Neuropsychiatric Sequelae of Traumatic Brain Injury

Table of Contents

ABSTRACT

The prevalence of traumatic brain injury (TBI) is increasing, particularly in the population of veterans. Many times, the motor and sensory consequences of TBI are addressed, but the post-TBI neuropsychiatric sequelae, which may be as, or even more devastating than the motor and sensory deficits, are left unattended. Cognitive, mood, anxiety, thought, impulse, and substance disorders, and a variety of personality disorders can be seen following TBI. The neuropsychiatric sequelae of TBI not only interfere with day-to-day function, but can severely impede rehabilitation efforts. To date, there have been few large-scale studies looking at the effectiveness of the various treatment modalities, including psychotherapeutic and pharmacological interventions.

KEYWORDS

Traumatic brain injury - concussion - neuropsychiatric sequelae - cognitive disorders - mood disorders - treatment

EPIDEMIOLOGY AND ETIOLOGY

Traumatic brain injury (TBI) is defined as traumatically induced physiological disruption of the brain, and is occurring with increasing frequency. The incidence is ~506 per 100,000 people.[1] Traumatic brain injury is being seen more often, particularly in patients injured in war. Many of the veterans with TBI whose other injuries would have been fatal in previous wars are now surviving because of improved protective gear.[2] The peak incidence is between the ages of 15 and 24 and older than the age of 64 years. Males are affected twice as often as females. In the civilian population, alcohol is involved in more than half the cases of TBI. People from lower socioeconomic groups are significantly more likely to be affected by TBI. Motor vehicle accidents (MVAs), particularly motorcycle accidents, account for the most frequent civilian cause of TBI. Falls are the next most common cause of head injury, with a high rate in the elderly. Recurrent head injury is common in patients with a history of alcohol abuse and individuals playing contact sports.[3] The estimated annual cost of TBI in the United States is $60 billion for treatment and lost productivity.

As significant as the epidemiology of TBI is, the prevalence of post-TBI syndromes is significant and includes post-traumatic stress disorder (PTSD), depression, mania, and aggression.[4] Post-TBI post-traumatic stress disorder occurs in up to 27%, including patients with no clear recall of the event.[5] [6] Post-TBI depression has an incidence of 15 to 33% and prevalence of 18 to 42%.[7] Post-TBI mania occurs in <10% of patients with TBI.[8] Post-TBI aggression (agitation, disinhibition, personality changes) occurs in variable frequencies depending on criteria, ranging from 20 to 49%.[9] [10] Although delusions and auditory hallucinations are common in the acute post-traumatic state, post-TBI psychosis occurs in <10% of the TBI population.[11] [12]

The prognosis following TBI is related to the initial Glasgow Coma Scale (GCS) score[13] [14] (Tables [1–3]).

Table 1 Glasgow Coma Scale Scores

Eyes

Open spontaneously = 4

Open to verbal stimuli = 3

Open to pain = 2

Do not open = 1

Verbal

Spontaneous speech, oriented = 5

Spontaneous speech, disoriented = 4

Nonsense speech = 3

Sounds = 2

No speech at all = 1

Motor

Spontaneous movement = 6

Localizes pain = 5

Withdraws from pain = 4

Decorticate posturing = 3

Decerebrate posturing = 2

No movement at all = 1

Table 2 Severity Grading of Traumatic Brain Injury[14]

	Glasgow Coma Scale Score	Loss of Consciousness (time)
Mild	13–15	Less than 30 min
Moderate	9–12	30 min to 1 wk
Severe	<9	More than 1 wk

Table 3 Prevalence and Prognostic Indicators for Traumatic Brain Injury[14]

Glasgow Coma Scale Score	Severity Percentage in Patients Admitted to Hospital (%)	Mortality (%)
Mild (13–15)	80	0
Moderate (9–12)	10	10
Severe ( <9)	10	60

