Assessing and Managing Head Injury

Two emergency physicians provide a head-to-toe review of prognostic clues, differentiate the major types of lesions, and describe the likely sequelae for the patient who has suffered a blow to the head.

By Allison R. Ashe, MD, and Jon D. Mason, MD

Dr. Ashe is a resident and Dr. Mason is an attending physician in the department of emergency medicine at Eastern Virginia Medical School in Norfolk, Virginia.

Head injuries present to the emergency department nearly as often as the everyday acute respiratory infection or lumbar muscle strain. There are more than 500,000 head injuries in the United States each year, both fatal and nonfatal, the highest rates occurring in the 15-to-29 and 65-to-70 age groups. More than half are associated with alcohol. Men's risk of such an injury is double that of women, and African Americans are up to twice as likely to suffer a head injury as other races. In inner-city populations, the leading cause of head injuries is violence, followed closely by falls. Overall, however, motor vehicle (including motorcycle) accidents are the leading cause of head injuries in general and of fatal head injuries in particular, causing 70% of all comas. Not surprisingly, 30% to 40% of all multitrauma cases feature head injury.

Mortality rates for head injury range from 17 to 30 per 100,000, accounting for 4% of deaths from all causes and 30% to 48% of all injury-related deaths. Half of all head-injury-related deaths occur less than two hours after injury, with approximately 70% occurring prior to arrival at the hospital. The number one prognostic factor in mortality risk is age. Patients more than 70 years old, for example, are 15 times more likely to die than a younger head-injured patient, which is attributed to a tripled risk of brain hemorrhage at that age.

Whether the patient is reporting a headache or mild dizziness after a minor fender bender or has lost consciousness after being thrown from a motor vehicle in a collision, the history and physical examination can often tell the physician as much as the CT scan. This article will review significant findings and their interpretation.

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Determining the Extent of Injury

Primary damage in head injury occurs at impact. Focal damage includes the coup/contrecoup (direct/indirect) injuries that occur when trauma causes the brain to strike the skull, including contusions, lacerations, and intracranial hematomas. Diffuse damage includes axonal injury, which can cause widespread neuroanatomical and neurophysiological interruption of brain function, and white matter shearing. Secondary damage results from hypoxia, hypercarbia, ischemia, hypothermia, increased intracranial pressure (ICP), intracranial hemorrhage, brain edema, and infection.

Head injury can be classified as mild, moderate, or severe, or it can be graded into one of four categories (see table, below).

The clinician can rate the probability of an intracranial injury based on symptoms and physical findings (see table, below).

Assessing the Likelihood of Intracranial Injury Low Risk Asymptomatic Isolated scalp injury Mild headache or dizziness Moderate risk Change in mental status Severe or progressive headache Alcohol or drug intoxication Posttraumatic seizures Protracted vomiting Multiple trauma Age less than 2yr Facial fracture High risk Lethargy Decreased level of consciousness Any focal neurologic deficit

As with any trauma patient, assessment should begin with the ABCs (airway, breathing, circulation). With head-injured patients, cervical spine stabilization is paramount. For patients who need airway assistance, the jaw thrust maneuver is appropriate to maintain cervical spine control. Physical examination should include temperature, blood pressure, oxygen saturation, pulse and respiratory patterns, and a full body assessment for clues to neurologic impairment (see table below), noting any identifiable patterns such as Cushing's reflex (hypertension with bradycardia) and determining the baseline Glasgow coma score (see sidebar below). Below we will focus on some of the key signs and symptoms the physician may encounter.

