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Clinical Case Conference   |    
Psychiatric Sequelae of Traumatic Brain Injury: A Case Report
Vani Rao, M.D.; Sharon Handel, M.D.; Sandeep Vaishnavi, M.D., Ph.D.; Shari Keach, L.C.P.C.; Beatrice Robbins, R.N., Ph.D.; Jennifer Spiro, M.S.; Julianna Ward, Ph.D.; Fred Berlin, M.D., Ph.D.
Am J Psychiatry 2007;164:728-735. doi:10.1176/appi.ajp.164.5.728

Traumatic brain injury is a significant cause of disability in the United States, with both neurological and psychiatric consequences (1). Although neurological sequelae usually stabilize with time, psychiatric disorders persist because of their propensity to produce chronic symptoms and to follow a relapsing course. Mood and behavioral problems after traumatic brain injury interfere with rehabilitation efforts and cause adverse outcomes such as unemployment, repeated hospitalizations, legal problems, and alienation from family and friends (2, 3). In addition, these effects are amplified by high rates of psychiatric comorbidity (4) (e.g., DSM axis I diagnoses) in patients with traumatic brain injury.

The case presented here of a 42-year-old man with a history of two traumatic brain injuries exemplifies the clinical and social complexities of traumatic brain injury. The formulation of multiple diagnoses and the design of a comprehensive treatment plan for this patient were challenging. As described by McHugh and Slavney in their book, The Perspectives of Psychiatry(5), the use of an organized approach and conceptual framework is important in psychiatric diagnosis and treatment. The four perspectives of psychiatry provide a framework for organizing a patient’s psychiatric history in a structured manner, independent of the etiology. The essence of each perspective defines how to approach a problem and design a solution. The four perspectives thus provide a roadmap for diagnosis and treatment.

This approach has been particularly useful in the effective clinical management of this patient. Our success with this patient emerges from the use of several distinct but complementary perspectives to understand his problems. We describe our patient’s history and treatment and then describe how using the four perspectives approach led to his arrival at an optimal level of functioning.

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Chief Complaint

“Mr. C” was a 42-year-old man who was referred for immediate admission to the inpatient neuropsychiatry unit at Johns Hopkins Hospital for evaluation and management of behavior problems associated with traumatic brain injury after initial treatment and rehabilitation at an outside hospital.

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Present Illness

Mr. C was doing well until he sustained a severe traumatic brain injury and right orbital wall fracture after falling from a 40-foot-high ladder. The duration of posttraumatic amnesia and the 24-hour Glasgow Coma Scale (6) score at the time of injury are unknown. Other than surgical repair of the orbital fracture, no other known medical or surgical postfall complications were diagnosed or treated at the outside hospital. He was not under the influence of illicit drugs or alcohol at the time of the fall. He was hospitalized for 3 weeks, during which time he was in a coma for approximately 2 weeks.

Upon discharge, he underwent 5 weeks of inpatient rehabilitation followed by several weeks of outpatient rehabilitative care. At this time, he attempted to return to work several times. However, he was unable to hold a job because of socially inappropriate behavior, such as arguing with male coworkers and inappropriately touching and groping female coworkers on multiple occasions. He was arrested twice and incarcerated once for 3 months because of these acts. Other behavior problems since the traumatic brain injury included frequent outbursts of anger and physically aggressive behavior, leading to separation from his wife and alienation from several family members. Mr. C received several trials of medication that were not effective (risperidone, 1 mg at bedtime; divalproex sodium, 750 mg b.i.d.; quetiapine, dose unknown; and methylphenidate, dose unknown) according to his family. There was no history of seizure after traumatic brain injury.

Mr. C’s behavior gradually became more disinhibited and physically aggressive, and he was referred to Johns Hopkins for evaluation and treatment recommendations. At the time of admission, he was most concerned about intermittent episodes of depression that had been occurring spontaneously for several years since the traumatic brain injury. He described a typical episode of depression as lasting for 2 to 4 weeks and characterized by persistent sadness, loss of interest in life, loneliness, feelings of worthlessness, anxiety about the future, fatigue, problems with inattention and memory, and passive suicidal thoughts. In addition, he also reported brief transient episodes of sadness that would last for a few hours and would occur after a stressful event, such as a confrontation with a family member.

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Family, Personal, and Social History

The patient’s family history was negative for known neuropsychiatric disorders. His birth and early development were reportedly normal. He graduated from high school and served in the Navy for 4 years, receiving an honorable discharge. Before sustaining his traumatic brain injury, he worked successfully as a subcontractor for homebuilders. He was married for only 6 months before his injury, and he separated from his wife. He had two young children who lived with his wife. He was receiving disability income. Mr. C drank socially and smoked tobacco and marijuana briefly before his traumatic brain injury. He converted his religion from Catholicism to born-again Christian after discharge from the military. However, he was ostracized by his church in 2003 secondary to sexually inappropriate behavior. He had had no legal problems before the second traumatic brain injury.

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Past Medical and Psychiatric History

Mr. C’s medical history was significant for a prior traumatic brain injury that occurred while he was playing baseball. He experienced a loss of consciousness of unknown duration after colliding with one of the other players. He suffered fractures of several facial bones on the right side and was hospitalized for approximately 4 days. His recovery was otherwise good, and he did not suffer any medical or psychiatric consequences after this injury. Since his second traumatic brain injury, he had undergone several corrective eye surgeries. Before this traumatic brain injury, Mr. C had no history of psychiatric symptoms or treatment, and his personality was described by his father as “happy-go-lucky” but conscientious. He had no history of inappropriate social or sexual behavior. He was now noted as having a “short fuse.” Additional medical comorbidities included a diagnosis of ankylosing spondylitis and arthritis.

