Back pain THEME
Lumbar
radicular pain
BACKGROUND Radicular pain is caused by
irritation of the sensory root or dorsal root
ganglion of a spinal nerve. The irritation causes
ectopic nerve impulses perceived as pain in the
distribution of the axon.
The pathophysiology is more than just mass
effect: it is a combination of compression
sensitising the nerve root to mechanical
stimulation, stretching, and a chemically
mediated noncellular inflammatory reaction.
OBJECTIVE This article discusses the clinical
features, assessment and management of lumbar
radicular pain (LRP).
DISCUSSION Lumbar radicular pain is sharp,
shooting or lancinating, and is typically felt as a
narrow band of pain down the length of the leg,
both superficially and deep. It may be associated
with radiculopathy (objective sensory and/or
motor dysfunction as a result of conduction block)
and may coexist with spinal or somatic referred
pain. In more than 50%
of cases, LRP settles with simple analgesics.
Significant and lasting pain relief can be achieved
with transforaminal epidural steroid injection.
Surgery is indicated for those patients with
progressive neurological deficits or severe LRP
refractory to conservative measures.
lthough commonly referred to as sciatica, the term
lumbar radicular pain (LRP) is anatomically more
correct. Lumbar radicular pain is a form of neuralgia
due to an irritation of the sensory root or the dorsal root
ganglion (DRG) of a spinal nerve. In contrast, sciatic
neuralgia specifically refers to pain in the distribution of
the sciatic nerve due to pathology of the nerve itself.1
By definition, radicular pain involves a region beyond the
spine. In individuals presenting both with spinal pain and LRP,
it is paramount that the characteristics and distribution of each
pain should be defined and diagnosed separately, as it is likely
they arise from different anatomical structures and are caused
by different pathomechanisms. In LRP, ectopic impulses generated in the DRG are perceived as pain arising in the territory
innervated by the affected axon. Somatic pain (nociception) is
evoked by noxious stimulation of nerve endings; somatic
referred pain is a function of interneuronal convergence within
the spinal cord. Neuropathic pain is evoked by ectopic
impulses generated in the axons of a peripheral nerve.1
Radicular pain should not be confused with radiculopathy. Radiculopathy is objective loss of sensory and/or
motor function as a result of conduction block; the features of which might include numbness, motor loss,
wasting, weakness, and loss of reflexes. Each can occur
simultaneously or independent of each other.2 Any lesion
that affects the integrity of the lumbosacral nerve root
can cause LRP, radiculopathy or both (Table 1).
Jay Govind,
MBChB, DPH (OH),
MMed, FFOM (RACP),
is VMO, Royal
Newcastle Hospital,
and research officer,
Department of Clinical
Research,
Bone and Joint Institute,
Royal Newcastle
Hospital, University of
Newcastle,
New South Wales.
Pathophysiology
Lumbar radicular pain is caused by more than a simple
mass effect. With the advent of computerised tomography (CT) and magnetic resonance imaging (MRI),
studies have confirmed that patients whose symptoms
of sciatica had resolved still showed the same mass
effect.3,4 Additionally, disc herniations or protrusions
evident on CT or MRI may not be associated with
either low back pain or LRP.5
Ectopic impulses, and hence perception of pain,
Reprinted from Australian Family Physician Vol. 33, No. 6, June 2004 409
Theme: Lumbar radicular pain
Table 1. Causes of radicular pain2
Disc herniation (commonest cause)
Spinal stenosis
Synovial cysts
Infection
Infestation
Tumour
Vascular abnormalities
Table 2. Distinguishing features of LRP and somatic referred pain2
Feature
Radicular pain
Somatic referred pain
Distribution Entire length of lower limb
BUT
below knee > above knee
Pattern
Narrow band
Travelling
Quasi segmental but not
dermatomal
Not distinguishable by segment
Quality
Depth
Shooting, lancinating,
like an electric shock
Deep as well as superficial
Anywhere in lower limb
BUT
proximal > distal
Wide area
Relatively fixed in location
Quasi segmental but not
dermatomal
Not distinguishable by segment
Boundaries difficult to define
Dull, aching, like an expanding
pressure
Deep only, lacks any cutaneous
quality
Table 3. Conditions mimicking radicular
pain2
Spinal cord tumours
Diabetic neuropathy
The prodromal phase of herpes zoster
Tabes dorsalis
Direct contusion of the sciatic nerve
Polyarthritis nodosa
Gluteal injections
Prolonged sitting
Penetrating wounds
Methyl methacrylate neuropathy following
hip replacement
may be generated as a result of:
mechanical deformation of DRG
mechanical stimulation of previously damaged
nerve roots
410Reprinted from Australian Family Physician Vol. 33, No. 6, June 2004
inflammation of DRG, and/or
possible ischaemic damage to DRG.
