Author(s): Martin A Samuels MD, FACP, FAAN
Edition: Seventh
ISBN: 0-7817-4646-9
Pub Date: March 2004
Pages: 592
By quack008
Copyright ©2004 Lippincott Williams & Wilkins
Samuels, Martin A.
Manual of Neurologic Therapeutics, 7th Edition
Edited by
Martin A. Samuels M.D., M.A.C.P., F.A.A.N.
Neurologist-in-Chief and Chairman
Department of Neurology, Brigham and Women
’
s Hospital, Professor of Neurology, Harvard Medical School, Boston, Massachusetts
Secondary Editors
James D. Ryan
Acquisitions Editor
Grace R. Caputo
Developmental Editor
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Production Editor
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Manufacturing Manager
Patricia Gast
Cover Designer
Compositor: Techbooks
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–
Crawfordsville
Printer

Harvard Medical School; Senior Neurologist, Department of Neurology, Brigham and Women
’
s Hospital, Boston, Massachusetts
Steven K. Feske M.D.
Assistant Professor of Neurology
Harvard Medical School; Director, Stroke Division, Department of Neurology, Brigham and Women
’
s Hospital, Boston, Massachusetts
Robert B. Fogel M.D.
Instructor in Medicine
Harvard Medical School; Physician, Division of Sleep Medicine, Brigham and Women
’
s Hospital, Boston, Massachusetts
Robert D. Helme F.R.A.C.P., Ph.D.
Professor of Neurology
University of Melbourne, Carlton, Victoria; Neurologist, Barbara Walker Centre for Pain Management, St. Vincent
’
s Hospital, Fitzroy,
Victoria, Australia
Galen V. Henderson M.D.
Instructor in Neurology
Harvard Medical School; Director, Critical Care and Emergency Neurology, Department of Neurology, Brigham and Women
’
s Hospital,
Boston, Massachusetts
Santosh Kesari M.D., Ph.D.
Instructor in Neurology
Harvard Medical School; Associate Neurologist, Department of Neurology, Brigham and Women
’
s Hospital, Boston, Massachusetts

Massachusetts
Patrick Y. Wen M.D.
Associate Professor of Neurology
Harvard Medical School; Director, Division of Neurooncology, Department of Neurology, Brigham and Women
’
s Hospital, Boston,
Massachusetts
David A. Wolk M.D.
Instructor in Neurology
Harvard Medical School; Associate Neurologist, Department of Neurology, Brigham and Women
’
s Hospital, Boston, Massachusetts
John W. Winkelman M.D., Ph.D.
Assistant Professor of Psychiatry
Harvard Medical School; Medical Director, Sleep Health Center, Newton, Massachusetts; Physician, Division of Sleep Medicine,
Department of Medicine, Brigham and Women
’
s Hospital, Boston, Massachusetts
Copyright ©2004 Lippincott Williams & Wilkins
Samuels, Martin A.
Manual of Neurologic Therapeutics, 7th Edition
DEDICATION
This book is dedicated to the original contributors to the Manual of Neurologic Therapeutics.
They were all members of a single group of residents in the neurology training program at the Massachusetts General Hospital when the
idea was hatched almost 30 years ago.
They have all gone on to distinguished careers in neurology.
Telmo M. Aquino
Raymond J. Fernandez
Robert D. Helme
Daniel B. Hier