His medications at the time of admission to the neuropsychiatry unit included divalproex sodium, 750 mg b.i.d.; sertraline, 75 mg/day; risperidone, 1 mg at bedtime; and indomethacin, 75 mg b.i.d. (for arthritis).

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Mental Status Examination

Mr. C was found to have adequate hygiene and grooming. He was cooperative during the evaluation and made good eye contact. He did not display psychomotor abnormalities or adventitious movements but was disinhibited and jocular. His speech was mildly dysarthric but fluent and grammatically correct with no paraphrasic errors. His thought processes were somewhat circumstantial, but there was no loosening of associations or evidence of a formal thought disorder. He described his mood as “anxious for having caused trouble to family.” His affect was labile and incongruent with his mood. He endorsed transient passive death wishes but denied active suicidal thoughts, intent, or plans. No other violent thoughts were elicited. His self-attitude and vital sense were normal. He had no delusions, hallucinations, obsessions, compulsions, or phobias. His insight into emotional difficulties was limited, and his judgment was poor, as evidenced by the socially inappropriate behavior. He scored 30 of 30 on the Mini-Mental State Examination.

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Physical Examination and Diagnostic Findings

Abnormalities upon neurological examination included the following:

  1. A mild upper motor neuron-type dysarthria

  2. Diplopia with disconjugate extraocular movements in all directions

  3. Diminished pinprick sensation on the right side of his face in areas innervated by all three branches of the trigeminal nerve

  4. Hyperreflexia (3+) in the lower extremities (of note, there was no clonus, and plantar reflexes were flexor bilaterally)

Testing performed during admission included brain magnetic resonance imaging, which showed diffuse cerebral volume loss and right frontal and left temporal areas of encephalomalacia and gliosis, a normal EEG, and normal blood tests (including a metabolic panel, a testosterone level, a thyroid-stimulating hormone level, and tests for HIV and syphilis).

A neuropsychological assessment revealed frontal-subcortical system dysfunctions with impairments in processing speed (i.e., the Symbol Digit Modalities Test [7], written and oral trials) and visual sequencing/set-shifting (i.e., the Trail Making Test, Part B [8]). Relative weaknesses were found in divided auditory attention (i.e., the Brief Test of Attention [9]), sustained visual attention (i.e., the Continuous Performance Test [10]), social judgment (i.e., the Dartmouth-Rabin Judgment Questionnaire [11]), verbal and visual learning and memory (i.e., the Hopkins Verbal Learning Test—Revised [12] and the Brief Visuospatial Memory Test—Revised [13]), and nondominant (left) hand fine motor coordination (i.e., the Grooved Pegboard test [14]). Visual memory improved to within the average range with provision of yes/no recognition testing, indicating a primary retrieval deficit. However, no such improvement was seen for verbal memory. Baseline verbal intellect was estimated to be in the average range. Quantitative assessment of psychiatric symptoms was also performed. The Geriatric Depression Scale (15) revealed mild to moderate symptoms of depression (score=18 of 30). On the Lawton Activities of Daily Living and Instrumental Activities of Daily Living Questionnaire (16), the patient rated himself as needing “some help” getting places that were not within walking distance, preparing meals, doing handyman work, and managing his medications and finances.

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Hospital Course

Mr. C was given a behavior plan detailing inappropriate behavior to minimize conflict with other patients and staff. With the structured activities and predictable routine that was provided on the inpatient unit, he remained compliant and had no behavior problems. Occasionally, there was evidence of inappropriate behavior, such as being overly familiar with visitors on the floor, but he was easily redirected in these instances. Because of prior lack of benefit, he was tapered from divalproex sodium and risperidone. Sertraline was titrated to 150 oral mg/day for symptoms of major depression. Considering his frontal lobe symptoms (i.e., impulsivity, poor social judgment, low frustration tolerance, and behavioral disinhibition), amantadine was started and gradually increased to a dose of 100 mg/day. Mr. C was discharged to the Johns Hopkins Bayview Brain Injury Clinic; the National Institute for the Study, Prevention, and Treatment of Sexual Trauma (formerly called the Johns Hopkins Sexual Disorders Clinic); and a psychosocial rehabilitation program.

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Outpatient Treatment

Even though Mr. C did very well in the structured inpatient setting, he found returning to the community difficult. Establishing realistic expectations was critical to his care, and the primary goals of therapy were to minimize existing disability and maximize productivity. The strategies employed to achieve these outcomes included pharmacotherapy (continuation of sertraline and amantadine), individual cognitive behavior therapy (once a week), group therapies (daily psychosocial rehabilitation program and weekly sexual behaviors group), and family therapy (every 3 months).

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Diagnostic Challenges

In summary, Mr. C was an unfortunate middle-aged man with a history of two traumatic brain injuries. He had been suffering from mood and behavior problems since the second incident. In addition, he had encountered several psychosocial stressors, including legal problems, separation from family and religious connections, unemployment, and increasing dependence on family members for assistance. Clearly, the patient’s case was complicated, and many would conclude that his prognosis was poor. Although the formulation of this patient’s case was challenging, successful treatment would emerge from disentangling his symptoms and their respective causes. Hence, we attempted to use an organized approach with four perspectives to define and treat all of the patient’s problems (5) (See Figure 1).

