THE

POCKET GUIDE TO
NEUROCRITICAL CARE:
A concise reference for the evaluation and
management of neurologic emergencies

by the

Editors-in-Chief:
Marin E. Darsie, MD
Asma M. Moheet, MD MHDS FNCS

Edition Editor:
Winnie Lau, MD
 THE
POCKET GUIDE TO
NEUROCRITICAL CARE:
A concise reference for the evaluation and
management of neurologic emergencies

Marin E. Darsie, MD
Assistant Professor of Emergency Medicine and Neurosurgery
University of Wisconsin School of Medicine and Public Health
Madison, WI, USA

Asma M. Moheet, MD MHDS FNCS

Neurointensivist
Ohio Health Riverside Methodist Hospital Columbus, OH, USA

Winnie Lau, MD
Assistant Professor of Neurology and Neurosurgery
University of North Carolina
Chapel Hill, NC, USA

ii
 For our families, our patients, and their families.
Thank you for teaching us.

Copyright © 2020 by Neurocritical Care Society

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,
mechanical, photocopying, recording, or otherwise, without the prior written
permission of the author.

Disclaimer:

This content was developed by the Neurocritical Care Society (NCS) and is
intended to be used as an educational tool and should not be construed as medical
advice. The editors and authors have made every effort to present accurate and
complete information at the time of publication, however new information on any of
the topics contained in this book may emerge. The authors, editors, publisher, or
any party involved in the production of this work cannot guarantee that all data
presented herein is complete or accurate, and these parties are not responsible for
any omissions or errors in this text or liable for outcomes due to use of this text.
Note that this includes drug information. The information
in this text cannot replace independent evaluation by a qualified medical
professional. Except when otherwise cited, the views expressed by the authors and
editors are their own and are not necessarily the views of any institution with which
the authors or editors are affiliated. Practitioners shouldrefer
to institutional policies and practices where appropriate. References have been
provided by chapter authors at the end of each chapter. NCS respects the
intellectual property rights of others and prohibits users from reproducing content
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written notification of such infringement to NCS.

ISBN-13: 978-1-943909-04-9

Library of Congress Control Number: 2019950961

Printed in the United States of America

iii
PREFACE
The Pocket Guide to Neurocritical Care was first conceived by NCS
members in training in 2016 after recognizing a need for a succinct
reference that reviewed the basics of neurologic emergencies and
neurocritical care. Spearheaded by the NCS Resident and Fellow
Committee with support from the Educational Products Committee,
40+ resident, fellow, and APP authors were recruited to develop the
product with the guidance of established leaders in the neurocritical
care field. This publication has become a recognizable part of NCS
courses, as well as some subspecialty
training courses.

The success of The Pocket Guide can be attributed to the original

mission of “written by trainees, for trainees.” This unique
characteristic ensures the content is high-yield, comprehensive, and
readily accessible to multiple levels of learning. With this edition, we
have continued that mission, taking feedback from trainees, and
adding new authors in training including those in pharmacy training.
We hope that this will be just the first of their many future
publication opportunities.

This book compiles 18 chapters of the highest-yield information as

suggested and recommended by providers and trainees across
multiple disciplines who all have a common interest in caring for
neurocritical care patients. It is not meant to be an exhaustive
reference, but to give readers a strong fund of knowledge in
neurocritical care to support their practice.

iv
ACKNOWLEDGEMENTS
Special thanks go to our editorial team: Anand Venkatraman,
Justin Barr, Kassi Kronfeld, Megan Barra, and Pouya Ameli.

We would like to recognize the members of the NCS Educational

Products Committee for their oversight and support in developing
this project, as well as their time spent editing and reviewing its
content for accuracy.

A special thank you to Angel Gindele who coordinated all the

authors, timeline, and editorial needs of this edition. Without her,
this could not be the comprehensive and refined product before
you.

Finally, we would like to thank our families. We are the best

versions of ourselves because of your love and support.