Calculation and Interpretation of the Glasgow Coma Score Developed in 1981, the Glasgow Coma Scale (GCS) tests level of consciousness by evaluating eye opening, verbal, and motor responses. It is most useful for following a patient's neurologic condition over time with serial Glasgow coma scores. Research on the GCS has found a 12-fold increase in mortality risk associated with scores of 8 to 12 and a hundredfold increase for scores below 8.     Of the three categories tested in the GCS, the motor response is the most sensitive. It verifies the ability to integrate information and perform motor tasks, thereby implying cortical function. If a patient is unable to respond or follow commands, a painful stimulus may elicit a response. Responses to painful stimuli include withdrawal, incomplete withdrawal (semipurposeful), decorticate (flexion) posturing, decerebrate (extension) posturing, or a combination of flexion and extension.     Purposeful and semipurposeful movement implies an intact motor system. Decorticate (flexion) posturing involves the rubrospinal pathway. It indicates an injury or disconnection between the cerebral cortex and the red nuclei. The GCS gives this response a motor score of 3 (see guide below). The patient will display flexion of the head and trunk, adduction and internal rotation of the arms, pronation and flexion of the forearm, flexion of the wrists and fingers, flexion of the hips, knees, ankles, and toes, internal rotation of the legs, and inversion of the feet.     Decerebrate (extension) posturing implies a lesion at the level of the midbrain or below. It is seen in more severe head injuries and implies a poorer prognosis for recovery. The mortality rate is approximately 70%. Affected patients will show extension and internal rotation of all four extremities and may also show extension of the body and head (opisthotonis). For such patients, damage to the midbrain-upper pons is indicated and the GCS motor score is 2.     A complete absence of motor response (flaccidity) implies an injury at the level of the pontomedullary junction. The GCS motor score is 1 and the mortality rate is approximately 75%. Eye opening Spontaneous 4 To voice 3 To pain 2 None 1 Verbal response Oriented 5 Confused 4 Inappropriate words 3 Incomprehensible words 2 None 1 Motor response Obeys commands 6 Localizes pain 5 Withdraws from pain 4 Flexion (decorticate) 3 Extension (decerebrate) 2 None 1 Scoring guide Minimum score 3 Maximum score 15 Mild brain injry 13 or higher Moderate brain injury 9 to 12 Severe brain injury 8 or lower

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What the Pupils Indicate

Basilar skull fracture and other head injuries may damage cranial nerve III, the oculomotor nerve. In that event, the patient will exhibit abnormalities of pupillary response, such as paralysis of light reflex, and other functional disturbances of sight. Pupillary dilation (mydriasis) indicates unopposed sympathetic activity due to impaired parasympathetic axons. This may reflect compression or distortion of the oculomotor nerve by either primary injury or herniation. Mydriasis also may be an effect of adrenergic stimuli such as epinephrine, anticholinergics, cocaine, PCP, and drug withdrawal. The classic fixed and dilated "blown pupil" is a unilateral phenomenon that may occur when a rapidly expanding intracranial mass, including blood from a hemorrhage, is compressing cranial nerve III. It may also represent herniation of the uncus of the temporal lobe.

Globe trauma is also a cause of unilateral mydriasis; however, unlike true cranial nerve III injuries, it is not associated with ocular muscle paresis.

Pupillary constriction (miosis) may be caused by opiates, metabolic encephalopathy, cholinergic toxicity, or pontine lesions. Miosis in pontine lesions is a consequence of unopposed parasympathetic activity due to inactivation of sympathetic pathways.

Contusion of the oculomotor nerve causes a dilated ipsilateral pupil. The patient will also have ptosis and adduction paresis, causing lateral deviation of the eye due to unopposed cranial nerve IV.

Hippus refers to spontaneous dilation and contraction of the pupil. This is often seen with Cheyne-Stokes respirations (tachypnea interspersed with periods of apnea). Dilation occurs with the apneic phase; constriction corresponds with tachypnea. Hippus indicates that both sympathetic and parasympathetic pathways are intact but autonomic tone is disinhibited.

Waxing and waning pupil size may indicate seizure activity, even without tonic-clonic movement. Midbrain injury may cause a loss of pupillary response, irregularly shaped pupils, or asymmetric pupil size. Brain stem injury may cause a unilateral Horner's pupil (miosis and ptosis). Midposition pupils with variable light reflexes may be seen in any stage of coma. Bilaterally dilated and fixed pupils are due to inadequate cerebral perfusion.

The oculocephalic and oculovestibular reflexes are tested to evaluate brain stem function and the reticular activating system, respectively. The oculocephalic response, or doll's eye reflex, is a measure of the pontine gaze center. Cervical spine injury must be ruled out before the test maneuver is done. After raising the head of the patient's bed 30°, the clinician rotates the patient's head briskly from side to side. In the normal doll's eye response, both eyes maintain position by moving in the direction opposite that of the rotation. If the eyes stay fixed and rotate with the head, brain stem function is impaired or absent.