Each perspective has a unique logic and set of principles that direct treatment in a very specific way. The perspective of disease is based on categories and asks, “What does the patient have?” This perspective explains mental disturbances as secondary to a “broken part” in the brain. The perspective of dimensions is based on the logic of gradation and quantification and asks, “What is the patient?” The dimensional perspective explains problems of mental life as arising out of the interaction between a person’s vulnerability (e.g., personality characteristics) and the demands of an environment to which that trait is mismatched or poorly suited. The perspective of behavior is based on the logic of goals and asks, “What is the patient doing?” The behavior perspective emphasizes the goal-directed aspects of behavior and how problem behaviors are gradually shaped by other factors (e.g., internal drives, environmental consequences). The perspective of the life story is based on the logic of narrative and asks, “What has the patient encountered?” The life story perspective highlights how a distressed state of mind could be the understandable result of disturbing life experiences.

Thus, the treatment for each type of problem is also different (see Figure 1): curative in the disease perspective by fixing the broken part, guiding and supportive in the dimensional perspective by strengthening the vulnerability and/or reducing the mismatch between patient traits and environmental demands, interpreting and converting in the behavior perspective by changing goals and reinforcements, and rescripting the patient’s narrative in the life story perspective by offering more encouraging interpretations of unfortunate events.

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The Disease Perspective

Several of Mr. C’s symptoms and problems could be explained by the damage caused to his brain. Mood disorders in patients with traumatic brain injury are associated with the disruption of brain circuits involving regions such as the prefrontal cortex, amygdala, hippocampus, basal ganglia, and thalamus (17). Studies in depression without traumatic brain injury have also found involvement of the frontal cortical regions and amygdala, suggesting that dysfunction of limbic prefrontal cortical structures impairs the modulation of the amygdala, leading to abnormal processing of emotional stimuli (18). Several studies have revealed frontal lobe damage in patients with impulse control problems similar to Mr. C’s, such as improper social etiquette and disinhibition (19–21).

The treatment approach in the disease perspective focused on curing the disease (5). In this case, the injury is irreversible, and it is not possible to cure the disease; however, symptoms of the pathology can be minimized. A literature review revealed that there is a limited evidence base to guide treatment of neuropsychiatric symptoms after traumatic brain injury; however, guidelines and reviews based on randomized controlled trials have been published. In particular, the Neurobehavioral Guidelines Working Group has recently done a comprehensive review of the evidence base for these disorders (22). Based on this analysis, tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) are recommended for depression after traumatic brain injury. There is insufficient evidence to support or refute use of any particular agent for mania or anxiety disorders after traumatic brain injury. For general cognitive functions, there is insufficient evidence to support any agent, but phenytoin in particular may make cognition worse. Agents found to enhance specific types of cognitive functioning include methylphenidate for attention and speed of cognitive processing, donepezil to enhance attention and memory, and bromocriptine for improving executive function. Beta blockers are recommended for aggression. Other treatment options for aggression include methylphenidate, cranial electrical stimulation, SSRIs, valproic acid, lithium, tricyclic antidepressants, and/or buspirone (22).

Mr. C’s major depression responded well to sertraline, an SSRI. Other researchers have recommended the use of sertraline for the treatment of major depression after traumatic brain injury (23–25). Symptoms of dysexecutive function, such as impulsivity and disinhibition, are being controlled by amantadine. There are several anecdotal reports on the use of amantadine, a dopaminergic agonist and an N-methyl-d-aspartate (NMDA) receptor antagonist, in patients with dysexecutive function after traumatic brain injury (26–28).

Thus, many of Mr. C’s problems (major depression, cognitive deficits) could be explained by the disease perspective. However, to formulate all of his problems as purely biological was to preserve the disease at the expense of the person. Also, relying solely on biological treatments to treat the symptoms was insufficient and not holistic. Other researchers also agree that psychiatric disturbances after traumatic brain injury have multiple causes: social, environmental, developmental, and behavioral (17, 29, 30). However, an approach for how to deal with these causes is usually not provided. We have attempted to address the emotional and cognitive problems in this patient by applying the four perspectives approach.

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The Dimensional Perspective

The central theme of the dimensional perspective is that emotional distress can be secondary to an individual’s cognitive or affective trait vulnerabilities (5). Studies have shown that patients with traumatic brain injury often have cognitive deficits and alterations in personality and emotional regulations that can have adverse outcomes (31). Common changes include disinhibition, irritability, apathy, agitation, aggression, indifference to surroundings, and problems with executive functioning (32). Disinhibition may be a particular problem in this patient population. In a study comparing patients with traumatic brain injury to normal comparison subjects on the Revised Diagnostic Interview for Borderlines (33), which is a measure of borderline traits, the patients with traumatic brain injury had more borderline-like traits than the comparison subjects on tasks of inhibition and object relations. The subjects with traumatic brain injury had a poorer performance on the “go/no go” task, indicating difficulty inhibiting their responses. The dimensional perspective includes assessing potential, provocation, and response. For example, Mr. C’s cognitive inefficiencies, such as inattention and poor memory, coupled with his personality traits after traumatic brain injury of low frustration tolerance and quickness to anger (potential) placed him at risk when stressed or challenged (provocation) to react aggressively or inappropriately (response). Although these cognitive and affective trait vulnerabilities were clearly a sequelae of traumatic brain injury, they were now the patient’s new persona or new baseline. Trauma to the brain often causes injury to the frontal-temporal regions with resultant cognitive, behavioral, and emotional impairments that can persist for decades after traumatic brain injury (34). These impairments can be further exaggerated by other factors, such as comorbid psychiatric disorders, substance abuse, and environmental factors, such as excessive stimulation and/or limited psychosocial support (34). Because there is no cure for traumatic brain injury, treatment for a dimensional problem should focus on factors precipitating the emotional distress and strategies used to reduce the emotional response. The dimensional approach helps recognize the patient’s vulnerabilities and provides guidance and strength to help the patient function to the fullest potential.

