Traumatic Brain Injury

How Does Head Trauma Cause Traumatic Brain Injury?

Direct Force

A blow to the head—by direct mechanical force (a coup injury [French, blow])—disrupts the underlying delicate brain tissue (the parenchyma ). As with strokes, trauma causes cell death by necrosis and its accompanying inflammatory changes, particularly mononuclear cell infiltration. (In contrast, neurodegenerative diseases, such as Huntington disease and amyotrophic lateral sclerosis [ALS], cause cell death by apoptosis [see Chapter 18 ].)

In addition to causing the coup injury, head trauma throws the brain against the opposite inner surface (table) of the skull, which causes a contrecoup injury of that surface of the brain. Damage from contrecoup injuries may surpass that from the coup injury. Contrecoup injuries frequently damage the temporal and frontal lobes because their anterior surfaces abut the sharp edges of the skull’s anterior and middle cranial fossae ( Fig. 22.1 ). Depending on its severity, damage to the frontal and temporal lobes characteristically leads to memory impairment and personality changes. In one exception to this mechanism, frontal trauma rarely leads to countercoup occipital lobe injuries because the occipital skull is relatively flat and smooth.

Bleeding Within the Skull but Outside the Brain

Head injury, ruptured aneurysms, and other insults often cause bleeding in the spaces between the three meninges, which are readily recalled using the mnemonic PAD: pia, arachnoid , and dura mater .

• Pia mater , the innermost layer, is a thin, translucent, vascular membrane adherent to the cerebral gyri. It follows gyri into sulci and thus allows for a generous region, the subarachnoid space , between it and the immediately overlying layer—the arachnoid mater.

• Arachnoid mater , also thin, spans the tops of gyri, capping the sulci. The subarachnoid space, which contains the cerebrospinal fluid (CSF), envelops the brain and, continuing downward within the spinal canal to the sacrum, the spinal cord and cauda equina. Neurologists performing a spinal tap or lumbar puncture (LP) insert a special needle into the subarachnoid space below the conus medullaris (lower end of the spinal cord), situated between the T12 and L1 vertebrae, to sample CSF (see Chapter 20 ).

• Dura mater, the outermost layer of the meninges, is a thick fibrous tissue adherent to the interior surface of the skull. Two of its infoldings, the falx and tentorium , support the brain and house most of its venous drainage. Neurologists designate the space between the skull and the underlying dura as the epidural space , and between the dura and the underlying arachnoid as the subdural space . Major head trauma may cause hematomas in either or both of these areas.

Epidural hematomas , which typically result from temporal bone fractures with concomitant middle meningeal artery lacerations, are rapidly expanding, high-pressure, fresh blood clots ( Fig. 22.2 ). They compress the underlying brain and force it through the tentorial notch, producing transtentorial herniation (see Fig. 19.3 ). Unless surgery can immediately arrest the bleeding, epidural hematomas are usually fatal.

As an example, a victim of an assault with a baseball bat lost consciousness when struck. After regaining consciousness for 1 hour, the patient lapsed into coma and developed fatal decerebrate posturing (see Fig. 19.3 ). A CT showed a temporal skull fracture and an underlying epidural hematoma (see Fig. 20.9D ). Neurologists label the period when the patient transiently regained consciousness the lucid interval .

In contrast, subdural hematomas usually result from slowly bleeding bridging veins, under relatively low pressure, into the subdural space (see Fig. 20.9A–C ). Dark, venous blood oozes into the extensive subdural space until the expanding hematoma encounters underlying brain. The brain dampens bleeding and suppresses further expansion of the subdural hematoma. However, if the hematoma continues to expand, it may lead to cerebral transtentorial herniation or cerebellar herniation through the foramen magnum. Survivors often have permanent brain damage from the initial trauma and the pressure from the subdural hematoma.

Acute subdural hematomas, which are most apt to occur in alcoholics, individuals medicated with warfarin, or the elderly (see later), produce headache, confusion, and a deteriorating level of consciousness over several hours to 1 or 2 days. Depending on the extent of the bleeding and time until the diagnosis, patients may develop focal signs and herniation. A history of head trauma need not necessarily precede the symptoms. CTs show acute, dense blood in the subdural space ( Fig. 20.9A ).

Chronic subdural hematomas, ones that have developed and persisted for weeks, usually have spread extensively in the subdural space ( Fig. 20.9B ). They typically give rise to insidiously developing headache, change in personality, and cognitive impairment, but only subtle focal physical deficits (see Chapter 19, Chapter 20 ). Although subdural hematomas may spontaneously resolve, they sometimes require surgical evacuation. Because subdural hematoma patients’ cognitive decline is rapid, but treatment usually reverses their symptoms, neurologists often include subdural hematomas in the differential diagnosis of “rapidly developing dementia” and as a “reversible cause of dementia” (see Chapter 7 ).