PREFACE TO THE FIRST EDITION
Until very recently the neurologist’s primary task was to categorize and organize the structure and pathologic alterations of the
nervous system. In fact, neurology has long been known as a discipline with elegantly precise and specific diagnostic capabilities but
little or no therapeutic potentiality. Further, many surgeons, pediatricians, and internists have traditionally thought of the neurologist
as an impractical intellectual who spends countless hours painstakingly localizing lesions while ignoring pragmatic considerations of
treatment. Perhaps this conception is largely attributable to the peculiar complexity of the nervous system and the consequent relative
naivete of physicians in their understanding of its functions.
Many of the classic descriptions of disease states in other medical disciplines were completed in the last century; in neurology, these
have only been described in the past generation, and only in the last ten years has neurology begun to be characterized by subcellular
mechanistic concepts of disease. This maturity has meant that the neurologist is now as much involved in the therapeutic aspects of his
specialty of medicine as any of his colleagues. Certain neurologic diseases, such as epilepsy, have been treatable for relatively long
periods of time, but understanding of the subcellular mechanisms of other diseases has led to newer, more effective forms of therapy.
An example of this is the enlarged understanding we now have of the biochemical alterations in Parkinson disease, and the resultant
therapeutic implications. Now, much as the endocrinologist treats diabetes with insulin and the cardiologist treats congestive heart
failure with digitalis, the neurologist treats Parkinson disease with l-dopa. In all these situations, the underlying condition is not cured;
rather, an attempt is made to alter the pathophysiologic processes by utilizing a scientific understanding of the function of the diseased
system.
This manual embodies a practical, logical approach to the treatment of neurologic problems, based on accurate diagnosis, that should
prove useful to both clinician and student. No attempt is made to reiterate the details of the neurologic examination; it is assumed that
the reader is competent to examine the patient
—
although particularly important or difficult differential diagnostic points are mentioned
when appropriate. In this regard, it should be emphasized that this manual is only a guide to diagnosis and therapy, and each patient
must be treated individually. The manual is organized to best meet the needs of the clinician facing therapeutic problems. Thus, the
first seven chapters are concerned with symptoms, such as dizziness and headache, while the last ten consider common diseases, such
as stroke and neoplasms.
I thank the many colleagues and friends whose criticism and comments were useful in the preparation of this book, in particular Drs. G.
Robert DeLong, C. Miller Fisher, George Kleinman, James B. Lehrich, Steven W. Parker, Henry C. Powell, E. P. Richardson, Jr., Maria
Salam, Bagwan T. Shahani, Peter Weller, James G. Wepsic, and Robert R. Young. In addition I am indebted to Sara Nugent and Helen
Hyland for their assistance in the preparation of the many manuscripts, and to Diana Odell Potter, formerly of Little, Brown and

The 7
th
edition contains an entire chapter on neurologic intensive care, now a well-defined subspecialty. Epilepsy management currently
involves not only an array of new drugs but also innovative strategies such as vagal nerve stimulation and a greater emphasis on
earlier surgical treatment. Neurootology encompasses the common complaint of dizziness, emphasizing both pharmacologic and
physical therapy approaches to treatment. Back and neck pain, still among the most common complaints in all of medicine, are now
evaluated with much improved diagnostic tests, which lead to more precise treatment. An entire chapter is dedicated to sleep
disorders, an enormous area of disability in which major new advances in therapy have occurred. Cancer neurology now involves a
complex array of chemotherapy, radiation therapy, and new cutting edge treatments using monoclonal antibodies. No area has changed
more substantively than multiple sclerosis, in which fresh magnetic resonance imaging-influenced diagnostic criteria and several
immunomodulatory drugs have substantively altered the clinical course of the disease. The area of neuromuscular diseases has been
influenced enormously by the use of potent treatment for immune-mediated diseases and better diagnostic precision using molecular
techniques applied to blood and muscle biopsy specimens. Pain management has become an art and science of its own, deserving of its
own chapter in this edition. The triptan drugs, currently numbering seven, have changed the approach to migraine, and many other
headache syndromes are now more clearly classified and specifically treated.
The management of acute stroke has dramatically changed even in the four years since the 6
th
edition, with widespread use of not only
intravenous thrombolytic drugs but also sophisticated interventional techniques aimed at extracting cerebral emboli and opening
narrowed vessels with angioplasty and stenting. The advances in Parkinson disease and other movement disorders reflect the
widespread availability of new dopamine receptor agonists and the use of deep brain stimulation in advanced and drug-resistant
disease. Even Alzheimer disease is now treated with some success using a class of anticholinesterase drugs, and other dementias are
more clearly classified and managed. Neuroophthalmology has become a major segment of neurologic practice, a fact that is reflected
in an entire chapter now dedicated to that group of disorders. The most prevalent of the toxic and metabolic disorders have undergone
an alteration in approach based on a better understanding of the nervous system
’
s reaction to perturbations in its milieu. Moreover,
the array of infectious agents affecting the nervous system continues to change as new diseases emerge and the approach with
antibiotics undergoes reassessment.
The 17 chapters of the 7

