Traumatic Brain Injury

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Chapter 22 Traumatic Brain Injury

Neurologists divide traumatic brain injury (TBI) into mild and severe categories. Following the classification scheme of the American Academy of Neurology, which is one of many, neurologists define mild TBI as “a trauma-induced alteration in mental status that may or may not involve loss of consciousness.” They expect that the altered mental status consists of confusion and amnesia that lasts seconds to minutes. Neurologists, who often substitute the everyday word concussion for mild TBI, also expect that the patient will have no focal neurologic signs, such as hemiparesis, cranial nerve abnormalities, and incoordination.

In contrast, neurologists define severe TBI as posttraumatic prolonged loss of consciousness (more than 12 hours) and radiographic signs of injury to brain, skull, or intracranial blood vessels. Civilians most at risk for severe TBI are 15–24-year-old men and individuals older than 75 years. For them, common causes include motor vehicle accidents (MVAs), athletic and recreational accidents, on-the-job injuries, falls, and violent assaults. At any age, alcohol plays a major role in causing TBI because it impairs judgment, coordination, and wakefulness. In the elderly, falls not only commonly cause TBI, they also pose several clinical problems. Strokes often cause the patient to fall and thereby sustain TBI deficits superimposed on stroke-induced ones. Falls may also cause bodily injury, such as a hip fracture, that leads to nonneurologic deficits. Also, fall-induced impairments and TBI in general may represent elder abuse.

The usual warfare injury that leads to severe TBI is head wounds from bullets and shrapnel. However, in the Afghanistan and Iraq wars, blasts rather than such penetrating missile wounds have been the predominant injury.

Major Head Trauma

How Does Head Trauma Cause TBI?

Epidural hematomas, which typically result from temporal bone fractures with concomitant middle meningeal artery lacerations, are essentially rapidly expanding, high-pressure, fresh blood clots (Fig. 22-2). They compress the underlying brain and force it through the tentorial notch, i.e., they produce transtentorial herniation (see Fig. 19-3). Unless surgery can immediately arrest the bleeding, epidural hematomas are usually fatal.

FIGURE 22-2 Meningeal arterial bleeding, which usually results from a blow forceful enough to fracture the skull, causes epidural hematomas. In contrast, venous bleeding, usually slower and under less pressure, causes subdural hematomas. Ruptured aneurysms and head trauma often cause subarachnoid hemorrhage (SAH). In SAH, blood spreads within the subarachnoid space over the convexities, between the gyri, into the interhemispheric fissure, and down into the spinal canal.

As an example, a victim of an assault with a baseball bat lost consciousness when struck. After regaining consciousness for 1 hour, the victim lapsed into coma and developed fatal decerebrate posture (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 victim 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. 20-9). Dark, venous blood generally 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 does not necessarily precede the symptoms. CTs show acute, dense blood in the subdural space (see Fig. 20-9).

Chronic subdural hematomas, ones that have developed and persisted for weeks, usually have spread extensively in the subdural space (see Fig. 20-9). They typically give rise to insidiously developing headache, change in personality, and cognitive impairment, but only subtle focal physical deficits (see Chapters 19 and 20). Although subdural hematomas may spontaneously resolve, they often require surgical evacuation. Because subdural hematoma patients’ cognitive decline is rapid, but treatment usually reverses their symptoms, neurologists often include subdural hematomas as an explanation for “rapidly developing dementia” and 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. Most importantly, age-related cerebral atrophy enlarges the subdural space: the capacious space allows hematomas to reach a considerable size before they encounter the resistance of the underlying brain.

Foreign Bodies

In addition to the disruption of brain tissue and intraparenchymal bleeding, gunshot wounds and other penetrating injuries leave bone, shrapnel, and other foreign bodies in the brain. These foreign bodies act either as a focus that generates seizures or a nidus for brain abscesses. Although desirable, neurosurgeons cannot remove all foreign bodies because many lodge in inaccessible areas.

Posttraumatic Coma and Delirium

Following head trauma, as well as at other times, neurologists often classify patients’ level of consciousness as alert, lethargic, stuporous, or comatose. They may also use the Glasgow Coma Scale (GCS), which 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. Moreover, physicians cannot appropriately include the GCS as part of a standard mental status examination for patients suspected of having dementia or circumscribed neuropsychologic deficits.

TABLE 22-1 The Glasgow Coma Scale (GCS)

Category		Score
Eyes opening	Never	1
	To pain	2
	To verbal stimuli	3
	Spontaneously	4
Best verbal response	None	1
	Incomprehensible sounds	2
	Inappropriate words	3
	Disoriented and converses	4
	Oriented and converses	5
Best motor response	None	1
	Extension*	2
	Flexion†	3
	Flexion withdrawal	4
	Patient localizes pain	5
	Patient obeys	6
Total		3–15

This standard scale quantitates the level of consciousness, with the lower scores indicating less neurologic function. Neurologists interpret scores of 3–8 as signifying severe traumatic brain injury (TBI) or coma; 9–12, moderate TBI; and 13–15, mild TBI. However, the GCS is not readily applicable to patients who have sustained cerebral hypoxia and, because they cannot make a verbal response, those who are intubated. Adapted, with kind permission, from Teasdale G, Jennett B. Assessment of coma and impaired consciousness: A practical scale. Lancet 1974;2:81–84.

