Head Trauma and Subdural Hematoma Part I: Emergency Management and Imaging Modalities

Authors: Danica N. Barron, MD, Alameda County Medical Center-Highland General Hospital, Department of Emergency Medicine, Oakland, CA; M. Andrew Levitt, DO, Associate Clinical Professor, University of California, San Francisco, Department of Medicine; Director of Research, Alameda County Medical Center-Highland General Hospital, Department of Emergency Medicine; R. Carter Clements, MD, Assistant Clinical Professor, University of California, San Francisco, Department of Medicine; Assistant Chief, Alameda County Medical Center-Highland General Hospital, Department of Emergency Medicine.

Peer Reviewers: David Kramer, MD, FACEP, Program Director, Associate Professor, Department of Emergency Medicine, York Hospital, Penn State University; David P. Sklar, MD, Professor and Chair, Department of Emergency Medicine, University of New Mexico School of Medicine, Albuquerque, NM.

Traumatic brain injury (TBI) is a serious public health problem that affects 2 million Americans annually. It is the leading cause of death in people younger than age 45. According to data from the Head Injury Task Force of the National Institute of Neurologic Disorders and Strokes, 500,000 victims are hospitalized annually as a consequence of their injuries. Approximately 100,000 people die, most of whom perish hours after the incident.1,2 Of the patients who survive, an estimated 70,000-90,000 will suffer from some form of significant, permanent neurological disability, and 2000 exist in a persistent vegetative state.3 As most victims of TBI are young and previously healthy, the cost to society in terms of disruption of families, lost productivity, and health care expenditures is enormous, exceeding $25 billion per year.3

Motor vehicle accidents are the most common cause of TBI (45.5%), followed by falls (15%) and assault (13.7).4 Although the proportion of penetrating TBI is difficult to ascertain, a recent review of 16,524 head injuries reveals that 4.6% of the injuries were caused by firearms and 0.4% were related to stab wounds.4 Suicide is the most common cause of gunshot wounds to the brain in the civilian population.5 The incidence of TBI is low in those younger than age 10, but dramatically increases during adolescence. Between ages 30 and 70, the incidence declines and then rises again in the elderly, which is largely attributed to increased incidence of falls. Elderly patients tend to have a higher incidence of brain contusions and multiple brain lesions,6 which is likely caused by greater motion of a smaller brain within the cranium. In children, bicycle accidents are common and account for 7% of all TBI cases.2 The frequency of assault-related TBI is inversely related to socioeconomic status and in many economically depressed neighborhoods, assault may be the leading cause of TBI.7 Alcohol use is noticeably linked with TBI, and alcohol intoxication is present in one-fourth to one-half of TBI patients.8-11 TBI is not an isolated injury, and at least 75% of cases involve serious injuries to other organ systems.12

In the past, TBI patients were judged unrecoverable. Few surgical and medical options existed. During "the decade of the brain," the 1990s, an enormous amount of new information was published on the pathophysiology of TBI which demonstrated that prompt and intensive management leads to a markedly better prognosis. In particular, early recognition and treatment of comorbid disorders, including hypoperfusion, ischemia, and high intracranial pressure in the injured brain, is crucial to good neurological outcome. The purpose of this article is to summarize the pathophysiology of TBI and its clinical classification, emergency management, and diagnostic imaging. This two-part series will review patterns of posttraumatic injuries and trends in future treatment modalities, with an emphasis on subdural hematoma, will be addressed. Pediatric injuries, a common and important problem in emergency medicine, have recently been addressed in American Health Consultants’ Trauma Reports (Current Concepts in the Emergency Management of Severe Traumatic Brain Injury in Children, 2000;1[1]:16;Current Concepts in the Management of Minor Closed Head Injury in Children, 2001;2[1]:1-12).— The Editor


Essential to the emergency care of TBI patients is an appreciation of the dynamic changes that occur at the time of impact and during the first hours following the injury. Traditionally, the description of pathophysiology of TBI has been temporally divided into primary injury, occurring at the moment of the injury; and secondary brain injury, resulting from processes that complicate the injury. Primary brain injury is the physical deformation of brain tissue caused by the inciting event. Secondary brain injury is defined as the biochemical and physiological changes that occur following primary brain injury. Secondary brain injury exacerbates the injured brain via hypoxemia, hypotension, edema, infection, and/or increased intracranial pressure.7,13 The processes that cause secondary brain injury result from damage from free radicals, receptor dysfunction, calcium-mediated damage, and inflammation.14,15 Exogenous or iatrogenic events, such as inadequate resuscitation of shock, nosocomial infections, and anesthetic agents, also may precipitate secondary injury.7