—
Oriented Localizes to pain
4 Spontaneous Confused Withdraws to pain
3 To speech Inappropriate Flexion (decorticate)
2 To pain Unintelligible Extensor (decerebrate)
1 None None None
a. This scale attempts to quantitate the severity of trauma on the basis of patient's best response in three areas: eye
opening, motor activity, and language.
b. The GCS scores range from 3 to 15. When the total score is 8 or less, the patient is considered to be in coma.
Components of the Examination
1. Level of consciousness should be described according to
a. Unresponsive.
b. Unresponsive to pain.
c. Responsive to voice.
d. Lethargic but spontaneously responsive classifications are best supplemented by a description of the stimuli used
and the nature of the responses.
2. Examination of the eyes
a. Ocular motility
1. Pupil size and reactivity.
2. Pupils are the most reliable means of distinguishing metabolic from structural disease.
3. Preserved pupillary reflexes with absent eye movements to vestibular stimulation or even respiratory
depression implicate metabolic coma.
4. Absent pupillary light reflexes indicate structural brainstem damage with important qualifications.
5. Symmetric or asymmetric impairment of the pupil's reaction to light usually indicates structural brainstem
disease. Pontine infarction or hemorrhages sometimes cause small,
“
pinpoint
”
pupils, but they can be seen
to react to light under magnification.

5. Blinking in response to a bright light, even through closed lids, does not indicate sparing of the visual cortex
since this reflex may be mediated at a brainstem level.
6. Blinking in response to a loud sound indicates integrity of the lower pons.
7. Absence of blinking to sound, threat, or light indicates severe metabolic compromise or structural damage of
the pontine tegmentum.
8. Bilateral lid closure and upward deviation of the eyes in response to strong corneal stimulation assures
function from the rostral midbrain right down to the medulla oblongata.
9. A combination of failure of lid closure with spared eye deviation on corneal stimulation signifies destruction of
the facial nerve or nucleus.
10. Loss of both lid closure and eye deviation on corneal (pain) stimulation is of little diagnostic help other than
indicating that brainstem depression is severe.
3. Skeletal motor and reflex signs
a. Patients who have hemispheric lesions typically lie in comfortable-appearing, relatively normal postures.
b. Patients who have brainstem lesions often display abnormal postures. The symmetry of spontaneous movement may
give a clue about the side of a focal lesion. Postures with some localizing significance are usually fragmentary and
may be elicited by noxious stimuli.
c. The terms decorticate and decerebrate rigidity refer to experimental studies of animals and do not accurately
reflect the clinicopathologic correlations that they imply.
1. Decorticate posturing: lower extremity extensions and internal rotation with flexion of both upper extremities
2. Decerebrate posturing: lower and upper extremity extensions
d. Upper extremity flexion reflects more superficial, less severe, and more chronic lesions at the level of the
diencephalon or above. Upper and lower extremity extension will often accompany brainstem lesions; however, as
mentioned, the upper extremity extension depends on the degree and acuteness of the lesion and being reflexively
driven, on the stimulus applied at the time of the examination. The responsible lesions may also be reversible, as in
severe toxic and metabolic encephalopathies.
e. Deep tendon reflexes and plantar responses may also suggest a lateralized lesion, but they, too, are often
misleading signs. Careful observation for subtle movements suggesting nonconvulsive seizures should be sought in
all cases of coma.
P.4
4. Responses respiratory pattern