There are two distinctive, but not mutually exclusive
pathomechanisms for LRP.
Nerve roots subjected to sustained compression for
protracted periods may become sensitised to mechanical stimulation. The resulting patho-anatomical changes
including focal demyelination, intraneural oedema,
impaired microcirculation, Wallerian degeneration,
partial axonal damage with or without neuroma in continuity, have the potential to generate ectopic impulses
from the affected nerve.2
Studies have also confirmed that while pain may correlate with the size of disc herniation, and limitation of straight
leg raising may correlate with pain, straight leg raising does
not correlate with the size of disc herniation.6 This implies
that tension in a sensitised nerve root is most likely cardinal
mechanism of pain rather than the effects of simple compression.
A complementary explanation implicates a chemically
mediated noncellular inflammatory reaction chemical
radiculitis implying irritation of the nerve root by perineural spread of nucleus pulposus, which might occur
through a disc rupture. Nucleus pulposus is inflammatogenic and leukotactic.7,8
Clinical features
Distinguishing between radicular pain and somatic pain
(local or referred) is essential to the diagnosis. Radicular
pain is often perceived in the territory innervated by the
affected nerve root, eg. in the lower extremity when
L4/5/S1 nerve roots are involved, and in the anterior
thigh in the case of L2/3. Implicitly, pain does not follow
the corresponding dermatomes and it is the sensory
loss that indicates the affected segment. Lumbar radicular pain travels through the lower limb along a narrow
band usually not more than 58 cm wide, and when
experimentally reproduced, the perceived pain is qualitatively sharp, shooting or lancinating. 9 It can be
experienced superficially and deeply.
In contrast, somatic referred pain is often felt deeply
as a dull aching pain. Radicular pain and somatic referred
pain are not mutually exclusive. They can co-exist.
Radicular pain may be superimposed on a background of
somatic referred pain. Hence, careful scrutiny is essential
to distinguish whether the patient is describing somatic
referred pain, radicular pain or a combination of both.
Although not absolute, certain features may assist
in distinguishing between somatic pain and radicular
pain (Table 2). Conditions that can mimic radicular pain
Theme: Lumbar radicular pain
without affecting the nerve roots are shown in Table 3.
Clinical examination
Clinical examination does not diagnose the cause of LRP,
but can establish the presence or absence of radiculopathy.
Although lumbar disc herniation is the commonest
cause of LRP, there are no distinctive features either in
the history or physical examination that would implicate
the intervertebral disc as the cause of pain. Definitive
diagnosis can only be made by imaging studies. The
straight leg raise clinical test has the best sensitivity,
but a low specificity with an average likelihood ratio of
1.5. Complementary testing procedures including dorsiflexion of the foot, impaired ankle reflex, sensory deficit
and muscle atrophy, have modest to poor sensitivities
and specificities. In younger and middle aged patients,
the pretest probability of disc herniation is high,
whereas in the elderly, foraminal stenosis or spinal
stenosis is more likely.