PATHOPHYSIOLOGY

The neuropathophysiology of TBI can be divided into biomechanical, biochemical, and biomolecular mechanisms. The acute injury results from primary (mechanical) physical disruption of the brain. Head injuries are divided into open, where there is a breach of the skull by fracture or penetrating injury, and closed, when the cranium is intact. Because of the brain's environment— floating in the cerebrospinal fluid (CSF) in the cranium—sudden acceleration, deceleration, or torsion injuries can cause the brain to strike the skull, causing injury. There are two basic types of brain injury: (1) direct trauma to the brain, causing contusions, hemorrhages, and lacerations; and (2) diffuse axonal injury, from stretch injuries to the deep white matter. Coup/contrecoup injuries occur when the brain is injured by a torsion injury of the head in which opposite sites in the brain are injured; for example, the left frontal and right parieto-occipital areas. The most commonly injured areas of the brain are the anterior poles of the frontal and temporal lobes, where they abut bony ridges of the skull.

Because the brainstem is fixed to the base of the skull, it turns as the skull does, but the cerebrum does not. This causes axonal shearing injuries in the long white matter tracts in the parasagittal areas, the corpus callosum, and the upper brainstem. This injury may range from neurapraxia, with focal demyelination, to axonotmesis with complete severing of the axon. The severity of the injury to the axons determines whether there will eventually be resumption of function.

Secondary (delayed, nonmechanical) postinjury factors include excitotoxic amino acid release, including glutamate. Oxidant injury from free radical release may result in secondary injury. Secondary causes of injury following the immediate head injury include physiological and pathological responses, such as alterations in cerebral blood flow and cerebral perfusion pressure. Reperfusion injury may result. Seizures may occur, along with centrally mediated systemic effects, which may include shock, electrolyte imbalances, and hypothermia. Hypoxia, brain edema, increased intracranial pressure, hemorrhage, ischemia, and infection (with open head injuries) may occur.

COURSE OF ILLNESS: ACUTE, SUBACUTE, AND LONG TERM

Acute Phase: Emergency Management

Emergency management in the acute phase of TBI includes GCS classification, documenting clinical findings, monitoring fluid balance, and maintaining airway and oxygenation. Pharmacological, surgical, and invasive interventions are also part of acute TBI management; however, the emergency care of TBI is beyond the scope of this article and is not discussed.

Subacute Phase: Post-Traumatic Delirium and Amnesia

In the subacute phase, during the period immediately following regaining consciousness following a TBI, patients go through a state during which they are delirious and of which they are amnestic. Risk factors for more severe and more prolonged delirium include older age,[15] hypoalbuminemia,[16] and prior neurological abnormalities.[17] As with delirium of other causes, there may be a fluctuating course with episodes of hyper- and hypoactivity. Patients with this condition demonstrate disorientation and impaired attention. Often they have a disrupted sleep-wake cycle, sleeping during the day and waking at night. The period of amnesia often outlasts the period of clear delirium. The duration of post-traumatic delirium varies with the number of lesions seen on computed tomography (CT) scan and fluid attenuated inversion recovery (FLAIR) sequence magnetic resonance imaging (MRI).[18] Magnetic resonance spectroscopy (MRS) shows decreased N-acetylaspartate and increased choline, which is due to the loss of neurons and increased glial cells.[19]

Treatment of the delirium includes treatment of any other contributing disorders such as metabolic or infectious disturbances. Providing orienting stimuli in the environment can help decrease confusion and disorientation. Atypical neuroleptics, except for clozapine, which lowers the seizure threshold and has significant anticholinergic properties, are the most useful pharmacological agents. There is some evidence that the typical neuroleptics may slow cognitive recovery.[20] The typical neuroleptics are more likely to cause extrapyramidal adverse effects, particularly in patients with TBI. Except when withdrawal from sedative-hypnotic medications is part of the cause of delirium, benzodiazepines should not be used because they worsen the delirium.