The application of force to the head causes an intricate cascade of mechanical and physiological phenomena. This force may be related to head-contact injuries, leading to local skull bending, volume changes, and propagation of shock waves. Injury that occurs following a penetrating object is chiefly imparted by the kinetic energy of the object, which is the square of the velocity. Velocities of less than 320 m/s induce injury through direct disruption and laceration of tissue. Fracture of the skull may cause penetration of a portion of this bone as a missile in its own right. At velocities greater than 320 m/s, shock waves emanate from the object and may create significant pressure gradients.16 In addition, centrifugal forces generated by the missile produce a temporary cavity as it passes through the tissue. This cavity, which may be more than 30 times the diameter of that of the object, produces substantial strains in surrounding tissue, disrupting vascular structures and causing severe axonal tears.17 Higher velocity injuries are seen with military weapons. Civilian shootings may involve hollow-point rounds, which expand their diameter on impact, causing a larger primary wound track and greater tissue destruction. Missiles involving a trajectory crossing the sagittal sinus are particularly devastating, as both cerebral hemispheres are affected. Alternately, a head-motion injury such as rapid acceleration, deceleration, and rotation of the head can create shearing injuries within the cranium. The brain is ill-equipped to handle inertial loading due to its viscoelastic structure. Severe strains or deformations of the brain at the surface may cause cortical contusions and/or a subdural hematoma (SDH) from the rupture of bridging veins between the cortical surface and the dural sinuses; if the injury is deeper within the parenchyma, diffuse axonal injury (DAI) may ensue.18-20 Reverberating shock waves may precipitate small intracerebral hemorrhages.21 Note that impact to the head is not necessary for SDH to occur; it is the acceleration of the brain relative to the skull and not the head contact per se that causes SDH.22 SDH and DAI are the most common culprits in fatal head injuries, with DAI almost entirely a consequence of vehicular accidents and most cases of SDH due to falls or assaults.13

Two different pathophysiological cascades may occur, resulting in either focal or diffuse brain injuries. Trauma causing focal brain injury, such as contusion or hematoma, may precipitate local mass effects and lead to brain shifts, herniation, and progressive brain stem compression. Adjacent to the localized area of tissue destruction is a concentric zone of ischemia and edema in which cytotoxic and inflammatory mechanisms may be triggered, expanding the area of original injury. In diffuse brain injuries, the original event causes a primary defect in the axonal membrane. Ionic shifts, especially the sudden load of calcium within the axonal interior, may cause the death of cells that were initially capable of surviving the mechanical insult. Most tissue injury does not result from the initial injury forces causing widespread structural degeneration, but via these tissue strains altering cell membrane function, axon neurofilaments, and axolemmal permeability. Thus, emergency physicians are dealing with not destroyed, but dysfunctional (and potentially salvageable) brain tissue.23

The changes in cell membrane and function resulting after TBI trigger a cellular response, ultimately producing physiological and supraphysiological concentrations of neurotransmitter and neurochemical mediators of injury. In particular, levels of glutamate and aspartate are increased in the extracellular space after TBI and are key components in a process known as cellular excitotoxicity involving the massive depolarization of brain cells. These neurotransmitters control the movement of sodium and/or calcium into and potassium out of the cell. Critical cellular processes are disrupted by excess intracellular calcium caused by the ionic shifts, such as phosphorylation of proteins and construction of proteases, enzymes, and microtubili. Ultimately, the membrane becomes increasingly permeable, the cytoskeleton dissolves, and the cell dies.24-26 Another major cause of brain injury aside from the excitotoxic mechanism appears to involve oxygen radicals and lipid peroxidation. During periods of hypoperfusion, hypoxia, and metabolic acidosis, oxidative pathways are activated. The radicals generated from these reactions are highly active and readily oxidize proteins, DNA, and more importantly, membrane fatty acids, leading to cellular dysfunction, cell lysis, and demise. It is believed that pharmacological agents prevent neuropathological changes in the injured brain by scavenging free radicals or decreasing membrane lipid peroxidation.27,28 Finally, the role of programmed cell death, apoptosis, is a topic of hot debate; it appears to halt this cascade by sacrificing injured cells.29,30