Marin Darsie, Asma Moheet, and Winnie Lau

May 2020

v
ABBREVIATIONS AVDO2 arterio-venous difference of
oxygen consumption
+ positive
AVM arteriovenous malformation
¯ decreased
BAL broncheoalveolar lavage
↑ increased
BCx blood culture
AAN American Academy of Neurology
BBB blood-brain barrier
Ab antibody
BID twice daily
ABCs airway, breathing, circulation
BiPAP bi-level positive airway pressure
ABG arterial blood gas
BMP basic metabolic panel
AC assist control
BP blood pressure
ACA anterior cerebral artery
BTF Brain Trauma Foundation
ACh acetylcholine
BSAS Bedside Shivering Assessment
AChEI acetylcholinesterase Scale
inhibitor(s)
C Celsius
AChR acetylcholinesterase
receptor(s) Ca2+ calcium

ACEI angiotensin-converting enzyme CAA cerebral amyloid angiopathy

inhibitor(s) CABG coronary artery bypass graft
ACLS Advanced Cardiac Life Support CAS carotid artery stenting
AComm anterior communicating artery CBC complete blood count
ADR alpha delta ratio CBF cerebral blood flow
AED anti-epileptic drug CCM cerebral cavernous
AF atrial fibrillation malformation

AG anion gap CEA carotid endarterectomy

AHA American Heart Association cEEG continuous EEG

AICA anterior inferior cerebellar artery CHF congestive heart failure

AIDS acquired immune deficiency CI continuous infusion

syndrome CIDP chronic inflammatory
AIS acute ischemic stroke demyelinating polyneuropathy

ALS amyotrophic lateral sclerosis COPD chronic obstructive pulmonary

disease
AKA also known as
CIM critical illness myopathy
ARDS acute respiratory distress
syndrome CIWA Clinical Institute Withdrawal
Assessment
aSAH aneurysmal subarachnoid
hemorrhage CKD chronic kidney disease

ASIA American Spinal Injury CMP comprehensive metabolic

Association panel

ASV adaptive support ventilation CMRO2 cerebral metabolic rate of

oxygen
ATLS Advanced Trauma Life Support

vi
CMV cytomegalovirus ECMO extracorporeal membrane
oxygenation
CN cranial nerve
ECT electroconvulsive therapy
CNS central nervous system
ED emergency department
CO cardiac output
EDH epidural hematoma
CPAP continuous positive pressure
ventilation EEG electroencephalogram
CPP cerebral perfusion pressure EKG electrocardiogram
CPR cardiopulmonary resuscitation EMG electromyography
CrCl creatinine clearance EMSE epidemiology based mortality
score
CSE convulsive status epilepticus
EN enteral nutrition
CSF cerebrospinal fluid
ENLS Emergency Neurologic Life
CSWS cerebral salt wasting syndrome Support
CT computerized tomography ENT ear/nose/throat or
CTA CT angiography otolaryngology

CTV CT venogram EOM extraocular muscles

CVR cerebral vascular resistance ETT endotracheal tube

CVST cortical vein sinus thrombosis EVD external ventricular drain

CXR chest x-ray FDA Federal Drug Administration

D day FFP fresh frozen plasma

DAI diffuse axonal injury FiO2 fraction of inspired oxygen

dAVF dural arteriovenous fistula FOUR Full Outline of

UnResponsiveness
DBP diastolic blood pressure
FVC forced vital capacity
DCD donation after circulatory death
GBS Guillain-Barré syndrome
DCI delayed cerebral ischemia
GCS Glasgow Coma Scale
DDAVP desmopressin
GI gastrointestinal
DH decompressive hemicraniectomy
GOS-E Glasgow Outcome Scale-
DI diabetes insipidus Extended
DKA diabetic ketoacidosis GPD generalized periodic discharge
DNI do not intubate GRE gradient echo
DNR do not resuscitate GTC generalized tonic-clonic
DOAC direct oral anticoagulant H hour
DSA digital subtraction angiography HCG human chorionic gonadotropin
DTR deep tendon reflexes HD hemodialysis
DVT deep vein thrombosis Hgb hemoglobin
EBV Epstein-Barr virus HIT heparin-induced
thrombocytopenia

vii
HIV human immunodeficiency virus LOS length of stay
HOB head of bed LP lumbar puncture
HSV Herpes simplex virus LR Lindegaard ratio
HTLV-1 Human T-lymphotropic virus LR Ringer’s lactate
type 1
MAP mean arterial pressure
HTN hypertension
MCA middle cerebral artery
HTS hypertonic saline
MCS minimally conscious state
IBW ideal body weight
MEP maximal expiratory pressure
ICA internal carotid artery
MFV mean flow velocity
ICH intracerebral hemorrhage
MG myasthenia gravis
ICP intracranial pressure
MH malignant hyperthermia
ICU intensive care unit
MHS malignant hemispheric stroke
IDSA Infectious Disease Society of
America MI myocardial infarction