The oculovestibular reflex is elicited by what is often referred to as the cold caloric test. Cold water injected into the ear canal acts to move the endolymph within the semicircular canals. The movement of the endolymph in turn prompts conjugate movement of the medial and lateral rectus muscles. To perform the test, the head of the patient's bed is raised 30° and 20 to 30 ml of cold water is injected into the ear.

A response should occur within 20 to 60 seconds. In an alert patient, there will be a slow horizontal movement of the eyes toward the stimulation (slow phase of nystagmus) followed by a fast horizontal movement of the eyes back to midline (fast phase of nystagmus). This indicates an intact reticular activating system. In a lethargic patient, one will still see the normal slow phase of nystagmus toward the stimulation; however, the fast phase is less pronounced. An obtunded patient will also exhibit the normal slow phase of nystagmus toward the stimulation but no fast phase of nystagmus back to midline. In a comatose patient, usually there will be no discernible response. A normal oculovestibular response in an unconscious patient indicates that the process causing the coma has spared the reticular activating system.

The clinician should always be alert for nystagmus in a head-injured patient. Vertical nystagmus may indicate damage to the brain stem. Dissociative nystagmus may indicate damage to either the brain stem or the cerebellum. Ocular bobbing‹coarse, rapid conjugate downward jerks with a slow return to horizontal‹may indicate a severe pontine lesion or anoxic encephalopathy.

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Clues in Respiratory Patterns

Distinct patterns such as Cheyne-Stokes breathing, central neurogenic hyperventilation, or Biot's breathing may indicate specific areas of trauma. Normal breathing, however, does not rule out the presence of a small, unilateral lesion.

Cheyne-Stokes breathing is seen with bihemispheric lesions or lesions in the basal ganglia. Central neurogenic hyperventilation, or sustained hyperventilation with respiratory rates greater than 40 per minute, is associated with lower midbrain or upper pontine injury. It must be distinguished from hyperventilation due to other common causes including hypoxia, acidosis, sepsis, drug toxicities, and anxiety.

Biot's breathing is an irregular or ataxic type of respiration. Breathing is chaotic with loss of regularity in the pace and depth of inspiration and expiration. It is seen with pontine or medullary dysfunction due to trauma.

In addition to abnormal breathing patterns, brain injury may also cause repetitive respiratory reflexes (sighing, yawning, hiccups), suggesting suppression of higher cortical function. These signs may also warn of impending herniation.

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Hemodynamics and Intracranial Pressure in Head Trauma

Cerebral blood flow is maintained by cardiac output (heart rate multiplied by stroke volume), cerebral perfusion pressure (mean arterial pressure minus intracranial pressure), and autoregulation. Autoregulation is the intrinsic ability of cerebral blood vessels to constrict or dilate in response to changes in mean arterial pressure. Disruption of autoregulation leads to an increased risk of cerebral ischemia if blood pressure falls and to disruption of the blood-brain barrier if blood pressure rises. In turn, disruption of the blood-brain barrier causes extravasation of protein and transudation of water, leading to cerebral edema.

Cushing's triad, which includes bradycardia, hypertension (with widened pulse pressure), and a change in respiratory pattern, is seen in head injuries with increased intracranial pressure (ICP).

Head injuries rarely cause hypotension, except in spinal cord injuries (hypotension with bradycardia); therefore, other causes of hypotension must be sought.

Normal ICP ranges from 0 to 15 mm Hg, depending on the total volume of brain tissue and the total volume of cerebrospinal fluid (CSF). Normal fluctuations in ICP are due to translocation of CSF into the subarachnoid space and to increased CSF absorption.

Possible triggers of a transient ICP increase in the clinical setting include prone positioning, suctioning, painful procedures, coughing, straining, REM sleep, and abnormal respiratory patterns. A sustained rise in ICP is seen when any added volume (mass, blood, abscess, cerebral edema) exceeds compensatory mechanisms. The magnitude of the increase depends on the amount and accumulation rate of the additional volume and the total volume of the intracranial cavity. The adverse effects of increased ICP are due to reduced cerebral blood flow, brain shift, and distortion. Signs and symptoms of increased ICP in addition to Cushing's triad include headache, vomiting, drowsiness, and lethargy. Studies have shown that common practices aimed at lowering ICP, such as intubation and hyperventilation, are often futile.

