TBI, referred to as a “silent epidemic,”² is one of the leading causes of death and disability in the United States.³ Nearly 1.4 million head injuries occur each year,² and of these, approximately 50,000 people die from their injuries, 235,000 require hospitalization, and 1.1 million are treated and released from the emergency department (ED).^2,⁴ An unknown number of additional patients with TBI are never seen at the hospital.⁵ Injury to the brain disrupts cognitive, physical, emotional, and behavioral function. These deficits may resolve within a few months or be permanent. While the majority of individuals who sustain a TBI recover, 80,000 to 90,000 Americans sustain permanent neuropsychiatric disabilities each year; most of those return home either directly from the ED or after a relatively brief hospitalization.² Even among these individuals, physical, cognitive, behavioral, and emotional impairments result in substantial disability and cause significant stress within families.³ Complications (e.g., suicide, divorce, chronic unemployment, economic strain, and substance abuse) increase after TBI.⁵ The consulting psychiatrist plays an important role in the evaluation and treatment of these patients at all stages of recovery.

EPIDEMIOLOGY AND RISK FACTORS

Among the most common causes of TBI are falls (28%) and motor vehicle accidents (20%).² Having the head struck by, or against, an object (19%), being assaulted (11%), and experiencing other (13%) or unknown (9%) problems make up the remaining cases.² Men sustain TBI at a rate 1.5 times higher than women and are hospitalized almost twice as frequently.² TBI occurs most frequently in children ages 0 to 4 years, followed by older adolescents (15 to 19 years of age).² The highest rates of hospitalization and death following TBI are found in adults over age 75.² Falls produce the most injuries for children younger than 15 years and for adults over age 55.² Motor vehicle accidents account for the most injuries among adolescents ages 15 to 19 and adults ages 20 to 55.² Earlier research has found that 56% of adults identified as having brain injuries had an elevated blood alcohol level (BAL) at the time of injury; 49% of them had a BAL at or above the legal level. Recurrent brain injury is common; the risk of a second injury is three times higher than it is for those in the general (noninjured) population.⁴ Following a second injury, the risk for a third injury becomes nearly 10 times higher than the risk for an initial injury.⁴ Finally, review of data from the United States National Health Interview, a national database used to estimate the incidence and features of persons with brain injury, found that the highest rates of injury occurred in families with the lowest income levels (Table 81-1).⁴

Table 81-1 Risk Factors for Traumatic Brain Injury in Adults

• Being male

• Having a motor vehicle accident

• Using alcohol

• Having a prior injury

• Having a lower socioeconomic status

PATHOPHYSIOLOGY

TBI is a spectrum disorder; injury can be focal, diffuse, or both.⁶ Damage can occur as a result of forces exerted on the brain at the time of injury, known as the primary injury,^1,^7,⁸ and from subsequent physiological processes (such as swelling or hypoxia) triggered by the initial insult; these are classified as secondary injuries.^7,⁸ Focal damage is typically the result of contusions or mass lesions.⁶ Most often they arise from contact injuries (such as falls or blows to the head)⁶ and result in skull fractures and hematomas (extradural, subarachnoid, subdural, or intracerebral hematomas).⁶ Hematomas may develop at the point of contact and at a point contralateral to the point of contact (known as coup-contrecoup contusions).¹ Contusions are seen more frequently in the poles of the frontal lobes, the inferior aspects of the frontal lobes, the cortex above and below the operculum of the Sylvian fissures, the temporal poles, and the lateral and inferior aspects of the temporal lobes.⁶ They may develop quickly within minutes of the injury or evolve slowly over several hours or days. The presence of these contusions contributes to neuronal necrosis and to elevated intracranial pressure (ICP).^5,⁶ In addition to contusions, contact forces can result in small or complete tears at the pontomedullary junction, damage to any of the cranial nerves, damage to the hypothalamus or pituitary gland, and damage to blood vessels.⁶ Moreover, there can be multiple areas of focal damage.