People older than 65 years are susceptible to chronic subdural hematomas for several reasons. They have a tendency to fall. They often take aspirin, anticoagulants, and other medications that increase their tendency to bleed. Age-related cerebral atrophy results in increased tension on the fragile bridging veins. Notably, elder abuse may be the explanation for repeated falls and traumatic subdural hematomas.

Once enough blood has collected, whether epidural, subdural, or even subarachnoid, increased intracranial pressure typically produces headache, confusion, nausea, vomiting, and focal neurologic signs. To avoid the often-fatal complication of herniation, neurologists try hyperventilation (patients are almost always intubated and artificially ventilated), infusions of hypertonic saline or mannitol to reduce cerebral blood volume, and, while controversial, even mild hypothermia. These measures temporize the situation while physicians prepare for surgical intervention.

Posttraumatic Coma and Delirium

Following head trauma, as well as in other settings, neurologists often classify patients’ level of consciousness as alert, lethargic, stuporous , or comatose . They may also use the Glasgow Coma Scale ( GCS ). It measures three readily obvious neurologic functions: eye-opening, speaking, and moving ( Table 22.1 ). In major head trauma, the GCS correlates closely with survival and neurologic sequelae; however, in minor head trauma, it correlates poorly. Neurologists do not include the GCS as part of a standard mental status examination for patients suspected of having dementia or circumscribed neuropsychologic deficits because patients undergoing evaluation for those impairments should be fully alert.

By the first day after TBI, patients who score 3 on the GCS, the lowest possible score, have a 90% chance of having a fatal outcome, and most of the remaining never regain consciousness. Of patients remaining comatose 4 weeks after TBI, almost all have an unsatisfactory outcome: death, partial recovery with consciousness, or evolution into a vegetative state ( Chapter 11 ). When in coma or the vegetative state, individuals cannot perceive pain and do not suffer.

When patients surviving major TBI emerge from coma, their mental state usually fluctuates and cognitive and personality changes emerge. In this twilight zone, they are often confused, disoriented, agitated, and combative. Their mental processes may be so disrupted and their behavior so counterproductive that they warrant treatment with antipsychotic agents.

During this time, physicians must keep in mind the role of drug and alcohol use in trauma and its aftermath. Not only may substance abuse have caused the trauma, but also because the effects of drugs and alcohol may persist for several days, patients may have substance-induced delirium comorbid with TBI in the immediate posttraumatic period. Then, during the recovery phase, alcohol or drug withdrawal may cause seizures, a markedly lower pain threshold, and abnormal behavior.

Even after recovery from TBI, drug and alcohol abuse stalks survivors. Substance abuse often remains a source of continued disability. In fact, binge drinking complicates the life of major TBI survivors 18 times more often than age-matched controls.

Preexisting dementia also leaves patients particularly susceptible to posttraumatic delirium. Sometimes dementia has led to the trauma, as when a patient with Alzheimer disease causes an MVA. Also, many trauma-related conditions may produce posttraumatic delirium, such as painful injuries, adverse reactions to antiepileptic drugs (AEDs), opioids, and other medications, and systemic complications, such as hypoxia, sepsis, electrolyte disturbances, burns, and fat emboli.

Physical Sequelae

TBI characteristically causes focal neurologic deficits, like hemiparesis, spasticity, and ataxia. Some studies, which remain controversial, assert that TBI may also cause involuntary movement disorders similar to Parkinson disease.

Recovery from physical deficits, to the extent it occurs, usually reaches a maximum within 6 months. During the recovery period and afterwards, patients can increase their functional abilities with physical and occupational therapy, braces, other mechanical devices, and modifications of their environment.

Damage to the special sensory organs and their cranial nerves, although not strictly speaking “brain injury,” adds to patients’ disability. These injuries may also lead to sensory deprivation, disfigurement, and functional impairment. Frontal head trauma, which is probably the most common injury, often shears the filaments of the olfactory nerves as they pass through the cribriform plate. Thus, patients sustaining frontal head trauma often develop combinations of anosmia along with personality and cognitive impairments. In addition, TBI that damages the hypothalamus disrupts patient’s sleep-wake cycle, which in turn leads to insomnia, inattention, and sometimes a requirement for additional medicines (see later).

Posttraumatic Epilepsy

Cerebral scars and residual foreign bodies routinely form epileptic foci. They generate posttraumatic epilepsy (PTE), one of the most commonly occurring complications of major TBI. As time passes after an injury, the prevalence of PTE increases, eventually reaching 50%. The prevalence is greater following penetrating rather than blunt or blast injury, and among patients who abuse alcohol. In contrast, PTE rarely complicates minor head trauma, like concussions (see later).