Although the complexities of the chemical interactions contributing to TBI have yet to be fully elucidated, the physiological consequences of these cellular changes are better understood and include alterations in cerebral perfusion, edema, and inflammation. Cerebral blood flow (CBF) is tightly controlled by cerebral vascular resistance and is largely unaffected by fluctuations in systemic arterial pressure or intracranial pressure (ICP). This phenomenon, termed cerebral autoregulation, is achieved by constriction and relaxation of arterioles and venules in response to neurotransmitters and local chemicals. Cerebral autoregulation also is intimately associated with the integrity of the blood-brain barrier (BBB), a formation of specialized cerebral vascular cells. In between these cells exist tight junctions that prevent passive diffusion of electrolytes, plasma proteins, and large molecules into the brain extracellular space. Cerebral autoregulation permits a constant flow of blood between a range of mean arterial pressure (MAP) of 50-140 mmHg.31 CBF is equal to the cerebral perfusion pressure (CPP) divided by cerebral vascular resistance. CPP is calculated as the difference between MAP and ICP. As the CBF is difficult to measure directly, the CPP is used as a guide for estimating cerebral perfusion. In healthy individuals, ICP ranges between 0 and 10 mmHg, and elevated ICP is defined as pressure in excess of 20 mmHg for 5 minutes or more.32 CPP values normally vary between 70 and 100 mmHg; due to cerebral autoregulation, ischemia in the non-injured brain does not occur until the CPP decreases below 40 mmHg.31 Following injury to the brain, however, mediators of injury may impair cerebral autoregulation and usually insignificant fluctuations in MAP can have a profound effect on CBF. In addition, as injured endothelial cells fail, the BBB may be compromised, affecting the diffusion of electrolytes, plasma proteins, and other molecules into the brain extracellular space.31,33

The brain is housed in a fixed space containing the parenchyma, cerebrospinal fluid (CSF), extracellular fluid, and blood. These tissues are largely incompressible. Following TBI, there is an increase in blood and tissue edema that increases the intracranial volume.34 Initially, elevations in intracranial volume are accommodated by movement of blood and CSF out of the vault. However, further increases in intracranial volume are met by sharp increases of ICP. Elevated ICP is not harmful unless it increases to a point where CPP falls below a critical value. Further lowering of CPP leads to cerebral ischemia causing neuronal injury and cerebral edema. The ensuing edema can cause further increases in ICP and exacerbate diminished CBF, leading to irreversible neuronal damage.35 Studies have shown that in patients with TBI, CBF may be reduced to less than one-half of that in normal individuals.36-38 The presence of blood collections in the tissues from epidural or subdural hematomas can be especially problematic, not only by increasing ICP, but also by releasing iron during decomposition and promoting oxidation.39 Furthermore, blood in the subarachnoid space can trigger vasospasm, worsening ischemia. Even after CBF is restored, however, damage also may occur during reperfusion of the injured area, via activation of mediators of injury causing edema.

The actual brain damage that occurs at the time of injury cannot be reversed; therefore, optimization of posttraumatic neurological function depends on alleviating factors contributing to secondary injury to the brain. As described above, the traumatized brain is especially vulnerable to ischemia due to metabolic and molecular derangements. Alterations in CBF and ischemia are central to the theme of secondary brain injury and may be caused by factors superimposed on the primary injury or as a consequence of extrinsic changes. These factors include hypotension, hypoxia, infection, hyperthermia, seizures, and electrolyte imbalances. The traumatic coma data show that the two most common secondary insults are hypoxia (paO2 < 60 mmHg) and hypotension (systolic blood pressure < 90 mmHg), which when present in combination may more than double mortality.40 Apnea is a frequent finding immediately following TBI, and alcohol and other drugs may exacerbate initial respiratory depression. Hemorrhage from internal or orthopedic injuries, decreased cardiac output from cardiac contusion, tamponade or tension pneumothorax, or neurogenic injury from a spinal cord insult may decrease CPP to critical levels. Wilberger and colleagues observed that one episode of hypotension in the prehospital/emergency department period can increase mortality by 50%.41 Proof of the significance of secondary neuronal injury is shown by the 30-40% of patients who talk or obey commands prior to death, indicating that the primary injury, by itself, was insufficient to cause mortality.42 Therefore, attenuation of these secondary factors and prevention of cerebral ischemia are important to maximizing neurological recovery.31