Diffuse damage involves multiple neurological structures. It is seen more frequently in injuries that involve rapid acceleration, deceleration, or rotational forces.¹ Diffuse damage can also result from disruption of vascular function and from hypoxia.⁶ Diffuse axonal injury (DAI) occurs at the level of the axons and disrupts cellular function and structures.⁵ Several structures (subcortical frontal and temporal white matter, the corpus callosum, and brainstem) are most frequently involved.⁶ It appears that the permeability of the axolemma is altered and results in impaired axonal transport and in subsequent swelling before the axon detaches from its downstream segment. While this process appears to be triggered by the mechanical forces of the original injury, it is one that evolves over several hours to days.^5,⁶ Because this damage occurs at a microscopic level, DAI is often missed on computed tomography (CT) scans.¹ It is more easily identified with magnetic resonance imaging (MRI), where the signature axonal swelling and axonal bulbs can be seen more readily, particularly if the brain is imaged several days after the injury.¹ Even with MRI, however, the absence of significant findings on radiological imaging does not mean that damage has not taken place.⁷

In addition to the primary injuries, further damage can occur as a result of complications associated with TBI (known as secondary injury).¹ Hematomas develop as a result of the hemorrhaging from torn blood vessels. Edema develops when there is an increase in intercellular or intracellular water concentration (or both), due to direct mechanical forces or changes in cell permeability.^8,⁹ Since the skull is fixed and unable to expand, hematomas and edema raise the ICP, which leads to further neurological damage as the surrounding (softer) structures become deformed. The pressure can push the brain through the base of the skull, causing damage to the brainstem.¹ The vascular system that supplies the brain is compressed, restricting the flow of blood, which results in ischemic damage.⁸ Compromised cardiopulmonary function, as either a direct result of brain damage or the structural damage sustained in the initial trauma, can lead to hypoxic injury. Hyper-release of catecholamines following TBI can produce transient hypertension, as well as changes in glucose, cortisol, and thyroid hormones, which further disrupts neurological function.⁹ Focal contusions can produce seizures (which convey the severity of the injury in that they are seen more frequently following a severe injury than with a moderate or mild injury).⁹

The brain’s plasticity, or neuroplasticity, produces structural and organizational changes that result in recovery of function.¹⁰ The hippocampus retains the ability to generate new neurons from dividing progenitor cells in the dentate gyrus.¹⁰ Surviving cortical structures take over the function of damaged areas.¹¹ Other adaptive and restorative processes include changes in the amount of neurotransmitters released, the number and distribution of postsynaptic receptors, the size and complexity of the dendritic trees of spared neurons, and their collateral sprouting of spared axons to innervate deafferented neurons.¹¹ These processes are dependent on purposeful and active interactions with the environment.¹⁰ Unfortunately, they are not well regulated, and can lead to maladaptive, as well as to beneficial, change.¹¹ While they are responsible for restoring function, they can result in maladaptive behavior and psychiatric disorders. In the case of mild TBI, symptoms will usually resolve within 6 months of injury.¹² In the case of moderate to severe TBI, the greatest amount of recovery typically takes place in the first 1 to 2 years following injury.¹ Recovery can continue, however, at an increasingly slower pace for many years following the injury.^5,⁹

TBI is typically classified as mild, moderate, or severe (Table 81-2) based primarily on the duration of altered mental status (including the degree of responsiveness, as measured by the Glasgow Coma Scale [GCS], and the duration of disrupted memory). These terms can be misleading as they reflect the degree of damage the brain has sustained; they do not necessarily reflect the severity of the disruption in the patient’s daily function. Individuals with a severe injury can make essentially full recovery, whereas others with mild to moderate injuries can remain significantly disabled for many years. The GCS, developed by Teasdale and Jennett, assigns points for increasingly complex levels of response to three dimensions (verbal and motor response and eye opening); the ratings in each domain are totaled to produce an overall score that can range from 3 to 15 (Table 81-3). Ratings can also be done serially to provide a measure of recovery. GCS scores have been predictive of ultimate outcome, with lower initial scores being associated with more severe injury and worse recovery.^1,⁴

Table 81-2 Classification of Traumatic Brain Injury

Table 81-3 Glasgow Coma Scale

Category	Score
Eye Opening
Spontaneous	4
To voice	3
To painful stimulus	2
None	1
Verbal Response
Oriented	5
Confused	4
Inappropriate words	3
Unintelligible sounds	2
None	1
Motor Response
Follows commands	6
Localizes pain	5
Withdraws from pain	4
Flexor response	3
Extensor response	2
None	1

From Teasdale G, Jennett B: Assessment and prognosis of coma after head injury, Acta Neurochir (Wien) 34(1-4):45-55, 1976.