a. Secondary destruction occurs in the brainstem tegmentum. In contrast to primary brainstem hemorrhage, which is
usually in the base of the pons, this damage occurs in the tegmentum.
b. The secondary changes lead to permanent coma and brainstem tegmental signs involving eye movements and the
pupils. The supratentorial pressure may compress the posterior cerebral arteries against the incisura of the
tentorium, causing infarction of the occipital lobes. Patients may survive this compressive effect to be left with
visual-field defects or blindness from damage to the striate cortex or geniculate bodies.
c. The mass itself may be remote from the visual pathways.
Ocular Response
Gaze Deviation
Deviation of the eyes implicates a structural cause of coma.
1. Tonic horizontal deviation
a. Eyes deviate conjugately toward the side of massive lesions in the cerebral hemisphere.
b. This ipsiversive deviation does not specify frontal lobe damage, but occurs more often with massive lesions in the
posterior hemisphere, especially the nondominant side.
c. In the acute phase, the eyes may be brought up to the mid position only by vigorous passive head turning and
oculocephalic maneuvers.
d. In the acute phase, it may be impossible to move the eyes to the opposite side for several hours, then the
vestibuloocular reflex (VOR) resumes a full range of
P.5
motion. The combination of cerebral hemispheric damage and anticonvulsant or sedative drugs can eliminate the
VOR.
2. Contraversive deviation
a. Unilateral damage in the pontine tegmentum causes contraversive deviation. Version of the eyes to the side
opposite cerebral hemispheric lesions (that is, toward the side of hemiparesis) signifies an irritative lesion, such as
an epileptic focus.
b. “ Wrong-way deviation” is usually a sign of thalamic hemorrhage and is commonly associated with intraventricular
hemorrhage and dissection into the brainstem suggesting that the wrong-way deviation might be caused by the
brainstem dissection.
c. Deviation of the eyes opposite to the lesion is also a feature of acute cerebellar damage.
3. Tonic vertical deviation

opposite side and can be brought up to the mid position only.
e. Caloric stimulation of the VOR is an integral part of the neuro-ophthalmic assessment of the comatose patient.
1. The head is elevated to 30 degrees on a pillow to make the horizontal semicircular canal vertical. Fifty to 100
mL or more of ice water is injected into the auditory canal until nystagmus or tonic deviation of the eyes
occurs.
P.6
2. In unconscious patients, nystagmus fast phases are absent and the eyes deviate in the direction of cold
stimulation.
3. Failure of deviation indicates structural interruption or severe metabolic depression of brainstem VOR
pathways.
4. Drug intoxication can paralyze the VOR in the early stages of coma. Discrete involvement of brainstem
connections by structural lesions can cause monocular paresis of adduction (INO).
5. Incomplete adduction as in INO may also result from metabolic- or drug-induced encephalopathy. Delayed
downward deviation in response to caloric stimulation of the horizontal VOR is another feature of barbiturate
coma.
6. With structural brainstem lesions, the eyes do not deviate at all or they move dysconjugately and
incompletely in response to vestibular stimulation.
7. Caloric testing should be combined with oculocephalic maneuvers if the caloric response is indefinite or
absent. For example, the patient may have peripheral vestibular damage from ototoxic drugs. In that case,
the neck proprioceptive reflexes may move the eyes. Normally the cervico-ocular reflex is negligible or
absent. In patients with bilateral peripheral damage, the gain of the cervico-ocular reflex (neck proprioceptive
reflex) may be increased to move the eyes normally. When testing the oculocephalic maneuvers, rotation
should be brisk since the VOR responds best to high-frequency rotation. Moreover, once deviated in response
to oculocephalic maneuvers, the eyes drift rapidly back to the mid position in coma since the eye velocity-to-
position integrator is leaky so that the VOR signal is not stored to maintain eccentric gaze. Reflex eye
movements are useful in evaluating the outcome of coma.
Roving Eye Movements
1. The presence of slow roving eye movements indicates metabolic coma or supratentorial structural lesions.
2. Roving occurs at a rate of four to six per minute.
3. They are slow drifting movements that may be conjugate or dysconjugate and are predominantly horizontal.

