendicular to the skin until the
needle is felt to impinge on superior pubic ramus. The depth of bony
contact is noted and the needle is withdrawn and redirected slightly lat-
erally and inferiorly. The current is set at 3–4 mA. The needle is advanced
¾ to 1 in deeper to place the needle in obturator canal. When there is
contraction of adductor muscles, the current is decreased to 0.5–0.8 mA
and if the contraction still persisted, 1–1.5 mL of 6% phenol is injected
(Photograph 34.2).

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

408 34. MANAGEMENT OF SPASTICITY

Posterior Tibial Nerve Block

The midpoint of popliteal fossa is identified. In prone position, needle
is advanced 2–5 mm deep just lateral to popliteal artery pulsations and
1 mL of 6% aqueous phenol is injected. Physiotherapy is avoided for
3 days.

Advantages of Phenol and Alcohol Motor Nerve Block

Unlike BTx A, phenol and alcohol do not provoke an immunologi-
cal reaction. Since the level and frequency of dosage is limited, larger
muscles may be treated more effectively. They are quite inexpensive com-
pared to BTx A.

Disadvantages of Phenol and Alcohol

The perineural injection of alcohol is often painful. The muscle near
the injection site is usually damaged along with target nerves. Damage
to sensory nerve may cause dysesthesia. There can be marked decrease in
muscle tone. Effectiveness and duration is similar to BTx from less than
1 month to more than 1 year.

Botulinum Toxin Type A

BTx A is a potent neurotoxin produced by the bacterium Clostridium
botulinum under anaerobic conditions. The effect of BTx A depends on the
high affinity of type A toxin to receptors on the human neuromuscular
junction. It binds to cholinergic nerve endings and inhibits the release of
neurotransmitter acetylcholine by blocking the binding of acetylcholine
vesicles to the plasma membrane of motor end plate (Fig. 34.1). Neuro-
transmission is then restored by the sprouting new nerve endings. It takes
about 3 months for the original nerve endings to be restored during which
time the newly sprouted nerve endings are removed. Thus, the effect of
BTx A is pharmacologically completely reversible. When injected into the
skeletal muscle, BTx A causes a dose-dependent, reversible chemodener-
vation of muscle.

Administration of BTx
BTx A is mainly used for hip adductors and gastrosoleus group of mus-
cles. Patient is placed in supine position with hips abducted and both hip
and knee flexed for adductor injection and prone position for gastrosoleus
injection (Photographs 34.3 and 34.4).
BTx A at a dose of 4 IU/kg body weight/muscle (maximum dose
300 IU) is injected by using palpation technique (Table 34.5). The muscle

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Principles of Spasticity Management 409

(a) (b)

FIGURE 34.1 Mechanism of action of botulinum toxin type A. (a) Normal Transmitter
release and (b) binding of botulinum toxins to cholinergic nerve endings and preventing
release of acetylcholine.

PHOTOGRAPH 34.3 Botulinum toxin A injection in gastrosoleus muscle.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

410 34. MANAGEMENT OF SPASTICITY

PHOTOGRAPH 34.4 Botulinum toxin A injection in hip adductor muscle.

belly is identified and five 1 in long 24 G needles are placed in the muscle
belly 1 cm deep to ensure the free and regular spread of BTx. Precaution is
taken so that the total dose does not exceed 300 IU/day and the injection
is repeated only after 3 months. The patients are followed up every month
for 1 year. Physiotherapy is avoided for 2 or 3 days.

Advantages
BTx temporarily weakens the specific muscle, allowing more of normal
limb positioning and function. Stretching exercises should be continued
throughout the treatment. The advantages of BTx over phenol chemode-
nervation include lack of sensory side effects, relative ease of administra-
tion and dose-dependent graded decrease in muscle tone.

Disadvantages
Disadvantages are development of mild flu-like symptoms, resistance
to BTx A due to antibody formation, high cost of the treatment, cannot be
used to treat widespread severe spasticity and contraindicated in myas-
thenia gravis and motor neuron disease patients.

INTRATHECAL BACLOFEN THERAPY

The use of baclofen in patients with spasticity has received great

attention in recent years. This system delivers a continuous infusion of
baclofen into the intrathecal space and allows for individual titration.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Intrathecal Baclofen Therapy 411

TABLE 34.5 Muscle Selection and Dosage Range: Suggested Adult Botulinum Toxin
A Dosage
Average Botulinum Number of
Potential muscle starting Toxin A dose injection
Clinical pattern involved dose/units units/visit sites

UPPER LIMBS
Adducted/internally Pectoralis complex 100 75–170 4
rotated shoulder
Latissimus dorsi 100 50–150 4

Teres major 50 25–75 1

Subscapularis 50 25–75 1

Flexed elbow Brachioradialis 50 25–75 1

Biceps 100 50–200 4

Brachialis 50 25–75 2

Pronated forearm Pronator quadratus 25 10–50 1

Pronator teres 40 25–75 1

Flexed wrist Flexor carpi radialis 50 25–100 2

Flexor carpi ulnaris 40 10–50 2

Thumb-in-palm Flexor pollicis longus 15 5–25 1

Adductor pollicis 10 5–25 1

Opponens 10 5–25 1

Clenched fist Flexor digitorum 50 25–75 4

superficialis

Flexor digitorum 15 25–100 2

profoundus

Intrinsic plus hand Lumbricals interossei 15 10–50/hand 3

LOWER LIMBS
Flexed hip Iliacus 100 50–150 2

Psoas 100 50–200 2

Rectus femoris 100 75–200 3

Flexed knee Medial hamstrings 100 50–150 3

Gastrocnemius (as 150 50–150 4

knee flexor)

Lateral hamstrings 100 100–200 3

Adducted thighs Adductor brevis/ 200/leg 75–300 6/leg

longus/magnus

Stiff (extended) knee Quadriceps 100 50–200 4

Continued

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412 34. MANAGEMENT OF SPASTICITY

TABLE 34.5 Muscle Selection and Dosage Range: Suggested Adult Botulinum Toxin
A Dosage—cont’d
Average Botulinum Number of
Potential muscle starting Toxin A dose injection
Clinical pattern involved dose/units units/visit sites

Equinovarus foot Gastrocnemius 100 50–200 4

medial/lateral

Soleus 75 50–100 2

Tibialis posterior 50 50–200 2

Tibialis anterior 75 50–150 3

Flexor digitorum 75 50–100 4

longus/brevis

Flexor hallucis longus 50 25–75 2

Striatal toe Extensor hallucis 50 20–100 2

longus
NECK
Sternocleidomastoid 30 15–75 2
(SCM)

Scalenus complex 30 15–50 3

Splenius capitis 60 50–150 3

Semispinalis capitis 60 50–150 3

Longissimus capitis 60 50–150 3

Trapezius 60 50–150 3

Levator scapulae 80 25–150 3

Dosing guidelines:
Total maximum dose per visit = 300 units.
Maximum dose per injection site = 50 units.
Maximum volume per site = 0.5 mL, except in select situations.
Reinjection > 3 months.
Note: The dose should be reduced by 50% if both SCM muscles are injected.

Desired goals of therapy include a decrease in spasticity to improve

function and alleviate spasm pain. This therapy is indicated for spastic-
ity that is clinically severe (≥3 on the Ashworth scale). Prior to implanta-
tion of pump, patients must respond favourably to a screening trial of
ITB. The standard procedure is to administer 50 microgram of baclofen
intrathecally. The bolus is slowly administered over 5 min. Onset of drug
action is within 30–60 min and lasts for 4–8 h. Positive response is defined
as 1 point decrease in either the average Ashworth score or Spasm score.
Dose through pump is usually set at twice the test dose 24 h. Adjustment
over several days to weeks is required, with dosage increase of 10–20%
at a time, until a satisfactory response is obtained.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

 Conclusion 413

Disadvantages of treatment include the physical presence of pump and

catheter, as well as the need for frequent hospital visits for medication
refills. Suitable candidates include those with moderate to severe spastic-
ity and who have failed oral medication. Dosages in ITB can be varied
throughout the day to address specific needs, such as increasing the dose
at night for comfortable sleep and decreasing the daytime dose if tone is
helpful in weight support and ambulation. Side effects include decline
in truncal tone, bladder dysfunction and daytime sleepiness. Compli-
cations arise out of surgery, unintended overdose and sudden infusion
discontinuation.

SURGICAL PROCEDURES FOR SPASTICITY

REDUCTION

Surgical procedures involve selective dorsal rhizotomy and neuroto-

mies. Surgical procedures in the lower extremities including tendon
release, tendon lengthening and osteotomies are often required in patients
with spasticity to treat the orthopaedic consequences of uncontrolled
spasticity, such as contractures and dislocations. The irreversibility of
some surgical treatments and their ‘all or none’ outcome make them inap-
propriate in a large number of patients, especially those who require some
spasticity for functioning.

CONCLUSION

Future treatment of spasticity will focus on prevention of spasticity as

well as effective permanent treatment at the level of brain. Until such solu-
tions are achieved, treatment occurs most effectively with a multidisci-
plinary approach to assessment and treatment. Adieu kind reader; maybe
we brought you

What you want to know,

What you ought to know,
What you got to know.

V. ADVANCED INTERVENTIONAL PAIN MANAGEMENT

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 A P P E N D I X

1
Definition of Commonly
Used Pain Terms

Discussion on pain involves many terms. The meaning and connota-

tion of these different terms may vary widely. Some authors use the term
pain to relate to a stimulus, others to a thing and still others to a response.
Such inconsistent usage creates difficulties in communication. As Merskey
noted, it would be most convenient and helpful if there were some con-
sensus on technical meanings and usage. IASP Classification of Chronic
Pain includes a set of definitions of commonly used pain terms. We also
follow the convention of IASP and use the below-mentioned definitions
in our clinical practice.

Pain: An unpleasant sensory and emotional experience associated with

actual or potential tissue damage or described in terms of such damage.
Note: The inability to communicate verbally does not negate the possi-
bility that an individual is experiencing pain and is in need of appropriate
pain-relieving treatment.

Pain, acute/chronic: Definitions of acute, chronic, recurrent and cancer

pain are not included in the IASP list of pain terms. We believe, how-
ever, that it is important to clarify these as they are commonly used in the
literature.
Traditionally, the distinction between acute and chronic pain has
relied on a single continuum of time with some interval since the onset
of pain is used to designate the onset of acute pain. Two most commonly
used chronologic markers to denote chronic pain have been 3 months
and 6 months since the initiation of pain; however, these distinctions are
arbitrary.
Another criterion for chronic pain is ‘pain that extends beyond the
expected period of healing’. This is relatively independent of time because
it considers pain as chronic even when it has persisted for a relatively

415
416 1. DEFINITION OF COMMONLY USED PAIN TERMS

brief duration. Unfortunately, how long the process of healing will take is
ambiguous.

Acute pain: Pain elicited by the injury of body tissues and activation
of nociceptive transducers at the site of local tissue damage. Local injury
alters the response characteristic of the nociceptors and perhaps their cen-
tral connections and the autonomic nervous system in the region. In gen-
eral, the state of acute pain lasts for a relatively limited time and generally
remits when the underlying pathology resolves.

Chronic pain: It is usually elicited by an injury but may be perpetuated

by factors that are both pathogenetically and physically remote from the
originating cause. This type of pain prompts patients frequently to seek
health care and it is rarely effectively treated. Because the pain persists, it
is likely that environmental and affective factors eventually interact with
tissue damage, contributing to the persistence of pain and illness behav-
iours. It is also possible that, just as the brain is modified by experience,
especially in early life, the brain may alter the way noxious information is
processed to reduce or augment its effect on subjective awareness.

Cancer pain: Pain associated with cancer includes pain connected with
disease progression as well as treatments. Pain associated with cancer can
have multiple causes, namely, disease progression, treatment (e.g. neuro-
pathic pain resulting from radiation therapy), and co-occurring diseases
(e.g. arthritis). Regardless of whether the pain associated with cancer
stems from disease progression, treatment, or a co-occurring disease, it
may be either acute or chronic. Thus, we do not advocate a separate clas-
sification of cancer pain as distinct from acute and chronic pain.

Recurrent pain: Recurrent pain is episodic or intermittent occurrences

of pain, with each episode lasting for a relatively short period of time but
recurring across an extended period of time.

Transient pain: Transient pain is elicited by activation of nociceptors in

the absence of any significant damage to local tissue. This type of pain is
ubiquitous in everyday life and rarely is a reason to seek health care. This
type of pain ceases as soon as the stimulus is removed.

Addiction: A behavioural pattern of psychoactive substance abuse,

addiction is characterized by overwhelming involvement with the use
of a drug (i.e. compulsive use), the securing of its supply, and the high
tendency to relapse. The compulsive use of the drug results in physical,
psychological and social harm to the user and its use continues despite
this harm.

APPENDIX
 1. DEFINITION OF COMMONLY USED PAIN TERMS 417

Allodynia: This is pain caused by a stimulus that does not normally pro-
voke pain.
Note: The term allodynia was originally introduced to separate from hyper-
algesia and hyperesthesia, the conditions seen in patients with lesions of the
nervous system where touch, light pressure or moderate cold or warmth
evoke pain when applied to apparently normal skin. Allo means ‘other’ in
Greek and is a common prefix for medical conditions that diverge from the
expected. Odynia is derived from the Greek word ‘odune’ or ‘odyne’, which
is used in ‘pleurodynia’ and ‘coccydynia’ and is similar in meaning to the
root from which we derive words with -algia or -algesia in them.

Analgesia: Absence of the spontaneous report of pain or pain behav-

iours in response to stimulation that would normally be painful. The term
implies a defined stimulus and a defined response. Analgesic responses
can be tested in animals as well as humans.

Anaesthesia dolorosa: This refers to spontaneous pain in an area or

region that is anaesthetic.

Central pain: Pain initiated or caused by a primary lesion or dysfunction

in the central nervous system.

Central sensitization: This is an increase in the excitability and respon-

siveness of neurons in the spinal cord.

CRPS type 1: Formerly known as reflex sympathetic dystrophy. It is a syn-

drome that usually develops after an initiating noxious event, is not lim-
ited to the distribution of a single peripheral nerve, and is apparently
disproportionate to the inciting event. It is associated at some point with
evidence of oedema, changes in skin blood flow, abnormal sudomotor
activity in the region of the pain, or allodynia or hyperalgesia.