Mild TBI (MTBI) may not show up on a CT scan, an MRI, or an electroencephalogram (EEG). Where there are positive radiological findings, the injury is classified as a complicated MTBI. Performance on a routine neurological examination (see Chapter 72), which tends to focus on sensorimotor function, may be essentially normal, although performance may represent a decline relative to preinjury performance.¹² Acute symptoms may persist for varying lengths of time. Physical symptoms often include nausea, vomiting, dizziness, headaches, blurred vision, an increased sensitivity to noise and light, diminished libido, sleep disturbance, quickness to fatigue, lethargy, or sensory loss (Table 81-4).⁷ Cognitive deficits typically involve attention, concentration, perception, memory, speech/language, or executive functions.^7,^12,¹³ These cognitive deficits are best identified through an in-depth neuropsychological evaluation. Behavioral changes (such as irritability, quickness to anger, disinhibition, or emotional lability) may follow.^7,^12,¹³ Symptoms generally resolve within 6 months of the injury. Physical, cognitive, emotional, and behavioral symptoms frequently persist, and cannot be accounted for by other peripheral injuries, or one’s emotional state or psychological reaction to physical or emotional stressors.¹²

Table 81-4 Symptoms of Mild Traumatic Brain Injury

Physical	Cognitive	Behavior
Nausea	Decreased attention	Irritability
Vomiting	Decreased concentration	Quick to anger
Dizziness	Problems with perception	Disinhibition
Headaches	Problems with memory	Emotional lability
Blurred vision	Problems with speech production
Increased sensitivity to noise and light	Problems with speech comprehension
Diminished libido	Executive dysfunction
Sleep disturbance
Reduced stamina
Lethargy
Sensory loss

While neurological damage can occur without formal loss of consciousness (LOC), LOC is considered a hallmark of most TBIs. The depth and duration of lost consciousness generally reflect the severity of injury. The longer the duration, the more severe the injury and more guarded the prognosis for recovery.⁹ No single path or pattern of recovery follows a brain injury,⁵ because there are so many variables involved (e.g., the location and extent of injury, the patient’s age and overall health, the presence of alcohol, the medical and psychological history, concurrent processes [such as infections or seizures], and availability of appropriate rehabilitation services and supports).

The Rancho Los Amigos Levels of Cognitive Functioning Scale (RLAS) is widely used in delineating the stages of recovery (Table 81-5).^1,⁵ It is an eight-point scale describing stages of cognitive and behavioral change used to track improvement following a TBI. While the scale provides a useful way of identifying a patient’s level of recovery, it has not been able to predict the ultimate rate or level of recovery. It has less relevance beyond level IV because patients show increasingly varied patterns of recovery beyond this level. Patients do not progress through the levels at a uniform or predictable rate. Individuals may progress through different levels at different rates. Progress in various domains is not universal; some levels of function (such as motor function) progress more rapidly and recover more fully than do language or memory.

Table 81-5 Ranchos Los Amigos Levels of Cognitive Functioning Scale (RLAS)

Level	Behavior
I	No response
II	Generalized response
III	Localized response
IV	Confused—agitated
V	Confused—inappropriate
VI	Confused—appropriate
VII	Automatic—appropriate
VIII	Purposeful and appropriate

CLINICAL FEATURES

No single profile characterizes the presentation of TBI (Table 81-6). A patient’s profile is the result of the location, depth, and volume of focal lesions and the extent of diffuse axonal injury. Age, previous injury, use of alcohol, and co-morbid conditions (such as hypoxia or hypertension) further contribute to the specific collection of deficits observed.¹⁴ Generally speaking, cognitive deficits, personality and behavioral changes, and psychiatric disorders follow TBI. The domains of attention, memory, language, and executive function are typically affected. Since they are somewhat hierarchical, deficits in more fundamental areas (such as attention) can limit performance in higher-level tasks of executive function. Day-to-day and within-day performance can vary considerably.¹⁵