Emergency Management of TBI

History. Table 1 lists key historical data that should be obtained from the patient and witnesses to the injury. Important comorbid factors include propensity toward coagulopathy (e.g., alcohol, anticoagulant therapy), prior history of TBI, and preexisting seizure disorders. Details regarding the mechanism of injury, including height of fall, landing surface, condition of car, deployment of airbags, use of seatbelt, and associated fatalities or severely injured people should be sought. Information regarding the patient’s condition postinjury and the patient’s condition upon arrival of first responders also should be determined.43 Any history of physiological anisocoria should be noted, as it is present in 10% of the general population. Finally, family members and/or acquaintances may be useful for documenting the patient’s baseline mental status.43

Table 1. Important Historical Facts in Head Injury
Mechanism of Injury
Condition of car (drivable, windshield, deployment of airbags, steering column)
Height of fall, landing surface, number of steps
Past medical history (coagulopathy, chronic alcoholism, hemophilia)
Medication history (warfarin)
Complaints preceding trauma (chest pain, dizziness, headache)
Drug/alcohol ingestion
Condition post injury
Duration of loss of consciousness
Repetitive questioning
Amnesia to event
Compared to baseline
Other injuries

Adapted from: Biros MH. Head Trauma. In: Rosen P, Barkin R, eds. Emergency Medicine: Concepts and Clinical Practice. 4th ed. Mosby-Year Book; 1998.

The Acute Neurological Examination. According to Advanced Trauma Life Support (ATLS) guidelines,44 the first tasks in the acute resuscitation of trauma victims involve airway, breathing, and circulation, and the TBI patient is no exception. A revised version of the ATLS guidelines is expected in July 2002. For this review, we have divided management of TBI according to the clinical spectrum of the disease. The initial resuscitation of patients with blunt and penetrating TBI is identical and specifics regarding airway management and fluid resuscitation are discussed in the section addressing severe head trauma.

A brief neurological examination should be performed early in the management as part "D" (deficit) in the initial "ABCs" of the ATLS primary survey. Accurate and objective assessment of neurological status serves as a basis that can be recorded and used for comparison during the resuscitation and further evaluation of the patient. Terms such as "obtunded," "stuporous," and "lethargic" should be avoided where possible. Stable patients who are awake may undergo a relatively comprehensive neurological examination, whereas critical patients may require a more efficient examination, which includes Glasgow Coma Scale (GCS) score (see Table 2), pupillary function, motor function, and mental status (see Table 3).

Table 2. The Glasgow Coma Scale
Eye opening
Spontaneously 4 Reticular activating system is intact; patient may not be aware
To verbal command 3 Opens eyes when told to do so
To pain 2 Opens eyes in response to pain
None 1 Does not open eyes to any stimuli
Verbal response
Oriented—converses 5 Relatively intact CNS. Aware of self and environment
Disoriented—converses 4 Well articulated, organized, but patient is disoriented
Inappropriate words 3 Random, exclamatory words
Incomprehensible 2 Moaning, no recognizable words
No response 1 No response or intubated
Motor response
Obeys verbal commands 6 Readily moves limbs when told to
Localizes to painful stimuli 5 Moves limb in an effort to remove painful stimuli
Flexion withdrawal 4 Pulls away from pain in flexion
Abnormal flexion 3 Decorticate rigidity
Extension 2 Decerebrate rigidity
No response 1 Hypotonia, flaccid: suggests loss of medullary function or concomitant spinal cord injury

Adapted from: Teasdale G, Jennett B. Assessment of coma and impaired consciousness: A practical scale. Lancet 1984;2:81-84.


Table 3. Abridged Neurological Examination in the Severe TBI Patient
Mental status
Glasgow Coma Scale
Pupils (size, responsiveness, asymmetry)
Motor exam (symmetry, abnormal movements, strength, reflexes)
Cranial nerves (gag reflex, corneal reflex)
Brainstem function (respiratory rate and pattern, eye movements)

Adapted from: Biros MH. Head Trauma. In: Rosen P, Barkin R, eds. Emer gency Medicine: Concepts and Clinical Practice. 4th ed. Mosby-Year Book; 1998.