CRPS type 2 (formerly, causalgia): A syndrome of sustained burning

pain, allodynia and hyperpathia after a traumatic nerve lesion, often com-
bined with vasomotor dysfunction, and later trophic changes.

Dysesthesia: An unpleasant abnormal sensation, whether spontaneous

or evoked.

Hyperalgesia: An increased response to a stimulus that is normally

painful.

Hyperesthesia: Increased sensitivity to stimulation, excluding special

senses.

APPENDIX
418 1. DEFINITION OF COMMONLY USED PAIN TERMS

Hyperpathia: A painful syndrome characterized by increased reaction to a

stimulus, especially a repetitive stimulus, as well as to increased threshold.

Hypoalgesia: Diminished pain in response to a normally painful

stimulus.

Hypochondriasis: An excessive preoccupation that bodily sensations

and fears represent serious disease despite reassurance to the contrary.

Impairment: Any loss of use of, or abnormality of psychological physi-

ological, or anatomical structure or function that is quantifiable. It is not
equivalent to disability. Impairment is to disability as disease is to illness.

Malingering: A conscious and wilful feigning or exaggeration of a dis-

ease or effect of an injury in order to obtain a specific external gain. It is
usually motivated by external incentives such as financial compensation,
avoiding work, or obtaining drugs.

Neuralgia: Pain in the distribution of a nerve or nerves.

Neuritis: Inflammation of a nerve or nerves.

Neurogenic pain: Pain initiated or caused by a primary lesion, dys-

function, or transitory perturbation in the peripheral or central nervous
system.

Neuropathic pain: Pain initiated or caused by a primary lesion or dys-

function in the nervous system.

Neuropathy: A disturbance of function or pathological change in a

nerve: in one nerve, mononeuropathy; in several nerves, mononeuropa-
thy multiplex; if diffuse and bilateral, polyneuropathy.

Nociceptor: A receptor preferentially sensitive to tissue trauma or to a

stimulus that would damage tissue if prolonged.

Nociception: Activation of sensory transduction in nerves by thermal,

mechanical, or clinical energy impinging on specialized nerve endings.
The nerve(s) involved conveys information about tissue damage to the
central nervous system.

Noxious stimulus: A stimulus that is capable of activating receptors for

tissue damage.

APPENDIX
 1. DEFINITION OF COMMONLY USED PAIN TERMS 419

Pain behaviour: Verbal or nonverbal actions understood by observers

to indicate that a person may be experiencing pain and suffering. These
actions may include audible complaints, facial expressions, abnormal
postures or gait, use of prosthetic devices, avoidance of activities, overt
expressions, and verbal or nonverbal complaints of pain, distress and
suffering.

Pain clinic: Facilities focusing on diagnosis and management of patients

with pain problems. It may specialize in specific diagnoses or pain related
to a specific area of the body.

Pain relief: Report of reduced pain after a treatment. It does not require
reduced response to a noxious stimulus and is not a synonym for analge-
sia. The term applies only to humans.

Pain threshold: The least level of stimulus intensity perceived as painful.

In psychophysics, pain threshold is defined as a level of stimulus intensity
that a person recognizes as painful 50% of the time.

Pain tolerance level: The greatest level of noxious stimulation that an

individual is willing to tolerate.

Pain sensitivity range: The difference between the pain threshold and
the pain tolerance level.

Paresthesia: An abnormal sensation, whether spontaneous or evoked.

Peripheral neurogenic pain: Pain initiated or caused by a primary

lesion or dysfunction or transitory perturbation in the peripheral nervous
system.

Placebo: A substance or procedure without therapeutic effect that is pro-

vided as a treatment. It is frequently used to control patients' expectations
for the efficacy in testing a treatment intervention.

Plasticity, neural: Nociceptive input leading to structural and functional

changes that may cause altered perceptual processing and contribute to
pain chronicity.

Psychogenic pain: Report of pain attributable primarily to psychologi-

cal factors usually in the absence of any objective physical pathology
that could account for pain. This term is commonly used in a pejorative
sense.

APPENDIX
420 1. DEFINITION OF COMMONLY USED PAIN TERMS

Rehabilitation: Restoration of an individual to maximal physical and

mental functioning in light of his or her impairment.

Symptom magnification: Conscious or unconscious exaggeration of

symptom severity in an attempt to convince an observer that one is truly
experiencing some level of pain. It differs from malingering as it is an
effort to be believed not necessarily to achieve a positive outcome (i.e.
secondary gain) such as financial compensation.

Suffering: Reaction to the physical or emotional components of pain

with a feeling of uncontrollability, helplessness, hopelessness, intolerabil-
ity, and interminableness. Suffering implies a threat to the wholeness of an
individual's self-concept, self-identify and integrity.

Tolerance: A physiological state in which a person requires an increased

dosage of a psychoactive substance to sustain a desired effect.

Wind-up, second pain: Slow temporal summation of pain mediated by

C fibres. Repetitive noxious stimulation at a rate less than one stimulus
per 3 s. It may cause the person to experience a gradual increase in the
perceived magnitude of pain.

Sensitization: Increased responsiveness of nociceptive neurons to their

normal input, and/or recruitment of a response to normally subthreshold
inputs.
Note: Sensitization can include a drop in threshold and an increase in
suprathreshold response. Spontaneous discharges and increases in recep-
tive field size may also occur. This is a neurophysiological term that can
only be applied when both input and output of the neural system under
study are known, e.g., by controlling the stimulus and measuring the neu-
ral event. Clinically, sensitization may only be inferred indirectly from
phenomena such as hyperalgesia or allodynia.

Central sensitization: Increased responsiveness of nociceptive neurons

in the central nervous system to their normal or subthreshold afferent
input.
Note: See note for sensitization and nociceptive neuron above. This may
include increased responsiveness due to dysfunction of endogenous pain
control systems. Peripheral neurons are functioning normally; changes in
function occur in central neurons only.

Peripheral sensitization: Increased responsiveness and reduced thresh-

old of nociceptive neurons in the periphery to the stimulation of their
receptive fields.

APPENDIX
 1. DEFINITION OF COMMONLY USED PAIN TERMS 421

TABLE A1.1 Categories of Pain and Possible Mechanisms

Transient pain

Nociceptor specialization

Tissue injury pain primary afferent sensitization

Recruitment of silent nociceptors, alteration in phenotype, hyperinnervation

Central sensitization recruitment, summation, amplification

Nervous system injury pain primary afferent

Acquisition of spontaneous and stimulus-evoked activity by nociceptor axons and

somata at loci other than peripheral terminals

Alteration in phenotype

Central nervous system-mediated central sensitization

Deafferentation of second-order neurons, disinhibition reorganization

MECHANISM-BASED CLASSIFICATION OF PAIN

The conventional classifications of pain disorders based on anatomy,

duration, and systems have drawn criticism for their deficiency in sensi-
bility for guiding treatment or research. A mechanism-based classification
of pain, proposing a potential list of pain mechanisms is given as below
(Table A1.1).
The mechanism-based classification of pain differs from the conven-
tional classification in that the former frees pain from diseases that may
accompany pain complaints. This classification is of immense help in
guiding treatment and in bridging research to clinical practice in pain
medicine.
Pain management specialists have seen rapid advances in the basic sci-
ences and clinical areas of pain medicine in the last two decades. Many
pain-related terms, once a major source of confusion, have received clear
definitions, helping efficient communication between researchers and
clinicians.

APPENDIX
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 A P P E N D I X

2
Common Abbreviations
in Pain Medicine

ABI Ankle-Brachial Index

Ach Acetylcholine
ACP Acupuncture
ACR American College of Rheumatology
ADL Activity of Daily Living
AIIMS All India Institute of Medical Sciences
ALARA As Low As Reasonably Achievable
ANS Autonomic Nervous System
AOSRA-PM Asian and Oceanic Society of Regional Anaesthesia and
Pain Medicine
AP Anteroposterior
APS Acute Pain Service
APTT Activated Partial Thromboplastin Test
ASO Arteriosclerosis Obliterans
AV Atrioventricular
BMD Bone Mineral Density
BPI Brief Pain Inventory
BTM Bone Tumor Markers
BTx A Botulinum Toxin Type A
CBT Cognitive-Behavioural Therapy
CCF Congestive Cardiac Failure
CLPM Conscious Laparoscopic Pain Mapping
CNS Central Nervous System
COX Cyclooxygenase
CP Cerebral Palsy
CPB Coeliac Plexus Blockade
CPP Chronic Pelvic Pain
CRPS Complex Regional Pain Syndrome

423
424 2. COMMON ABBREVIATIONS IN PAIN MEDICINE

CSA Continuous Spinal Analgesia

CSEA Combined Spinal Epidural Analgesia
CSF Cerebrospinal Fluid
CT Computed Tomography
DCS Dorsal Column Stimulation
DDS Descriptor Differential Scale
DEXA Dual-Energy X-ray Absorptiometry
DHE Dihydroergotamine
DPN Diabetic Poly neuropathy
DREZ Dorsal Root Entry Zone
DRG Dorsal Root Ganglion
DSA Digital Subtraction Angiography
EA Epidural Analgesia
EEG Electroencephalogram
EHL Extensor Hallucis Longus
EMF Electromagnetic Field
EMG Electromyograph
EMLA Eutectic Mixture of Local Anaesthetics
ESI Epidural Steroid Injection
ESR Erythrocyte Sedimentation Rate
FBSS Failed Back Surgery Syndrome
FMS Fibromyalgia Syndrome
FRAX Fracture Risk Assessment Tool
GABA Gamma Amino Butyric Acid
GI Gastrointestinal
GN Glossopharyngeal Neuralgia
GnRH Gonadotropin-Releasing Hormone
HNP Herniated Nucleus Pulposus
5-HT 5-Hydroxytryptamine
IASP International Association for Study of Pain
IBS Irritable Bowel Syndrome
IDET Intradiscal Electrothermal Coagulation
IM Intramuscular
INR International Normalized Ratio
IPG Implantable Pulse Generator
ISSP Indian Society of Study on Pain
ITB Intrathecal Baclofen Therapy
IV Intravenous
IVRA Intravenous Regional Analgesia
LA Local Anaesthetic
LANSS Leeds Assessment of Neuropathic Symptoms and Signs
LASER Light Amplification by Stimulated Emission of Radiations
LAT Lateral
LBA Low Back Ache

APPENDIX
 2. COMMON ABBREVIATIONS IN PAIN MEDICINE 425

LBP Low Back Pain

LTR Local Twitch Response
MAO Monoamine Oxidase
MAOIs Monoamine Oxidase Inhibitors
MMP Metalloproteinase
MMPI Minnesota Multiphasic Personality Inventory
MPQ McGill Pain Questionnaire
MPS Myofascial Pain Syndrome
MRI Magnetic Resonance Imaging
MSkP Musculoskeletal Pain
NAMS North American Menopause Society
NCPB Neurolytic Coeliac Plexus Blockade
NCV Nerve Conduction Velocity
NICE National Institute of Clinical Excellence
NMDA N-methyl-D-Aspartate
NO Nitric Oxide
NOF National Osteoporosis Foundation
NRS Numerical Rating Scale
NSAIDs Nonsteroidal Anti-inflammatory Drugs
OA Osteoarthritis
OT Operation Theatre
PA Posteroanterior
PABA Para-aminobenzoic Acid
PCA Patient Controlled Analgesia
PCEA Patient Controlled Epidural Analgesia
PCRA Patient Controlled Regional Analgesia
PDN Peripheral Diabetic Neuropathy
PEG Pneumoencephalogram
PET Positron Emission Tomography
PFPS Pelvic Floor Pain Syndrome
PFS Primary Fibromyalgia Syndrome
PG Prostaglandins
PHN Post Herpetic Neuralgia
PID Pelvic Inflammatory Disease
PIVD Prolapsed Intervertebral Disc
PMMA Polymethylmethacrylate
PNB Peripheral Nerve Block
PNS Peripheral Nervous System
PPI Present Pain Intensity
PRI Pain Rating Index
PRTG Percutaneous Radiofrequency Trigeminal Gangliolysis
PT Physical Therapy
PVD Peripheral Vascular Disease
PVR Peripheral Vascular Resistance

APPENDIX
426 2. COMMON ABBREVIATIONS IN PAIN MEDICINE

QOL Quality of Life

RA Rheumatoid Arthritis
RF Radiofrequency
RFK Racz-Finch Kit
RFTC Radiofrequency Thermocoagulation
RICE Rest, Ice pack application, Compression bandage,
and limb Elevation
ROM Range of Motion
RPZ Referred Pain Zone
RSD Reflex Sympathetic Dystrophy
SC Subcutaneous
SCS Spinal-cord Stimulation
SGB Stellate Ganglion Block
SI Sacroiliac
SIP Sympathetically Independent Pain
SLE Systemic Lupus Erythematosus
SLRT Straight Leg Raising Test
SMP Sympathetically Maintained Pain
SNRB Selective Nerve Root Block
SNS Sympathetic Nervous System
SP Substance P
SPECT Single Photon Emission Computed Tomography
SPG Sphenopalatine Ganglion
SPGB Sphenopalatine Ganglion Block
SSEP Somatosensory Evoked Potentials
SSRI Selective Serotonin Reuptake Inhibitors
SSS Spinal Segmental Sensitisation
TAO Thromboangiitis Obliterans
TCA Tricyclic Antidepressants
TENS Transcutaneous Electrical Nerve Stimulation
TeP Tender Point
TMJ Temporomandibular Joint
TN Trigeminal Neuralgia
TNF Tumour Necrosis Factor
TP Trigger Point
TTH Tension Type Headache
UAB University of Alabama, Birmingham
UMN Upper Motor Neuron
VAS Visual Analogue Scale
VIP Vasoactive Intestinal Peptide
WHO World Health Organization

APPENDIX
 A P P E N D I X

3
Equipment for
Pain Management:
Interventional and
Noninterventional
Techniques

PHOTOGRAPH 1 Fluoroscope for guided interventions (C-arm).

427
428 3. EQUIPMENT FOR PAIN MANAGEMENT

PHOTOGRAPH 5 Hydrocision discec-

tomy console/kit.