IgA immunoglobulin A Min minute

IIC ictal-interictal continuum mL milliliter

IM intramuscular MMR measles, mumps, rubella

INR international normalized ratio MOA mechanism of action

IO intraosseous MRI magnetic resonance imaging

I&O input and output mRS modified Rankin Scale

IV intravenous MRV magnetic resonance venogram

IVC inferior vena cava MV mechanical ventilation

IVF intravenous fluids NCCU Neurocritical Care Unit

IVH intraventricular hemorrhage NCS nerve conduction study OR

Neurocritical Care Society
IVP intravenous push
NCSE nonconvulsive status epilepticus
IVIg intravenous immunoglobulin
NG nasogastric
IVP intravenous push
NIF negative inspiratory force
IV tPA intravenous tissue plasminogen
activator NIPPV noninvasive positive pressure
ventilation
KCI potassium chloride
NM neuromuscular
LE lower extremity
NMBA neuromuscular blockade agent
LCMV lymphocytic choriomeningitis
virus NMJ neuromuscular junction

LDH lactate dehydrogenase NMO neuromyelitis optica

LFTs liver function tests NMS neuroleptic malignant syndrome

LKWT last known well time NORSE new onset status epilepticus

LMWH low-molecular-weight heparin NPi neurologic pupillary index

viii
NS normal saline PTT partial thromboplastin time
NSAID nonsteroidal anti-inflammatory PVS persistent vegetative state
drugs
QID four times daily
O2 oxygen
QOD every other day
OG orogastric
RA rheumatoid arthritis
OHCA out-of-hospital cardiac arrest
RAAS renin-angiotensin-aldosterone
OOB out of bed system
OSA obstructive sleep apnea RAS renin-angiotensin system
OSM osmolar RAS reticular activating system
OT occupational therapy or therapist RASS Richmond Agitation and
Sedation Scale
PbtO2 brain tissue oxygen tension
R/O rule out
PCA posterior cerebral artery
RCT randomized control trial
PCC prothrombin complex
concentrate RN registered nurse
PComm posterior communicating artery ROM range of motion
PCR polymerase chain reaction ROSC return of spontaneous circulation
PD periodic discharge RR respiratory rate
PE pulmonary embolus RSE refractory status epilepticus
PEEP positive end expiratory pressure RSI rapid sequence intubation
PEG percutaneous endoscopic RT respiratory therapy or therapist
gastrostomy
RTA renal tubular acidosis
PFO patent foramen ovale
RVR rapid ventricular response
PICA posterior inferior cerebellar artery
SAH subarachnoid hemorrhage
PICC peripherally inserted central
catheter SBP systolic blood pressure

PIP peak inspiratory pressure SC subcutaneous

PIV peripheral intravenous line SCA superior cerebellar artery

PLEX plasmapheresis SCD sequential compression device

Pplat plateau pressure SCI spinal cord injury

PRBCs packed red blood cells SDH subdural hematoma

PRES posterior reversible Se sensitivity

encephalopathy syndrome SE status epilepticus
PRIS propofol infusion syndrome Sec second
PRN pro re nata, as needed SIADH syndrome of inappropriate
PRVC pressure regulated volume antidiuretic hormone secretion
control SIMV synchronized intermittent
PT physical therapy or therapist mechanical ventilation
SLE systemic lupus erythematosus

ix
s/p status post management
Sp specificity U units
SpO2 peripheral capillary oxygen UA urinalysis
saturation
UCx urine culture
SRSE super refractory status
epilepticus UE upper extremity