de-afferented
”
but remains
conscious.
a. The only way the patient can express his or her alertness is by communication through intact voluntary eyelid and
vertical eye movements.
b. Midbrain involvement can cause the locked-in syndrome accompanied by bilateral ptosis and third nerve palsies The
only clue that the patient is conscious is some remnant of movement such as the orbicularis oculi in response to
command.
c. These patients require meticulous nursing and psychological care.
d. Survival may be prolonged and recovery is possible in patients depending on the lesion type and extent of damage.
Vegetative State
1. This state has many eponyms—vegetative state, coma vigil, apallic syndrome, and akinetic mutism.
2. Coma seldom lasts more than 2 to 4 weeks.
3. Eyes eventually open and sleep
–
awake cycles appear.
4. Caloric and rotational nystagmus quick phases are regained if the brainstem is intact.
5. Patients do not obey verbal commands but they open their eyes on alerting.
a. Seen with damage of the frontal limbic syndrome, deep midline lesions that disconnect the frontal lobe from the
thalamus, or extensive cortical anoxic damage.
b. If the damage is predominantly frontal, the patient's eyes may follow the examiner (i.e., tracking). It is the eyes
open, sometimes with preserved ocular-following responses, that gives the appearance of coma vigil.
Psychogenic Unresponsiveness
The eyes are particularly important in distinguishing psychogenic unresponsiveness and catatonia from coma and the
vegetative state.
1. If the patient lies with the eyes closed, lifting the eyelids results in a slow closure in genuine coma but rapid closure of
the eyes is nonphysiologic.
2. Roving eye movements are a type of smooth eye movement and smooth eye movements cannot be produced voluntarily.
3. The patient with psychogenic unresponsiveness never has roving eye movements.

• Obtain blood for CBC, PT/PTT, chemistry panel, toxic screen, blood cultures, anticonvulsant levels
Threatening conditions to be considered for possible early therapy
•
Elevated ICP
→
head CT
•
Meningitis, encephalitis or both
→
antibiotics, LP, blood cultures
•
Myocardial infarction
→
ECG
•
Hypertensive encephalopathy
→
early therapy
•
Status epilepticus
→
EEG
•
Acute stroke
→
consider thrombolytic therapy
IV, intravenous; CBC, complete blood count; PT, prothrombin time; PTT, partial thromboplastin time; ICP,
intracranial pressure; CT, computed tomography; LP, lumbar puncture; ECG, electrocardiogram; EEG,
electroencephalogram.
From Neurologic Clinics, Neurologic Emergencies, May 1998, with permission.

f. Seizures (postictal state, nonconvulsive status epilepticus)
g. Others
i. Basilar migraines
ii. Transient global amnesia
iii. TTP and other syndromes of medical illness
iv. Sleep deprivation
v. Situational (i.e., ICU psychosis)
vi. Psychiatric (conversion, depression, mania, catatonia)
ICH, intracranial hemorrhage; MS, multiple sclerosis; ADEM, acute disseminated encephalomyelitis; ICP,
intracranial pressure; ICU, intensive care unit; SAH, subarachnoid hemorrhage; TTP, thrombotic
thrombocytopenic purpura.
From Neurologic Clinics, Neurologic Emergencies, May 1998, with permission.
2. The ABCs (airway, breathing, and circulation) of acute resuscitation top the list.
3. Acute cervical stabilization is crucial whenever there is any possibility of cervical trauma or instability caused by medical
disease, as in rheumatoid arthritis.
4. Maneuvers that require neck movement should be modified to minimize movements or should be avoided (oculocephalics
stimulation) until after adequate radiographs have eliminated any concern of cervical instability.
2. They are often difficult to visualize on plain skull films or axial computed tomography (CT) scans. The diagnosis is often
based on clinical signs and symptoms.
3. There is a risk of meningitis if the dura is penetrated; however, prophylactic antibiotics are not indicated.
4. Anterior fossa fractures generally involve the frontal bone and ethmoid and frontal sinuses.
a. Characterized by bilateral periorbital ecchymosis (
“
raccoon eyes
”
).
b. Anosmia from damage to the olfactory apparatus is common.
c. Rhinorrhea occurs in 25% of patients, usually lasts 2 to 3 days, and is often self-limiting with conservative
measures (e.g., elevating the head of the bed, cautioning the patient against blowing his/her nose, lumbar drain
placement).