In accordance with the dimensional perspective, Mr. C received guidance through instruction, practice, and support during individual and group therapy sessions. During these sessions, Mr. C was educated about brain injury and its consequences. Guidance included encouraging Mr. C to acknowledge his deficits and to recognize a “new” baseline. During therapy sessions, his strengths (e.g., motivation to get better, desire to be self-sufficient, absence of substance abuse) and weaknesses (cognitive deficits and specific personality traits) were discussed. Modeling and role playing were used to demonstrate how his vulnerabilities could lead to trouble. Discussing his strengths improved his self-esteem and helped him stay motivated. Guidance also included training to improve his interpersonal relationships, with an emphasis on learning to listen, exercising self-control when angry, and making conversation in a polite and responsible manner. Group counseling was useful in providing actual interactions with peers and opportunities for socialization to offset the loneliness that often provoked Mr. C’s distress. This supportive and structured setting gave Mr. C an opportunity to obtain safe feedback from peers. In addition, regular family meetings were held to provide additional instruction and support.

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Behavior Perspective

Even though the disease and the dimensional perspectives could explain many of Mr. C’s behavioral problems, some of them, such as the sexually inappropriate behavior, were better explained using the behavior perspective. Sexually inappropriate behavior can be particularly troublesome in this patient population. Simpson et al. (35) related patients with traumatic brain injury with sexually inappropriate behavior to comparison subjects with traumatic brain injury without the behavior to identify social, cognitive, and medical correlates. They found a higher incidence of psychosocial impairment and failure to return to work after traumatic brain injury in subjects with traumatic brain injury with sexually inappropriate behavior. Premorbid temperament or postinjury medical or cognitive variables were not significantly more common in the traumatic brain injury group with sexually inappropriate behavior. The researchers warn against having “a simplistic explanation,” such as frontal lobe damage or psychosocial disturbance before traumatic brain injury, as the cause for sexually inappropriate behavior that emerges after injury.

The behavior perspective identifies conditions that represent problems of choice and control and is governed by a triad of physiological drive, conditioned learning, and choice. Motivated behaviors, such as eating, drinking, sleeping, and sexuality, all depend on learning and maturation. However, these normal behaviors can become a “disorder” when carried to excess in form or frequency. These abnormal motivated behaviors are often sustained by rewarding consequences. Mr. C’s inappropriate sexual behavior is a typical example of an abnormal goal-directed behavior. Even though injury to the frontal lobes may have resulted in impulsivity and disinhibition, making him vulnerable to hypersexual acts, this behavior is probably shaped and maintained by positive reinforcements that Mr. C receives when he indulges in touching others. The rewards, such as joy and/or attention, that he receives may also be a distorted form of sexual outlet.

Treatment involves stopping or converting the problematic behavior. This approach involves confronting behavior, challenging the patient’s reluctance to change, and adopting the new goal of striving to end it. The behavioral approach has been shown to help in this patient population. Fyffe et al. (30) described a case of a 9-year-old boy diagnosed with traumatic brain injury who continued to maintain inappropriate sexual behavior secondary to positive reinforcement in the form of social attention. A behavioral intervention in the form of functional communication training and extinction led to a reduction of the inappropriate behavior. Zencius et al. (36) described the effectiveness of simple strategies such as feedback and “scheduled massage” to decrease hypersexual behavior in brain-injured subjects. Bezeau et al. (37) reviewed the various types of sexually intrusive behavior following traumatic brain injury and discussed methods for assessment and management.

Evaluation and treatment of inappropriate sexual behavior is often frustrating and challenging for the therapist and awkward, embarrassing, and sometimes even shameful for the patient and/or his family. In the behavioral approach, these behaviors should be addressed respectfully and in a professional manner, and the therapist should be sensitive to the feelings of the person/family (38). The person should be told in a clear, straightforward manner that the behavior is unacceptable. Family members should be educated about the frequency of socially and sexually inappropriate behaviors after traumatic brain injury.

Management of Mr. C’s hypersexual behavior included a combination of pharmacotherapy and psychotherapy. The increased sexual drive was reduced pharmacologically with leuprolide. There is a significant literature on the use of medroxyprogesterone and leuprolide acetate for the treatment of paraphilias and hypersexual behavior in patients with and without traumatic brain injury (39–42). Psychotherapy included group therapy and individual therapy focused on providing clear recommendations about acceptable and unacceptable behavior. Examples include avoiding people and places where he was likely to be vulnerable to hypersexuality, encouraging him to have a responsible person supervise him when he was meeting with friends, role-playing his actions before his dates, modeling and providing feedback, and encouraging repetition of appropriate behavior. Regular discussion in simple language about the feelings and rights of the person being touched and the legal consequences he had to suffer because of his actions also helped. Mr. C’s strong religious beliefs helped to reduce and keep this behavior in check.