Table 81-6 Cognitive Changes

Cognitive Impairments

Impaired attention is one of the most common deficits associated with TBI involving the reticular activating system and the prefrontal or connecting white matter.¹⁴ Individuals with attentional difficulties report decreased concentration, being unable to follow conversations in a group setting, losing track of what they are reading, being distractible, being unable to do more than one thing at a time, and being unable to sustain attention.^1,¹⁴ Reduced speed of processing, while not strictly an attention deficit, limits the amount of information that can be processed, the ability to respond quickly, and the ability to complete tasks within traditional time frames.

Impaired memory is also common following TBI.¹⁶ The duration of posttraumatic amnesia (PTA), the inability to recall information presented after the accident, correlates with the severity of one’s injury. While some patients have a period of retrograde amnesia (i.e., the inability to recall information acquired before the trauma), problems acquiring, storing, and retrieving new information are more common.¹⁶ Memory is not a unitary construct; there are different forms of memory that may be affected to differing degrees depending on the nature and the location of injury.^1,¹⁶ Because different neuroanatomical structures are involved with these various forms, there is typically sparing of some forms of memory. Procedural memory (i.e., memory for motor sequences that occur outside of conscious awareness) is typically less affected than is memory for more language-based or visual information.^1,¹⁶ This also means that there is not a specific profile of memory deficit associated with TBI. Declarative memory (i.e., the ability to recall events [episodic memory] and specific facts [semantic memory]) is more vulnerable to damage because of the active processes and neural structures involved. Encoding, consolidating, and retrieving new information involves a degree of effortful, controlled, and generally conscious processing.¹⁴ Much of this activity appears to involve the hippocampus, as well as the prefrontal, temporal, and frontal structures. The hippocampus is particularly vulnerable to diffuse axonal injury. The prefrontal and frontal areas, due to their anatomic location and their proximity to orbital cranial structures, are also vulnerable to contusions and hematoma formation.¹⁴ The ability to retrieve old or previously learned information typically returns before the ability to acquire new information. For a period of time amnestic individuals may confabulate,¹ or generate false memories, which can be problematic because they can be indistinguishable from “real memories.” False memories typically have elements of truth embedded within them, as people involved may actually exist or events recalled may really have happened. The memories, however, contain significant distortions. The affected individual may recall a visit the day before from a friend who has been dead for many years, or may report returning from a trip the day before that had taken place a number of years ago. Confabulation is distinguished from being delusional in that the confabulation is often more isolated, less organized, and often more transient than are delusions. Confabulation typically resolves as the patient’s overall memory improves. The ability to recall new information typically takes more time to resolve and may be a persistent or permanent deficit.¹⁴ Acquisition, storage, and retrieval of new information are procedures that involve attention, sensory function, language, and executive function. Deficits in any of these areas limit the ability to participate in new learning. Even in individuals with mild TBI, new learning is less efficient, thus requiring more effort than was required before their injury.¹⁴ This inefficiency and increased effort makes it harder for an individual to sustain performance relative to his or her preinjury levels.

Impaired language results from damage to frontal and temporal areas. The nature of the deficits will depend on the location and extent of the injury.¹⁷ Disruption of language (both receptive and expressive) occurs more frequently after moderate to severe injuries than after mild TBI. In mild TBI, disturbances tend to be limited to difficulties with word finding and with decreased fluidity when speaking. Global aphasia (total loss of both receptive and expressive language) is relatively rare. More commonly, specific aphasic syndromes include anomic aphasia (in which an individual has difficulty naming specific objects and proper names), paraphasic errors, and circumlocution. In addition to these primary language impairments, patients with TBI tend to generate less speech, are less efficient in their discourse, and have more trouble managing the interpersonal pragmatics of speech (such as taking turns, maintaining a topic of conversation, taking a listener’s perspective, and interpreting the nonverbal elements of communication).¹⁴