1. Classification
a.
“
Acute
”
is used for those less than 3 days old.
b.
“
Subacute
”
if they are 3 days to 3 weeks old.
c.
“
Chronic
”
if they are more than 3 weeks of age.
2. Acute subdural hematoma (ASDH) is the most common traumatic intracranial hematoma and carries the highest
associated mortality (as high as 60% in some series).
3. ASDHs usually arise from venous bleeding caused by tearing of bridging veins in the subdural space between the dura
and the arachnoid.
4. There is a fourfold increase in the mortality rate if surgery to evacuate the hematoma was delayed 4 hours or more after
injury compared with patients who had surgery within 2 hours.
5. Surgical treatment options include burr holes or formal craniotomy and evacuation of the clot.
Epidural Hematoma
1. Epidural hematoma (EDH) is most commonly caused by arterial bleeding into the epidural space, between the skull and
dura.
2. Associated with temporal bone fractures causing a tear in middle meningeal artery. Arterial blood rapidly accumulates,
and patients can deteriorate quickly (so-called
“
talk and die

or more than 30 mL of EDH, regardless of GCS score.
b. Those who may be considered for nonoperative management include those with an EDH that is
1. Less than 30 mL in volume, less than 15 mm thick, and less than 5 mm of midline shift, as long as the GCS
score is above 8.
2. These patients should undergo serial CT scanning and close observation.
Intracerebral Hematoma
1. Intraparenchymal hemorrhages (IPHs) are unusual in nonpenetrating head trauma.
2. Enlarging cerebral contusions can coalesce into frank intraparenchymal clots requiring surgical intervention.
3. It is more common to see IPH with penetrating injuries (i.e., gunshot and stab wounds).
4. The lesion size and patient status dictate treatment.
Diffuse Axonal Injury
1. Deceleration and rotation of the brain may result in shearing of nerve axons.
2. Mortality after diffuse axonal injury (DAI) is as high as 50%.
3. DAI is the most common cause of a posttraumatic vegetative state.
4. The findings of the initial CT scan are normal in 50% to 85% of patients.
5. Magnetic resonance imaging (MRI) is more sensitive than CT scanning for detecting the hallmark small punctate
hemorrhages that are caused by shearing of small perforating arteries.
6. Many believe that involvement if the corpus callosum is a sine qua non of DAI.
Cerebral Edema
1. Cerebral edema leads to increased brain volume from increased water content.
2. Steroids should not be used to treat posttraumatic edema (see below).
Herniation Syndromes
1. Herniation is the shifting of brain tissue to an abnormal area and is secondary to ICP differentials.
2. The associated signs and symptoms depend on the location of herniation and anatomy of the structures being
compressed.
3. The most commonly seen syndromes are cingulate/subfalcine herniation, uncal/tentorial herniation, and tonsillar
herniation.
a. Cingulate (or
“
subfalcine

TREATMENT
Prehospital Management
1. The evaluation and treatment of traumatic injuries should be initiated from the time prehospital emergency personnel
arrive at the scene and continue during transport and through acute management in the emergency department.
2. The priorities for assessment and treatment of the patient with a head injury can be summarized as the ABCs: airway,
breathing, and circulation.
a. Airway/breathing
1. Securing and maintaining an airway is top priority to ensure adequate oxygenation and ventilation.
2. Airway patency is often compromised by the presence of foreign objects; obstruction by the tongue and/or
pharyngeal/laryngeal soft tissue; accumulation of blood, secretions, or vomitus; and airway collapse by direct
trauma.
3. Ventilation can be compromised by pulmonary contusions, rib fractures (flail chest), diaphragmatic rupture,
presence of hemo- or pneumothorax, brainstem injury affecting the respiratory centers, or cervical cord injury
affecting phrenic nerve function.
4. In the absence of airway obstruction, supplemental oxygen should be given via face mask. Otherwise, an
airway should be secured via endotracheal or nasotracheal intubation.
5. Direct tracheotomy or cricothyroidotomy offer alternatives in the presence of massive facial trauma or upper
airway swelling.
6. If needed, respiration can be supported with bag ventilation either via face mask or tracheal tube.
7. Do not prophylactically hyperventilate. Present evidence, including a randomized clinical trial that
demonstrated an adverse effect on neurologic outcome in patients with head injury undergoing prophylactic
hyperventilation, strongly suggests that aggressive prophylactic hyperventilation may actually worsen tissue
hypoxia and lead to secondary brain injury.
b. Circulation
1. In concert with securing the airway and procuring ventilation, blood flow to the brain and other organs must
be rapidly and aggressively supported.
2. Hemodynamic collapse in the trauma setting is most often associated with blood loss, although cardiac
dysfunction and neurogenic causes are also common.
3. External hemorrhage should be controlled via direct wound pressure
—