Cerebral edema is not uncommon after head injuries. The cause may be cytotoxic, vasogenic, or ischemic. Cytotoxic edema is associated with neuronal degeneration. Each neuron is equipped with a sodium pump to maintain fluid and electrolyte balance. Traumatic injury can cause dysfunction of this pump and consequent influx of sodium and water into the cells. Vasogenic edema is due to compromise of the blood-brain barrier by damaged capillaries that allow plasma leakage into brain tissue. Ischemic edema is due to a combination of cytotoxic and vasogenic processes.

Cerebral edema is the major cause of reduced blood flow to the brain. It is also a major contributor to increased ICP. Cerebral edema occurs between 1 and 18 hours after injury, peaking at day 3. Alcohol promotes cerebral edema by increasing the permeability of the blood-brain barrier. Common radiographic signs include small or absent sulci, low attenuation within adjacent white matter, compression of the ventricles, and poor gray-white differentiation.

The combination of increased ICP and cerebral edema with an expanding lesion is the cause of various herniation syndromes. The most common is tentorial herniation, in which the uncus of the temporal lobe is pushed over the edge of the tentorial notch. Typical findings include ipsilateral pupillary dilation, loss of light reflex, and ptosis due to compression of cranial nerve III. With compression of the midbrain as herniation progresses, patients will also have a decreased level of consciousness. Projectile vomiting is common. If the cerebral peduncles are also compressed, patients may display contralateral posturing. Patients have also been described as having Cheyne-Stokes respirations or central neurogenic hyperventilation.

A variant worth noting is cerebellar tonsil herniation syndrome, meaning that the cerebellar tonsils are being forced through the foramen magnum. This syndrome is usually associated with lesions in the posterior fossa. Respiratory arrest ensues as the respiratory centers are compressed in the medulla.

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Common Traumatic Lesions

The major types of injury likely to result from head trauma are variously located hematomas, subarachnoid or intraventricular hemorrhage, contusion, diffuse axonal injury, and concussion.

Brain injuries as seen via computed tomography. Clockwise from upper left, these CT scans show a left frontal epidural hematoma; a right frontal subdural hematoma with midline shift and ventricular compression; a subarachnoid hemorrhage in the left sylvian fissure; diffuse axonal injury with diffuse edema, obliteration of the ventricular system, and scattered hyperdense foci throughout the parenchyma (consistent with shear injury); and a second example of subdural hematoma.

Epidural hematoma. Acute epidural hematomas are also known as extradural hematomas. Most commonly, these arise from arterial hemorrhage into the potential space superficial to the dura. The bleeding is usually due to injury to the middle meningeal artery in the temporal area. Skull fracture is found in 76% to 85% of patients with this type of hematoma. The lesion is a focal, biconvex (lens shaped) collection with high attenuation. Blood can cross the sinuses with this type of lesion. People with epidural hematoma are commonly referred to as patients who "talk and die" because they usually have a lucid phase followed by rapid deterioration. The overall mortality rate ranges from 9% to 33%. Operative decompression is the standard treatment.

Subdural hematoma. A subdural hematoma is a hemorrhage, usually venous, in the space deep to the dura. There is an associated intracranial contusion or hemorrhage in up to 65% of cases. The blood does not cross the sinuses (in contrast with acute epidural lesions) and displaces the brain away from the calvarium. It appears as a crescent-shaped, high-attenuation lesion on a CT scan. There may be associated ventricular compression, midline shift, and compression of brain tissue as the blood acts like an expanding lesion. Subdural hematoma results from a fall or an assault in 72% of cases; only 24% are due to motor vehicle collisions.

Subdural hematomas are classified as acute, subacute, and chronic. Acute refers to active bleeding or clotted blood up to 72 hours after injury. Subacute subdural hematoma is clotted blood formed between 72 hours to 3 weeks after injury. Residual blood or fluid noted more than three weeks after the injury is termed chronic subdural hematoma.

Subdural hematoma can even occur months after injury. In these cases it becomes encapsulated and usually increases very slowly over time, which allows for some degree of compensation that prevents a significant rise in ICP up to a certain point. Beyond that threshold, the combination of the expanding lesion with increased ICP can cause distortion and herniation. Chronic subdural hematomas are most commonly seen in the elderly. The classic story is that of an elderly patient with cerebral atrophy who presents with a change in level of consciousness and is found to have a history of a fall in the preceding weeks. With either subacute or chronic subdural hematoma, blood flow and cellular metabolism are reduced in the area of the hematoma and ischemia develops due to local compression of the microcirculation.

