How Does Head Trauma Cause TBI?

Direct Force

A blow – by its direct mechanical force (a coup injury) – disrupts the underlying, delicate brain tissue (the parenchyma). As with strokes, trauma causes cell death by necrosis and its accompanying inflammatory changes, particularly monocular cell infiltration. (In contrast, neurodegenerative diseases, such as Huntington disease and amyotrophic lateral sclerosis, 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 frequently surpasses that from the coup injury. Contrecoup injuries frequently damage the temporal and frontal lobes because their anterior surfaces abut against the sharp edges of the skull’s anterior and middle cranial fossae (Fig. 22-1). Depending on its severity, damage of the frontal and temporal lobes characteristically leads to memory impairment and personality changes.

FIGURE 22-1 In this drawing, a hammer blow to the back of the head inflicts a coup injury to the occipital region and, through the contrecoup, a typically more extensive injury to the inferior surface of the frontal and anterior tips of the temporal lobes.

In one exception to this mechanism, frontal trauma rarely leads to countercoup occipital lobe injuries because the occipital skull is relatively flat and smooth. Thus, TBI rarely causes long-lasting visual impairments.

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 insert a special needle into the subarachnoid space below the conus medullaris (lower end of the spinal cord), which is situated between the T12 and L1 vertebrae, to sample CSF.

• 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 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.

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)

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.

Other Mental Disturbances

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.

Nonaccidental Head Injury

Nonaccidental head injury (NAHI) and abusive head trauma, more legally acceptable terms, mean child abuse. An infant’s brain, compared to one of an adult, is especially vulnerable to trauma because it has a greater water content, much less myelin, and a covering of only the soft, thin skull. NAHI often leaves no external sign of trauma, such as face or scalp abrasions or burns. Rages of violent shaking or even direct blows typically injure only the brain, retinas, and internal organs.

The shaken baby syndrome, which is another form of abusive head trauma, consists of the injuries inflicted by violent back-and-forth throws, without direct impact. In this violence, rotational (angular) deceleration produces diffuse axonal shearing, hemorrhages in the brain’s delicate parenchyma and subdural space, and retinal hemorrhages (Fig. 22-3).

FIGURE 22-3 Head trauma causes small hemorrhages throughout the retina – not just around the disk as in papilledema.

Although children may accidentally fall backward and injure their occiput, if they fall forward, they reflexively extend their arms to shield their face and eyes. Therefore, facial, ocular, and anterior skull injuries more strongly suggest NAHI than occipital injuries. Spiral fractures of long bones and fractures of different ages, accompanying head trauma, certainly suggest NAHI.

Physicians must perform a fundoscopic examination to find retinal hemorrhages. In the absence of external injuries, retinal hemorrhages may be the sole clinical indication that a child has sustained NAHI; however, they are not pathognomonic. For example, bleeding diatheses, spontaneous subarachnoid hemorrhages, arteriovenous malformations, and sepsis, as well as genuine accidental trauma, also cause retinal hemorrhages.

MRIs may detect and approximate the chronicity of intracranial bleeding. They can show hemorrhages in the subarachnoid, subdural, and epidural spaces and in the cerebrum and brainstem. Nevertheless, as in most acute head trauma, neurologists and neurosurgeons usually immediately obtain a head CT because, compared to MRI, hospitals can perform it rapidly with little or no sedation, and it shows the skull.

Children who survive NAHI often have residual cognitive impairment, behavioral difficulties, learning disabilities, developmental delay, and seizures. Sometimes neuropsychologic sequelae may not appear for several years. As discussed above, many NAHI survivors have either had ADHD before abuse or develop it afterwards.

Elder Abuse

Elder abuse, child abuse’s geriatric counterpart, usually results from family members or other caregivers mistreating older individuals. Chronic neurologic and psychiatric disorders, particularly dementia, are risk factors. Physicians must be cautious: Even without mistreatment, older individuals are prone to falls, fractures, and subdural hematomas.