PHOTOGRAPH 2 Ultrasound machine

for US guided blocks (point of care).

PHOTOGRAPH 6 RF kit for ablation.

PHOTOGRAPH 3 Radio frequency le-

sion generator (RF/PRF) with RF needle.

PHOTOGRAPH 7 Racz's epidural cath-

eter for adhesiolysis.

PHOTOGRAPH 4 Ozone generator (for PHOTOGRAPH 8 Special curved epi-

ozone discectomy). dural needle for adhesiolysis.

APPENDIX
 3. EQUIPMENT FOR PAIN MANAGEMENT 429

PHOTOGRAPH 9 Programmable pump

with intraspinal catheter.

PHOTOGRAPH 12 Ambulatory infu-

sion pump.

PHOTOGRAPH 10 Nerve locator for re-

gional analgesia.

PHOTOGRAPH 13 Omnipaque non-

ionic contrast agent.

PHOTOGRAPH 11 Regional analgesia PHOTOGRAPH 14 Continuous plexus

needle. block set with catheter.

APPENDIX
430 3. EQUIPMENT FOR PAIN MANAGEMENT

PHOTOGRAPH 15 Long spinal needles.

PHOTOGRAPH 18 Epidural stimula-
tion (percutaneous and surgical paddle)
leads used for spinal cord stimulation.

PHOTOGRAPH 16 Spinal macro cath-

eter for continuous intrathecal anaesthesia.

PHOTOGRAPH 19 Programmer for spi-

nal cord stimulation and intrathecal pump
p­rogramming.

PHOTOGRAPH 17 Implantable Port

with intraspinal catheters.

APPENDIX
 3. EQUIPMENT FOR PAIN MANAGEMENT 431

PHOTOGRAPH 20 Implantable spinal cord pulse generator.

APPENDIX
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 A P P E N D I X

4
Professional Journals,
Magazines and
Newsletters on Pain

American Journal of Hospice & Palliative Medicine (http://ajh.

sagepub.com/) Peer-reviewed journal provides an essential academic
forum across the spectrum of palliation and hospice care from the
medical and pharmaceutical to the administrative and social.

Anaesthesia and Intensive Care (Journal) (http://www.aaic.net.

au/) This Australian journal presents original articles of scientific
and clinical interest in the specialties of anesthesia, intensive care, pain
therapy, and related disciplines.

Anesthesia and Analgesia (Journal) (http://www.anesthesia-

analgesia.org/) Published monthly by the International Anesthesia
Research Society (IARS), this journal includes peer-reviewed, original
clinical and research articles, providing practicing physicians,
researchers, and allied medical personnel in anesthesiology and related
fields with a wealth of information.

Anesthesiology (Journal) (http://www.anesthesiology.org/pt/re/

anes/home.htm)

433
434 4. PROFESSIONAL JOURNALS, MAGAZINES AND NEWSLETTERS ON PAIN

Annals of the Rheumatic Diseases (Journal) (http://ard.bmj

journals.com/) An international peer review journal covering all
aspects of rheumatology, which includes the spectrum of musculoskeletal
conditions, arthritic disease, and connective tissue disorders. ARD
publishes basic, clinical, and translational scientific research.

Applied Neurology (http://www.appneurology.com/) Peer

reviewed publication providing neurologists, neurosurgeons, and other
physicians with a combination of information and news that is clinically
relevant, practical, and useful.

Arthritis Care and Research (Journal) (http://www3.interscience.

wiley.com/cgi-bin/jhome/76509746) The official journal of the
Arthritis Health Professions Association. Link connects to "Arthritis and
Rheumatism (Arthritis Care & Research section)." Back issues ofArthritis
Care and Research : the Official Journal of the Arthritis Health Professions
Association are also included here.

BMC (BioMed Central) Complementary and Alternative Medicine

(http://www.biomedcentral.com/bmccomplementalternmed/) This
is an open access journal featuring peer-reviewed research articles
focusing on interventions and resources that complement or replace
conventional therapies, with a specific emphasis on research that
explores the biological mechanisms of action, as well as their efficacy,
safety, costs, patterns of use and/or implementation.

BMC (BioMed Central) Palliative Care (Journal) (http://www.

biomedcentral.com/bmcpalliatcare/) Open-access journal offers
original research articles in clinical, scientific, ethical and policy issues,
local and international, regarding all aspects of hospice and palliative
care.

CA: A Cancer Journal for Clinicians (http://onlinelibrary.

wiley.com/journal/10.3322/(ISSN)1542-4863) A peer-
reviewed journal of the American Cancer Society providing cancer
care professionals with up-to-date information on all aspects of cancer
diagnosis, treatment, and prevention.

APPENDIX
 4. PROFESSIONAL JOURNALS, MAGAZINES AND NEWSLETTERS ON PAIN 435

Canadian Journal of Anesthesia (http://www.cja-jca.org/) Peer

reviewed publication on the latest advances in anesthesia and Pain
Management.

Cancer Pain Release (http://www.whocancerpain.wisc.

edu) The publication of the World Health Organization global
communications program to improve cancer pain control, and palliative
and supportive care.

Clinical Journal of Pain (http://www.clinicalpain.com/) Explores

all aspects of pain and its effective treatment, bringing together
insights of leading anesthesiologists, surgeons, internists, neurologists,
orthopedists, psychiatrists and psychologists, clinical pharmacologists,
and physical and rehabilitation therapist.

Clinical Rheumatology (Journal) (http://www.springer.

com/sgw/cda/frontpage/) An international journal devoted to
publishing original clinical investigations and research in the general
field of rheumatology with focus on clinical aspects at postgraduate
level.

Community Oncology (Journal) (http://www.communityoncology.

net/) Publishes articles related to clinical research in the community
setting, the translation of research outcomes into delivery of high-quality
care, and practice management issues.

Continuing Education in Anaesthesia Critical Care and Pain

(http://ceaccp.oxfordjournals.org/subscriptions/) A bimonthly
publication containing structured, authoritative articles covering core
knowledge, current controversies, and future trends. Basic science is also
included, but with a clinical emphasis.

European Journal of Pain (http://www.europeanjournal

pain.com) International journal that serves as a global forum on all
major aspects of pain and its management. The journal differs from
existing pain journals in its clinical and educational emphasis.

APPENDIX
436 4. PROFESSIONAL JOURNALS, MAGAZINES AND NEWSLETTERS ON PAIN

European Journal of Palliative Care (EJPC) (http://www.ejpc.eu.

com/aboutEJPC.asp) This is a multidisciplinary journal of the
EAPC published six times a year both in English and French. The journal
concentrates on reviews and current awareness of palliative care on the
European scene.

Headache Currents (Journal) (http://www.blackwellpublishing.

com/journal.asp?ref=1743-5005&site=1) A publication from
the American Headache Society, the International Headache Society, and
Blackwell Publishing, featuring state-of-the-art scientific reviews in the
field of migraine science.

Headache: The Journal of Head and Face Pain (http://www.black

wellpublishing.com/journal.asp?ref=0017-8748&site=1) Publishes
original articles on all aspects of head and face pain, including: clinical and
basic research, diagnosis and management, epidemiology, genetics, and
pathophysiology of primary and secondary headaches, cranial neuralgias,
and pains referred to the head and face.

Journal of Cancer Pain & Symptom Palliation (http://www.info

rmaworld.com/smpp/title∼content=t792304017∼db=all) This
journal addresses nontraditional methods of pain and symptom relief,
including: physical modalities and complementary and alternative
medicine; interventional techniques in treatment approaches; and
present and future analgesic agents.

Journal of Clinical Oncology (JCO) (http://www.jco.org/) JCO

publishes original research and reviews in breast cancer, gastrointestinal
cancer, hematologic malignancies, molecular oncology, lung cancer,
genitourinary cancer, head and neck cancer, pediatric oncology,
neurooncology, supportive care and quality of life issues, prevention,
and phase I and clinical pharmacology.

Journal of Musculoskeletal Pain (http://www.informaworld.com

/smpp/title∼content=t792304019∼db=all) For 10 years, this peer-
reviewed journal has presented research findings, case reports, literature and
book reviews, and professional announcements on fibromyalgia, myofascial
pain, and other types of chronic soft-tissue pain.

APPENDIX
 4. PROFESSIONAL JOURNALS, MAGAZINES AND NEWSLETTERS ON PAIN 437

Journal of Neuropathic Pain & Symptom Palliation (http://www.

informaworld.com/smpp/title∼content=t792304021∼db=all) This
publication examines current clinical research on treatment options,
diagnosis, and assessment methods for various pain syndromes and
associated symptoms that impair the quality of life for patients with
neurologic conditions.

Journal of Opioid Management (http://www.opioidmanagement.

com/) Designed to meet the challenge faced by pain management
professionals as they prescribe opioids. This publication is intended to
fill what's been called "a dangerous gap" in medical literature at a time
when the Federal spotlight has been switched on to the rising problem of
abuse and addiction tied to these prescription painkillers.

Journal of Oncology Practice (JOP) (http://www.jopasco.org/) The

mission of this journal is to provide oncologists and other oncology
professionals with information, news, and tools to enhance practice
efficiency and promote a high standard for quality of patient care.

Journal of Orofacial Pain (http://www.quintpub.com/journals/jop/

gp.php?journal_name=JOP&name_abbr=JOP) This journal
combines the work of dental and medical professionals involved in
treating temporomandibular disorders. It discusses prevailing research,
diagnostic techniques, and treatment therapies for orofacial pain,
headache, mandibular dysfunction, and occlusion. Pharmacology,
physical therapy, surgery, and other pain management methods are
covered.

Journal of Pain (http://www.ampainsoc.org/pub/journal/) This

is the official journal of the American Pain Society, providing peer-
reviewed articles focusing on issues related to clinical and basic research,
patient care, education, and health policy.

Journal of Pain & Palliative Care Pharmacotherapy (http://www.

informaworld.com/smpp/title∼content=t792304028∼db=all) This
is an interdisciplinary, peer-reviewed, quarterly publication that
addresses advances in acute, chronic, and end-of-life symptom
management.

APPENDIX
438 4. PROFESSIONAL JOURNALS, MAGAZINES AND NEWSLETTERS ON PAIN

Journal of Pain & Symptom Management (http://journals.elsevier

health.com/periodicals/jps) Provides professionals with the results
of important new research and clinical information related to pain
management and palliative care.

Journal of Palliative Medicine (http://www.liebertpub.com/publi

cation.aspx?pub_id=41) This bimonthly interdisciplinary journal
reports on the clinical, educational, legal, and ethical aspects of care for
seriously ill and dying patients.

Lupus (Journal) (http://lup.sagepub.com) International journal

devoted exclusively to lupus (and related disease) research. Includes
new clinical and laboratory-based studies from leading specialists in all
lupus-related disciplines.

Molecular Pain (Journal) (http://www.molecularpain.com/) An

open access, peer-reviewed, online journal of research that addresses
physiological and pathological pain at the cellular, subcellular, and
molecular levels. These studies integrate pain research with molecular
biology, genomics, proteomics, modern electrophysiology, and neurobiology.

Oncology News International (http://oni/cancernetwork.com

/home) This publication provides oncologists, oncology nurses, and
other cancer specialists with practical information about important news
and developments in oncology.

Oncology Nursing Forum (ONF) (http://www.ons.org/publi

cations/ONF) ONF publishes manuscripts that focus on nursing
achievements in the field of oncology including, but not limited
to: clinical advances, research findings, educational developments,
administrative issues, and role and theory development.

Pain (Journal) (http://www.sciencedirect.com/science/journal/

03043959) This is the official publication of the International
Association for the Study of Pain and publishes original research on the
nature, mechanisms and treatment of pain.

APPENDIX
 4. PROFESSIONAL JOURNALS, MAGAZINES AND NEWSLETTERS ON PAIN 439

Pain Clinical Updates (http://www.iasp-pain.org/PCUOpen.

html) This official and brief publication of the IASP appears 4
times a year. Each issue covers one or two topics of wide medical
interest for practitioners in a number of specialties, patients, and their
families.

Pain Digest (http://www.springer.com/sgw/cda/frontpage/

0,11855,1-10093-70-1104521-0,00.html) A bimonthly
international multidisciplinary journal on pain providing up-to-date
information of research, evaluation methods, and techniques of pain
management [German site].

Pain Management Nursing (Journal) (http://www.medscape.com

/viewpublication/947_index) A peer-reviewed journal focusing on
pain management as it applies to nursing. Additional features include
practice guidelines and pharmacology updates.

Pain Medicine (Journal) (http://www.blackwellpublishing.com

/journal.asp?ref=1526-2375&site=1) This is the official journal
of the American Academy of Pain Medicine, an organization devoted to
the advancement of pain management, education, and research, and also
of the Faculty of Pain Medicine of the Australia New Zealand College of
Anesthetists.

Pain Medicine News (Newsletter) (http://www.painmedicinenews.

com/index.asp) Published 6 times per year, plus special supplements,
Pain Medicine News is a free offering designed to meet the needs of pain
medicine clinicians, including: primary care physicians, neurologists,
orthopedic surgeons, pain management specialists, rheumatologists,
oncologists, and more.

Pain Physician (Journal) (http://www.painphysicianjournal.

com/) This is a quarterly peer-reviewed, multi-disciplinary journal
directed to an audience of interventional pain physicians, clinicians,
and basic scientists with an interest in pain medicine. It is the
official publication of the American Society of Interventional Pain
Physicians.

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Pain Practice (Journal) (http://www.blackwellpublishing.com/

journal.asp?ref=1530-7085&site=1) This is the official
journal of the World Institute of Pain. It publishes international
multidisciplinary articles on pain that provide readers with up-to-date
knowledge of the research, evaluation methods, and techniques of pain
management.

Pain Research & Management (Journal) (http://www.pulsus.com

/Pain/home2.htm) The official journal of the Canadian Pain Society;
peer reviewed.

Palliative Medicine (Journal) (http://www.palliativemedjournal.

com/) This is an international interdisciplinary journal dedicated
to improving knowledge and clinical practice in the palliative care of
patients with far advanced disease.