Intracerebral hematoma. Often occurring directly beneath an external injury, the intracerebral hematoma can also occur as a contrecoup injury. This is in contrast with intracerebral hemorrhages that occur deep in the gray matter during a hypertensive bleed (hemorrhagic stroke). The blood appears as a high attenuation area with sharp margins. The most common locations are the frontal and temporal lobes. The hematoma is due to direct rupture of intrinsic cerebral vessels.

Intraventricular hemorrhage. Rare in traumatic head injury (occurring in only 3% to 5% of cases), intraventricular hemorrhage suggests a severe brain insult. The blood is shown as high attenuation in the ventricles.

Subarachnoid hemorrhage. Trauma is the number one cause of subarachnoid hemorrhage. Blood is seen on CT scan as high attenuation areas within the sulci and basal cisterns. Unlike subdural hematoma, blood in subarachnoid hemorrhage interdigitates within the sulci. A well known complication of subarachnoid hemorrhage is vasospasm, thought to be due to the effects of vasoactive substances in the displaced blood, which can contribute to local ischemia. Notably, half of all patients with subarachnoid hemorrhage also have intracranial hematomas.

Contusion. Direct injury to the brain tissue itself, due either to bruising or crushing, is common in areas where the brain abuts rough surfaces of the calvarium or directly beneath skull trauma. Contusion is described as having a "salt and pepper" appearance due to areas of petechial hemorrhage interspersed with edema and tissue necrosis. The most severe contusions occur in the temporal and frontal lobes.

Diffuse axonal injury. The stretching and tearing of axons secondary to trauma is termed diffuse axonal injury. It tends to be complicated by subsequent swelling that further injures the white matter or the tracts that connect groups of cells. The usual cause of diffuse axonal injury is a deceleration trauma. Diffuse axonal injury may cause only temporary loss of function, but long-term disability is not unusual. This diffuse injury is thought to be responsible for postconcussive syndrome (discussed below). Often, there is no macroscopic abnormality noted on CT. It is detected on the basis of neuropsychological tests, which reveal impairments in vigilance, selective attention, memory, stamina and cognition. Common signs and symptoms of diffuse axonal injury include irritability, hypochondria, depersonalization, frustration, phobias, alienation, apathy, decreased affect, and depression.

Concussion. Concussion refers to a transient loss of consciousness. There is no structural cerebral injury. It has been defined as a reversible traumatic paralysis of nervous system function. Affected patients experience an immediate loss of consciousness, suppression of reflexes, a brief period of apnea, and a brief period of bradycardia. Recovery occurs in seconds to hours. These patients will have amnesia (retrograde, anterograde, or both) for the traumatic event. The severity of the concussion often correlates with the duration of the amnestic period.

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Head Injury Sequelae

Major sequelae for which the head-injured patient may be at risk are postconcussive syndrome, amnesia, headache, vomiting, and seizures.

Postconcussive syndrome. A constellation of signs and symptoms that are commonly noted after head trauma is referred to as postconcussive syndrome. It is very common even after relatively minor injuries. Often beginning 24 to 48 hours after injury, the syndrome typically includes headache, dizziness, irritability, insomnia, anxiety, impaired attention, impaired memory, and sound sensitivity. Other possible signs and symptoms are vertigo, tinnitus, decreased hearing, blurred vision, diplopia, photophobia, reduced taste and smell, depression, change in personality, fatigue, sleep disturbances, reduced libido, decreased appetite, decreased attention, and increased information-processing time. Physical findings may include nystagmus, internuclear ophthalmoplegia, cranial nerve V sensory impairment, asymmetric muscle reflexes, abnormal plantar reflexes, asymmetric hearing loss, altered blood flow in the cerebral circulation, and electroencephalographic abnormalities. Exertion and stress can aggravate the symptoms.

The occurrence and severity of postconcussive syndrome is not related to type or severity of injury, duration of posttraumatic amnesia, or duration of loss of consciousness. The neurologic abnormalities are thought to be due to diffuse axonal injury. The syndrome has been categorized into two subtypes. Type 1 encompasses benign injuries with good prognosis for recovery and adjustment. Affected patients return to premorbid functioning within three to five months. Type 2 is conceived as a syndrome of symptoms that persist for more than five months.