Long-Term Neuropsychiatric Sequelae

Once the patient is beyond the acute and subacute phases, many are left with neuropsychiatric sequelae of TBI. Underscoring the importance of addressing TBI sequelae, Robert Karol warns that treatment providers who attend “only to cognitive and physical deficits after brain injury and downplay emotional concerns are unlikely to ameliorate behavioral dyscontrol.”[21] We divide the discussion of post-TBI issues into social/self, symptoms and syndromes.

Self/social issues include vocation/financial, physical skills, appearance, intelligence/thought, relationships, and sexual functioning. Post-TBI job loss results in loss of income, sometimes a supportive spouse, and a disability application. Physical skills lost sometimes include physical strength, speed, dexterity, athleticism, and difficulties with spasticity, paralysis, balance, visuospatial function, visual praxis, and adjusting to equipment. Issues associated with appearance include scars from injury and from surgery and verbal expression difficulty. Formerly high-functioning patients are sometimes devastated by the impact of mild TBI on their thinking and intelligence. Attention, reasoning, language, memory, planning, and tracking (executive functioning) all can be affected by TBI. A commonly overlooked area in TBI is the effect on relationships and sexual functioning. Family, friends, work, and community of faith may be estranged due to new frustrations or behaviors or bolstered as supports after TBI.

Common issues related to symptoms include behavioral outbursts, emotional adjustments, cognitive deficits, and physical concerns. The link between ability to adjust to TBI and the capacity to do so is complicated by a major factor. In addition to having to adjust to dysregulation in behavior, emotions, thinking, and physical challenges, persons with TBI must make these adjustments with a brain that processes information poorly. A person with limited coping skills may become frustrated with his or her mood variability or with limb weakness, and may as a result have outbursts. Trouble with attention, decreased ability to understand, and difficulty remembering things may impact an individual's ability to adjust to deficits. The patient may lose the information given at the doctor's office, or may forget to use the assistive device. He or she may have problems with perceiving situations or assign incorrect motives to other people's actions.

Common syndromes seen post-TBI include: behavioral disinhibition, depression/anxiety/psychosis, substance abuse, attention/cognitive disorders, and motor/sensory disorders. Given the lack of controlled treatment studies for post-TBI syndromes, the information provided here is from studies from the literature with the caveat that there currently are no U.S. Food and Drug Administration (FDA)-approved interventions for post-TBI neuropsychiatric syndromes. Key rules of thumb for these syndromes are to start lower and go slower. Brain injury confers increased sensitivity to the active agents of the central nervous system (CNS); therefore, treatment and side effects may be accentuated at lower doses in patients after TBI. Second, to systematically approach treatment in TBI beyond pharmacological interventions, three areas are important to keep in mind: (1) identification of target symptoms, (2) consideration of coexisting medical problems and iatrogenic contributions, and (3) implementation of nonpharmacological treatment.[22]

The initial steps of treatment include a comprehensive neuropsychiatric evaluation and testing. This may include neurological and psychiatric examination to document baseline deficits, diagnoses, and functioning. A neuropsychological battery documents the cognitive skills and limitations, and provides a baseline from which gains in cognitive rehabilitation can be benchmarked. Neurophysiological tests may show brain dysfunction and seizures.[23] When indicated, neuroimaging may be of benefit to show ischemia, hemorrhage, encephalomalacia, neuronal loss, and altered cerebral metabolism or perfusion[24] (Fig. [1]; Table [4]).