The behavior perspective may also help patients with traumatic brain injury with various other inappropriate behaviors. Hegel and Ferguson (43) demonstrated a significant reduction in aggressive behavior using the technique of “differential reinforcement of other behaviors” in a brain-injured man. Tiersky et al. (44) compared the effectiveness of individual cognitive behavior psychotherapy and individual cognitive remediation therapy to regular follow-up treatment in patients with mild to moderate traumatic brain injury. A total of 20 subjects were followed for 11 weeks. They found that the group that received cognitive behavior therapy/cognitive remediation therapy had reduced emotional distress and improved attention at 1 and 3 months posttreatment. Bell et al. (45) used a novel but simple method of scheduled telephone intervention with counseling and education. In this study, 85 patients with traumatic brain injury were selected at random for telephone intervention, and 86 patients with traumatic brain injury, for usual outpatient care. The telephone interventions consisted of motivational counseling and education and counseling regarding follow-up appointments and medications. At the end of 1 year, those who received telephone intervention fared significantly better on several behavioral outcomes and overall quality of life. Cox et al. (46) also demonstrated the effectiveness of systematic motivation counseling to treat substance abuse in patients with traumatic brain injury. Those who received systematic motivation counseling had a significant reduction in negative affect and substance abuse compared to patients with traumatic brain injury without systematic motivation counseling. Other types of behavioral interventions found to be helpful for patients with traumatic brain injury include natural setting behavior management, in which the focus is on education and individualized behavior modification in the natural community setting (47), and multidisciplinary treatment (48). The latter study revealed that targeting patients with traumatic brain injury with pre-injury psychiatric problems is effective in reducing depressive symptoms postinjury.

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The Life Story Perspective

The transient episodes of sadness and hopelessness that Mr. C experienced are less satisfactorily explained by any of the previous perspectives and are best explained by the life story perspective. This perspective takes into account events that have taken place in a person’s life and tries to explain their distress as an outcome of this narrative (5). In other words, the life story perspective attempts to make sense of emotional problems as meaningful responses to life encounters. McHugh and Slavney (5) defined the life story perspective as the triad of setting, sequence, and outcome. In the case presented, the setting is the brain injury; sequences include the loss of his job, separation from his wife, family conflicts, and legal problems; and outcomes are the demoralized states of sadness, loneliness, helplessness, and rage.

The goal of therapy in the life story perspective is to “rescript” events and the negative meanings adopted by the patient. Individual and group therapy often help the person to “reinterpret” his or her life by providing an understanding of the “setting” and “sequence” and coping skills and compensatory strategies to modify the outcome. Ultimately, the patient is encouraged to continue his or her life with an acceptance of past events and renewed optimism about the potential for future successes that will lead to a satisfying and fulfilling life.

Studies indicate that patients with traumatic brain injury face numerous psychosocial problems, such as those experienced by Mr. C, that contribute to emotional distress, anger, and aggression (29, 49). When compared to those with other chronic medical illnesses, people with traumatic brain injury have a unique set of problems that increases the risk for emotional distress. First, traumatic brain injury strikes suddenly, causing a dramatic change in functional, social, and occupational life. Second, because of this acute onset, family members have not made any preparations to take care of the handicapped brain-injured person. This often results in family relationships faltering. Third, because the physical sequelae of traumatic brain injury often resolve or stabilize, the psychiatric disturbances continue to persist or relapse, which many families of patients with traumatic brain injury have difficulty understanding. Fourth, many patients with traumatic brain injury are unable to obtain rehabilitation services that they need because of poor finances, lack of insurance, or difficulty finding an appropriate place. Finally, impaired self-awareness is a common problem in traumatic brain injury (50). Patients with traumatic brain injury with impaired self-awareness when compared to those without impaired self-awareness show more psychopathological symptoms, worse neuropsychological function, and decreased functional independence (51). Sherer et al. (52) noted that decreased self-awareness after traumatic brain injury is secondary to multiple disruptions of the integrated, broadly distributed neural network associated with awareness rather than lesions in particular brain regions. Others, however, have noted specific abnormalities in the right anterior prefrontal region in patients with traumatic brain injury with impaired self-awareness in relation to normal comparison subjects (53). Lack of insight can be particularly challenging in the treatment of neuropsychiatric symptoms after traumatic brain injury. Hurt (54) has proposed three specific strategies to improve self-awareness. They include identification of the strengths and limitations of people with traumatic brain injury by formal vocational testing, confrontation of behavior problems through group therapy, and involvement in a work setting to learn compensatory strategies and rebuild self-esteem. Other methods to improve awareness include education in brain-behavior relations, goal and journal group therapy, and video feedback therapy (55).

Mr. C had limited self-awareness, perhaps because of the right frontal injury. Regular education, individual and group therapy, and gentle confrontation of inappropriate behavior all played a role in improving Mr. C’s awareness of his deficits and improvement in behavior.