Practical Pain Management (Magazine) (http://www.ppmjournal.

com/default.asp) As the name implies, this journal has the
practitioner in mind, providing tutorial articles and editorial
commentary designed to help diagnose and treat various aspects of pain.
Subscriptions are free to qualifying healthcare professionals, or issues
can be purchased at a reasonable price.

Psycho-Oncology (Journal) (http://www3.interscience.wiley.

com/cgi-bin/jhome/5807) This journal is concerned with the
psychological, social, behavioral, and ethical aspects of cancer.

Regional Anesthesia and Pain Medicine (Journal) (http://www.

rapm.org/) Publishes scientific information for physicians and
scientists engaged in regional anesthesia for surgery, obstetrics, and pain
medicine.

Reviews in Analgesia (Journal) (http://www.cognizantcom

munication.com/) Reviews in Analgesia (formerly Analgesia) is an
international journal that publishes in English original reviews by
experts on topics related to the basic mechanisms and therapeutics of
pain relief. See journal index at website for listing.

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Spine (Journal) (http://www.spinejournal.com/) This

international, peer-reviewed, bi-weekly periodical is a leading
subspecialty journal on the treatment of spinal conditions.

Techniques in Regional Anesthesia and Pain Management

(Journal) (http://www.techreganesth.org/) A quarterly journal
with the illustrative aspects of a procedure-oriented atlas. Exact
techniques are well-illustrated, giving precise drug dosages and helpful
clinical information. In addition, common complications of regional
anesthesia and pain management procedures and their appropriate
treatments are described.

The Journal of Headache and Pain (http://www.springer.com/

sgw/cda/frontpage/0,,5-10054-70-1151225-0,00.html) Official
Journal of the Italian Society for the Study of Headaches, which
publishes original papers, reviews, rapid communications, brief reports,
and letters pertinent to the various aspects of headache and pain.

The Journal of Pain (http://www.jpain.org/) Journal of the

American Pain Society publishes original articles related to all aspects
of pain, including clinical and basic research, patient care, education,
and health policy. In addition, the journal features invited critical
reviews, including meta analyses of drugs for pain management,
invited commentaries on reviews, and exceptional case studies.

The Oncologist (Journal) (http://theoncologist.alphamedpress

.org/) This international peer-reviewed journal publishes original
papers, reviews, and commentaries addressing the multimodality
diagnosis, treatment, and quality of life of the cancer patient.

The Pain Practitioner (Magazine) (http://www.aapainmanage.

org/literature/PainPrac.php) This quarterly publication is the
official magazine of the American Academy of Pain Management. It is
provided free with Academy membership, while others may subscribe
for a nominal fee. Each issue contains useful information on current
pain topics of importance from an interdisciplinary perspective, and the
publication is sufficiently non-technical to be of interest to anyone in a
healthcare setting.

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Topics in Pain Management (Journal) (http://www.lww.com/

product/?0882-5646) This publication reports news on a wide
range of pain management topics gleaned from a survey of dozens of
journal articles. Individual articles are not accessible via this website.

GENERAL PAIN INTEREST SITES

American Academy of Neurology: Chronic Pain (http://www.aan.

com/professionals/) Provides resources for medical specialists
worldwide who are committed to improving the care of patients with
neurological diseases.

American Academy of Orofacial Pain (http://www.aaop.org) An

organization of health care professionals dedicated to alleviating
pain and suffering through the promotion of excellence in education,
research and patient care in the field of orofacial pain and associated
disorders.

American Academy of Orthopaedic Surgeons (AAOS) (http://

www.aaos.org) Founded at Northwestern University as a not-
for-profit organization in 1933, the AAOS provides education and
practice management services for orthopaedic surgeons and allied
health professionals. The Academy also serves as an advocate for
improved patient care and informs the public about the science of
orthopaedics.

American Academy of Pain Management (AAPM) (http://www.

aapainmanage.org/) This is the largest multidisciplinary membership
organization in the United States for pain practitioners. It is an inclusive,
interdisciplinary organization and serves the needs of clinicians who treat
people with pain through education, setting standards of care, and advocacy.

American Academy of Pain Medicine (http://www.painmed.

org/) The Academy is the medical specialty society representing
physicians practicing in the field of Pain Medicine. As a medical specialty
society, the organization is involved in education, training, advocacy, and
research in the specialty of Pain Medicine.

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American Academy of Physical Medicine and Rehabilitation

(AAPM&R) (http://www.aapmr.org/) This is the American
medical society representing more than 7,000 physicians (physiatrists)
specializing in the field of physical medicine and rehabilitation.

American Chiropractic Association (ACA) (http://www.acatoday.

org/) The purpose of the ACA is to provide leadership in health care
and a positive vision for the chiropractic profession and its natural
approach to health and wellness.

American College of Rheumatology (ACR) (http://www.rheuma

tology.org) ACR is the professional organization of rheumatologists
and associated health professionals who share a dedication to healing,
preventing disability, and curing the more than 100 types of arthritis
and related disabling and sometimes fatal disorders of the joints,
muscles, and bones.

American Massage Therapy Association (AMTA) (http://www.

amtamassage.org/) This organization represents more than
53,000 massage therapists in 27 countries. AMTA works to establish
massage therapy as integral to the maintenance of good health and
complementary to other therapeutic processes.

American Neuromodulation Society (http://www.neuromodulation.

org/) Dedicated to advancing the field of Neuromodulation (implanted
devises such as “stimulators” and “pumps”) through clinical research,
education, and print material within the United States.

American Pain Society (APS) (http://www.ampainsoc.org/) The

APS is a multidisciplinary organization of basic and clinical scientists,
practicing clinicians, policy analysts, and others. The organization's
mission is to advance pain-related research, education, treatment and
professional practice.

American Physical Therapy Association (APTA) (http://www.

apta.org/) This is a national professional organization representing
more than 66,000 members. Its goal is to foster advancements in physical
therapy practice, research, and education.

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American Society of Anesthesiologists (ASA) (http://www.asahq.

org) Since its founding in 1905, the Society has been an important
voice in American Medicine and the foremost advocate for all patients
who require anesthesia or relief from pain This site provides educational
resources and clinical information for patients and professionals.

American Society of Interventional Pain Physicians (http://www

.asipp.org/) The society serves more than 3,500 members nationwide
with advocacy efforts, educational programs, publications, and
communications.

American Society of Pain Educators (ASPE) (http://www.pain

educators.org/) ASPE is a nonprofit professional organization
dedicated to improving pain management through the education and
training of healthcare professionals to become Certified Pain Educators
(CPEs). As the only organization focusing on pain-educator training,
the Society teaches healthcare professionals to serve as resources
in educating their clinical peers, as well as patients, families, and
caregivers on ways to relieve pain by the safest means possible. For more
information about the CPE Examination, visit the ASPE Web site.

American Society of Pain Management Nursing (http://www.

aspmn.org) This site offers a comprehensive bibliography in addition
to a list of new features that are under development including an area
to acknowledge member achievements, a place to share policies, a list of
institutions offering preceptor sites, chapter educational offerings and a
State of the Science section on current topics.

American Society of Regional Anesthesia & Pain Medicine

(ASRA) (http://www.asra.com/) ASRA is the largest subspecialty
society in anesthesiology. There are approximately 7,400 members,
including physicians and scientists and a rich international distribution.
Member information, web-based CME, and fellowship opportunities are
some of the highlights.

Anterior Knee Pain Project (http://www.ucalgary.ca/∼kneepain/) A

research project to develop clinical practice guidelines sponsored by the
University of Calgary Sport Medicine Centre.

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Association of Rehabilitation Nurses (http://www.rehabnurse.

org) This site promotes and advances professional rehabilitation nursing
practice through education, advocacy, collaboration, and research to
enhance the quality of life for those affected by disability and chronic illness.

Chronic Pain Anonymous (CPA) (http://www.chronicpainano

nymous.org/) Founded in 2004 and following a traditional 12-Step
recovery model, CPA is a nonprofit fellowship of men and women who
share their experience, strength, and hope with each other so that they
may solve their common problem and help others recover from the
disabling effects of chronic pain and chronic illness.

City of Hope Pain/Palliative Care Resource Center (http://

prc.coh.org/) The purpose of the COHPPRC is to serve as a
clearinghouse for disseminating information and resources to assist
others in improving the quality of pain management and end of life
care. Established in 1995, this site is a central source for a variety
of materials, including: pain assessment tools, patient education
materials, quality assurance materials, end of life resources, research
instruments, and other resources.

Complementary/Integrative Medicine (CIM) (http://www.mdand

erson.org/topics/complementary) Linked through the MD Anderson
Cancer Center site, this website contains detailed evidence-based reviews
of complementary or alternative cancer therapies, as well as links to
other sources. The scientific reviews help health care professionals guide
patients using complementary therapies alongside conventional treatment.

Delhi Pain Management Centre (www.pain-india.com) Official

website of Delhi Pain Management Centre, a state of the art centre for
chronic pain management in New Delhi, India. This website offers
diverse information for patients suffering from chronic pain.

Emerging Solutions in Pain (ESP) (http://www.emergingsoluti

onsinpain.com/) This site is a comprehensive initiative designed to
meet the needs of physicians, pharmacists, nurses, and other health care
professionals who are actively involved in pain management, and in
working with patients who are prescribed opioids.

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For Grace – Empowering Women in Pain (http://www.forgrace.

org/women/in/pain_home/) For Grace is a nonprofit organization
devoted to ensuring the ethical and equal treatment of all women in pain,
by empowering women to become better advocates for their pain care,
informing heath care professionals about the gender disparity in pain
treatment, and educating public policy makers.

In The Face of Pain (http://www.inthefaceofpain.com/) Industry-

sponsored, but non-commercial, site offers an advocacy toolkit and other
materials to support the rights and better treatment for persons with pain.
The site also features a Pain Advocacy Community e-Newsletter. Purdue
is a Pain Treatment Topics educational supporter.

Institute for Chronic Pain (ICP) (http://www.institutefor

chronicpain.org/) The mission of ICP is to change the culture of
how chronic pain is treated by promoting the theory and practice of
chronic pain rehabilitation. The organization’s staff and fellows are
specialists in chronic pain management as well as healthcare policy and
management.

Institute for the Study and Treatment of Pain (ISTOP) (http:

//www.istop.org/) An international non-profit organization based in
Canada and dedicated to the understanding and treatment of soft tissue
pain through the use of Intramuscular Stimulation, which is a form of
acupuncture.

Masterdocs.org (Taylor Micro Technology [TMT]) (http://master

docs.org) Nonprofit pain-focused website provides a number of free
questionnaires for pain conditions that can be answered by patients
and a report is automatically generated containing the responses
together with a differential diagnosis for physician review. The site also
has medical summaries of painful conditions and regularly updated
news.

MayoClinic.com (http://www.mayoclinic.com/health/pain/
PN99999) The Pain Management Center offers diverse information
and resources for pain patients.

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MD Anderson Cancer Center (http://www.mdanderson.org/topics/

paincontrol/) Pain management resource and treatment center at
the University of Texas; with information for physicians and patients
regarding palliative care, postoperative pain, pain management, and more.

Memorial Sloan-Kettering Pain Control Program (http://www.

mskcc.org/mskcc/html/474.cfm) The pain section of the Memorial
Sloan-Kettering Cancer Center website presents the current information
on the Institute's approaches to pain management.

MGH Cares About Pain Relief (http://www.massgeneral.org/

painrelief/) The mission of MGH Cares About Pain Relief is to
support all Massachusetts General Hospital (MGH) educational, clinical,
and research programs related to pain. The website provides educational
programs and resources for clinical educators, practicing clinicians in all
disciplines, administrators, and patients and their families.

Michigan Department of Community Health (MDCH) – Pain

& Symptom Management (http://www.michigan.gov/painman
agement) This website was developed to increase the general public's
and health professional's awareness of pain and symptom management.
It provides information via professional papers, articles, related statutes,
and numerous links to organizations with expertise in the area of pain
and symptom management.

National Center for Complementary and Alternative Medicine

(NCCAM) (http://www.nccam.nih.gov) NCCAM is dedicated to
exploring complementary and alternative healing practices in the context
of rigorous science, training complementary and alternative medicine
(CAM) researchers, and disseminating authoritative information to the
public and professionals.

National Institute of Arthritis and Musculoskeletal and Skin

Diseases (NIAMS) (http://www.niams.nih.gov) The mission of this
U.S. government agency is to support research into the causes, treatment,
and prevention of arthritis and musculoskeletal and skin diseases, the
training of basic and clinical scientists to carry out this research, and the
dissemination of information on research progress in these diseases.

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National Institute of Neurological Disorders and Stroke

(NINDS) (http://www.ninds.nih.gov) This agency of the
U.S. National Institutes of Health conducts, fosters, coordinates, and
guides research on the causes, prevention, diagnosis, and treatment of
neurological disorders and stroke, and supports basic research in related
scientific areas.

National Institutes of Health (NIH) Pain Consortium (http:

//painconsortium.nih.gov/) The NIH Pain Consortium was
established to enhance pain research and promote collaboration
among researchers engaged in activities addressing pain. This website
provides free access to many vital resources of importance in the pain
management field.

National Pain Foundation (http://www.nationalpainfoundation

.org/) An on-line educational and support community for persons in
pain, their families and physicians. A source for treatment options and
pain information that is peer reviewed by leading pain specialists.

North American Spine Society (http://www.spine.org) This

organization addresses the clinical problems faced by spine patients and
their physicians.

Opioids911-Safety: Help for Safely Using Opioid Pain Relievers

(http://Opioids911.org) Is an independent, noncommercial,
Internet-based educational activity from Pain Treatment Topics for patients
and their family caregivers focusing on the proper and safe use of opioid
pain relievers. The mission is to provide an understanding of opioid
analgesics and their various risks, and to suggest specific actions for
preventing opioid-related problems, including: misuse, abuse, addiction,
diversion, adverse reactions, overmedication, and life-threatening
overdose. Instruction is provided on recognizing opioid problems if they
do occur and on being prepared for what to do during an emergency.

Pain and Policy Studies Group (Univ. of Wisconsin) (http://www.

painpolicy.wisc.edu/) A World Health Organization Collaborating
Center for Policy and Communications in Cancer Care at the
University of Wisconsin; facilitates public access to information about
pain relief and public policy.