This abridged version is not a substitute for a comprehensive examination that should be performed when the patient is more stable. The importance of repeated neurological exams cannot be emphasized enough, as the clinical status of TBI patients can change rapidly. An expanding hematoma may cause rapid deterioration of an awake, talking patient within minutes. Likewise, severely inebriated patients may soon awaken if the coma is related to alcohol rather than severe TBI. While not included in the evaluation of GCS score, assessment of pupillary function may provide important information. Pupillary asymmetry is especially concerning and is thought to result from transtentorial herniation causing mechanical compression of the third cranial nerve and subsequent brainstem compromise. Bilateral, nonreactive pupillary dilation usually is associated with severe TBI and a poor prognosis. The Brain Trauma Foundation recommends a pupillary size of greater than 4 mm as diagnosis for a "blown" pupil.45 A recent study demonstrated that anisocoria of 1 mm or greater is associated with intracranial lesions in 30% of patients, whereas patients with anisocoria of 3 mm or greater harbored intracranial lesions in 43% of cases. A higher incidence of lesions occurred in older patients injured as a result of something other than being occupants of vehicles involved in accidents.46 Of note, paralytic agents do not alter pupillary function. In the comatose patient, loss of extraocular eye movements is not uncommon, but eyes may deviate toward the side of an intracranial lesion. Roving eye movements or disconjugate gaze also may be seen in TBI. Identification of seizure in TBI patients can be subtle and noted by small, rhythmic eye movements or persistent nystagmus. Loss of corneal and oculocephalic reflexes in association with TBI suggests severe brainstem dysfunction. In the unconscious patient, an unequal motor exam suggests hematoma or significant damage to the contralateral cerebral hemisphere. The mechanism of injury also is important, as 80% of patients with focal motor findings may require surgery if their mechanism was unrelated to a motor vehicle accident, as compared with 30% of patients who were either occupants, pedestrians, or motorcyclists.21

Classification of TBI. Numerous attempts have been made to classify TBI in terms of severity for directing management and assessing prognosis. Although studies have shown changes in levels of biological markers following TBI, there are no easily measured markers to guide the clinician.47 Brain stem auditory evoked potentials, single photon emission computed tomography (SPECT), and magnetic resonance imaging (MRI) may prove to be useful, but are difficult to perform in the emergent setting. At this point, the GCS score (see Table 2), developed in 1974 by Teasdale and Jennett, enables assessment of the TBI patient with regard to neurological function.48 In the early 1980s, Rimel and colleagues divided the GCS score into three categories: scores of 8 or less were "severe," 9-12 were "moderate," and 13-15 were "mild."49 However, data suggest that patients with GCS scores of 13 may have complication rates more consistent with moderately classified injuries.50-55 Therefore, the term "mild" TBI is generally reserved for patients with GCS scores of 14-15.56-58

Imaging in TBI

Computed Tomography Scanning. The advent of computed tomography (CT) scanning in the 1970s revolutionized the work-up of TBI by providing timely anatomic and pathologic information used to identify TBI patients with surgical conditions. Skull radiographs, although still in use in many countries, have been almost completely superseded by head CT scanning in North America. Newer machines have reduced the scanning time to less than two minutes, which allows clinicians not only to determine at-risk patients earlier, but also to scan potentially less stable patients. Although there is little debate regarding the clinical utility of CT scanning, significant controversy exists as to which patients should be scanned. There is little argument that TBI patients with GCS scores of less than 13 need to be scanned and early in its history, the CT scan was a scarce resource that was reserved for such individuals.

As CT scanning became more widely available, studies demonstrated that scanning even minor TBI patients was less expensive than admitting patients for observation.59 Debate then arose over the need to immediately identify all patients with intracranial lesions vs. emphasis on cutting costs. One group demonstrated that home observation of TBI patients might be unreliable,60 further emphasizing the need to identify those patients at risk prior to discharge. The indications for performing a head CT scan will be discussed in the section addressing minor head trauma.

TBI patients can deteriorate suddenly; therefore, adequate resuscitation is important to avoid further cerebrovascular compromise while the patient is in the relatively inaccessible environment of the CT scanner. Prevention of deterioration in TBI patients who initially appear to be at low risk appears to cause the greatest reduction of morbidity and mortality in head traumatized patients.61 Rapid CT scan may be performed in patients who respond to resuscitation, regardless of initial hypotension and subsequent need for surgery.62 In cases of massive hemorrhage that is unresponsive to fluid administration, however, correction of homeostasis is priority. Severely injured (GCS score < 9) or combative patients may require adequate sedation, paralysis, and intubation prior to CT to eliminate motion artifact and protect the patient’s airway. Conscious sedation with parenteral benzodiazepines may suffice for less severe TBI patients (GCS scores 9-13).