Traumatic brain injury is a complex condition associated with several psychiatric problems, some of which could be direct manifestations of brain damage, and others, associated with the person’s inherent cognitive or personality traits. In addition, patients with traumatic brain injury may also indulge in abnormal goal-directed behaviors, which can further increase their emotional distress and cause social, occupational, or legal problems. Finally, their negative reactions and sense of pessimism may be understood by their changing life circumstances and the associated new challenges.

We used four distinct but complementary perspectives in formulating and treating Mr. C’s psychiatric problems after traumatic brain injury. This organized approach helped to identify and differentiate the independent aspects of his illness and provide the necessary pharmacological and nonpharmacological treatments. Mr. C has made significant improvement since he began treatment in our clinic. Although Mr. C is by no means cured, his treatment was individually designed to help him attain the goal of improving his overall quality of life.

We presented this case report to highlight the importance of using a structured formulation to diagnose and treat the psychiatric sequelae of traumatic brain injury. To clearly demonstrate the effectiveness of this organized approach, future studies should include larger numbers of subjects and well-validated research instruments to assess mood and cognitive and behavioral outcomes.

+Received July 13, 2006; revision received Jan. 25, 2007; accepted Feb. 7, 2007. From the Divisions of Geriatric Psychiatry and Neuropsychiatry and Medical Psychology and the Department of Psychiatry, Johns Hopkins School of Medicine, Baltimore; and the Community Psychiatry Program, Johns Hopkins Bayview Medical Center, Baltimore. Address correspondence and reprint requests to Dr. Rao, Suite 308, 550 N. Broadway, Baltimore, MD 21205; vrao@jhmi.edu (e-mail).

+Ms. Spiro is a consultant for Respironics, Inc. Dr. Rao has received NIH grants and grants from Pfizer and Forest. The remaining authors report no competing interests.

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28.Kraus MF, Smith GS, Butters M, Donnell AJ, Dixon E, Yilong C, Marion D: Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj 2005; 19:471–479
 
29.Bay E, Kirsch N, Gillespie B: Chronic stress conditions do explain posttraumatic brain injury depression. Res Theory Nurs Pract 2004; 18:213–228
 
30.Fyffe CE, Kahng S, Fittro E, Russell D: Functional analysis and treatment of inappropriate sexual behavior. J Appl Behav Anal 2004; 37:401–404
 
31.Warriner EM, Velikonja D: Psychiatric disturbances after traumatic brain injury: neurobehavioral and personality changes. Curr Psychiatry Rep 2006; 8:73–80
 
32.Kim E: Agitation, aggression, and disinhibition syndromes after traumatic brain injury. NeuroRehabilitation 2002; 17:297–310
 
33.Gagnon J, Bouchard MA, Rainville C, Lecours S, St-Amand J: Inhibition and object relations in borderline personality traits after traumatic brain injury. Brain Inj 2006; 20:67–81
 
34.Jorge RE: Neuropsychiatric consequences of traumatic brain injury: a review of recent findings. Curr Opin Psychiatry 2005; 18:289–299
 
35.Simpson G, Tate R, Ferry K, Hodgkinson A, Blaszczynski A: Social, neuroradiologic, medical, and neuropsychologic correlates of sexually aberrant behavior after traumatic brain injury: a controlled study. J Head Trauma Rehabil 2001; 16:556–572
 
36.Zencius A, Wesolowski MD, Burke WH, Hough S: Managing hypersexual disorders in brain-injured clients. Brain Inj 1990; 4:175–181
 
37.Bezeau SC, Bogod NM, Mateer CA: Sexually intrusive behaviour following brain injury: approaches to assessment and rehabilitation. Brain Inj 2004; 18:299–313; erratum, 18:517
 
38.Lawrie B, Jillings C: Assessing and addressing inappropriate sexual behavior in brain-injured clients. Rehabil Nurs 2004; 29:9–13
 
39.Britton KR: Medroxyprogesterone in the treatment of aggressive hypersexual behavior in traumatic brain injury. Brain Inj 1998; 12:703–707
 
40.Briken P: Pharmacotherapy of paraphilias with luteinizing hormone-releasing hormone agonists. Arch Gen Psychiatry 2002; 59:469–470
 
41.Krueger RB, Kaplan MS: Depot-leuprolide acetate for treatment of paraphilias: a report of twelve cases. Arch Sex Behav 2001; 30:409–422
 
42.Saleh FM, Berlin FS: Sex hormones, neurotransmitters, and psychopharmacological treatments in men with paraphilic disorders. J Child Sex Abus 2003; 12:233–253
 
43.Hegel MT, Ferguson RJ: Differential reinforcement of other behavior (DRO) to reduce aggressive behavior following traumatic brain injury. Behav Modif 2000; 24:94–101
 
44.Tiersky LA, Anselmi V, Johnston MV, Kurtyka J, Roosen E, Schwartz T, Deluca J: A trial of neuropsychologic rehabilitation in mild-spectrum traumatic brain injury. Arch Phys Med Rehabil 2005; 86:1565–1574
 
45.Bell KR, Temkin NR, Esselman PC, Doctor JN, Bombardier CH, Fraser RT, Hoffman JM, Powell JM, Dikmen S: The effect of a scheduled telephone intervention on outcome after moderate to severe traumatic brain injury: a randomized trial. Arch Phys Med Rehabil 2005; 86:851–856
 
46.Cox WM, Heinemann AW, Miranti SV, Schmidt M, Klinger E, Blount J: Outcomes of systematic motivational counseling for substance use following traumatic brain injury. J Addict Dis 2003; 22:93–110
 