Table 4 Ancillary Testing in Traumatic Brain Injury

1. Neuropsychological testing: cognitive functioning, language testing, tests of motivation and malingering, tests for premorbid functioning

• Types of attention include selected, sustained, and divided

• Types of memory disturbances can be anterograde, which is loss of the ability to lay down new memories, or retrograde, in which there is loss of previously acquired memories

• Executive functions often affected by TBI include judgment, reasoning, concept formation, planning, organizing, set maintenance and flexibility, and impulse control

• Language

• Tests for motivation and malingering, required especially when litigation is potentially involved

• Tests to determine the level of premorbid functioning

2. Electrophysiological: EEG and QEEG, evoked potentials including ERPs

• EEG: used to assess for post-traumatic epilepsy or encephalopathy

• QEEG: sometimes used, but is of questionable utility[23]

• ERPs

3. Neuroimaging

• CT: useful for examining blood and bone status

• MRI: excellent resolution of structural lesions

• fMRI: used in research presently; shows localization of task-specific operations

• PET: shows level of cerebral metabolic activity; heterogeneous pattern may indicate TBI among other conditions in the differential diagnosis

• SPECT: shows level of cerebral perfusion; heterogeneous pattern may indicate TBI among other conditions in the differential diagnosis

• MRS: shows areas of cerebral neuronal loss

• DTI/FT: shows cerebral white matter tracts

TBI, traumatic brain injury; EEG, electroencephalography; QEEG, quantitative EEG; ERPs, evoked response potentials; CT, computed tomography; MRI, magnetic resonance imaging; PET, positron emission tomography; fMRI, Functional MRI; SPECT, single-photon emission computerized tomography; MRS, magnetic resonance spectroscopy; DTI/FT, diffusion tensor imaging and fiber tractography.

Figure 1 Neuroimaging in traumatic brain injury (TBI). Transaxial images from non-contrast head CT and single-photon emission computerized tomography (SPECT) images showing intraventricular hemorrhage and large parenchymal hematoma in right parieto-occipital area and hypoperfusion in the same area. (Image courtesy of Alan Siegel, Dartmouth Medical School, Nuclear Medicine.)

COGNITIVE DYSFUNCTION

The severity of post-traumatic cognitive disturbance depends on the degree of diffuse axonal injury[25] as well as the volume and location of focal injuries. Diffuse axonal injury is more often associated with generalized cognitive dysfunction, such as attention disorder, whereas focal injuries cause specific deficits, such as aphasia.

Patients with generalized cognitive dysfunction have difficulties following conversations. They tend to be perseverative but have problems maintaining their train of thought. Because of difficulties with selective and divided attention, patients with a history of TBI have difficulty with multitasking. Declarative memory for events is more affected than implicit memory. Working memory and prospective memory (remembering to pay one's bills) are impaired, particularly after damage to the frontal lobes. Functional magnetic resonance imaging (fMRI) shows alttered patterns of activation of the brain during memory tasks in patients with TBI.[26]

Executive function involving the frontal lobe–basal ganglionic–thalamic circuits is responsible for establishing goals, planning, initiating, sequencing, and inhibiting responses.[27] Frontal lobe injuries impair executive function, conceptual reasoning, and decision making. Patients with frontal lobe damage have difficulty with self monitoring and regulation. These deficits may significantly interfere with a patient's ability to cooperate with any type of psychotherapy or behavioral therapy.

Small studies have shown cholinesterase inhibitors,[28] stimulants,[29] L-dopa,[30] tricyclic antidepressants,[31] and lamotrigine[32] to be helpful in treating cognitive deficits.

MOTIVATION

Motivation refers to how behavior is started, energized, and sustained. Abulia, or lack of motivation, is common following significant head injury. Orbitofrontal and medial frontal cortical injuries affect motivation as well as injuries to the ventral pallidum and ventral tegmentum.[33] The mildest degree of impairment of motivation sometimes is erroneously referred to as apathy. Apathy is defined as a lack of emotion or feeling. Apathy is sometimes manifested as abulia as a quantitative rather than a qualitative change in drive, characterized by diminished overt behavior, goal-related cognition, and emotional responses. On examination, psychomotor retardation may be observed in mild to moderate TBI. With abulia, the ability to plan and react is preserved, but diminished in force. A more extreme form of abulia is characterized by a poverty of behavior and speech, lack of initiative, loss of emotional responses, and severe psychomotor slowing. Akinetic mutism can be observed in TBI as an extreme form of a deficit of motivation in which the patient is awake and able to track visually with no other responses.