The CT scan has revolutionized the management of TBI; however, it is a low contrast study. Specifically, the CT scan is excellent for demonstrating intracranial hemorrhages but is poor at defining non-hemorrhagic injured areas. Therefore, TBI patients with severe DAI and a low presenting GCS score may have a relatively normal-appearing initial head CT scan. As a consequence, the initial head CT scan reading poorly correlates with the eventual neurologic outcome of the TBI patient.63 Furthermore, the CT scan provides information on neither the functional nor the metabolic status of the brain or CBF. Notwithstanding, the CT scan is rapid, readily available, and fortunately identifies most surgically amenable lesions.

Magnetic Resonance Imaging. Almost all studies have used the head CT scan as the gold standard for identifying intracranial pathology. However, MRI is superior to the head CT scan for identifying hemorrhages in brain parenchyma, defining nonhemorrhagic areas (DAI, cortical contusions, subcortical gray matter injury) and brainstem lesions, and permitting better approximation of the total degree of injury.18,64 Similar to CT scanning, though, studies have shown that MR scan findings do not accurately predict eventual neurological outcome. However, data suggest that the presence of hemorrhage in DAI-type lesions and traumatic space-occupying lesions have a poorer prognosis.65 MRI does take markedly longer to perform than head CT scan; one study found an average time of 2-5 minutes for head CT scan and 45 minutes for head MRI.66 Therefore, it is not feasible in the initial management of the TBI patient. As technology improves, the enhanced detail provided by MRI may become important in the future management of early TBI.

Angiography. Penetrating TBI frequently causes vascular lesions, such as carotid-cavernous or arteriovenous fistula, arterial occlusion, arterial transection, or traumatic aneurysm. Traumatic aneurysms are particularly prone to rupture, producing delayed traumatic intracerebral hematoma and/or subarachnoid hemorrhage.67,68 The incidence of traumatic aneurysms ranges from 3% to 33% of the penetrating TBI population.67,69-70 Patients with penetrating or perforating TBI involving the sphenoid bone, temporal bone, or posterior fossa may have injuries to the carotid and/or vertebral arteries, or major venous sinuses. These individuals should undergo cerebral angiography to exclude vascular occlusion, traumatic dissection, or false aneurysm. Angiography also may be considered in the presence of delayed intracerebral hemorrhage or otherwise unexplained subarachnoid hemorrhage, particularly in association with a deteriorating neurological examination.71


1. Bennett BR, Jacobs LM, Schwarz RJ. Incidence, cost and DRG-based reimbursement for traumatic brain injured patients: A 3-year experience. J Trauma 1989;29:566-565.

2. Jennett B, Frankowski RF. The epidemiology of brain injury. In: Braakman R, ed. Handbook of Clinical Neurology. St. Louis, MO: Elsevier Science; 1990.

3. Borzuck P. Neurologic emergencies: Mild head trauma. Emerg Med Clin North Am 1997;15:563-577.

4. Gennarelli TA, Champion HR, Sacco WJ, et al. Mortality of patients with head injuries and extracranial injury treated in trauma centers. J Trauma 1989;29:1193-1201.

5. No authors listed. Part 2: Prognosis in penetrating brain injury. J Trauma 2001;51:S44-S86.

6. Pennings JL, Bachulis BL, Simons CT, et al. Survival after severe brain injury in the aged. Arch Surg 1993;128:787-793.

7. Zink BJ. Critical resuscitations: Traumatic brain injury. Emerg Med Clin North Am 1996;14:116-150.

8. Dikmen SS, Machamer JE, Donovan DM, et al. Alcohol use before and after traumatic head injury. Ann Emerg Med 1995;26:167-176.

9. Kraus JF, Morgenstern H, Fife D, et al. Blood alcohol tests, prevalence of involvement, and outcomes following brain injury. Am J Public Health 1989;79:294-299.

10. Jagger J, Fife D, Vernberg K, et al. Effect of alcohol intoxication on the diagnosis and apparent severity of brain injury. Neurosurgery 1984;15:303-306.

11. Brismar B, Engstrom A, Rydberg U. Head injury and intoxication: A diagnostic and therapeutic dilemma. Acta Chir Scand 1983;149:11-14.

12. Miller JD. Changing patterns in acute management of head injury. J Neurol Sci 1991;103:S33-S37.

13. Pearl GS. Forensic pathology, part 1: Traumatic neuropathology. Clin Lab Med 1998;18:39-64.

14. Graham DI, Adams JH, Nicoll JAR, et al. The nature, distribution and causes of traumatic brain injury. Brain Pathol 1995;5:397-406.