SSEPs somatosensory evoked UFH unfractionated heparin

potentials UMN upper motor neuron
SSRI selective serotonin reuptake US ultrasound
inhibitor
UTI urinary tract infection
SSS sick sinus syndrome
VALI ventilator associated lung injury
ST speech therapy or therapist
VBG venous blood gas
STESS status epilepticus severity score
VC volume control
SWI susceptibility-weighted imaging
VF ventricular fibrillation
TB tuberculosis
VPA valproic acid
TBI traumatic brain injury
VS vegetative state
TCA tricyclic antidepressant
VT tidal volume
TCD transcranial doppler ultrasound
VT ventricular tachycardia
TH therapeutic hypothermia
VTE venous thromboembolism
TIA transient ischemic attack
VZV Varicella zoster virus
TMJ temporomandibular joint
w/ with
TMP-SMX trimethoprim-sulfamethoxazole
WFNS World Federation of Neurological
TOF train-of-four Surgeons
tPA tissue plasminogen activator WNV West Nile virus
TPN total parenteral nutrition w/o without
TSH thyroid stimulating hormone yo years old
TTM targeted temperature

x
CONTENTS
COMPONENTS OF THE COMA EXAM .......................................... 1
Anand Venkatraman, MD
Edward Manno, MD MS

ACUTE SPINAL CORD INJURY ................................................... 13

Shola Aluko, MD
Ribal Bassil, MD
Deborah M. Stein, MD MPH FACS FCCM

NEUROMUSCULAR EMERGENCIES .......................................... 24

Marin Darsie, MD
J. Dedrick Jordan, MD PhD FNCS

STATUS EPILEPTICUS ................................................................ 33

Alexis Steinberg, MD
Anh Nguyen, MD
Jan Claassen, MD PhD FNCS

MENINGITIS AND ENCEPHALITIS .............................................. 45

Tachira Tavarez, MD
Maria Muzammil, MD MBBS
Barnett Nathan, MD

NEUROLOGIC CARE AFTER CARDIAC ARREST...................... 57

Christian Hernandez, MD
Romergryko Geocadin, MD FNCS

ACUTE ELEVATED INTRACRANIAL PRESSURE

& HYDROCEPHALUS ................................................................... 65
Deepa Malaiyandi, MD
Lori Shutter, MD FNCS FCCM

SUBARACHNOID HEMORRHAGE............................................... 77
Jennifer A. Kim, MD PhD
Ashutosh Mahapatra, MD
Paul Vespa, MD FCCM FAAN FANA FNCS

INTRACEREBRAL HEMORRHAGE ............................................. 92

Tobias Kulik, MD
J. Claude Hemphill III, MD FNCS

xi
ACUTE ISCHEMIC STROKE ...................................................... 104
Winnie Lau, MD
Kassie Kronfeld, MD
Wade Smith, MD PhD FNCS

TRAUMATIC BRAIN INJURY ..................................................... 118

Chitra Sivasankar, MD
Catherine Albin, MD
Kristine O’Phelan, MD

BRAIN DEATH IN ADULTS ........................................................ 130

Sherri A. Braksick MD
Eelco F. M. Wijdicks, MD FNCS

MULTIMODAL MONITORING ..................................................... 139

Masoom Desai, MD
Kara R. Melmed, MD
Chad Miller, MD FNCS

HIGH-YIELD MEDICATIONS IN NEUROCRITICAL CARE ........ 149

Yasmin Ali O’Keefe, MD
Feras Akbik MD PhD
Gretchen M. Brophy, PharmD BCPS FCCP FCCM FNCS

MECHANICAL VENTILATION .................................................... 165

Junling Dong, DO
Krista Lim-Hing, MD
Amol Patil, MD

ACID-BASE & ELECTROLYTE DISTURBANCES ..................... 184

Brittny Medenwald, PharmD
Michael Halstead, MD MPH
Jose I. Suarez, MD FNCS

TOXIDROMES ............................................................................. 204

Megan Barra, PharmD BCPS BCCCP
Melissa Squires, MD MPH
Thomas Bleck, MD MCCM

INTERDISCIPLINARY PATIENT CARE IN THE NCCU.............. 228

Megan A Brissie, DNP RN ACNP-BC CEN
Helen M. Nester, MSN RN ACNP-BC
Mary Kay Bader, MSN RN CNNS FNCS FAHA

xii
 CHAPTER 1
COMPONENTS OF THE COMA EXAM

Anand Venkatraman & Edward Manno

The examination of a comatose patient is one of the most important

responsibilities in the care of neurocritically ill patients. We describe key
components of the coma exam and review common findings.
………………………