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Pain Connection (http://pain-connection.org/) This non-profit,

patient-centered organization aims to improve the quality of life of
those suffering from chronic pain, decrease their sense of isolation and
alienation, increase control of their condition and treatment, and help
them to maintain their independence.

Pain and the Law (http://www.painandthelaw.org/) This site

was been developed by the Center for Health Law Studies at Saint Louis
University and the American Society of Law, Medicine and Ethics under
a grant from The Mayday Fund.

Pain Relief Connection (Newsletter) (http://www.massgeneral.

org/painrelief/Newsletter/mghpain_connection.htm) Pain Relief
Connection is a very timely and informative newsletter with extensive
links published monthly by MGH (Massachusetts General Hospital)
Cares About Pain Relief. Current and past issues are archived as
PDF files, and future issues are added at the time of publication.
Individuals may register for a free e-mail subscription at the site.

Pain Relief Network (PRN) (http://www.painreliefnetwork.

org/) PRN is a public network of patients and their family members,
physicians, attorneys, and activists who are working toward affording all
people in pain dignity and compassion in the treatment of their medical
conditions.

Pain.com (http://www.pain.com/) Extensive, industry-sponsored

site providing free access to educational resources for professionals and
patients, including: web-based CME, articles, and pain journals.

painACTION.com (http://www.painaction.com/) This website

has been designed to help patients manage their chronic pain. It provides
free access to pain journals, responses to common questions, and
interactive support and educational tools. From the same organization
that produces PainEDU.

PAINClinician.com (http://painclinician.com) PAINClinician.

com™ is an independently-funded forum committed to improving clinician
access to high quality pain education resources. Sponsorship of the site is
vague and free registration is required to access some content.

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PainEDU.org (http://www.painedu.org/) PainEDU.org is

developed by Inflexxion, Inc. through an unrestricted educational grant
from Endo Pharmaceuticals. It is an educational website for clinicians,
teaching about pain assessment and management. The information
included at this site focuses on clinician interests, best practices in the field,
and a desire to deliver health education in an interactive manner.

PainKnowledge.org (NIPC) (http://painknowledge.org) This

site is part of the National Initiative on Pain Control (NIPC®), which
offers innovative, interactive, and practical activities providing guidance
in pain assessment, and offer proven strategies for pain management, all
with the aim of improving patient outcomes.

Partners Against Pain (http://www.partnersagainstpain.

com/) Industry-sponsored, but non-commercial, site offers a wide
variety of evidence-based resources for healthcare professionals and
patients. Purdue is a Pain Treatment Topics educational supporter.

Spine-Health (http://www.spine-health.com/) Provides

thousands of physician written and reviewed articles for patients on
back pain, neck pain, and related disorders; videos; discussion forums;
an online contact service; and more.

SpineUniverse (http://www.spineuniverse.com/) This primarily

consumer-oriented site provides medical information reviewed by
leading orthopedic and neurosurgeons from around the world focusing
on painful conditions of the back and neck.

Tame the Pain (http://www.medtronic.com/neuro/ttp/) An

advocacy and awareness campaign funded by Medtronic, although generally
noncommercial, and designed to improve chronic pain management by
providing information primarily on non-pharmacologic therapies.

The Legal Side of Pain (http://www.legalsideofpain.com/) This

organization, a division of the J. Bolen Group LLC, specializes in the
education of health care providers and office staff, with an emphasis on
the development and implementation of compliance programs related
to the use of controlled substances to treat pain, and the office-based
treatment of opioid addiction.

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The Mayday Pain Project (http://www.painandhealth.org) This

site includes information, research, and resources on a variety of subjects
relating to pain; however, many links are to sources of information via the
mass media or other resources that may or may not be evidence-based.

The Oxford Pain Internet Site (http://www.medicine.ox.ac.uk

/bandolier/booth/painpag/index2.html) Draws from the most up-
to-date evidence-based resources available via Pubmed and through the
Cochrane Library to evaluate and discuss pain management topics.

The Pain Community (TPC) (http://paincommunity.org) This

nonprofit, organization founded in 2013 provides support to patients
through an online community where education and advocacy for people
living with pain are promoted. TPC also works collaboratively with
other organizations to advocate for optimal pain care for all people with
pain.

U.S. Pain Foundation (http://uspainfoundation.org/) Founded

by a fellow pain sufferer, U.S. Pain Foundation support groups and
other hands-on programs help build a caring community through
educational resources and valuable information about local, regional,
and national events. A Pain Treatment Topics affiliate organization.

WebMD Pain Management Health Center (http://www.webmd.

com/diseases_and_conditions/pain.htm) Consumer-oriented
site offers current information on chronic pain treatments, as well as
natural ways to manage chronic pain. One feature is an online support
group.

PAIN TREATMENT TOPIC SUPPORTERS

American Academy of Pain Management (http://www.aapainma

nage.org/) The American Academy of Pain Management (AAPM)
is the largest multidisciplinary membership organization in the United
States for pain practitioners. With more than 6,000 members, the
nonprofit Academy provides credentialing of healthcare providers in
pain management, accreditation of facilities, networking opportunities,
continuing education, and an annual clinical meeting.

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American Association for the Treatment of Opioid Dependence

(http://www.aatod.org) The American Association for the Treatment
of Opioid Dependence (AATOD) is a nonprofit organization for healthcare
professionals founded in 1984 to enhance the quality of patient care in
addiction treatment programs by promoting the growth and development
of comprehensive medication-assisted therapy services throughout the
United States and internationally.

American Chronic Pain Association (http://www.theacpa.

org) Founded in 1980, this organization’s mission is to facilitate peer
support and education for individuals with chronic pain and their
families so that these individuals may live more fully despite their pain
and to raise awareness among the health care community, policy makers,
and the public at large about issues of living with chronic pain. The
ACPA website features a variety of unique educational materials and
other resources for patients, their families, and healthcare professionals.

American College of Apothecaries (http://www.americancoll

egeofapothecaries.com/) The American College of Apothecaries
(ACA) focuses on the dissemination of knowledge, research data, and
recent developments in professional pharmacy practice for the benefit
of pharmacists, pharmacy students, and the public. Within the ACA,
a specialty practice group for pharmacists interested in strengthening
their practices in hospice care and pain management was established in
January 2006.

American Society of Pain Educators (http://www.paineducators.

org/) The American Society of Pain Educators (ASPE) is a nonprofit
professional organization dedicated to improving pain management
through the education and training of healthcare professionals to
become Certified Pain Educators (CPEs). As the only organization
focusing on pain-educator training, the Society teaches healthcare
professionals to serve as resources in educating their clinical peers, as
well as patients, families, and caregivers on ways to relieve pain by
the safest means possible.

EUROPAD — European Opiate Addiction Treatment

Association (http://www.europad.org/) This organization was
founded in Geneva, Switzerland in 1994. With approximately 800

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members, it is a nonprofit organization with a mission to improve the

lives of opioid drug misusers and their families, and to reduce the
impact of illicit drug use on society as a whole. The interface of pain and
addiction is a special interest.

National Fibromyalgia & Chronic Pain Association (http://fmcp

Aware.org/) The National Fibromyalgia & Chronic Pain Association
(NfmCPA) is a not for profit organization working to support people
who have chronic pain illnesses and their families and friends by
contributing to caring, professional, and community relationships.
Through continuing education, networking with support groups/
advocates, and affiliations with professional organizations, the members
of the NfmCPA have a place to be informed, get involved, and recognize
achievements in helping persons with pain.

National Fibromyalgia Association (http://www.fmaware.

org/) A nonprofit organization founded in 1997 and dedicated
to informing and educating communities, patients, and healthcare
professionals about fibromyalgia through special events, a magazine and
newsletter, and other awareness programs.
Professional Resource Center (http://www.FibromyalgiaHCP.org) This
was created by the NFA specifically for healthcare professionals (HCPs) to
help them find information on new fibromyalgia research, NIH and FDA
updates, advocacy issue, CME/CE resources, NFA programs, and other
resources.

Reflex Sympathetic Dystrophy Syndrome Association (http://

www.rsds.org/) Founded in 1984, the Reflex Sympathetic Dystrophy
Syndrome Association (RSDSA) promotes greater public and professional
awareness and earlier recognition of Complex Regional Pain Syndrome
(CRPS, formerly RSD). The organization educates those afflicted with the
syndrome, their families, friends, insurance and healthcare providers on
the disabling pain it causes.

The Foundation For Peripheral Neuropathy (http://foundation

forpn.org) Established in 2007, this nonprofit organization is
committed to fostering collaboration among gifted and dedicated
neuroscientists and physicians. Through its various publications,
meetings, conferences, and collaborative research efforts, the

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organization serves as a catalyst for advancing therapeutic developments

and accelerating a cure for painful neuropathies. Additionally, the
Foundation raises awareness of peripheral neuropathy through outreach
programs to patients, their families, and healthcare professionals.

TNA – The Facial Pain Association (http://endthepain.org) This

nonprofit organization was founded in 1990, and the mission of the
TNA-The Facial Pain Association is to serve as an advocate for patients
living with trigeminal neuralgia (TN) and related facial pain conditions by
providing information, encouraging research, and offering support.

U.S. Pain Foundation (http://uspainfoundation.org/) Founded

by a fellow pain sufferer, the U.S. Pain Foundation believes strongly in
the importance of connecting those who share the feelings, frustrations,
and daily challenges of living with pain. The organization’s support
groups and other hands-on programs help build a caring community
through educational resources and valuable information about local,
regional, and national events.

SPECIALITY PAIN WEBSITES

Academy of Psychosomatic Medicine (APM) (http://www.apm.

org/) The APM has as its central focus patients with comorbid medical
and psychiatric illness and the interaction between them. This focus
entails clinical work, research, and teaching, as well as leadership in the
provision of medical-surgical psychiatry services.

Aftershingles.com (http://www.aftershingles.com) Site with

extensive information focusing on shingles and post-herpetic neuralgia.

American Behcet's Disease Association (http://www.behcets.

com) As the name implies, this nonprofit organization focuses on
awareness and education regarding Behcet's Disease, an autoimmune
condition that typically manifests as painful vasculitis.

American Academy of Orofacial Pain (AAOP) (http://www.aaop.

org/) Organization of professionals whose aim is to promote education
and awareness of orofacial pain and associated disorders.

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American Holistic Nurses Association (AHNA) (http://www.ahna.

org/) This organization serves as a bridge between traditional medical
paradigms and universal complementary and alternative healing
practices. AHNA supports the concepts of holism; a state of harmony
among body, mind, emotions, and spirit within an ever-changing
environment.

American Psychosomatic Society (http://www.psychosomatic.

org/) This organization, founded in 1942, is a worldwide community
of scholars and clinicians dedicated to the scientific understanding of the
interaction of mind, brain, body, and social context in promoting health
and contributing to the pathogenesis, course, and treatment of disease.

Foundation for Peripheral Neuropathy (http://foundationforpn.

org/) This nonprofit organization works to educate the public and
healthcare professionals, provide state-of-the-art treatment for patients
with peripheral neuropathy, and serves as a catalyst for advancing
innovative therapeutic developments and accelerating a cure for painful
neuropathies.

Geriatric Pain (http://www.geriatricpain.org/) This site is a

one-stop resource, sharing free best-practice tools and resources that
support recommendations for good pain assessment and management
in older adults, including implementation of quality improvement
processes focused on pain management. It is intended for nurses and
administrators working in long-term care environments.

Hormones and Pain Care Information Network (http://www.

hormonesandpaincare.com/) This noncommercial site for
healthcare providers organized by Forest Tennant, MD, DrPH, focuses
on how chronic pain can be a severe biologic stressor that affects the
hypothalamus–pituitary–adrenal–gonadal axis. Resources describe
neurosteroid therapies that may be effective adjuncts for current pain
treatment regimens.

National Organization for Rare Disorders (NORD) (http://www.

rarediseases.org/) A unique federation of voluntary health
organizations dedicated to helping people with rare "orphan" diseases
(affecting fewer than 200,000 people) and assisting the organizations

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that serve them. NORD is committed to the identification, treatment,

and cure of rare disorders through programs of education, advocacy,
research, and service.

National Vulvodynia Association (NVA) (http://www.nva.

org) Nonprofit organization organized around helping women affected
by vulvar pain disorders. Site contains: teaching CD, newsletter, and other
services.

Reflex Sympathetic Dystrophy Syndrome Association (http://

www.rsds.org/) Founded in 1984, the Reflex Sympathetic Dystrophy
Syndrome Association (RSDSA) promotes greater public and
professional awareness and earlier recognition of Complex Regional
Pain Syndrome (CRPS, formerly RSD). The organization educates
those afflicted with the syndrome, their families, friends, insurance and
healthcare providers on the disabling pain it causes.

Spondylitis Association of America (http://www.spondylitis.

org/) A nonprofit organization and the largest resource for people
affected by spondylitis, advancing education, research and treatment for
ankylosing spondylitis (AS) and related painful diseases.

The Neuropathy Association (http://www.neuropathy.org) This

organization was founded by patients committed to raising awareness of
peripheral neuropathy and supporting the research to find its cure.

The Vulvar Pain Foundation (http://www.vulvarpainfoundation.

org/) Nonprofit organization supporting women with vulvar pain.

TMJ Association, Ltd (http://www.tmj.org/) Association

fostering research and education on TMJ disorders.

TNA-The Facial Pain Association (http://endthepain.org) This

nonprofit organization was founded in 1990, and the mission of
TNA-The Facial Pain Association is to serve as an advocate for
patients living with trigeminal neuralgia (TN) and related facial pain
conditions by providing information, encouraging research, and
offering support.

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VZV Research Foundation (VZRF) (http://www.vzvfoundation.

org/) This nonprofit organization is dedicated to the fight against
the varicella-zoster virus (VZV) and related painful infections
through research and education. It sponsors scientific conferences
and develops educational materials for scientists, physicians, and the
general public.

INTERNATIONAL PAIN ORGANIZATIONS

Action for ME (http://www.afme.org.uk/) UK organization

founded by people with Myalgic Encephalomyelitis/Encephalopathy
(ME) and dedicated to improving their lives.

Action on Pain (http://www.action-on-pain.co.uk/) A British

national charity dedicated to providing support and advice for people
who are affected by chronic pain.