15. Miller JD. Head injury. J Neurol Neurosurg Psychiatry 1993;56: 440-447.

16. Hopkinson DAW, Marshall TK. Firearm injuries. Br J Surg 1967; 54:344-353.

17. Rosenwasser RH, Andrews DW, Jiminez DF. Penetrating craniocerebral trauma. Surg Clin North Am 1991;71:305-317.

18. Gentry LR. Imaging of closed head injury. Radiology 1994;191:1-17.

19. Povlishock JT. Pathobiology of traumatically induced axonal injury in animals and man. Ann Emerg Med 1993;22:280-286.

20. Povlishock JT. Traumatically induced axonal injury: Pathogenesis and pathobiological implications. Brain Pathol 1992;1:1-12.

21. Gennarelli TA. Mechanisms of brain injury. J Emerg Med 1993;11: 5-11.

22. Gennarelli TA, Thibault LE. Biomechanics of acute subdural hematoma. J Trauma 1982;22:680-686.

23. Zink BJ. State of the art: Traumatic brain injury outcome: Concepts for emergency care. Ann Emerg Med 2001;37:318-332.

24. Bullock R, Kuroda Y, Teasdale GM, et al. Prevention of post-traumatic excitotoxic brain damage with NMDA antagonist drugs: A new strategy for the nineties. Acta Neurochir 1992;55:49-55.

25. Hayes RL, Dixon CE. Neurochemical changes in mild head injury. Semin Neurol 1994;14:25-31.

26. Siesjo BK. Basic Mechanisms of traumatic brain damage. Ann Emerg Med 1993;22:959-969.

27. Braughler JM, Hall ED. Central nervous system trauma and stroke I: Biochemical considerations of oxygen radical formation and lipid peroxidation. Free Radic Biol Med 1989;6:289-301.

28. Hall ED, Braughler JM. Central nervous system trauma and stroke II. Physiological and pharmacological evidence for involvement of oxygen radicals and lipid peroxidation. Free Radic Biol Med 1989; 6:303-313.

29. White BC, Sullivan JM. Apoptosis. Acad Emerg Med 1998;5:1019-1031.

30. Cairns CB. Apoptosis: only the good die young. Acad Emerg Med 1998;5:948-950.

31. Marik P, Chen K, Varon J, et al. Management of increased intracranial pressure: A review for clinicians. J Emerg Med 1999;17:711-719.

32. Miller JD, Butterworth JF, Gudeman SK, et al. Further experience in the management of severe head injury. J Neurosurg 1981;75:685-693.

33. Fessler RD, Diaz FG. The management of cerebral perfusion pressure and intracranial pressure after severe head injury. Ann Emerg Med 1993;22:998-1003.

34. Bouma GJ, Muizelaar JP, Fatouros P. Pathogenesis of traumatic brain swelling: Role of cerebral blood volume. Acta Neurochir Suppl (Wien) 1998;71:272-275.

35. Shapiro HM. Intracranial hypertension: Therapeutic and anesthetic considerations. Anesthesiology 1975;43:445-471.

36. Bouma GJ, Muizelaar JP, Choi SC. Cerebral circulation and metabolism after severe traumatic brain injury: The elusive role of ischemia. J Neurosurg 1991;75:685-693.

37. Jaggi JL, Obrist WD, Gennarelli TA. Relationship of early cerebral blood flow and metabolism to outcome in acute head injury. J Neurosurg 1990;72:176-182.

38. Raichle ME, Plum F. Hyperventilation and cerebral blood flow. Stroke 1972;3:566-575.

39. Gutteridge JMC, Rowley DA, Holliwell B. Superoxide-dependent formation of hydroxyl radicals in the presence of iron salts. Detection of free iron in biological systems by using bleomycin-dependent degradation of DNA. Biochem J 1981;199:263-165.

40. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216-222.

41. Wilberger JE. Contemporary treatment paradigms in head injury. Clin Neurosurg 2000;46:143-152.

42. Menon DK. Cerebral protection in severe head injury: Physiological determinants of outcome and their optimization. Brit Med Bull 1999;55:226-258.

43. Biros MH. Head Trauma. In: Rosen P, Barkin R, eds. Emergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby-Year Book; 1998.

44. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors. 6th ed. American College of Surgeons: Chicago, IL; 1997.

45. Anonymous. The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Pupillary diameter and light reflex. J Neurotrauma 2000;17:583-590.

46. Chestnut RM, Gautille T, Blunt BA, et al. The localizing value of asymmetry in pupillary size in severe head injury: Relation to lesion type and location. Neurosurgery 1994;34:840-846.