^*Decerebrate rigidity (Fig. 19-3).

^†Decorticate rigidity (Fig. 11-5).

By the first day after TBI, of patients who score 3 on the GCS, which is the lowest possible score, 90% have a fatal outcome and most of the remaining never regain consciousness. By 4 weeks, almost all TBI comatose patients die, partially recover and regain consciousness, or evolve into the vegetative state (see Chapter 11). When in coma or the vegetative state, individuals cannot perceive pain and do not suffer.

As 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. During the recovery phase, alcohol or drug withdrawal may cause seizures and a markedly lower pain threshold, as well as abnormal behavior from substance withdrawal delirium superimposed on TBI.

Even after recovery from TBI, alcohol abuse stalks survivors. It and other substance abuse often remains a source of continued disability. Binge drinking complicates the life of major TBI survivors 18 times more often than age-matched controls.

Pre-existing dementia also leaves patients particularly susceptible to posttraumatic delirium. In fact, dementia may have led to the trauma, as when a patient with Alzheimer disease causes a MVA. Also, numerous 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, and fat emboli.

Physical Sequelae

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

Recovery from physical deficits, to the extent that 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, such as the eye, ear, or nose and their cranial nerves, although not strictly speaking “brain injury,” adds to patients’ neurologic disability. It 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 and personality and cognitive impairments. In addition, TBI that damages patients’ hypothalamus disrupts their sleep–wake cycle, which causes 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), which is 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.

Seizures that occur either within the first 24 hours (immediate posttraumatic seizures) or the first 7 days (early posttraumatic seizures) 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 prophylaxis following severe TBI reduces early posttraumatic seizures, but no AED clearly reduces the prevalence of PTE. PTE remits in only 25–50% of cases. PTE usually takes the form of complex partial seizures that undergo secondary generalization (see Chapter 10). Not only does PTE cause disability and carry the risk of further head injury, AEDs may exacerbate TBI-induced cognitive and personality changes.

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).

Of those TBI patients who regain consciousness, many still have residual 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 preliminary version of 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 their immediate posttraumatic depth of coma, as measured by the GCS. However, their deficits more strongly correlate 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 important caveat remains: Self-reported cognitive complaints correlate closer 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 with medications causing or adding to delirium in the immediate posttraumatic period, numerous AEDs, muscle relaxants, and opioids may further depress cognitive function. These medicines may 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 TBI causing debilitating cognitive impairments, some epidemiologic studies suggest that it also constitutes a risk factor for Alzheimer disease. Studies have shown that severe head trauma causes increased levels of soluble 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 apolipoprotein E4 (Apo-E4) alleles correlates with a marked increased risk of developing Alzheimer disease (see Chapter 7). Surviving moderate TBI, individuals with two Apo-E4 alleles may have twice the risk of developing Alzheimer disease, and surviving severe TBI, those individuals may have four times the risk. (A confounding issue for some of these studies is that individuals with Alzheimer disease are prone to cause an accident in which they sustain TBI and come to medical attention.)

TBI-induced memory impairment, posttraumatic amnesia, is the most consistent neuropsychologic TBI-induced deficit. It includes memory loss for the trauma, immediately preceding events (retrograde amnesia), and, to a less extent, newly presented information (anterograde amnesia). Even compared to the depth or duration of coma, the duration of posttraumatic amnesia provides the most reliable predictor for overall neuropsychologic outcome, including cognitive impairments.

Treatment Strategies for Posttraumatic Cognitive Impairment

Neurologists and other physicians who work with TBI patients with cognitive impairment administer medications that hopefully increase their attentiveness, if not reverse their learning and memory impairments. Of the numerous medicines that purportedly help, few have undergone rigorous trials that have documented their value. For example, many trials have indicated that methylphenidate and other dopamine-enhancing medications increase patients’ attention and directly or indirectly memory. Anticholinesterases may also improve TBI patients’ memory, at least those who have suffered severe memory deficits (see Chapter 7). Treatment of comorbid PTSD, if present, may improve cognitive impairments and other posttraumatic neuropsychologic changes. At the same time, physicians should, if possible, reduce or eliminate medicines that may interfere with attention and memory, such as AEDs, antipsychotics, and minor tranquilizers. They should always bear in mind that multiple medicines are likely to lead to adverse interactions and unwanted, occasionally fatal, outcomes.

Patients do well with cognitive, behavioral, physical, and occupational rehabilitation, i.e., nonpharmacologic treatment. Exposure therapy, for example, may provide greater benefit for PTSD than psychotropics. Multidisciplinary teams have a role in restoring patients’ intellectual functioning and returning them to their place in the family and work. Classic strategies – physical, occupational, and speech therapy, identification and treatment of depression, anxiety, and insomnia, and social interactions with peers – enhance remaining functions, reduce impediments, and provide compensatory mechanisms for injured ones.