DISORDERS OF CONSCIOUSNESS

Consciousness is comprised of 2 components: arousal and awareness. Two

connected anatomic pathways coordinate consciousness: the ascending RAS
within the brainstem, and arousal centers in the bilateral thalami which project
diffusely to cortical neurons. Impairment of awareness can lead to a spectrum of
disorders, which include MCS and VS. Coma, on the other hand, is caused by
impaired arousal which leads to impaired awareness. Consciousness is not an all-
or-nothing phenomenon, and gradations do exist. Newer technologies, such as
functional MRI, are beginning to provide the ability to image and interpret brain
processing in a more advanced and high-resolution fashion. This is shedding light
on the gradations of consciousness and may alter how we evaluate and treat
patients that may be “functionally locked-in” or have Unresponsive Wakefulness
Syndrome, but the bedside neurologic exam remains a highly valuable standard
assessment tool for all clinicians.

DIFFERENTIAL DIAGNOSIS
It is important to differentiate coma from other disorders of consciousness,
including VS, MCS, and locked-in syndrome (Table 1). The prognosis of disorders
of consciousness varies widely, and depends on clinical factors, cause of brain
injury, and the duration of the consciousness impairment. For patients with PVS
(defined as vegetative state with duration of > 1 month), the prognosis is poorest.
Some patients with MCS will show recovery over time. Locked-in syndrome
usually results from a lesion that interrupts the descending motor pathways,
leaving cognitive function and consciousness intact, but with severe limitations on
the patient’s ability to interact with the examiner.

POSSIBLE CAUSES OF COMA

Bihemispheric phenomena: medication or drug toxicities, SE or NCSE, metabolic
disorders, meningoencephalitides (w/ or w/o focal neurologic findings).

1
Focal anatomic brain lesions: affecting the thalamus or brain stem which
contain crucial arousal-supporting neurons. May be associated with focal
neurologic findings.

It is essential to rule out reversible causes of coma in cases when the etiology
is not known (Table 2).

NEUROLOGIC EXAM IN COMA

The initial exam is important for localization and identifying the cause of coma.
Serial exams to assess interval change are equally important. Acute neurologic
deterioration can signal AIS, ICH, seizure, worsening edema, hydrocephalus,
or elevated ICP. Hourly vital sign assessments and neurologic checks are the
norm in newly-admitted NCCU patients. In some, such as those admitted after
surgical or endovascular procedures, the frequency of assessments may need
to be more often.

We recommend the use of standardized scales to assess disorders of

consciousness. The best known is the GCS, of which the arbitrary definition of
coma is GCS ≤ 8 (E2V2M4). See Table 3 for reference.

Limitations of GCS:
 Can miss locked-in states and subtle changes in consciousness
 Does not assess pupillary and other brainstem reflexes
 Patients with similar scores may go on to have different outcomes
 Assigns greater weight to motor response than eye opening and verbal
responses
 Intubated patients default to a T score on the verbal component and aphasic
patients have a low verbal score, each of which make the total GCS less
reliable
 Some studies suggest only moderate inter-rater reliability, especially for
motor response

FOUR score can also be used, and addresses some shortcomings of the GCS:
 Incorporates brainstem function and respiratory pattern, allowing for better
localization
 Can help recognize a locked-in state
 Can recognize various stages of herniation
The calculation of the FOUR Score is illustrated in Figure 1 and is also
described in Table 4.

2
Figure 1. Calculation of the FOUR Score (used with permission from the Mayo
Foundation for Medical Education and Research)

SPECIFIC STEPS OF THE COMA EXAM

The patient’s mental status, cranial nerve exam, motor exam (including response to
noxious stimulus), tone, and reflexes should be assessed.

Cranial Nerves (CN)

Pupils:
 Afferent: CN II, Efferent: CN III
 Observe pupils in low light. Then, shine a light into both pupils alternately and
observe for briskness of response. Assess for both direct and consensual light
reflexes. A pupillometer is a useful adjunct, especially with abnormal pupils

Asymmetric pupils: consider compressive lesions of CN III, such as due to

herniation and/or PComm aneurysms
 Unilateral dilated, non-reactive pupil: CN III dysfunction (rule out compression) vs
unilateral medication effect or post-surgical pupil
 Nonreactive, dilated pupils: consider severe brainstem damage or medication
side effect (Table 5)
 Pinpoint pupils: consider opioid use, pontine stroke or hemorrhage,
organophosphate poisoning, clonidine overdose, pilocarpine eye drop use, and
occasionally mirtazapine and olanzapine
 Sluggish pupils: NMBA, recent mydriatic administration, or albuterol use
Corneal responses:
 Afferent: CN V, Efferent: CN VII
 Gently hold the patient’s eyelids open and drop 1-2 saline drops onto the cornea
of each eye
 Cotton swabs can be used with caution as repeated testing with this method
can lead to corneal ulceration