47.Carnevale GJ, Anselmi V, Johnston MV, Busichio K, Walsh V: A natural setting behavior management program for persons with acquired brain injury: a randomized controlled trial. Arch Phys Med Rehabil 2006; 87:1289–1297
 
48.Ghaffar O, McCullagh S, Ouchterlony D, Feinstein A: Randomized treatment trial in mild traumatic brain injury. J Psychosom Res 2006; 61:153–160
 
49.Bay E, Hagerty BM, Williams RA, Kirsch N, Gillespie B: Chronic stress, sense of belonging, and depression among survivors of traumatic brain injury. J Nurs Scholarsh 2002; 34:221–226
 
50.Hart T, Sherer M, Whyte J, Polansky M, Novack TA: Awareness of behavioral, cognitive, and physical deficits in acute traumatic brain injury. Arch Phys Med Rehabil 2004; 85:1450–1456
 
51.Noe E, Ferri J, Caballero MC, Villodre R, Sanchez A, Chirivella J: Self-awareness after acquired brain injury: predictors and rehabilitation. J Neurol 2005; 252:168–175
 
52.Sherer M, Hart T, Whyte J, Nick TG, Yablon SA: Neuroanatomic basis of impaired self-awareness after traumatic brain injury: findings from early computed tomography. J Head Trauma Rehabil 2005; 20:287–300
 
53.Schmitz TW, Rowley HA, Kawahara TN, Johnson SC: Neural correlates of self-evaluative accuracy after traumatic brain injury. Neuropsychologia 2006; 44:762–773
 
54.Hurt P: Mild brain injury: critical factors in vocational rehabilitation. J Rehabil 1990; 57:36–45
 
55.Wesolowski MD, Zencius AH: A Practical Guide to Head Injury Rehabilitation: A Focus on Postacute Residential Treatment. New York and London, Plenum Press, 1994
 
 
Figure 1. The Four Perspectives of Psychiatry
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3.Warriner EM, Velikonja D: Psychiatric disturbances after traumatic brain injury: neurobehavioral and personality changes. Curr Psychiatry Rep 2006; 8:73–80
 
4.Hibbard MR, Uysal S, Kepler K, Bogdany J, Silver J: Axis I psychopathology in individuals with traumatic brain injury. J Head Trauma Rehabil 1998; 13:24–39
 
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12.Brandt J, Benedict RHB: Hopkins Verbal Learning Test—Revised (HVLT-R): Professional Manual. Lutz, Fla, Psychological Assessment Resources, 2001
 
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15.Yesavage JA, Brink TL, Rose TL, Lum O, Huang V, Adey MB, Leirer VO: Development and validation of a geriatric depression screening scale: a preliminary report. J Psychiatr Res 1983; 17:37–49
 
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17.Jorge RE, Starkstein SE: Pathophysiologic aspects of major depression following traumatic brain injury. J Head Trauma Rehabil 2005; 20:475–487
 
18.Drevets WC: Prefrontal cortical-amygdalar metabolism in major depression. Ann NY Acad Sci 1999; 877:614–637
 
19.Cato MA, Delis DC, Abildskov TJ, Bigler E: Assessing the elusive cognitive deficits associated with ventromedial prefrontal damage: a case of a modern-day Phineas Gage. J Int Neuropsychol Soc 2004; 10:453–465
 
20.Chow TW: Personality in frontal lobe disorders. Curr Psychiatry Rep 2000; 2:446–451
 
21.Sandel ME, Williams KS, Dellapietra L, Derogatis LR: Sexual functioning following traumatic brain injury. Brain Inj 1996; 10:719–728
 
22.Warden DL, Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, Drake A, Gentry T, Jagoda A, Katz DI, Kraus J, Labbate LA, Ryan LM, Sparling MB, Walters B, Whyte J, Zapata A, Zitnay G: Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. J Neurotrauma 2006; 23:1468–1501
 
23.Lee H, Kim SW, Kim JM, Shin IS, Yang SJ, Yoon JS: Comparing effects of methylphenidate, sertraline and placebo on neuropsychiatric sequelae in patients with traumatic brain injury. Hum Psychopharmacol 2005; 20:97–104
 
24.Turner-Stokes L, Hassan N, Pierce K, Clegg F: Managing depression in brain injury rehabilitation: the use of an integrated care pathway and preliminary report of response to sertraline. Clin Rehabil 2002; 16:261–268
 
25.Fann JR, Uomoto JM, Katon WJ: Sertraline in the treatment of major depression following mild traumatic brain injury. J Neuropsychiatry Clin Neurosci 2000; 12:226–232
 
26.Nickels JL, Schneider WN, Dombovy ML, Wong TM: Clinical use of amantadine in brain injury rehabilitation. Brain Inj 1994; 8:709–718
 
27.Kraus MF, Maki PM: Effect of amantadine hydrochloride on symptoms of frontal lobe dysfunction in brain injury: case studies and review. J Neuropsychiatry Clin Neurosci 1997; 9:222–230
 
28.Kraus MF, Smith GS, Butters M, Donnell AJ, Dixon E, Yilong C, Marion D: Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj 2005; 19:471–479
 
29.Bay E, Kirsch N, Gillespie B: Chronic stress conditions do explain posttraumatic brain injury depression. Res Theory Nurs Pract 2004; 18:213–228
 