Other Mental Disturbances

Aggression

Many severe TBI patients, particularly those with frontal lobe damage, remain reticent, docile, and dependent. On the other hand, some patients tend toward either verbal or physical aggression.

Premorbid factors as well as the location of the TBI and its other sequelae are risk factors for posttraumatic aggression. For example, premorbid poor social functioning and, in some studies, substance abuse are a risk factor for TBI-induced aggression. Injury of the frontal lobes more than other brain regions is a risk factor. The most powerful risk factor is probably TBI-induced depression.

Although antidepressants usually have a therapeutic role, they alone may be insufficient. β-blockers more reliably suppress aggressive behavior. AEDs, especially ones with mood-stabilizing effects, such as valproate and carbamazepine, reportedly suppress violent outbursts.

Personality Changes

Personality changes, presumably from frontal and temporal lobe damage, often lead to patients developing an abrupt, suspicious, or argumentative manner. In some cases, frontal lobe damage impairs inhibitory centers. The lack of inhibition – disinhibition – allows unbridled aggressiveness, loquaciousness, impulsivity, and hyperactivity.

In addition to altering patients’ personality and possibly cognitive capacity, frontal lobe injury may disable their executive abilities. Just as with patients who sustain anterior cerebral artery infarctions, those who sustain frontal lobe trauma have impaired ability to solve abstract problems, plan sequenced actions, or execute responses. Moreover, patients who develop pseudobulbar palsy, another complication of frontal lobe trauma, may display emotional incontinence with easily precipitated fits of pathologic laughing or crying, and unexpected sudden switches between them (see Chapter 4).

Depression

Posttraumatic depression consists of an ill-defined combination of depressive symptoms. Developing in about 25–50% of TBI patients, posttraumatic depression has a weak correlation with the severity of TBI. Several preinjury factors – substance abuse, depression, and poor social functioning – predispose TBI patients to posttraumatic depression. Several trauma-induced factors – cognitive impairments, PTE, and impaired physical, occupational, and social skills – further increase its incidence. Once present, posttraumatic depression predicts poor quality of life.

If depression complicates trauma, it interferes with patients’ rehabilitation and compliance. It also reduces patients’ chance of making a complete recovery and is a risk factor or comorbidity for PTSD. Moreover, depression following TBI represents a risk factor for aggression.

Depressed TBI patients invariably require psychopharmacology. They may benefit from selective serotonin reuptake inhibitors, mood stabilizers, and anxiolytics. They also often need a full array of ancillary services, including physical and occupational therapy, financial assistance, and psychologic support.

Psychosis

Posttraumatic psychosis takes the form primarily of delusions, paranoia, and auditory hallucinations. Impairments in cognition, especially memory, and executive ability are frequent comorbidities of posttraumatic psychotic disorder.

Most cases of TBI-induced psychosis develop in males, within the first 2 years after the trauma, and usually in the aftermath of moderate to severe TBI. Risk factors include a family history of psychosis and a long duration of unconsciousness. Overall, about 20% of severe TBI survivors develop psychosis.

Treatment usually entails not only typical or atypical antipsychotics, but also the addition of antidepressants or AEDs. As with depressed TBI patients, those with psychosis require extensive ancillary services.

Trauma in Childhood

Compared to TBI in adults, TBI in children has somewhat different features. For example, children are frequent victims of deliberately inflicted (nonaccidental) head injury. Also, children with attention deficit hyperactivity disorder (ADHD) or behavior disorder, compared to unaffected ones, are more likely to have engaged in dangerous activities as well as having suffered nonaccidental injuries. Similarly, children with learning disabilities, compared to those without such disabilities, are more apt to sustain sports-related TBI. Then, in a reciprocal relationship, TBI is likely to exacerbate learning disabilities.

The prognosis for children with TBI generally surpasses that for adults with comparable TBI. The severity and extent of brain damage in children largely determine their prognosis, but the GCS is not a suitable guide. Other prognostic factors include the family’s socioeconomic status and psychiatric history.

As with adults, children’s memory is particularly vulnerable to TBI and the duration of their posttraumatic amnesia correlates with their ultimate cognitive impairment and behavioral disturbances. In addition, TBI-induced social problems and behavioral disturbances handicap children as well as adults. Sometimes their residual injuries do not appear until they confront the academic and social demands of successive school years. In this case, as children “grow into their deficits,” TBI may limit their cognitive and psychosocial development.

When TBI occurs before growth spurts, affected limbs may fail to achieve their normal, expectable size. The limbs’ growth arrest resembles the spastic hemiparesis with foreshortened limbs that characterizes congenital cerebral injuries (see Fig. 13-4). If dominant hemisphere injury were to occur before age 5 years, the opposite hemisphere would usually assume control of language. For example, a left-sided cerebral injury in a 4-year-old child will probably not result in aphasia because the plasticity of the brain allows the right cerebral hemisphere to develop language centers. If TBI affects the dominant hemisphere of someone age 5 years or older, it is likely to cause language impairments, if not clear-cut aphasia.

In another potential scenario, TBI in children may damage the hypothalamic–pituitary axis. Resulting endocrine disturbances may lead to obesity, precocious puberty, or delayed puberty.