Treatment of amotivational syndromes involves both pharmacological treatment and behavioral interventions. Stimulants and dopaminergic medications, as well as activating antidepressants such as bupropion or monoamine oxidase inhibitors (MAOIs), may increase motivation. Selective serotonin reuptake inhibitors (SSRIs) and typical neuroleptics may worsen amotivational syndromes.[34] Nonpharmacological treatments include rewarding goal-directed behavior, psychological prostheses such as lists and prompting, behavior modification, and family intervention. Lack of motivation, as with cognitive deficits, can be a major obstacle to success in rehabilitation.

MOOD DISORDERS

Following TBI, up to 50% of patients have symptoms of depression, with 20% meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria for major depression. The incidence of depression in patients with TBI is approximately twice that of other patients who were as badly injured but without a head injury.[7] Patients with TBI have a significantly increased risk of suicide. There is controversy about whether the laterality of the injury makes a difference in the occurrence of depression, with some studies suggesting that right hemispheric lesions are more likely to be associated with depression, but neither left nor right-sided lesions consistently reveal associations.[35] Mania can occur in patients with TBI but is much less common and is usually of short duration. Anxiety disorders, discussed later, are also common, particularly in patients with depression.

The differential diagnosis includes apathy, emotional lability, PTSD, and pathological laughing and crying, which may be symptoms of pseudobulbar affect.

Tricyclic antidepressants (TCAs) may be of benefit in treating anxiety and depression,[36] but they should be limited to agents with the least anticholinergic activity, the least sedation, and the least effect on the seizure threshold. With their safety profile, low histamine, cholinergic, and α-adrenergic binding SSRIs are preferred for mood and anxiety; however, side effects of sexual dysfunction, dyspepsia, drowsiness, and irritability may limit their use in TBI. Stimulants, amantidine, and anticholinesterase drugs have been shown to be helpful in some studies.[37] [38] [39] Clonidine, carbamazepine, and divalproex are the drugs of choice for post-traumatic mania, with lithium being reserved for patients with a prior history of mania.[40] Pseudobulbar affect is treated with TCAs[41] and with combination dextromethorphan hydrobromide and quinidine sulfate.[42]

PSYCHOTIC DISORDERS

Approximately 1.5% of TBI patients develop psychotic symptoms. The onset is generally quite delayed following the injury, around 4 years.[43] The psychoses are characterized by hallucinations and delusions with retained insight. Although non-delirium associated hallucinations can occur post-TBI, the absence of Schneiderian first-rank symptoms—such as thought insertion and thought withdrawal—distinguishes TBI psychosis from schizophrenia. Other factors distinguishing TBI psychosis from schizophrenia include a later age of onset, less premorbid psychiatric disturbance, briefer duration, less common family history, better response to neuroleptics, less need for maintenance medication, and a better prognosis.[44] In some patients, post-TBI psychosis may be an ictal-related process. Post-TBI psychosis has the same features as interictal psychosis.

Treatment for post-TBI psychosis with neuroleptics should be initiated at one third to one half the usual doses because of potential adverse reactions.[45] There is some evidence that neuroleptics may impede cognitive recovery.[46] Atypical neuroleptics, except for clozapine, which is strongly anticholinergic and lowers the seizure threshold, are the drugs of choice. Benzodiazepines should be used sparingly, if at all.