3
 There is a blinking response if this pathway is intact
Blink to threat:
 Afferent: CN II, Efferent: CN VII
 Briskly move your hand into the patient’s visual field while holding his/her eyelid
open. The patient should blink

Gaze:
 Hold eyes open and observe direction of gaze in neutral head position
 Eye movements involve coordinated functioning of multiple CN, frontal lobe and
brainstem centers
 Gaze deviation also occurs due to involvement of frontal eye fields in each
hemisphere: destructive lesions cause ipsilateral gaze deviation, stimulation
causes contralateral deviation
□ Cortical ischemic stroke patients demonstrate gaze directed towards
hemisphere of the stroke
□ Seizure patients demonstrate gaze directed away from seizing hemisphere,
and may have gaze towards the hemisphere post-ictally
 Brainstem strokes can cause impaired gaze towards the side of the stroke
 Forced downgaze may be seen in thalamic hemorrhages, pineal mass lesions,
and severe hydrocephalus
 Bilateral CN VI palsy seen in ↑ ICP
EOMs:
 Innervation of extraocular muscles: Lateral Rectus CN VI, Superior Oblique CN
IV, All others CN III
 Fixation and tracking are normal findings
 Fixation: eyes looking at an object and not moving from that position
 Tracking: eyes moving as the object or the examiner moves, to follow them
 Roving eye movements: slow and conjugate to-and-fro movements
□ Can be seen in toxic and metabolic conditions where brainstem is intact.
Light stages of sleep and lighter coma also cause this
 Nystagmus: fast, beating movements to one side (may indicate ongoing
seizures)
□ Other causes: phenytoin toxicity, brain lesions like those seen in stroke or
multiple sclerosis, inner ear disorders, and metabolic disorders like thiamine
deficiency
□ Down-beating nystagmus may be seen in disorders of the craniocervical
junction or cerebellar flocculus
□ Up-beating nystagmus may be seen in cerebellar vermis involvement, and
sometimes in lesions of the medulla
□ Acute lesions in the pons can cause rapid downward jerking of the eyes with
slow return to normal position, called ocular bobbing

4
Fundoscopy:
 Evaluate optic disc and nerve
 Blurring of optic disc margins is indicative of ↑ ICP, but absence of blurring
does not automatically indicate normal ICP. Subhyaloid hemorrhages can also
be seen with ↑ ICP. The presence of spontaneous venous pulsations implies a
normal ICP, but the absence of these pulsations is uninformative
□ Terson syndrome: subhyaloid hemorrhage in SAH
Oculocephalic reflex or “doll’s eyes”:
 Afferent: CN VIII and proprioceptive pathways from the cervical level,
Efferent: CN III and VI
 Confirm stability of cervical spine, then move head briskly in one direction and
then the other with the eyelids held open
 Interpretation of OCR responses in a comatose patient:
□ In a normal OCR, eyes move conjugately in the direction opposite to head
movement
□ In abnormal OCR, eyes stay in fixed position in the head, implying
brainstem disease

Oculovestibular reflex or “cold calorics”:

 Afferent: CN VIII, Efferent: CN III and VI
 Do this if OCRs are absent; also useful in cases where cervical spine
instability is suspected
 Ensure patency of ear canal and ability of water to reach tympanic membrane
 Instill 50-60 mL of ice-cold water into each ear over 1 minute using a syringe
 Test each side individually with several minutes between testing each side
 Normal: slow conjugate deviation towards the irrigated side and fast
horizontal nystagmus tothe contralateral ear
 Abnormal: no fast nystagmus in patients with cerebral damage but intact
brainstem reflexes. No slow deviation and no fast nystagmus imply brainstem
damage

Gag reflex:
 Afferent: CN IX, Efferent: CN X
 Tested by stimulating the back of the patient’s throat with a tongue depressor
or suction catheter
 Gag reflex is of limited utility since many patients with normal brainstem lack a
gag reflex. If a gag reflex is present, and on subsequent testing it is lost, that
might be of clinical value