Head Trauma in Sports

Sports-induced TBIs usually consist of concussions, the most common form of minor head trauma. When assessing injured athletes, neurologists rate concussions as transient confusion – shorter or longer than 15 minutes – with or without loss of consciousness (lasting minutes or less).

After a concussion, athletes’ confusion usually consists of inattention, slowed responses to inquiries, disorientation, and impaired memory. They frequently report headache and nausea, and, on examination, have dysarthria, impairment of tandem gait, and loss of dexterity. However, neurologists do not require that the athlete have physical symptoms or signs to diagnose a concussion.

Sometimes the head trauma damages one or both trochlear (fourth) cranial nerves, causing diplopia (see Chapter 4). Head trauma may also damage the inner ear’s labyrinthine system. This injury causes vertigo, which patients may describe as “dizziness.” Patients rapidly moving their head or changing position induces this symptom. A neurologic examination of vertiginous patients may show nystagmus.

These physical deficits usually diminish by 1 week after the injury. Afterwards, only subjective problems comprise the postconcussion picture.

At 1 week, athletes with a headache, the most common postconcussion symptom, will usually still show impairments in memory and other neuropsychologic functions. Their other postconcussion symptoms may include irritability, mood changes, and sleep disturbances. Physicians assess injured athletes with various screening or computerized tests, but the Mini-Mental Status Examination (MMSE) (see Chapter 7) is not helpful.

During the time that postconcussion symptoms persist, which may extend to several months, neurologists routinely bar athletes from returning to play. For concussions that involved loss of consciousness, neurologists may bar athletes from playing for the entire season.

Studies justify such a stringent policy. They show that athletes who sustain a concussion are more apt than uninjured ones to have additional concussions. Even allowing for a full recovery from a concussion, subsequent concussions have a cumulative or multiplicative effect. Athletes cannot decide for themselves if they are ready to return to play. For a variety of reasons, athletes tend to underreport symptoms. Many are too young to have the judgment. They may deny injuries so that they remain eligible. The injury itself may not allow them to appreciate it.

Physicians and other supervisors must enforce a stringent policy mostly because athletes who have received a concussion are vulnerable to the second impact syndrome. In this condition, an additional blow, received within days of the original injury, leads to destructive and potentially fatal cerebral edema. It affects children and teenagers more frequently and more severely than adults, and leads to death in almost 50% of cases.

The intercollegiate sports with the greatest risk of concussion are ice hockey, football and both men’s and women’s soccer. High-school TBI risks are greatest for football, but also significant for wrestling, basketball, field hockey, and soccer. The risk in soccer probably relates to players, unlike those in most other contact sports, not wearing helmets despite their routine head-to-head collisions and heading the soccer ball.

Professional and amateur soccer players have subtle but undeniable impairments in memory, visual perception, and other cognitive functions. College football players develop neuropsychologic impairments and exacerbation of pre-existing learning disabilities. Professional football players who sustain concussions are 1.5–3 times more likely to develop depression than their teammates who do not have head injuries. Results of brain imaging and neuropsychiatric testing in retired players are similar to the results in TBI patients. In addition, autopsies of deceased players show excess cerebral tau protein and plaques and tangles – the same pattern present in brains of Alzheimer disease patients.

The American Academy of Neurology, which released a Position Statement on Sports Concussion Management in 2010, recommends immediate removal of an athlete who has sustained a concussion until all symptoms have abated and a doctor has performed an evaluation.

Patients, parents, and psychiatrists should weigh the risks of TBI in contact sports against those in equally vigorous noncontact sports. At the least, parents and psychiatrists should steer children with learning disabilities and other academic impediments away from the risk of TBI.

Dementia Pugilistica

Boxers (pugilists) generally receive blows to the head that frequently leave them dazed. Repeated episodes of such TBI lead to cognitive impairment, often reaching the severity of dementia, and Parkinson disease-like physical deficits (see dementia pugilistica, Chapter 18). Overall, depending on the length of their career, boxers have approximately a 20% risk of dementia.