Finally, impaired executive function can be seen at all levels of TBI. These skills are the functions of the frontal lobes and their projections, which are particularly prone to injury.¹⁸ Executive function encompass those skills needed to operate independently in the world (i.e., to identify goals, to plan, and to organize behavior to meet those goals). They involve initiating and monitoring behavior, inhibiting competing impulses or behaviors, and correcting behavior in response to feedback. They are essential for self-determination, self-direction, and self-regulation. Problems with regulation of attention, working memory, insight and empathy, verbal fluency, decision-making, perseveration, and inflexibility frequently follow damage to the frontal lobes.^1,¹⁹

Personality and Behavioral Changes

In many respects the changes in behavior and personality that follow TBI, particularly when there is frontal lobe involvement, are more disabling than are the cognitive changes (Table 81-7).^1,²⁰ They limit an individual’s ability to participate in therapy, they are a source of significant stress on families and caretakers,²⁰ and they can prevent the individual from returning home and returning to work.²¹ The individual may appear to move about aimlessly, become preoccupied with seemingly trivial matters, or perseverate on topics or concerns in an obsessional manner. The individual may fail to be aware of, or take in, information from the environment or alter his or her behavior in response to feedback. As a result the individual may have a difficult time learning from his or her mistakes. Because of deficits in executive function, several functions (e.g., planning, sequencing, and initiating behavior in a goal-directed manner) become difficult. Looking ahead and anticipating the implications or consequences of one’s actions becomes difficult following frontal lobe damage; this can interfere with participation in therapy because the individual fails to grasp the long-term benefits of treatment in the absence of more immediate gratification. Deficits in the modulation of affect, self-awareness, and self-monitoring result in behavior that is socially inappropriate. Temper outbursts and mood swings, often dysphoric in nature, are common after temporal lobe damage.¹ Flatness of affect and indifference, belligerence and aggression, childishness, euphoria and abnormal jocularity, irritability and reduced tolerance for frustration, disinhibition, and lack of empathy may arise, interfering with normal social relationships.²² Individuals have a difficult time identifying and initiating activities that foster social interaction. Previously active people will be content to sit and watch television for hours on end. Individuals may begin to avoid social gatherings because the demands of selectively attending, shifting attention, self-monitoring, and comprehending language and emotive expression are overwhelming. All of these deficits are subject to the effects of fatigue and environmental variables (such as supportive structure, level of sensory stimulation, and degree of familiarity). An individual’s behavior is seen as erratic and difficult to predict. Social isolation becomes common as friends and even family withdraw from behavior that can be disruptive, embarrassing, and even dangerous. The burden these behaviors place on families who are already stressed by changes in financial resources and the demands of physical care and increased dependence can be enormous.¹

Table 81-7 Personality and Behavioral Changes Associated with Traumatic Brain Injury

Aggression	Need for immediate gratification
Apathy	Mood lability
Withdrawal	Erratic and difficult to predict
Lack of goal-directed activity	Temper outbursts and mood swings
Lack of empathy	Abnormal jocularity
Distractible	Irritability and reduced tolerance for frustration
Difficulty learning from mistakes	Disinhibition
Impulsivity

Aggressive behavior is perhaps the most disruptive of the behavioral changes observed after TBI. Agitated, combative, disinhibited behavior is common during the initial stages of posttraumatic delirium ²³ and is one of the defining features of the Ranchos Los Amigos Level IV. Agitated behavior at this stage tends to be reactive in nature, and often arises in response to seemingly minor or trivial stimuli. It is neither planned nor serves a purpose other than to eliminate the source of irritation. The behavior is often explosive and occurs with little buildup or warning. Brief outbursts alternate with long periods of calm. Where the individual is aware of the behavior, he or she is often upset or embarrassed by it.²⁴ Early agitation tends to resolve as cognition improves.

Agitated and aggressive behavior can persist beyond the acute phase of recovery; it has been observed following severe TBI in 31% to 71% of cases studied and in 5% to 71% of cases involving mild TBI.²³ Agitated and aggressive behaviors persist in 31% to 71% of patients from 1 to 15 years after injury.²⁴ Aggressive behavior has been associated with damage to the inferior orbital surface of the frontal lobes, the anterior temporal lobes, the hypothalamus, and limbic structures.^23,²⁴

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