Australian & New Zealand Society of Palliative Medicine

(http://www.anzspm.org.au/) This ANZ/SPM website is a useful
center for information exchange among society members as well as
being an information resource for medical practitioners and volunteers
working in palliative care.

Australian Pain Society (http://www.apsoc.org.au) Formed

in 1979 with members from many medical specialties including
researchers and clinicians active in the pain management field.

British Pain Society (http://www.britishpainsociety.org/) The

society represents all UK professionals involved in the management
and understanding of pain. It promotes education, training, research
and development in all fields of pain and facilitates the exchange of
information and experience.

Canadian Anesthesiologists Society (CAS) (http://www.cas.

ca/) CAS is a not-for-profit, voluntary organization, for the benefit of
its member anesthesiologists. Canadian anesthesiologists are specialist
physicians in peri-operative medicine, critical care, and pain management.

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Canadian Association of Psychosocial Oncology (http://capo.ca/

eng/index.asp) CAPO is dedicated to the understanding, treatment
and study of the social, psychological, emotional, spiritual and quality-
of-life aspects of cancer.

Canadian Pain Society (CPS) (http://www.canadianpainsociety.

ca/) A chapter of the International Association for the Study of Pain,
that includes as members all professional and lay persons with an
interest in the field of pain.

Chronic Pain Australia (http://www.chronicpainaustralia.org.

au/) This advocacy group seeks to reduce the unnecessary suffering
and isolation caused by chronic pain in the Australian community. The
organization provides access to helpful information and resources to help
patients effectively manage their pain in a manner promoting dignity and
self-respect.

Endometriosis UK (http://www.endometriosis-uk.org) UK
charity devoted to funding research on endometriosis, and raising
awareness among medical professionals and the general public. This
website also hosts information and support for patients.

European Association for Palliative Care (EAPC) (http://www.

eapcnet.eu) Established in 1988 to promote palliative care in Europe
and act as a focus for all who work or have an interest at the scientific,
clinical, and social levels in the field of palliative care.

European Society of Anaesthesiology (http://www.esahq.

org) This organization promotes improvements in safety and quality
of care of patients who are treated by anesthesiologists inside and
outside the operating room by coordinating activities of anesthesiology
societies throughout Europe.

Fibromyalgia Association UK (http://www.fibromyalgia-

associationuk.org/) A nonprofit organization that works towards
raising awareness of fibromyalgia in the United Kingdom.

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Headache Network Canada (HNC) (http://www.headachenetwork.

ca/) This website was developed to make available to individuals with
headache and health professionals scientifically based information on the
diagnosis and treatment of headache. It represents a partnership between
Headache Network Canada and The Canadian Headache Society.

Healing Touch International (http://www.healingtouchinterna

tional.org/) This organization establishes standards of practice, and
offers certification of healing touch practitioners and instructors. Thei
focus is on nurturing energy therapy that assists in balancing physical,
mental, emotional, and spiritual well-being.

International Association of Hospice and Palliative Care (http://

www.hospicecare.com/) The site offers professional forums,
publications, world reports, and a manual of palliative care.

International Association for Pain & Chemical Dependency

(IAPCD) (http://www.iapcd.org/) The IAPCD is an international
organization dedicated to promoting appropriate and effective treatment for
all patients with pain, including individuals with substance abuse, mental
health or other co-occurring problems that may make treatment more
challenging. The association encourages cooperation among professionals
in the fields of healthcare, policy and regulation, law enforcement, law,
politics and the media to improve communication and education for the
appropriate use of controlled substances in pain treatment.

International Association for the Study of Pain (IASP)

(http://www.iasp-pain.org) This non-profit professional organization
is the largest multidisciplinary international association in the field of
pain and is dedicated to furthering research on pain and improving the
care of patients with pain. Membership is open to scientists, physicians,
dentists, psychologists, nurses, physical therapists, and other health
professionals actively engaged in pain research and to those who have
special interest in the diagnosis and treatment of pain. Provides access to
web-based learning, grants/awards, employment opportunities, etc.

International Children’s Palliative Care Network (ICPCN) (http:

//www.icpcn.org.uk/) Children and young people with life-limiting
or life-threatening conditions have very specific and unique palliative

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care needs, often different to those of adults. The International Children’s

Palliative Care Network (ICPCN) shares a vision that these total
needs should be met to encompass physical, emotional, spiritual, and
developmental aspects of care.

International Neuromodulation Society (INS)

(http://www.neuromodulation.com/) The International
Neuromodulation Society (INS), founded in 1989, is a nonprofit group
of clinicians and scientists focusing on the alteration of nerve activity to
relieve pain through electrical stimulation or chemical agents delivered
to targeted sites of the body.

International Pelvic Pain Society (IPPS) (http://www.pelvicpain.

org/) Site aims to educate health care professionals on how to
diagnosis and manage chronic pelvic pain in women and men, raising
public awareness and impacting individual lives.

International Society on Complementary Medicine Research

(ISCMR) (http://www.iscmr.org/) A worldwide not-for-
profit professional association devoted to fostering co-operative and
multidisciplinary research and development as well as the application of
knowledge in the fields of Complementary, Traditional, and Integrated
Medicine.

International Spine Intervention Society (http://www.spinal

injection.com/) An association of physicians interested in the
development, implementation and standardization of percutaneous
techniques for the precision diagnosis of spinal pain.

National Back Pain Society (Backcare) (http://www.backcare.

org.uk/) UK charity dedicated to educating people on how to avoid
preventable back pain, and supporting those living with back pain.

Oxford Pain Internet Site (http://www.medicine.ox.ac.uk/ba

ndolier/booth/painpag/index2.html) This site is for anyone with
a professional or personal interest in pain and analgesia. It is firmly
based on principles of evidence-based medicine and has pulled together
systematic reviews focusing on pain.

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Pain Concern (http://www.painconcern.org.uk/) UK charity that

provides information and support for pain sufferers and their caregivers.

Pain in Europe (http://www.painineurope.com/) Seeks

to provide access to information for both patients and healthcare
professionals, offering more understanding of pain and its management,
and providing support to patients and their families.

Pain Relief Foundation (http://www.painrelieffoundation.

org.uk/) UK charity that funds research into the causes and treatment
of human chronic pain and continuing education of physicians and
nurses in pain management.

Pain Research Institute (http://www.liv.ac.uk/pri/) Funded by

the Pain Relief Foundation and is part of the Department of Neurological
Science at the University of Liverpool.

Pain Web (http://www.thepainweb.com/) UK resource for health

professionals involved with research, assessment and the treatment of pain.

The International Society of Nurses in Cancer Care (ISNCC)

(http://www.isncc.org) This organization of oncology nurses has more
than 60 member groups in 33 countries. Their goal is to improve standards
of cancer care through the provision of education, research, and training.

HEADACHE / MIGRAINE

American Council for Headache Education (ACHE) (http://www.

achenet.org/) A nonprofit patient-healthcare professional
partnership dedicated to advancing the treatment and management
of headache and to raising the public awareness of headache as a
valid, biologically-based illness. Advocates individualized treatments,
which combine the best of traditional medicine, alternative medicine,
drug, and non-drug therapies.

American Headache Society (http://www.americanheadacheso

ciety.org) A professional society of health care providers dedicated

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to the study and treatment of headache and face pain bringing together
physicians and other health providers from various fields and specialties
to share concepts and developments about headache and related
conditions. Offers CME courses and other resources.

Help for Headaches (http://www.headache-help.org) An

Ontario, Canada non-profit organization committed to educational
services for those suffering from and treating headaches. Contains an
extensive resource library for research.

Migraine Awareness Group: A National Understanding for

Migraineurs (MAGNUM) (http://www.migraines.org) The
National Migraine Association site provides comprehensive information
about migraines, focusing on the nature of migraines as well as other
headache and head-pain issues.

Migraine Resource Network (http://www.migraineresourcenet

work.com/) Migraine Resource Network is an industry-sponsored
website established in 2008 to provide practicing clinicians with up-to-
the-minute interactive programs, information, and clinical perspectives
on the latest developments in the field of migraine.

National Headache Foundation (http://www.headaches.

org/) Nonprofit organization with a divided site offering resources for
either healthcare professionals (latest information in headache diagnosis
and treatment) or headache sufferers (providing headache causes/
treatments, self management tips, and support groups). NHF sponsors
Migraine Masterpieces National Art Contests.

CHRONIC PAIN AND FIBROMYALGIA

American Chronic Pain Association (ACPA) (http://www.theac

pa.org) Founded in 1980, this organization’s mission is to facilitate peer
support and education for individuals with chronic pain and their families
so that these individuals may live more fully despite their pain and to
raise awareness among the health care community, policy makers, and the
public at large about issues of living with chronic pain. The organization’s
website features a variety of unique educational materials and other
resources for patients, their families, and healthcare professionals.

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Arthritis Foundation (http://www.arthritis.org/) A consumer-

oriented site, the Arthritis Foundation is the only national not-for-
profit organization that supports the more than 100 types of arthritis
and related conditions with advocacy, programs, services and
research.

Chronic Pain Association of Canada (CPAC) (http://chronicpain

canada.com) The Chronic Pain Association of Canada is Canada's
largest independent, not-for-profit charitable organization serving
people affected by pain, through education, information, and support
advocacy. CPAC's programs include a website, a nationwide support
group network; a quarterly newsletter for members, and patient
access to information.

Fibromyalgia Information Foundation (FIF) (http://www.myalgia.

com) A website offering research and treatment information from
an Oregon-based foundation whose directors are Oregon Health and
Science University researchers engaged in the day to day management of
fibromyalgia patients.

Fibromyalgia Network (http://www.fmnetnews.

com/) Educational materials, including an extensive quarterly
newsletter containing research studies, interviews and information to
provide ideas for coping and new therapies to try.

Institute for Chronic Pain (http://www.instituteforchronicpa

in.org) The mission of this organization is to change the culture
of how chronic pain is treated by promoting the theory and practice
of chronic pain rehabilitation. Its staff and fellows are specialists
in chronic pain management, as well as healthcare policy and
management.

National Fibromyalgia & Chronic Pain Association (http://fmcp

Aware.org/) The National Fibromyalgia & Chronic Pain Association
(NfmCPA) is a not for profit organization working to support people
who have chronic pain illnesses and their families and friends by
contributing to caring, professional, and community relationships. A Pain
Treatment Topics affiliate organization.

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National Fibromyalgia Partnership (NFP) (http://www.fmpartner

ship.org) An educational organization that makes medically accurate,
quality resource information concerning etiology, pathophysiology and
management of fibromyalgia available to healthcare professionals and
the community at-large.

National Fibromyalgia Research Association (NFRA) (http:

//www.nfra.net) The website of an activist organization located in
Salem, Oregon dedicated to education, treatment and finding a cure
for fibromyalgia.

CANCER PAIN

American Cancer Society (ACS) (http://www.cancer.org) A

nationwide community-based voluntary health organization dedicated
to eliminating cancer as a major health problem by preventing cancer,
saving lives, and diminishing suffering from cancer, through research,
education, advocacy, and service. Extensive site with information for
patients, families, and healthcare professionals.

American Society of Clinical Oncology (ASCO) (http://www.

asco.org/) ASCO's membership is composed of clinical oncologists
representing all oncology disciplines (medical, surgical, and radiologic
oncology) and subspecialties; physicians and healthcare professionals
participating in approved oncology training programs; oncology nurses;
and other health-care practitioners with a predominant interest in
oncology. This site offers extensive resources including database and
publications access.

Association of Oncology Social Work (AOSW) (http://www.aosw.

org/) This non-profit, international organization is dedicated to the
enhancement of psychosocial services to people with cancer and their
families. The site contains message boards and online courses.

BreakthroughCancerPain.org (http://www.breakthroughcancer
pain.org/) This website is a collaboration between healthcare
professionals and 5 pharmaceutical companies that are developing/
marketing products for the treatment of breakthrough cancer pain. It is

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maintained by an independent communications company in Europe and

the content is overseen by an independent medical editorial board.

BreastCancer.org (Pain Section) (http://www.breastcancer.org/

treatment/pain/) This website section is for women affected by breast
cancer and for whom overcoming pain can be a major part of dealing
with the disease and its treatment.

Cancer Care (http://www.cancercare.org/) Nonprofit

organization designed to provide free, professional counseling,
education, financial assistance and practical help to cancer patients,
caregivers, children, loved ones, and the bereaved.

CancerIndex (Guide to Internet Resources for Cancer)

(http://www.cancerindex.org/) The aim of this site is to make
it easier to find more specific information quickly by providing a
comprehensive directory of cancer-related sites and pages.

Cancer Pain Education Resources (http://www.caper.tufts.

edu/) A resource site for use by educators regarding cancer pain;
includes problem based learning cases, syllabus, links, and resources for
patients and families.

Cancer-Pain.org (http://www.cancer-pain.org) A site for cancer

pain patients and their caregivers detailing the various options available
for cancer pain treatment.

Cancer Pain Management in Children (http://www.childcancer

pain.org/) The design and development of this website and its
contents were funded by a grant from the Texas Cancer Council as a
resource focused on pain management for health professionals who care
for children with cancer.

Intercultural Cancer Council (ICC) (http://iccnetwork.

org/) This organization at Baylor College of Medicine promotes policies,
programs, partnerships, and research to eliminate the unequal burden

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of cancer among racial and ethnic minorities, as well as underserved

populations in the United States and its associated territories.

Leukemia Society of America (http://www.leukemia.org/) The

Leukemia & Lymphoma Society is the world's largest voluntary health
organization dedicated to funding blood cancer research, education and
patient services. Site provides extensive information, including advocacy
networking and free information.

Memorial Sloan-Kettering Cancer Center (http://www.mskcc.

org) The site offers comprehensive information on cancer treatments,
patient care, research, education and training.

National Cancer Institute (NCI) (http://www.nci.nih.

gov) Component of NIH that regulates the National Cancer
Program which conducts and supports research, training, health
information dissemination, and other programs with respect to the
cause, diagnosis, prevention, and treatment of cancer, rehabilitation
from cancer, and the continuing care of cancer patients and the
families of cancer patients.