Postconcussion Syndrome

The most common sequela of minor head trauma consists of an admixture of symptoms that neurologists place into a catch-all term, postconcussion syndrome. This disorder probably falls under the rubric of the preliminary DSM-5 term, Neurocognitive Disorder due to Traumatic Brain Injury. Lacking a strict definition, neurologists base a diagnosis of postconcussion syndrome on one or more of several core symptoms – headache, memory impairment, and insomnia – lasting more than 2–3 months. These and other symptoms of postconcussion syndrome remain entirely subjective and often nonspecific, variable, and occasionally unending.

Neurologists find that postconcussion syndrome patients have a normal physical and neurologic examination, CT, and MRI. Although the electroencephalogram often shows minor abnormalities, the changes are generally inconsistent, insignificant, and often attributable to medications. Similarly, neuropsychologic tests often reveal minor and uneven abnormalities, and those changes may be attributable to inattention, depression, exaggeration, lack of education, or even malingering.

Proposed etiologies of the postconcussion syndrome include diffuse axonal shearing, excitatory neurotransmitter imbalance, and subtle cerebral contusions. In addition, any coexistent whiplash injury (see later) may cause head and neck pain. No matter which postconcussion symptoms predominate, they distract patients, interfere with patients’ sleep, and require them to take medicines that may impair their mood and cognition.

Although neurologists routinely diagnose and treat patients with the postconcussion syndrome, individual patients regularly provoke skepticism. Prolonged symptoms are associated with psychiatric and socioeconomic factors as much as with neurologic injury. They do not correlate with either the estimated force of impact or the usual neurologic parameters of TBI – GCS scores and duration of amnesia. Among compensation claimants undergoing neuropsychologic tests, their effort or socioeconomic status often has more of an effect than the severity of the TBI on their scores. For example, assembly-line workers dissatisfied with their workplace typically fare poorly after head trauma; however, children, soldiers, self-employed workers, and professionals rarely report prolonged or incapacitating symptoms. Finally, treatment that is usually effective for headache and insomnia generally fails to alleviate these symptoms in posttraumatic patients.

The postconcussion syndrome may last unbelievably long. Patients with premorbid intellectual and personality abnormalities tend to have permanent symptoms. For some patients, symptoms seem inextricably linked to litigation and other unsettled issues.

On the other hand, some reports indicate that the postconcussion syndrome results predominantly from neurologic injury. Support for this position is the finding that postconcussion symptoms are similar from patient to patient. In addition, the syndrome strikes many self-employed and highly motivated people, including physicians. In addition, according to some data, symptoms correlate poorly with outstanding litigation and persist after legal claims are settled.

Many children and some adults may not report postconcussion symptoms because they are unable to describe them, have a stoic disposition, or substitute other symptoms. For example, rather than complaining of posttraumatic headaches, children may have somnolence, inattention, or hyperactivity. Professionals unable to describe their feelings may develop unusual irritability.

Headache

The signature of postconcussion syndrome is a dull, generalized, endless headache. Movement, bending, work, and alcohol use usually worsen it. In 50% of patients, postconcussion headache lasts longer than 1 year, and in 25%, longer than 3 years. Surprisingly, postconcussion headache occurs more frequently in mildly injured individuals than in moderately or severely injured individuals. One consideration in patients with continuous postconcussion headache is that the trauma may have exacerbated pre-existing migraine. Another is that use of analgesics, prescribed for any aspect of the injury, for as few as 15 days each month for 3 months has created chronic daily headache (see Chapter 9).

Memory Impairment

Patients with postconcussion syndrome characteristically describe mild amnesia accompanied by inattention or easy distractibility, slowed information processing, and difficulty completing complex mental tasks. As with other postconcussion symptoms, the amnesia shows little correlation with the severity of trauma.