Degrees of Certainty
Standards
—
Accepted principles of patient management that reflect a high degree of clinical certainty.
Guidelines
—
A particular strategy or range of management strategies that reflect moderate clinical
certainty.
Options
—
The remaining strategies for patient management for which there is unclear clinical certainty.
Initial Management
Standard: None.
Guideline: None.
Option: Rapid, physiologic resuscitation
–
sedation and neuromuscular blockade for specific indications
(e.g., airway compromise, elevated ICP). Mannitol or hyperventilation (never to Paco
2
< 25 mm Hg) only if
there are signs of life-threatening herniation.
Resuscitation of Blood Pressure and Oxygenation
Standard: None.
Guideline: Avoid SBP < 90 mm Hg arterial oxygen saturation < 90%.
Option: Maintain SBP to keep CPP (the mean arterial pressure less the intracranial pressure) > 70 mm Hg.
Endotracheal intubation if GCS score is <8 (coma).
Indications for ICP Monitoring
Standard: None.
Guideline: Severe TBI (GCS<8) with an abnormal CT scan, or with a normal CT if > 40 years old,
posturing, or SBP <90 mm Hg; ICP monitoring may be used in selected noncomatose patients.

Option: Use with ICP monitoring and signs of tentorial herniation or progressive neurologic deterioration.
Avoid hypovolemia, maintain euvolemia
Keep serum osmolarity <320 mOsm
Use of Barbiturates in Control of Intracranial Hypertension
Standard: None
Guideline: High-dose barbiturate therapy may be considered in patients with severe TBI with intracranial
hypertension refractory to maximal medical and surgical therapy.
Role of Steroids
Standard: The use of steroids is not recommended in severe TBI.
Guideline: None.
Option: None.
Role of Antiseizure Prophylaxis
Standard: Prophylactic use of anticonvulsants is not recommended to prevent late (> 7 d) posttraumatic
seizures.
Guideline: None.
Option: Phenytoin and carbamazepine are effective in preventing early (< 7 d) posttraumatic seizures.
Stop prophylaxis 7 d after injury. There is no evidence that antiseizure prophylaxis improves outcome.
Nutrition
Standard: None.
Guideline: Provide 140% of estimated calories to nonparalyzed and 100% of estimated calories to
paralyzed patient with severe TBI.
Option: Utilize jejeunal alimentation.
ICP, intracranial pressure; SBP, systolic blood pressure; CPP, cerebral perfusion pressure; GCS, Glasgow coma
scale; TBI, traumatic brain injury; CT, computed tomography; CBF, cerebral blood flow.
From the Brain Trauma Foundation, the American Association of Neurological Surgeons (AANS), and the Joint
Section on Neurotrauma & Critical Care of the AANS and Congress of Neurological Surgeons.
1. Starts by repeating what was done in the field
—
the ABCs are reassessed, and further respiratory support is given via
supplemental oxygen with a nasal canula or intubation.