Cough reflex:
 Afferent: CN X, Efferent: CN X
 In an intubated patient can be tested by touching the carina with a suction
catheter passed through the patient’s ETT or tracheostomy tube

5
Motor
A normal patient should follow commands. In a comatose patient it is often
necessary to administer noxious stimuli, which may include sternal rub or
supraorbital ridge pressure. Do not perform supraorbital ridge pressure in the
presence of facial fractures. If there is no response to this noxious stimulus,
peripheral stimulus (such as application of nailbed pressure) should be performed.
There is a range of movements which may be seen.
 Patients may localize to the stimulus, withdraw away from the stimulus, flex,
extend, or have no response at all. Grimacing may also be observed
 Spinal reflexes may lead to lower extremity movements even in patients with
severe brain damage or brain death (e.g. triple flexion response of hip, knee, and
ankle flexion)
 Decorticate posturing: upper extremity flexion and lower extremity extension,
typically from a lesion above the red nucleus of the midbrain
 Decerebrate posturing: upper and lower extremity extension is typically from a
lesion below the red nucleus
 Unilateral or bilateral posturing may be seen based on location of lesion causing
it
 Post-anoxic myoclonus is common in patients following cardiac arrest.
Occasionally it may indicate ongoing seizure activity, and EEG is recommended

Tone and reflexes

Increased tone, brisk reflexes, and upgoing toes are indicative of a lesion in the
spinal cord or brain.
 If unilateral, usually indicates a lesion on the opposite side
 Symmetric hyperreflexia can be normal, especially in young patients, but may
also indicate bilateral lesions, especially in the brainstem and spinal cord. In
rare instances, symmetric hyperreflexia might indicate conditions like
serotonin syndrome
 Neuro-intact people with brisk reflexes usually do not have upgoing toes, so
this can be a good way to differentiate pathological cases from physiologic
hyperreflexia
 Brisk reflexes and ↑ tone in lower extremities but not upper extremities are
indicative of lesion below the level of the cervical spinal cord
 Very early on, brain and spinal cord lesions might present with flaccid
paralysis

RESPIRATORY PATTERNS IN COMATOSE PATIENTS

Medication side effects should be ruled out first. Sedating medications tend to
cause slow regular breathing, whereas salicylate overdose can cause rapid
breathing. In intubated patients, assess synchrony with the ventilator and degree
of effort, including actual vs set respiratory rate. Abnormal breathing may
manifest more prominently on spontaneous ventilator modes.
Types of abnormal breathing include:
 Cheyne-Stokes: oscillation between fast and slow breathing (multiple causes
including bilateral hemispheric lesions, heart failure, etc.)

6
 Apneustic: rapid breathing with inspiratory pauses (pontine lesions)
 Biot’s: quick shallow breaths followed by pause after four to five cycles
(medullary damage). Also known as ataxic breathing
 Cluster: regular cycles of deep breaths with variable periodicity
 Kussmaul: rapid, deep and labored breaths (metabolic acidosis)
USEFUL ANCILLARY TESTS IN COMATOSE PATIENTS
 Laboratory tests: serum electrolytes, glucose, hormone levels (such as TSH),
ammonia, and toxicology tests should be considered to evaluate for potentially
reversible causes of coma (see Table 2)
 CT: primary value is to rule out ICH or large mass, and to assess for edema,
hydrocephalus, and herniation
 MRI: requires significantly more time than CT and can be contraindicated or
difficult to obtain in unstable patients, but is helpful in diagnosis of demyelinating
lesions, meningoencephalitides, small strokes (especially evaluation of posterior
fossa), and some metabolic disorders
 EEG: should be performed in all patients who are unresponsive without a clear
etiology to evaluate for nonconvulsive or electrographic seizures. Most common
finding in coma is “generalized slowing.” Focal slowing can indicate a structural
lesion. Triphasic waves are often seen in metabolic encephalopathies
(classically in liver failure). Cefepime is another common cause of triphasic-like
waves on EEG and alteration of consciousness in ICU patients, especially those
with impaired renal function
 LP: measurement of opening pressure and diagnostic evaluation of CSF for
infectious or inflammatory etiologies may assist in narrowing the differential
diagnosis