47. Romner B, Ingebrigsten T, Kongstad P, et al. Traumatic brain damage: Serum S-100 protein measurements related to neuroradiological findings. J Neurotrauma 2000;17:641-647.

48. Teasdale G. Jennett B. Assessment of coma and impaired consciousness: A practical scale. Lancet 1984;2:81-84.

49. Rimel RW, Giordani B, Barth JT, et al. Disability caused by minor head injury. Neurosurgery 1981;9:221-228.

50. Hsiang JNK, Yeung T, Yu ALM, et al. High-risk mild head injury. J Neurosurg 1997;87:234-238.

51. Borczuk P. Predictors of intracranial injury in patients with mild head trauma. Ann Emerg Med 1995;25:731-736.

52. Gomez PA, Lobato RD, Ortega JM. Mild injury: Difference in prognosis among patients with a Glasgow Coma Scale score of 13 to 15 and analysis of factors associated with abnormal CT findings. Br J Neurosurg 1996;10:453-460.

53. Culotta VP, Sementilli ME, Gerold K, et al. Clinicopathological heterogeneity in the classification of mild head injury. Neurosurgery 1996;38:245-250.

54. Tellier A, Della Malva LC, Cwinn A, et al. Mild head injury: A misnomer. Brain Inj 1999;13:463-475.

55. Wang MY, Griffith P, Sterling J, et al. A prospective population-based study of pediatric trauma patients with mild alterations in consciousness (Glasgow Coma Scale score 13-14). Neurosurgery 2000;46:1093-1099.

56. Narayan RK, Greenberg RP, Miller JD, et al. Improved confidence of outcome prediction in severe head injury. A comparative analysis of the clinical examination, multimodality evoked potentials, CT scanning, and intracranial pressure. J Neurosurg 1981;54: 751-762.

57. Stein SC, Ross SE. Mild head injury: Plea for routine early CT scanning. J Trauma 1992;33:11-33.

58. Stein SC, Ross SE. Minor head injury: A proposed strategy for emergency management. Ann Emerg Med 1993;22:1193-1196.

59. Stein SC, O’Malley KF, Ross SE. Is routine computed tomography scanning too expensive for mild head injury? Ann Emerg Med 1991;20:1286-1289.

60. Saunders CE, Cota R, Barton CA. Reliability of home observation for victims of mild closed-head injury. Ann Emerg Med 1986;15:160-163.

61. Klauber MR, Marshall LF, Luerssen TG, et al. Determinants of head injury mortality: Importance of the low risk patient. Neurosurgery 1989;24:31-36.

62. Winchell RJ, Hoyt DB, Simons RK. Use of computed tomography of the head in the hypotensive blunt-trauma patient. Ann Emerg Med 1995;25:737-742.

63. Cheung DS. Evidence based emergency medicine: Evaluation and diagnostic testing. Evaluation of the patient with closed head trauma: An evidence based approach. Emerg Med Clin North Am 1999;17:9-23.

64. Sklar EM, Quencer RM, Bowen BC, et al. Magnetic resonance applications in cerebral injury. Radiol Clin North Am 1992;30:353-366.

65. Paterakis K, Karantanas AH, Komnos A, et al. Outcome of patients with diffuse axonal injury: The significance and prognostic value of MRI in the acute phase. J Trauma 2000;49:1071-1075.

66. Ogawa T, Sekino H, Uzura M, et al. Comparative study of magnetic resonance and CT scan imaging of cases of severe head injury. Acta Neurochir Suppl (Wien) 1992;55:8-10.

67. Aarabi B. Traumatic aneurysms of brain due to high velocity missile head wounds. Neurosurgery 1988;22:1056-1063.

68. Haddad FS, Haddad GF, Taha J. Traumatic intracranial aneurysms caused by missiles: Their presentation and management. Neurosurgery 1997;28:1-7.

69. Amirjamshidi A, Rahmat H, Abbassioun K. Traumatic aneurysms and arteriovenous fistulas of intracranial vessels associated with penetrating head injuries occurring during the war: Principles and pitfalls in diagnosis and management—a survey of 31 cases and review of the literature. J Neurosurg 1996;84:769-780.

70. Jinkins JR, Dadsetan MR, Sener RN, et al. Value of acute-phase angiography in the detection of vascular injuries caused by gunshot wounds to the head: Analysis of 12 cases. Neurosurgery 1991;29: 67-72.

71. Pruitt BA, Jr, ed. Vascular complications of penetrating brain injury. J Trauma 2001;51:S26-S28.