POST-TRAUMATIC STRESS DISORDER AND OTHER ANXIETY DISORDERS

Patients who have suffered a TBI may have anxiety presenting as insomnia, inability to concentrate, free-floating anxiety, phobias, and panic attacks. Subthreshold PTSD symptoms are common in civilians,[47] and PTSD is now being seen increasingly in veterans who sustained TBI.[48] Patients may be particularly anxious in situations in which they know they cannot perform as well as they did before their injury. It is important that family members and coworkers realize and accept that the patient is not the same person they knew before the trauma. This is important not only to decrease the patient's performance anxiety, but also to help the patient realize and accept his or her limitations. Approximately 10% of patients with TBI suffer from a generalized anxiety disorder. Travel phobias are seen in 25% of patients with TBI who were injured in MVAs. Interestingly, PTSD is less common in patients who lost consciousness as a result of their injury.[6] [49]

Treatment includes family therapy to help family members adjust to the “new” person in their lives. Behavior therapy, including desensitization, can be helpful. A short course of a short-acting benzodiazepine may help in an acute stress situation. Although SSRIs may be helpful, they may also exacerbate apathy and cause sexual dysfunction. Antiepileptic drugs (AEDs) may also be useful, particularly in patients who are aggressive. As noted earlier, neuroleptics are more likely to cause adverse reactions in patients with TBI and may slow down cognitive recovery.

SOMATOFORM DISORDERS

An understudied, but prevalent condition found in some patients with TBI is somatization. This may manifest itself with ill-defined symptoms, including dizziness, vertigo, gait instability, headache, fatigue, malaise, tinnitus, visual disturbances, cognitive “fogginess,” non-neuroanatomical paresthesias, weakness, focal deficits, and nonepileptic events. Patients in this category are often classified as having “postconcussional syndrome.”[50] Interestingly, 30% of patients with nonepileptic seizures report a prior history of TBI.[51] [52] Treatments for somatoform disorders are lacking, but preliminary evidence in non-TBI populations shows benefits of cognitive behavior therapy (CBT).[53] [54]

COGNITIVE DISORDERS

Cognitive impairments are among the most commonly occurring sequelae in TBI, and post-traumatic cholinergic deficits are thought to contribute to the development of post-traumatic cognitive impairments.[55] A randomized double-blind placebo-controlled study of a cholinesterase inhibitor in 157 post-TBI patients failed to show a difference from placebo on both primary cognitive and secondary outcome measures.[56]

PERSONALITY CHANGE DUE TO A MEDICAL CONDITION

The most disruptive consequences of TBI at 1, 5, and 15 years after the event are personality changes. Such changes may include lability, disinhibition, aggression, apathy, and paranoia. The personality changes are most often exaggerations of premorbid personality traits. The “pseudoborderline” personality is characterized by impulsivity, lack of empathy, loss of a sense of self, and inability to monitor one's own behavior. Patients who display mania, euphoria, and impulsivity are labeled as “pseudosociopathic.” This syndrome is associated with damage to the orbitofrontal cortex. Medial frontal damage may cause a “pseudodepressed” personality disorder with severe apathy. Explosive personality disorders in which patients are irritable and subject to sudden rages and violence are commonly seen, particularly in patients who use alcohol.

Environmental management is essential for personality disorders, which can be affected by pain and fatigue. Management includes sleep hygiene; avoiding caffeine, alcohol, and illicit substances; avoiding chronic opiates for pain; and maintaining an exercise plan and stretches. Treatment of these various personality changes must include counseling. Pharmacological treatment with tricyclic and SSRI antidepressants may help with lability. Low-dose stimulants, L-dopa, and dopamine agonists have been shown in some studies to be helpful with impulsivity.[57]

AGGRESSIVE DISORDERS

In different studies, the incidence of aggression post-TBI is between 35 and 90%.[58] [59] Agitation occurs commonly in the delirious subacute phase of recovery. Chronic irritability and aggression are seen in ~40 to 70% of patients with TBI. Aggression in patients with TBI is generally reactive without premeditation, and is nonpurposeful, explosive, periodic, and egodystonic; that is to say, the patients are genuinely remorseful after the event.[60] Damage to the limbic system, orbitofrontal cortex, left anteromedial frontal lobe, and anterior cingulate have been particularly associated with aggressive behavior.[61] Studies have found increased amounts of CSF norepinephrine[62] and decreased amounts of serotonin in violent patients.[63]

Behavior modification is probably the most effective treatment for these patients. Careful observation and documentation of the patient's aggressive outbursts may reveal triggers of and secondary gains from this behavior.