lack of proven neurologic benefit.
2. Outcomes are worse if methylprednisolone is administered more than 8 hours after injury.
P.18
d. Main drug interactions
1. Methylprednisolone increases circulating glucose levels.
2. Decreases effect of phenytoin and phenobarbital.
3. Rifampin increases clearance of methylprednisolone.
e. Main side effects
1. Hypersensitivity
2. Increased risk of infection
Surgical Treatment
1. The role of surgery in the treatment of acute spinal cord injury remains controversial.
2. The goals of surgery for spinal cord injuries are spinal cord decompression, correction of spinal column deformity, and
spinal column stabilization.
3. The goals sound straightforward; however, little evidence supports exactly how or when this should be done.
4. Surgical stabilization and decompression
a. Anterior operations or posterior operations.
b. Instrumentation such as plates, wires, and rods plays an important role in ensuring spinal column stabilization.
c. Instrumentation can be placed either through an anterior procedure or a posterior procedure.
d. In the absence of definitive data, the selection of the most appropriate procedure and its timing remains the realm
of individual surgical judgment.
Prevention of Complications
1. Aspiration precautions: Placement of a nasogastric tube is used to reduce the risk of aspiration and pneumonia.
2. Urinary retention: Placement of a Foley catheter reduces the risk of hydronephrosis and renal impairment.
3. Warming blanket: Hypothermia can promote systemic complications and is commonly seen in trauma victims and patients
with spinal cord injury.
4. Cervical immobilization
a. The short-term goal of immobilization is to prevent further misalignment and additional injury to the spinal cord.
b. Immobilization can be achieved by bed rest, traction, or spinal orthosis.
c. Orthosis for immobilization of the spine allows early mobilization of the patient and can help in achieving spinal

less then 70 mm Hg, or a Pco
2
greater that 45 mm Hg, intubation should be
accomplished.
d. Contraindications: In the case of major facial or skull base trauma, tracheotomy should be preformed instead of
nasal or endotracheal intubation.
e. Complications: Endotracheal intubation may worsen a cervical spine cord injury in cases with unstable cervical
spine fractures or ligament injury.
f. Special points: Most high cervical injuries will require intubation.
1. Intubation is indicated with lesions at or above C-3 because there is no diaphragmatic or intracostal muscle
function.
2. Lower cervical or upper thoracic injuries may require intubation because of delayed ascending cord swelling.
8. Blood pressure: The treatment objective is to maintain or enhance blood flow to the injured cord, and treat shock if
present.
Patient Placement, Catheters, and Vasopressors
1. Neurogenic shock can happen with injuries above T-6.
a. The sympathetic outflow tracts are found from T-1 to L-2.
b. Lesions at T-6 (or above) disrupt a significant proportion of these tracts, which results in the loss of sympathetic
nervous system control over peripheral vascular tone. This results in pooling of blood and reduces central venous
return.
c. Examination reveals warm extremities, good urine output, and vital signs that show bradycardia and hypotension.
2. Standard procedure: Placement of the patient in Trendelenburg position (head down) helps reduce the pooling of blood in
the lower extremities.
a. A Swan
–
Ganz catheter or central venous catheter is used to assess and regulate fluid status.
b. Vasopressors are used to augment blood pressure.
3. Contraindications: relative contraindication in those patients with impaired cardiac function.
4. Complications: development of heart failure from fluid overload.
5. Special points: Hypovolemic shock is commonly seen in patients with spinal cord injury and additional systemic trauma.

d. Complications: During the course of reduction, an acute disc herniation may occur adding further injury to the
spinal cord.
2. Open reduction
a. Special points: Surgical reduction (open reduction) is indicated in those patients with neurologic compromises
because of a compressive lesion. It may be also preformed when closed reduction has failed.
b. There is controversy about the speed with which reduction should be accomplished. Many neurosurgeons believe
that cervical dislocation should be reduced within a few hours, although thoracic and lumbar dislocations (which
frequently require extensive surgical procedures) are best treated in a semielective fashion.
Imaging
The patient's clinical history and physical examination findings dictate the radiographs physicians should obtain. The most
common radiographs used today are plain films, CT, and MRI.
1. Plain films: A cervical spine series should be obtained on all patients with suspected cervical spine injury.
a. Odontoid, anteroposterior, and lateral films. All seven cervical vertebrae down to the C7-T1 junction should be
seen.
b. Plain films remain the fastest and least expensive way to obtain an initial assessment that allows visualization of
the entire spine.
2. CT: Plain films do not provide detail of the bony anatomy and may not reveal fractures.