One potential explanation for amnesia in postconcussion syndrome is that the trauma propelled the anterior poles of the frontal and temporal lobes against the rough, bony inner surfaces and edges of the anterior and middle cranial fossae. Comorbid PTSD, depression, anxiety, treatment with opioids and other medications, and substance abuse might also contribute to postconcussion amnesia.

Insomnia

Postconcussion syndrome patients regularly report inability to fall or remain asleep. They also describe excessive daytime sleepiness, but neither nighttime sleep nor daytime naps restore their full normal wakefulness. For patients with postconcussion insomnia, comorbid physical and psychiatric conditions – pain, anxiety, depression, and PTSD – sometimes exacerbate, if not cause, the insomnia. Also, patients’ tendency to consume excessive caffeine, alcohol, opioids, and other medications makes the problem worse.

On the other hand, whatever the cause, physicians might consider that a pre-existing sleep disorder actually led to the TBI. For example, patients with sleep apnea, narcolepsy, or sleep deprivation might cause an MVA or be unable to avoid one (see Chapter 17).

Other Symptoms

Postconcussion syndrome patients often report that they have dizziness. In most cases, their symptom is not authentic vertigo, but a nonspecific sensation with variable, idiosyncratic meanings that substitutes for lightheadedness, anxiety, unsteadiness, or lassitude. Except for patients who have vertigo because they sustained labyrinth damage, posttraumatic dizziness remains difficult to define and almost impossible to treat.

Patients also commonly have exquisite sensitivity to light (photophobia) and sound (phonophobia). They cannot tolerate even everyday levels of sunlight, street noise, or workplace activity. The hypersensitivity intensifies patients’ headaches, distracts them from work-related tasks, and pushes them into seclusion.

In addition, patients often describe symptoms of depression, anxiety, irritability, and moodiness, but perhaps not in a few words. They also frequently report that their injuries reduce their desire for sex and other previously enjoyable activities.

In contrast, some patients with the postconcussion syndrome may minimize their symptoms. Whether stoic or in denial, they fail to acknowledge memory impairments, other cognitive deficits, personality changes, or physical impediments. Using poor judgment, they may resume their work at demanding jobs.

Mild TBI has a problematic relationship to PTSD. For example, the incidence of PTSD is similar among individuals who sustained mild TBI and those who did not. Also, the most powerful risk factor for PTSD is not TBI, but pre-TBI affective or anxiety disorder.

Treatment and Recovery

Almost all patients improve to a greater or lesser extent. About 85% fully recover and none deteriorate. Although recovery from postconcussion symptoms often follows a nonlinear and uncertain course, it should take place by 3 months in uncomplicated cases.

Neurologists attempt to educate and reassure the patient and family about the nature, extent, and course of postconcussion syndrome. Many urge patients with minor or vague symptoms to attempt to return to work with a reduced load, but patients with demanding or dangerous jobs to take a medical leave. With symptoms refractory to treatment and the passage of time, neurologists often decline to challenge the patient’s and family’s beliefs, but accept that symptoms exist without necessarily agreeing that they originate in TBI.

Perhaps more than in other syndromes, the symptoms of postconcussive syndrome seem to present in an inextricable group. No single medicine or other treatment relieves all elements of the syndrome. Moreover, many medicines, such as analgesics, directed at one symptom may exacerbate another symptom, such as sleepiness. One strategy is to work with the patient to identify the most troublesome symptom and target it for treatment with specific medicines.

For headaches, neurologists prescribe often mild, nonaddicting analgesics similar to those used for muscle contraction headaches. They typically prescribe nonsteroidal anti-inflammatory drugs (NSAIDs) and tricyclic antidepressants. These medications may alleviate insomnia and neck pain as well as headaches. Even when only a minimal migraine component exists or the patient has a history of migraine, antimigraine medicines may help (see Chapter 9).