National Coalition for Cancer Survivorship (NCCS) (http://www.

canceradvocacy.org/) Advocating quality cancer care for all
Americans and empowering cancer survivors. NCCS believes in
evidence-based advocacy for systemic changes at the federal level in how
the nation researches, regulates, finances and delivers quality cancer care.

Oncolink (http://www.oncolink.com/) This website was founded

in 1994 by University of Pennsylvania cancer specialists with a mission
to help cancer patients, families, health care professionals, and the
general public get accurate cancer-related information at no charge.

Oncology Nursing Society (ONS) (http://www.ons.org/) The

largest professional oncology association of registered nurses and other
healthcare providers dedicated to excellence in patient care, education,
research, and administration in oncology nursing. Information resources
target both professionals and affected individuals.

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Supportive Care in Cancer (http://www.springer.com/medicine/

oncology/journal/520) Provides members of the Multinational
Association of Supportive Care in Cancer (MASCC) and all other
interested parties with the most recent scientific and social information
on all aspects of supportive care in cancer patients.

END OF LIFE/PALLIATIVE CARE

Aging with Dignity (http://www.agingwithdignity.org) This

nonprofit organization provides practical information, advice and legal
tools to help improve patient quality of care, aiming to preserve the
rights of the sick.

American Academy of Hospice and Palliative Medicine

(AAHPM) (http://www.aahpm.org) Members are physicians and
other professionals from many medical specialties who are committed
to furthering and fostering the practice of hospice/palliative care for
the terminally ill and their families. The site includes: certification,
fellowships, and other opportunities.

American Hospice Foundation

(http://www.americanhospice.org/) This organization seeks to
improve access to quality hospice care through public education,
professional training, and advocacy on behalf of consumers.

Caring Connection (http://www.caringinfo.org/) Caring

Connections, a program of the National Hospice and Palliative Care
organization (NHPCO), develops networks of people, communities, and
organizations working to improve timely access to quality end-of-life care.

Center for Palliative Care Education (http://depts.washington.

edu/pallcare/about/index.shtml) This is an educational resource
center and training program for improving palliative care in people with
HIV/AIDS by increasing the knowledge, skills, and comfort level of
clinicians to provide this care.

Center to Advance Palliative Care (CAPC) (http://www.capc.

org/) A national initiative that provides health care professionals with

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the tools and training necessary to start and sustain successful palliative
care programs.

Children’s Hospice International (CHI) (http://www.chionline.

org/) CHI is a nonprofit organization founded in 1983 to promote
hospice support through pediatric care facilities, and encourage the
inclusion of children in existing and developing hospice, palliative, and
home care programs.

Compassion & Choices (http://www.compassionandchoices.

org) This is a nonprofit organization working to improve care and
expand choice at the end of life.

Contemporary Long-Term Care (http://www.hcpro.com/) An

online information center for administrators, directors of nursing,
medical directors, pharmacists and other professionals in the long term
care industry.

EndLink (End of Life Care Education) (http://endoflife.northwe

stern.edu/index.cfm) EndLink is hosted at Northwestern University
and was developed as an educational resource for people involved in
end-of-life care. The vast content of the site is primarily for healthcare
professionals who work with dying patients and their families.

End of Life/Palliative Education Resource Center (EPERC)

(http://www.mcw.edu/palliativecare/EPERC.htm) The purpose
of EPERC is to share educational resource material among the community
of health professional educators involved in palliative care education.

End of Life Nursing Education Consortium (ELNEC) (http://

www.aacn.nche.edu/ELNEC/) The ELNEC project is administered
by the American Association of Colleges of Nursing (AACN) and the City
of Hope National Medical Center of Los Angeles as a national education
initiative to improve end-of-life care in the United States. The project
provides undergraduate and graduate faculty to teach this essential
information to nursing students and practicing nurses.

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GetPalliativeCare.org (http://www.getpalliativecare.org) This

site is sponsored by the Center to Advance Palliative Care (CAPC) and
provides information and resources for patients and clinicians.

Growthhouse.org (Improving Care for the Dying) (http://www.

growthhouse.org/) This Growth House, Inc., website is a
portal to resources for life-threatening illness and end of life care.
The organization’s primary mission is to improve the quality of
compassionate care for people who are dying through public education
and global professional collaboration.

Hospice Association of America (HAA) (http://www.nahc

.org/HAA/) This national organization represents more than
2,800 hospices and thousands of caregivers and volunteers who
serve terminally ill patients and their families and is the largest
lobbying group for hospice, advocating the industry's interests before
Congress, the regulatory agencies, other national organizations, the
courts, the media, and the public.

Hospice & Palliative Nurses Association (http://www.hpna.

org) The nation's largest and oldest professional nursing organization
dedicated to promoting excellence in pain management and end-of-life
care.

Hospice Education Institute (http://www.hospiceworld.

org/) The Institute is an independent, not-for-profit organization,
serving members of the public and healthcare professionals with
information and education about the many facets of caring for the
dying and the bereaved.

Hospice Foundation of America (HFA) (http://www.hospice

foundation.org/) This organization, chartered in 1982, provides
leadership in the development and application of hospice and
its philosophy of care with the goal of enhancing the American
health care system and the role of hospice within it. HFA conducts
programs relating to professional development, public education and
information, research, publications and health p­olicy issues.

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Last Acts (http://www.rwjf.org) In 2005, Last Acts – a highly

acclaimed Robert Wood Johnson Foundation national program – came to
a close and the program's website, www.lastacts.org, ceased publication at
that time. Much of the content of the Last Acts Web site is still archived here.

National Hospice and Palliative Care Organization (http://www.

nhpco.org) A nonprofit membership organization representing
hospice and palliative care programs and professionals. The organization
is committed to improving end-of-life care and expanding access to
hospice care with the goal of profoundly enhancing quality of life for
people in America dying and their loved ones.

National Palliative Care Research Center (NPCRC) (http://www.

npcrc.org/) The NPCRC is committed to stimulating, developing, and
funding research directed at improving care for seriously ill patients and
their families. The NPCRC has collaborated with the Center to Advance
Palliative Care (see link above) to rapidly and directly translate its
research findings into improved clinical care.

PalliativeDrugs.com (http://www.palliativedrugs.com/) This

site, based in the UK, provides essential, comprehensive, and independent
information for health professionals about the use of various drugs in
palliative care. Free registration is required to view most site contents.

Pallimed (http://www.pallimed.org/) The goal of this excellent

blog/website run by professionals in the field is to review current
palliative medicine, hospice, and end-of-life research with a particular
focus on publications not from the major palliative care journals. They
also highlight important events and news regarding end-of-life care from
the mass media.

StopPain.org (Palliative Care Focus) (http://www.stoppain.

org/) Sponsored by Beth Israel Hospital, New York, the mission
of this website is to advance the educational aims of pain medicine
and palliative care. This website represents an evolving process to
meet the needs of an ever-increasing online audience of healthcare
consumers and professionals seeking accurate, reliable information on
treatment options.

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SUBSTANCE ABUSE AND ADDICTION

Addiction Recovery Guide (http://www.addictionrecoverygu

ide.com) Assists individuals struggling with drug addiction and
alcoholism find programs and resources that best suit their needs.

Addiction Treatment Forum (http://www.ATForum.

com) Addiction Treatment Forum is an industry-sponsored site that has
reported on substance abuse and addiction therapies, research, news,
and events of interest to both healthcare professionals and patients since
1992. Many treatment options of concern are discussed, and an important
focus is on methadone maintenance for opioid-addiction treatment.

American Academy of Addiction Psychiatry (AAAP) (http://www.

aaap.org) AAAP, founded in 1985 and with approximately 1,000
members internationally, consists of psychiatrists who work with addiction
and mental health disorders in their practices, faculty at academic
institutions, non-psychiatrist professionals who are making a contribution
to the field of addiction psychiatry, and others. The organization specializes
in bringing together the academic and private practice communities with
the common goal of providing the most effective training for physicians
and treatment for individuals suffering from addictive disorders.

American Association for the Treatment of Opioid Dependence

(AATOD) (http://www.aatod.org) This nonprofit organization for
healthcare professionals was founded in 1984 to enhance the quality of
patient care in addiction treatment programs by promoting the growth
and development of comprehensive medication-assisted therapy services
throughout the United States.

American College of Psychiatrists (http://www.acpsych.org/) A

non-profit honorary association of psychiatrists who promote and
support the highest standards in psychiatry through education, research,
and clinical practice.

American Society of Addiction Medicine (ASAM) (http://www.

asam.org/) This site strives to Increase access to and improve the
quality of addictions treatment by educating physicians, medical and
osteopathic students, and the public and to promote research and
prevention.

APPENDIX
472 4. PROFESSIONAL JOURNALS, MAGAZINES AND NEWSLETTERS ON PAIN

Canada Centre on Substance Abuse (CCSA) (http://www.ccsa.

ca) Provides objective, evidence-based information and advice that
will help reduce the health, social, and economic harm associated with
substance abuse and addictions.

Center for Addiction and Mental Health (CAMH) (http://www.

camh.net) The Centre for Addiction and Mental Health (CAMH) is
Canada's leading addiction and mental health teaching hospital. CAMH
succeeds in transforming the lives of people affected by addiction and
mental illness, by applying the latest in scientific advances, through
integrated and compassionate clinical practice, health promotion,
education and research.

College on Problems of Drug Dependence (CPDD) (http://views.

vcu.edu/cpdd) This organization serves as an interface among
governmental, industrial and academic communities maintaining
liaisons with regulatory and research agencies as well as educational,
treatment, and prevention facilities in the drug abuse field

National Mental Health Association (http://www.nmha.

org/) Leading advocate for tolerance and awareness of mental
illness, which is often a confounding factor in pain disorders and their
treatment.

Pain Management and Chemical Dependency: A Critical Link

(http://www.stoppain.org/pcd/default.asp) This site from the Pain
Division at Beth Israel Medical Center, New York, focuses on information
regarding the interface of pain management and chemical dependency.

United Nations Office on Drugs & Crime (http://www.unodc.

org/) Informative site from a global leader in the fight against illicit
drugs, the international illicit drug trade, and addictive disorders.

World Health Organization (WHO) – Substance Abuse (http:

//www.who.int/substance_abuse) This web site contains
information pertaining to psychoactive substance use and abuse, and
also information about the World Health Organization's projects and
activities in the areas of substance use and substance dependence.

APPENDIX
 Bibliography and
Suggested Further
Readings

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.

Philadelphia: Lippincott Williams & Wilkins; 2005.
Dureja GP, Madan R, Kaul HL, editors. Regional anaesthesia and pain management: current
perspectives. New Delhi: B.I. Churchill Livingstone; 2000.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Lennard TA, editor. Pain procedures in clinical practice. Hanley & Belfus Inc; 2001.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain. Lon-
don: Churchill Livingstone; 2013.
Raj PP, editor. Pain medicine: a comprehensive review. Mosby; 1996.
Raj PP, editor. Practical management of pain. Mosby; 2008.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Raj PP, Lou L, Erdine S, Staats PS. Radiographic imaging for regional anesthesia and pain
management. Philadelphia: Churchill Livingstone; 2003.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD, editor. Atlas of pain management injection techniques. Philadelphia: Saunders,
W.B. Company; 2012.
Waldman SD, editor. Pain management. Philadelphia: Saunders W.B. Company; 2011.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

1. Evaluation of the Pain Patient

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2012.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Raj PP, editor. Pain medicine: a comprehensive review. Mosby; 1996.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

2. Pain Measurement and Assessment

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Doctor JN, Slater MA, Atkinson JH. The descriptor differential scale of pain intensity: an
evaluation of item and scale properties. Pain 1995;61:251–260.

473
474 Bibliography and Suggested Further Readings

Elleland CS, Ryan KM. Pain assessment: global use of the brief pain inventory. Ann Acad
Med Singapore 1994;23:129–138.
Fishman B, Pasterrnak S, Wallensteing SL, et al. The memorial pain assessment card: a valid
instrument for evaluation of cancer pain. Cancer 1987;60:1151–1158.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain
1975;1:277–299.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

3. Radiography and Imaging in Pain Medicine

Atlas SW, editor. Magnetic resonance imaging of the brain and spine. New York: Raven
Press; 1996.
Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Raj PP, editor. Radiographic imaging for regional anesthesia and pain management.
Philadelphia: Churchill Livingstone; 2002.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.

4. Ultrasonography in Pain Medicine

Greher M, Eichenberger U, Gustorff B. Sonographic localization of an implanted infusion
pump injection port: another useful application of ultrasound in pain medicine. Anesthe-
siology January 2005;102(1):243.
Huntoon MA. Ultrasound in pain medicine: advanced weaponry or just a fad? Reg Anesth
Pain Med September–October 2009;34(5):387–388.
Narouze S, Peng PW. Ultrasound-guided interventional procedures in pain medicine: a re-
view of anatomy, sonoanatomy, and procedures. Part II: axial structures. Reg Anesth Pain
Med July–August 2010;35(4):386–396.
Narouze SN, Provenzano D, Peng P, et al. The American Society of Regional Anesthesia and
Pain Medicine, the European Society of Regional Anaesthesia and Pain Therapy, and the
Asian Australasian Federation of Pain Societies Joint Committee recommendations for
education and training in ultrasound-guided interventional pain procedures. Reg Anesth
Pain Med November–December 2012;37(6):657–664.
Narouze SN. Ultrasound-guided interventional procedures in pain management: evidence-
based medicine. Reg Anesth Pain Med March–April 2010;35(2 Suppl.):S55–S58.
Neal JM, Brull R, Chan VW, et al. The ASRA evidence-based medicine assessment of ultra-
sound-guided regional anesthesia and pain medicine: executive summary. Reg Anesth
Pain Med March–April 2010;35(2 Suppl.):S1–S9.
Peng PW, Cheng P. Ultrasound-guided interventional procedures in pain medicine: a re-
view of anatomy, sonoanatomy, and procedures. Part III: shoulder. Reg Anesth Pain Med
November–December 2011;36(6):592–605.
Peng PW, Narouze S. Ultrasound-guided interventional procedures in pain medicine: a re-
view of anatomy, sonoanatomy, and procedures: part I: nonaxial structures. Reg Anesth
Pain Med September–October 2009;34(5):458–474.
 Bibliography and Suggested Further Readings 475
Peng PW. Ultrasound-guided interventional procedures in pain medicine: a review of
anatomy, sonoanatomy, and procedures. Part IV: hip. Reg Anesth Pain Med July–August
2013;38(4):264–273.
Ramlogan R, Manickam B, Chan VW, et al. Challenges and training tools associated with the
practice of ultrasound-guided regional anesthesia: a survey of the American society of re-
gional anesthesia and pain medicine. Reg Anesth Pain Med March–April 2010;35(2):224–226.
Sites BD, Chan VW, Neal JM, et al. The American Society of Regional Anesthesia and Pain
Medicine and the European Society of Regional Anaesthesia and Pain Therapy joint com-
mittee recommendations for education and training in ultrasound-guided regional anes-
thesia. Reg Anesth Pain Med March–April 2010;35(2 Suppl.):S74–S80.