30.Fyffe CE, Kahng S, Fittro E, Russell D: Functional analysis and treatment of inappropriate sexual behavior. J Appl Behav Anal 2004; 37:401–404
 
31.Warriner EM, Velikonja D: Psychiatric disturbances after traumatic brain injury: neurobehavioral and personality changes. Curr Psychiatry Rep 2006; 8:73–80
 
32.Kim E: Agitation, aggression, and disinhibition syndromes after traumatic brain injury. NeuroRehabilitation 2002; 17:297–310
 
33.Gagnon J, Bouchard MA, Rainville C, Lecours S, St-Amand J: Inhibition and object relations in borderline personality traits after traumatic brain injury. Brain Inj 2006; 20:67–81
 
34.Jorge RE: Neuropsychiatric consequences of traumatic brain injury: a review of recent findings. Curr Opin Psychiatry 2005; 18:289–299
 
35.Simpson G, Tate R, Ferry K, Hodgkinson A, Blaszczynski A: Social, neuroradiologic, medical, and neuropsychologic correlates of sexually aberrant behavior after traumatic brain injury: a controlled study. J Head Trauma Rehabil 2001; 16:556–572
 
36.Zencius A, Wesolowski MD, Burke WH, Hough S: Managing hypersexual disorders in brain-injured clients. Brain Inj 1990; 4:175–181
 
37.Bezeau SC, Bogod NM, Mateer CA: Sexually intrusive behaviour following brain injury: approaches to assessment and rehabilitation. Brain Inj 2004; 18:299–313; erratum, 18:517
 
38.Lawrie B, Jillings C: Assessing and addressing inappropriate sexual behavior in brain-injured clients. Rehabil Nurs 2004; 29:9–13
 
39.Britton KR: Medroxyprogesterone in the treatment of aggressive hypersexual behavior in traumatic brain injury. Brain Inj 1998; 12:703–707
 
40.Briken P: Pharmacotherapy of paraphilias with luteinizing hormone-releasing hormone agonists. Arch Gen Psychiatry 2002; 59:469–470
 
41.Krueger RB, Kaplan MS: Depot-leuprolide acetate for treatment of paraphilias: a report of twelve cases. Arch Sex Behav 2001; 30:409–422
 
42.Saleh FM, Berlin FS: Sex hormones, neurotransmitters, and psychopharmacological treatments in men with paraphilic disorders. J Child Sex Abus 2003; 12:233–253
 
43.Hegel MT, Ferguson RJ: Differential reinforcement of other behavior (DRO) to reduce aggressive behavior following traumatic brain injury. Behav Modif 2000; 24:94–101
 
44.Tiersky LA, Anselmi V, Johnston MV, Kurtyka J, Roosen E, Schwartz T, Deluca J: A trial of neuropsychologic rehabilitation in mild-spectrum traumatic brain injury. Arch Phys Med Rehabil 2005; 86:1565–1574
 
45.Bell KR, Temkin NR, Esselman PC, Doctor JN, Bombardier CH, Fraser RT, Hoffman JM, Powell JM, Dikmen S: The effect of a scheduled telephone intervention on outcome after moderate to severe traumatic brain injury: a randomized trial. Arch Phys Med Rehabil 2005; 86:851–856
 
46.Cox WM, Heinemann AW, Miranti SV, Schmidt M, Klinger E, Blount J: Outcomes of systematic motivational counseling for substance use following traumatic brain injury. J Addict Dis 2003; 22:93–110
 
47.Carnevale GJ, Anselmi V, Johnston MV, Busichio K, Walsh V: A natural setting behavior management program for persons with acquired brain injury: a randomized controlled trial. Arch Phys Med Rehabil 2006; 87:1289–1297
 
48.Ghaffar O, McCullagh S, Ouchterlony D, Feinstein A: Randomized treatment trial in mild traumatic brain injury. J Psychosom Res 2006; 61:153–160
 
49.Bay E, Hagerty BM, Williams RA, Kirsch N, Gillespie B: Chronic stress, sense of belonging, and depression among survivors of traumatic brain injury. J Nurs Scholarsh 2002; 34:221–226
 
50.Hart T, Sherer M, Whyte J, Polansky M, Novack TA: Awareness of behavioral, cognitive, and physical deficits in acute traumatic brain injury. Arch Phys Med Rehabil 2004; 85:1450–1456
 
51.Noe E, Ferri J, Caballero MC, Villodre R, Sanchez A, Chirivella J: Self-awareness after acquired brain injury: predictors and rehabilitation. J Neurol 2005; 252:168–175
 
52.Sherer M, Hart T, Whyte J, Nick TG, Yablon SA: Neuroanatomic basis of impaired self-awareness after traumatic brain injury: findings from early computed tomography. J Head Trauma Rehabil 2005; 20:287–300
 
53.Schmitz TW, Rowley HA, Kawahara TN, Johnson SC: Neural correlates of self-evaluative accuracy after traumatic brain injury. Neuropsychologia 2006; 44:762–773
 
54.Hurt P: Mild brain injury: critical factors in vocational rehabilitation. J Rehabil 1990; 57:36–45
 
55.Wesolowski MD, Zencius AH: A Practical Guide to Head Injury Rehabilitation: A Focus on Postacute Residential Treatment. New York and London, Plenum Press, 1994
 
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