Levy et al provide an overview of pharmacological management of agitation in TBI,[64] and many of the agents used for agitation are also used for aggression. Antipsychotic medications do not help with chronic, nonpsychotic aggression. In fact, akathisia, a common adverse reaction to typical neuroleptics, may actually increase violent behavior. As noted previously, neuroleptics have been shown to slow recovery from TBI. Benzodiazepines may cause a paradoxical response in TBI patients, as they do in children. Low-dose buspirone has been tried in some patients, but it may also cause a paradoxical reaction. Antipsychotic agents should be reserved for patients who are truly psychotic. Carbamazepine, valproic acid, gabapentin, and oxcarbazepine have been used successfully in some patients. Lithium is useful in patients who are clearly manic or who display cyclic violence. Antidepressant medications, including TCAs and SSRIs, have been shown to be helpful in small studies. High-dose propranolol, up to 12 mg/kg/d, has been very helpful in some patients.[65]

SUBSTANCE DISORDERS

A history of substance abuse predicts increased disability, poorer prognosis, and delayed recovery. Although consensus in the literature indicates that substance-abuse rates decline following injury, conflicting literature shows a significant history of brain injury in patients with addictions.[66] More recent literature reveals that when combined with difficulties in psychosocial adjustment and coping skills, cognitive impairments may increase the risk for chronic substance abuse in a subset of patients with TBI. Substance abuse significantly complicates TBI rehabilitation and recovery.

Traumatic Brain Injury and the Family

Patients who have suffered a TBI need a social support system to help them adapt to their new lives. The family is usually the source of this support; communities of faith and local or national brain injury support groups are also used. Daily structure is of benefit with vocational rehabilitation and volunteer programs if the patient is unable to return to work. Despite the TBI sequelae, it should be emphasized to the patient and the family that he or she must be able to behave appropriately within the family and social settings. The spouse has the double responsibility of not only caring for the patient, but also becoming the primary or only bread-winner. For the family, the patient with TBI is often a different person than the one they knew before the injury, even though they may look exactly the same. Unfortunately, these changes are usually for the worse. Often the patients are less caring, more irritable, and prone to violence as well as depressed, anxious, and withdrawn. The patient's lack of awareness or angry denial of any deficits or personality changes leads him or her to feel like people are picking on him. The patient may then become more angry and aggressive, further alienating the family members who may ultimately abandon the patient. It is important that the family realizes that the patient may struggle to control his or her behavior and fully function in the same manner as before the trauma.

This does not mean the family has to accept the behavior, but to deal with it by working to modify the behavior by emphasizing that it is the behavior that is wrong, not the person. “Time-outs” and rewarding good behavior may make a significant difference in the patient's actions and ease the tensions within the family. Individual and family therapy can address issues of limit setting, boundaries, and forgiveness. Clearly, alcohol and substance use, which further disinhibits patients, is discouraged and is a prescription for disaster. The safety of the family and the individual has to be ensured for the benefit of all in the support system.

CONCLUSION

Traumatic brain injury can cause not only focal deficits of motor activity or language, but also a variety of potentially disabling psychiatric symptoms and syndromes. These include mood and anxiety disorders; personality disturbances; aggression; and, occasionally, psychosis. Treatment is complicated by cognitive deficits, lack of motivation, and lack of awareness of deficits. Controlled treatment trials for TBI are lacking. Pharmacological treatment may include a wide range of medications, such as antidepressants, antipsychotics, mood stabilizers, and stimulants. Family and individual counseling is particularly important in helping the patient and the family reconcile themselves to the reality of the behavioral changes in the patient post-TBI.

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