5. Pharmacotherapeutics (Drugs) in Pain Management

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Florian S, Driver LC, Burton AW. Update on adjuvant medications for chronic nonmalignant
pain. Pain Pract 2003;3(4).
Lennard TA, editor. Pain procedures in clinical practice. Hanley & Belfus Inc; 2001.
Raj PP, editor. Pain medicine: a comprehensive review. Mosby; 1996.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.

6. Neurolytic Agents
Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.

7. How to Set up a Pain Clinic?

American Chronic Pain Association (ACPA): Managing Chronic Pain.
womenshealth.gov: Pain.
American Society of Anesthesiologists (ASA): The Management of Acute, Chronic and
Cancer Pain.
Bonica JJ, editor. The management of pain. 2nd ed. Philadelphia: Lea and Febiger; 2011.
Loeser JD: Desirable characteristics for pain treatment facilities: Report of the IASP taskforce.
In Bond MR, Charlton JE, Woof CJ (eds): Pain research and clinical management, vol. 4.
1991, pp. 411–415.
Scripps Health: Pain Management. www.scripps.org/services/pain-management.

8. Acute Pain Management: Practical Guidelines

Acute pain management guideline panel. Acute pain management: operative or medical
procedures and trauma – clinical practice guideline, Pub No. 92-0032. Rockville, MD:
Agency for Health Care Policy and Research; February 1992, US Department of Health
and Human Services.
Barsan WG, Tomassoni AJ, Seger D, et al. Safety assessment of high dose narcotic analgesia
for emergency department procedures. Ann Emerg Med 1993;22:1444.
476 Bibliography and Suggested Further Readings

Bonica JJ. Biology, pathophysiology and treatment of acute pain. In: Lipton S, Miles J, editors.
Persistent pain: modern methods of treatment, vol. 5. Orlando, FL: Grune & Stratton;
1985.
Cohen Sp, Christo PJ, Moroz L. Pain management in trauma patient. Am J Phys Med Rehabil
2004;83:142–161.
Ducharme J. Emergency pain management: a Canadian Association of Emergency Physi-
cians (CAEP) consensus document. J Emerg Med 1994;12:855.
Dykes EH. Paediatric trauma. Br J Anaesth 1999;83:130–138.
General considerations of chronic pain. In: Bonica JJ, editor. The management of pain. 2nd ed.
Philadelphia: Lea & Febiger; 1900. p. 189–196.
Hedderich R, Ness TJ. Analgesia for trauma and burns. Crit Care Clin 1999;15:167–180.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Ready LB, Edwards WT. Management of acute pain: a practical guide, International Associa-
tion for the Study of Pain, Seattle IASP Publications; 1992.
Sinatra RS. Pathophysiology of acute pain. In: Sinatra RS, Hord AH, Cinberg B, editors.
Acute pain: mechanisms & management. St. Louis: Mosby; 1992.
Whipple J, Lewis K, Quebbeman E, et al. Analysis of pain management in critically ill pa-
tients. Pharmacotherapy 1995;15:592–599.

9. Myofascial Pain Syndromes

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain. L­ondon:
Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD, editor. Atlas of pain management injection techniques. Philadelphia: W.B.
Saunders Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

10. Headache
Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Evans RW, Mathew NT, editors. Handbook of headache. Philadelphia: Lippincott Williams
& Wilkins; 2000.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Robert J Joynt, Adolph L. Sahs, MD (1906–1986). Arch Neurol 1987;44(5):562.
Raj PP, editor. Text book of regional anaesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD, editor. Atlas of pain management injection techniques. Philadelphia: WB
Saunders Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.
 Bibliography and Suggested Further Readings 477

11. Neck and Shoulder Pain

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Raj PP, editor. Text book of regional anaesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD. Atlas of pain management injection techniques. Philadelphia: W.B. Saunders
Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

12. Back Pain

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD, editor. Atlas of pain management injection techniques. Philadelphia: WB
Saunders Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

13. Facetogenic Pain

Bogduk N. International Spinal Injection Society guidelines for the performance of spinal
injection procedures. Part 1: zygapophysial joint blocks. Clin J Pain 1997;13:285–302.
Bogduk N. Low back pain. Clinical anatomy of the lumbar spine and sacrum. 3rd ed. New
York: Churchill Livingstone; 1997. p. 187–214.
Bogduk N, McGuirk B. Management of acute and chronic neck pain. Evidence-based approach.
Elsevier; 2006.
Bogduk N. The zygapophysial joints. Clinical anatomy of the lumbar spine and sacrum. 3rd ed.
New York: Churchill Livingstone; 1997. p. 33–41.
Boswell MV, Colson JD, Sehgal N, Dunbar E, Epter R. Systematic review of therapeutic facet
joint interventions in chronic spinal pain. Pain Physician 2007;10:229–253.
Cohen SP, Raja SN. Pathogenesis, diagnosis, and treatment of lumbar zygapophysial (facet)
joint pain. Anesthesiology March 2007;106(3):591–614.
Dreyfuss P, Schwarzer AC, Lau P, et al. Specificity of lumbar medial branch and L5 dorsal
ramus blocks. Spine 1997;22:895–902.
Fujiwara A, Lim T, An HS, et al. The effect of disc degeneration and facet joint osteoarthritis
on the segmental flexibility of the lumbar spine. Spine 2000;25:3036–3044.
Ghormley RK. Low back pain with special reference to the articular facets, with presentation
of an operative procedure. JAMA 1933;101:1773–1777.
Harris RI, Macnab I. Structural changes in the lumbar intervertebral discs; their relationship
to low back pain and sciatica. J Bone Joint Surg Br May 1954;36-B(2):304–322.
Hirsch C, Ingelmark BE, Miller M. The anatomical basis for low back pain. Studies on the
presence of sensory nerve endings in ligamentous, capsular and intervertebral disc struc-
tures in the human lumbar spine. Acta Orthop Scand 1963;33:1–17.
478 Bibliography and Suggested Further Readings

Interventional techniques: evidence-based practice guidelines in the management of chronic

spinal pain. Pain Physician 2007;10:7–111; ISSN 1533-3159.
Jackson RP, Jacobs RR, Montesano PX. Volvo award in clinical sciences. Facet joint injection
in low-back pain. A prospective statistical study. Spine September 1988;13(9):966–971.
Manchikanti L, Singh V, Pampati V, et al. Evaluation of the relative contributions of various
structures in chronic low back pain. Pain Physician 2001;4:308–316.
Sehgal N, Shah RV, McKenzie-Brown AM, Everett CR. Diagnostic utility of facet (zyg-
apophysial) joint injections in chronic spinal pain: a systematic review of evidence. Pain
Physician 2005;8:211–224.
Schwarzer AC, Wang SC, O'Driscoll D, et al. The ability of computed tomography to iden-
tify a painful zygapophysial joint in patients with chronic low back pain. Spine 15 April
1995;20(8):907–912.
Vernon-Roberts B, Pirie CJ. Degenerative changes in the intervertebral discs of the lumbar
spine and their sequelae. Rheumatol Rehabil 1977;16:13–21.

14. Knee Pain

McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anaesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD. Atlas of pain management injection techniques. Philadelphia: WB Saunders
Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

15. Neuropathic Pain: Mechanisms and Management

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Bridges D, Thompson SWN, Rice ASC. Mechanisms of neuropathic pain. Br J Anaesth
2001;87:12–26.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

16. Herpetic Neuralgia

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.
 Bibliography and Suggested Further Readings 479

17. Orofacial Pain

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Fromm GH, Terrence CF, Chattha AS. Baclofen in the treatment of trigeminal neuralgia:
double-blind study and long-term follow-up. Ann Neurol. 1984 Mar;15(3):240-4.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD. Atlas of pain management injection techniques. Philadelphia: W.B. Saunders
Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

18. Scar Neuralgia/Painful Scars

Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.

19. Complex Regional Pain Syndrome

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Dureja GP, Madan R Kaul HL, editors. Regional anaesthesia and pain management: current
perspectives. New Delhi: B.I. Churchill Livingstone.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
Forouzanfar T, Koke AJ, VanKleef M, Weber WE. Eur J Pain 2002;6:105–122.
Harden RN. Br J Anaesth 2001;87:99–106.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raja SN, Grabow TS. Anesthesiology 2002;96:254–260.
Raj PP, editor. Text book of regional anaesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

20. Pelvic Pain

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
Fishman SM, Ballantyne Jane, Rathmell James, editors. Bonica’s management of pain.
Philadelphia: Lippincott Williams & Wilkins; 2009.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anaesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
480 Bibliography and Suggested Further Readings

Waldman SD. Atlas of pain management injection techniques. Philadelphia: W.B. Saunders
Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

21. Perineal Pain

Ballantyne J, editor. The massachusetts general hospital handbook of pain management.
Philadelphia: Lippincott Williams & Wilkins; 2005.
McMohan S, Koltzenburg M, Tracey I, Turk DC. Wall and Melzack’s textbook of pain.
London: Churchill Livingstone; 2013.
Raj PP, editor. Text book of regional anesthesia. Philadelphia: Churchill Livingstone; 2002.
Tollison CD, Satterthwaite JR, Tollison JW, editors. Practical pain management. Philadelphia:
Lippincott Williams & Wilkins; 2002.
Waldman SD, editor. Atlas of pain management injection techniques. Philadelphia: W.B.
Saunders Company; 2012.
Weiner RS, editor. Pain management. Boca Raton: CRC Press; 2005.

22. Peripheral Vascular Diseases

Waldman SD, editor. Atlas of pain management injection techniques. Philadelphia: WB
Saunders Company; 2012.

23. Pain Management in Rheumatological Diseases

Cossmann M, Kohnen C. General tolerability and adverse event profile of tramadol hydro-
chloride. Rev Contemp Pharmacother 1995;6:513–531.
Graven-Nielsen T, Arendt-Nielsen L. Peripheral and central sensitization in musculoskeletal
pain disorders: an experimental approach. Curr Rheumatol Rep 2002;4:313–321.
Singh G, Triadafilopoulos G. Epidemiology of NSAID induced gastrointestinal complica-
tions. J Rheumatol 1999;26(Suppl. 26):18–24.
Ytterberg SR, Mahowald ML, Woods SR. Codeine and oxycodone use in patients with chron-
ic rheumatic disease pain. Arthritis Rheum 14 May 2004;41(9):1603–1612.

24. Pain Management in the Elderly

AGS Panel on Chronic Pain in Older Persons, American Geriatrics Society. The management
of chronic pain in older persons. Geriatrics 1998;53(Suppl. 3):S8–S24.
Feinberg SD. Prescribing analgesics: how to improve function and avoid toxicity when treat-
ing chronic pain. Geriatrics 2000;55(9):44–62.
Freedman GM. Chronic pain. Clinical management of common causes of geriatric pain.
Geriatrics May 2002;57(5):36–41.
Gallagher RM, Verma S, Mossey J. Chronic pain: sources of late-life pain and risk factors for
disability. Geriatrics 2000;55(9):40–47.
Gibson MC, Schroder C. The many faces of pain for older, dying adults. Am J Hosp Palliat
Care 2001;18(1):19–25.
Gibson SJ, Helme RD. Cognitive factors and the experience of pain and suffering in older
persons. Pain 2000;85(3):375–383.
Gibson SJ. IASP global year against pain in older persons: highlighting the current status
and future perspectives in geriatric pain. Expert Rev Neurother June 2007;7(6):627–635.
Gibson SJ, Katz B, Corran TM, et al. Pain in older persons. Disabil Rehabil 1994;16(3):127–139.
Gloth III FM. Concerns with chronic analgesic therapy in elderly patients. Am J Med
1996;101(1A):19S–24S.
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Gloth III FM. Geriatric pain. Factors that limit pain relief and increase complications. Geriat-
rics 2000;55(10):46–48; 51–54.
Gloth III FM. Pain management in older adults: prevention and treatment. J Am Geriatr Soc
2001;49(2):188–199.
Helme RD, Katz B, Gibson SJ, et al. Multidisciplinary pain clinics for older people. Do they
have a role? Clin Geriatr Med 1996;12(3):563–582.
Nikolaus T. Assessment of chronic pain in elderly patients. Ther Umsch 1997;54(6):340–344.
Robinson CL. Relieving pain in the elderly. Health Prog January–February 2007;88(1):48–53; 70.

25. Osteoporosis
American Association of Clinical Endocrinologists. Medical guidelines for clinical prac-
tice for the prevention and treatment of postmenopausal osteoporosis. Endoc Pract
2003;9(6):544–564.
American College of Obstetricians and Gynecologists. Osteoporosis. ACOG Practice Bulletin
No. 50. Obstet Gynecol 2004, reaffirmed 2008;103(1):203–216.
Anderson JJB. Nutrition and bone health. In: Mahan LK, Escott-Stump S, editors. Krause's
food and nutrition therapy. 12th ed. St. Louis: Saunders Elsevier; 2008. p. 614–635.
Bell KJL, et al. Value of routine monitoring of bone mineral density after starting bisphospho-
nate treatment: secondary analysis of trial data. BMJ 23 June 2009. Published online. http
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26. Pain Management by Rehabilitative Approaches

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27. Cancer Pain

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28. Cancer Pain Management

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29. Advanced Interventional Pain Management Modalities

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30. Spinal Cord Stimulation for Management of Chronic

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31. Continuous Intrathecal Drug Delivery Systems

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32. Radio Frequency Ablation in Pain Management

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33. Vertebroplasty and Kyphoplasty

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34. Management of Spasticity

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