Physicians must cautiously treat insomnia. They should avoid prescribing hypnotics because they easily lead to excessive daytime sleepiness, mimic symptoms of TBI, or worsen depression and cognitive impairment. They may prescribe modafinil to counteract excessive daytime sleepiness, but it will not alleviate fatigue. Whatever medicines physicians prescribe, they should prohibit alcohol because it may induce disturbances in personality, behavior, sleep, and judgment. Nonpharmacologic strategies, which have some advocates, include relaxation training, cognitive behavioral therapy, and instituting basic memory devices, such as checklists.

Some patients have symptoms that persist or, in a small proportion of cases, incapacitate the patient. Risk factors for incomplete recovery from postconcussion syndrome include the following:

Mechanism of Action

The common MVA is the rear-end collision. In these MVAs, the sudden impact snaps the driver’s and passengers’ head and neck backwards and then forwards. It causes a flexion–extension neck injury (whiplash) (Fig. 22-4) because it wrenches the neck’s soft tissues, including ligaments, tendons, and the trapezius, paraspinal, and numerous, small, delicate muscles.

FIGURE 22-4 Cervical flexion–extension injuries, popularly called “whiplash,” may tear the anterior and posterior longitudinal ligaments (blue) and other soft tissues, herniate intervertebral disks, and exacerbate cervical spondylosis (see Chapter 5).

Whiplash may also aggravate degenerative spine disease and herniate cervical intervertebral disks (see Chapter 5). A severe rear-end MVA may fracture or dislocate cervical vertebrae, which can even transect the spinal cord.

If MVA victims wear their seatbelt, they should not sustain concomitant direct head trauma. However, because whiplash often jostles the brain within the skull, some MVA patients develop the postconcussion syndrome as well as a whiplash.

Symptoms

As in the postconcussion syndrome, the development, severity, and duration of whiplash symptoms do not correlate with the MVA’s forcefulness, as calculated from its speed. The primary symptom of whiplash is neck pain. It typically radiates upward towards the head and downward towards the shoulders, arms, and lower back. With simultaneous head trauma and whiplash, symptoms reverberate.

Even without head trauma, whiplash patients also often report suffering from cognitive impairments, mood changes, inattention, and dizziness. (Despite the large number of individuals who sustain whiplash injury and the regularity of their cognitive and mood symptoms, the preliminary DSM-5 does not define this disorder unless psychiatrists might consider it as a variety of Neurocognitive Disorder due to Traumatic Brain Injury.) When trauma herniates cervical intervertebral disks, patients typically have radicular pain (pain that radiates along the nerve roots), weakness, and loss of deep tendon reflexes in their arms. MRI can detect herniated disks as well as fractures and vertebral dislocations. Electromyograms (EMGs) may establish the presence of a nerve root injury. However, numerous other techniques, including thermography, surface EMGs, and ultrasound, which have crept into the field, lack diagnostic reliability.

Approximately 50% of whiplash patients recover by 3 months and 75% by 6 months, which is approximately the course of postconcussive symptoms. Still, 20% have symptoms for 2 years or longer. Risk factors for prolonged disability include middle age, pre-existing degenerative spine disease, persistent headache, and psychiatric comorbidity, particularly anxiety, depression, and PTSD. In addition, compensation and other forms of litigation, looking at the population at large, constitute one of the most powerful risk factors in the United States. As an example of the effects of litigation, after Saskatchewan, Canada converted its tort compensation system to a no-fault plan, its citizens enjoyed a markedly reduced incidence of whiplash and, if it developed, a better prognosis.

Treatment

Treatment of whiplash remains largely empiric and variable. In fact, patients may improve with little or no treatment. Many respond to reassurance, rest, at-home exercising, or simple physical measures, such as massage and heat. Patients should avoid vigorous cervical manipulation, as occurs as part of chiropractic treatment, because it may lead to spinal cord injury or vertebral artery dissection. Although protecting the head and neck from further abrupt movement is obviously reasonable, the purported benefits of a restraining soft cervical collar remain controversial. Medications for whiplash include muscle relaxants, NSAIDs, nonopioid analgesics, and – for their analgesic and sedative, as well as their mood-elevating, effects – antidepressants. Migraine medications, according to some reports, may help.