Posttraumatic amnesia. The head-injured patient sometimes develops impairment of information storage and integration, which leads to confusion and disorientation. Diffuse axonal injury is thought to be the cause. This posttraumatic amnesia may be anterograde, meaning an inability to consolidate information about new and ongoing events, or retrograde, meaning an inability to recall information concerning times before the injury. Posttraumatic amnesia can last hours to weeks. Its duration, which tends to correlate with the duration of loss of consciousness, is indicative of severity of injury (see table below) and is predictive of outcome.

Correlation of Amnesia with Injury Severity Duration of post-traumatic amnesia Severity of head injury Less than 5 min very mild 5-60 min mild 1-24 hrs moderate 1-7 d severe 1-4 wk very severe More than 4 wk extremely severe

Posttraumatic headache. Headache is the most common complaint after head injury. In patients with postconcussive syndrome, the incidence is close to 100%. The types of headache include tension, occipital neuralgia, migraine, supraorbital, and infraorbital. In the majority of cases there is no intracranial abnormality that would explain the symptoms. Of course, traumatic hemorrhage must always be ruled out. More than 50% of patients report that this sequela resolves within five months. Some correlation between duration of headaches and injury severity has been found. Treatment options for posttraumatic headache include NSAIDS, tricyclic antidepressants, biofeedback techniques, counseling, stress management, behavioral training, rehabilitation, and reassurance that there is no structural abnormality.

Posttraumatic vomiting. One in six patients with head injury experiences vomiting. Its incidence is unrelated to injury severity, loss of consciousness, or the presence of an intracranial lesion. There is, however, an association between vomiting and increased ICP.

Posttraumatic seizures. Seizures occur after head injury at a rate more than 12 times that of the general population. They can happen immediately after the traumatic event or up to years later. Risk has been linked to the severity of the injury. There is an increased risk of seizures in head-injured patients with any of the following: posttraumatic amnesia, skull fracture (especially depressed skull fracture), focal neurologic deficits, and intracranial hematoma. Within one year of the injury, 35% to 57% of head-injured patients experience seizures; in half of these cases, the seizures appear within six months. Eight out of 10 head-injured patients who develop seizures after trauma do so within 24 months of the injury. There is an increased risk of recurrent seizures (epilepsy) for patients with early onset seizures, two or more seizures within the first week after injury, or three or more seizures within the first year.

The actual mechanism of posttraumatic seizures is unknown, but one theory proposes an association with mechanical shearing of fiber tracts leading to loss and degeneration of inhibitory neuronal function. Another theory holds that there is an association with synaptic reorganization that increases electrical excitation in the brain.

Prophylaxis for posttraumatic seizures is controversial. The commonly used agents are phenytoin, phenobarbital, and carbamazepine. Many studies have shown that prophylactic treatment early in the management of head injury has no effect against any later development of seizures, and exposes the patient to serious drug side effects. There are also psychological effects associated with being labeled an epileptic. The decision on whether to initiate an anticonvulsant regimen for a head-injured patient therefore tends to be individualized and dependent on the physician's judgment.

Suggested Reading Becker DP and Gudeman SK: Textbook of Head Injury. Philadelphia, W.B. Saunders Co., 1989. Bernad PG: Closed Head Injury. Charlottesville, Virginia, The Michie Company, 1994. Cooper PR: Head Injury, 3rd ed. Baltimore, Williams & Wilkins, 1993. Feske S: Neurologic Emergencies. Neurologic Clinics 16:237, 1998. Goldberg S: Clinical Neuroanatomy Made Ridiculously Simple. Miami, MedMaster, Inc., 1995. Greenberg J: Handbook of Head and Spine Trauma. NewYork, Marcel Dekker, Inc.; 1993. Lee E, et al.: Factors influencing the functional outcome of patients with acute epidural hematomas: analysis of 200 patients undergoing surgery. Trauma 45:946, 1998. McCrory P and Berkovic S: Video analysis of acute motor and convulsive manifestations in sport-related concussion. Neurology 54:1488, 2000. Tintinalli JE, et al.: Emergency Medicine: A Comprehensive Study Guide. 4th ed. New York, McGraw-Hill, 1996.

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