The natural history
On average, patients with LRP can expect a dramatic
reduction in the severity of pain with treatment limited
to simple analgesics. At 12 months, at least 50% of
patients can expect to be free of leg pain, but at least
6070% will continue to experience low back pain.10
Investigations
Imaging
Given the favourable natural history, authorities recommend that in the absence of other indications, imaging
is not required for 46 weeks after the onset of LRP.11
Imaging is best reserved for patients who do not
respond to conservative treatment, and for whom
surgery is contemplated. In patients with a history of
sciatica or in whom a red flag condition seems likely,
appropriate imaging should be requested. Generally,
MRI is the investigation of choice. Not only does it
provide a comprehensive survey of all possible causes,
MRI is radiation free.
Electrophysiological studies
In the absence of clinically proven peripheral neuropathy, electrophysiological studies in patients presenting
with acute LRP are generally not indicated. These
tests cannot accurately determine the precise spinal
nerve level associated with disc herniations and radicular pain cannot be explained by neurophysiological
testing. Furthermore, electromyogram studies correlate poorly with the anatomical level of a disc
herniation. Studies may be indicated to exclude a more
distal nerve damage, verify suspected muscle weakness by needle electromyogram, and to assess
pre-operative baseline muscle status in cases of recurrent disc operation.11
Treatment
Generally bed rest is no more effective than watchful
waiting. Depending on the severity and response to
medication, the early resumption of daily activities
should be encouraged.
Clinical studies have shown that neither piroxicam,10
indomethacin,12 nor oral dexamethasone,13 offer greater
analgesia than placebo. For severe pain, opioids can be
used judiciously.
The efficacy of physical modalities including manipulation and traction remains controversial,11 and there is
no compelling evidence to encourage their utilisation.
Injection techniques such as botulinum toxin,
prolotherapy, or facet joint injections are irrational
and illogical.
Epidural steroid injection
Epidural steroids are not indicated for the treatment
of low back pain. The efficacy of steroid injection
for the treatment of LRP may be due to its antiinflammatory effect on inflamed nerve roots,
inherent local anaesthetic properties, 14 or as a
membrane stabiliser suppressing ectopic
impulses. 15 Steroids injected transforaminally may
offer substantial pain relief for a protracted
period. 6,17 The results are less impressive if given by
the caudal or interlaminar route.
Chemonucleolysis
In carefully selected patients, chemonucleolysis has been
demonstrated to be effective with chronic symptoms, but
residual back and leg pain are troublesome features. At
least 20% of patients will proceed to surgery.18
Surgery
For the management of LRP alone, surgery may be
considered where:
severe unrelenting and disabling pain remains
refractory to conservative measures after at least 6
weeks, but not more than 34 months
neurological signs are present in the radicular distribution, and
leg pain follows a radicular distribution and is the
dominant complaint when compared with back pain.11
Reprinted from Australian Family Physician Vol. 33, No. 6, June 2004 411
Theme: Lumbar radicular pain
Conclusion
Back pain is not synonymous with LRP. These are two
separate entities. In more than 50% of patients, LRP
settles with simple analgesics and patients are encouraged to resume daily activities. Where feasible and
practical, a transforaminal epidural injection of long acting
local anaesthetic and steroid should be considered
given the potential for significant and lasting relief of pain.
Regular review assists in identifying any progressive neurological deficit. In such instances, early referral for
surgical review is necessary.
Summary of important points
LRP is caused by irritation of the sensory root or
DRG.
Disc prolapse is the commonest cause of LRP, but
foraminal or spinal stenosis is more likely in the
elderly.
LRP needs to be distinguished from spinal pain and
somatic referred pain.
Clinical examination will not identify the cause of
LRP but can establish the presence or absence of
radiculopathy (sensory or motor deficit).
Investigation is only indicated for those who do not
respond to conservative measures, as a preparation
for surgery, or to exclude red flag conditions.
If required, MRI is the investigation of choice.
Steroids injected transforaminally can give significant and lasting pain relief.
Surgery is indicated for severe leg pain associated
with neurological deficit not responding to conservative measures.
Conflict of interest: none declared.
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Email: jaygovind@bigpond.com.au
AFP