Seizures that occur either within the first 24 hours (immediate posttraumatic seizures) or the first 7 days (early posttraumatic seizures) following TBI do not fall within the definition of PTE because neurologists label them “provoked seizures.” Only seizures that occur (and recur) more than 7 days after the traumatic injury fall into the definition of PTE. Of note, 1 week of phenytoin or levetiracetam prophylaxis following severe TBI reduces early posttraumatic seizures, but no AED clearly reduces the prevalence of PTE, which may account for 5% to 6% of all epilepsy cases. PTE remits in approximately only 25% to 50% of cases. PTE usually takes the form of focal seizures with impaired awareness (previously named complex partial seizures) that undergo secondary generalization (see Chapter 10 ). Not only does PTE cause disability and carry the risk of further head injury, but AEDs may also exacerbate TBI-induced cognitive and personality changes. Complicating the assessment and treatment of seizures following TBI is some studies have shown an increase of psychogenic non-epileptic seizures in patients with mild TBI (see Chapter 10 ).

Cognitive Impairment

TBI-induced coma usually lasts, at most, 4 weeks. By then, most patients have either succumbed to their injuries or recovered at least some cognition. However, many patients remain in a twilight state with their eyes open, but unconscious. These patients are incapable of thinking, communicating, or deliberately moving. They cannot perceive pain and do not suffer. Most of them linger in the persistent vegetative state (see Chapter 11 ). Neurologists use the term permanent vegetative state once 3 months have passed without change.

Of those TBI patients who regain consciousness, many have permanent incapacitating cognitive impairments. They remain reticent, responsive to only simple requests, and capable of initiating only rudimentary bodily functions. Moreover, physical deficits and PTE accompany their cognitive impairments.

The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, (DSM-5) has updated its previous edition’s term Dementia Due to Head Trauma to Neurocognitive Disorder due to Traumatic Brain Injury .

As a general rule, severely injured patients have profound cognitive deficits. To some extent their deficits correlate with the depth of their immediate posttraumatic coma, as measured by the GCS. However, their deficits correlate more strongly with the duration of the posttraumatic amnesia, which includes the patient’s time in coma. Cognitive deficits include not only memory impairment (see later), but also apraxia, impulsivity, inattention, and slowed information processing. One remaining caveat: self-reported cognitive complaints correlate more closely with premorbid low educational status, emotional stress, and poor physical condition than with neuropsychological test results.

Surprisingly, the trauma’s location, with one important exception, correlates inconsistently with cognitive impairment. Left temporal lobe injuries, the exception, routinely produce vocabulary deficits similar to anomic aphasia (see Chapter 8 ).

Just as medications can cause or add to delirium in the immediate posttraumatic period, so too numerous AEDs, muscle relaxants, and opioids may further impair cognitive function. These medicines can also alter the patient’s personality, mood, and sleep-wake cycle. Similarly, comorbid posttraumatic stress disorder (PTSD) may worsen cognitive impairment.

Recovery of motor and language skills usually reaches a maximum within 6 months, but intellectual recovery may not peak until 18 months. Older patients generally recover more slowly and less completely than younger ones.

In addition to causing debilitating cognitive impairments, some epidemiologic studies suggest TBI also constitutes a risk factor for Alzheimer disease. Studies have shown severe head trauma causes increased levels of insoluble amyloid and deposition of amyloid plaques, one of the hallmarks of Alzheimer disease. Several, but not all, studies also suggest that moderate and severe head trauma in individuals with two Apo-E4 alleles correlates with a markedly increased risk of developing Alzheimer disease (see Chapter 7 ). Individuals with two Apo-E4 alleles who survive moderate TBI may have double the risk of developing Alzheimer disease, and those surviving severe TBI may have four times the risk. (A confounding issue for some of these studies is individuals with Alzheimer disease are prone to cause an accident in which they sustain TBI and come to medical attention.) Studies of older veterans with a history of TBI revealed a 60% increase in risk of developing dementia compared to veterans without a TBI history.

TBI-induced memory impairment, posttraumatic amnesia , is the most consistent neuropsychologic TBI-induced deficit. It includes memory loss for the trauma and immediately preceding events (retrograde amnesia) ; this period of amnestic time diminishes during recovery to the point where patients will frequently remember all preceding details except for the actual traumatic event. Amnesia for newly presented information (anterograde amnesia) is uncommon with mild TBI, but very common with moderate to severe TBI. Because this amnesia represents information that has failed to be encode in a patient’s memory, this period is never recovered. Even more than the depth or duration of coma, the duration of posttraumatic amnesia provides the most reliable predictor for neuropsychological outcome, including cognitive impairments.