Psychosomatics 48:67-70, January-February
doi: 10.1176/appi.psy.48.1.67
© 2007 Academy of Psychosomatic Medicine
Affective Disorder and Personality Change in a Patient With Traumatic Brain Injury
Sharon F. Handel, M.D.,
Linda Ovitt, M.S.N.,
Jennifer R. Spiro, M.S., and
Vani Rao, M.D.
Received January 4, 2006; revised February 10, 2006; accepted March 20, 2006. From the Division of Geriatric Psychiatry and Neuropsychiatry, Dept. of Psychiatry, Johns Hopkins School of Medicine, Baltimore, MD, and the Brain Injury Clinic, Community Psychiatry Program, Dept. of Psychiatry, Johns Hopkins Bayview Medical Center, Baltimore, MD. Send correspondence and reprint requests to Vani Rao, M.D., Assistant Professor, Dept. of Psychiatry and Behavioral Sciences, Division of Geriatric Psychiatry and Neuropsychiatry, 550 N. Broadway, The Johns Hopkins Hospital, Baltimore, MD 21205. e-mail: vrao{at}jhmi.edu
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INTRODUCTION
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Traumatic brain injury (TBI) is a major public health problem in the United States. The medical and psychiatric consequences of TBI are often dire, and these consequences permeate the patient’s life at all levels. Although medical disabilities usually stabilize after rehabilitation, psychiatric consequences can cause chronic handicaps that often do not receive appropriate attention and treatment. Common post-TBI psychiatric comorbidities include affective, cognitive, and behavioral disorders.1 The prevalence of psychiatric diagnoses in these patients is much higher than in the general population,2 and up to 44% of patients suffer from more than one psychiatric disorder.3 Unfortunately, the symptoms of psychiatric conditions are often accepted as "normal" reactions to a devastating event. Without a diagnosis, TBI patients are deprived of appropriate treatment for prolonged periods. During this critical period, symptoms worsen and the consequences are compounded.
A comprehensive evaluation to determine the presence of psychiatric disorders is essential for TBI patients. The detection of psychiatric phenomena affects crucial decisions that will set the pace for treatment and increase the likelihood of successful rehabilitation. We present a case that demonstrates how one patient suffered from several psychiatric conditions after a TBI. As each problem arose, reevaluation and reformulation were essential in order to institute an appropriate and effective treatment plan. Furthermore, close follow-up was important so as to ensure that that his progress in rehabilitation would be sustained. Despite their characterization as a group with poor prognosis, TBI patients not only benefit from treatment but also can return to meaningful and productive lives. Our case represents this expectation of optimism and is an example of our wider clinical experience.
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Case Report
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"Mr. K" is a 58-year-old married white man who was referred to our Brain Injury Clinic for evaluation of mood and behavioral changes that developed after a motorcycle accident. His family history is unknown because he was adopted. His birth and early childhood development were reportedly unremarkable. He obtained a bachelor’s degree in electronic technology and worked as an electrical technician for over 20 years, achieving the level of supervisor/manager. After his company closed, he worked as a truck driver until his accident. He has been happily married for 31 years and has no children. He has no history of alcohol or illicit drug abuse. Before the accident, he had no significant medical problems or past psychiatric history. His premorbid personality was described by his wife as lively and outgoing, as a "chronic kidder and joke-teller," and a "go-getter with workaholic tendencies."
In 2000, Mr. K sustained a traumatic brain injury in a motorcycle accident. There were no witnesses at the scene. He was air-lifted to a local hospital, where he remained for about 2 weeks. There is no record of the Glasgow Coma Scale score. The initial head computerized tomography (CT) scan revealed a subarachnoid hemorrhage, primarily involving the left fronto-parietal regions, which did not require neurosurgical intervention. He was maintained in an induced coma for 13 days, after which he was transferred to a rehabilitation center for another 10 days. He was then discharged home, where he continued his rehabilitation. Less than 1 year after the accident, he attempted to return to work as a truck driver. He had difficulty following instructions and was easily overwhelmed when attempting multi-step tasks. He became withdrawn and excessively worried about money despite the couple’s financial stability. He developed nihilistic delusions about his lack of resources and convictions about impoverishment. His mood, sleep, appetite, interest in self-care, and participation in day-to-day activities declined. Eventually, he stopped working. Mr. K was then seen for the first time by a psychiatrist, who started him on mirtazapine and olanzapine.
A medical work-up done at this time showed a normal EEG. Neuropsychological tests revealed a full-scale IQ on the WAIS–III of 115. Scores on verbal subtests of abstract reasoning, general fund of information, social judgment/reasoning, numerical reasoning, and auditory attention/concentration were normal except for reciting digits in reverse order (37th percentile), consistent with difficulty attending to, maintaining, and manipulating auditory material over a brief period of time. Scores on the performance subtests ranged from normal to superior, except for the symbol-digit task (37th percentile), which was correct but slow, consistent with difficulty in cognitive speed and efficiency. On more specific tests of executive functioning, performance on Trails A and B were normal. However, his performance on nonverbal abstract reasoning and problem-solving tests showed perseverative errors (19th percentile), consistent with difficulty conceptualizing alternative approaches with abstract material. Spontaneous word-production was quite impaired (3rd percentile). His performance on measures of memory functioning ranged from low-average to high-average scores. He also had difficulty on tests of fine motor manipulation and gross motor strength (3rd–16th percentiles).
When several months passed with minimal progress, he was referred to our brain injury clinic. His primary symptoms at this time included depression, insomnia, lethargy, loss of interest in usual activities, inability to make decisions, lack of motivation, and feelings of worthlessness. He would sit for hours at a time doing nothing, and there was real concern that patient had an abulic syndrome as a result of injuries to his frontal lobes. After a complete neuropsychiatric evaluation, he was diagnosed with major depression. An MRI scan of the brain revealed cerebral atrophy with left frontal and right fronto-parietal encephalomalacia. Since he had had some response to the mirtazapine at 15 mg, it was titrated up to 30 mg, and the olanzapine was discontinued. On this higher dose, the patient’s initiative, motivation, and mood gradually returned to baseline. He continued regular follow-up. However, about 1 year later, he asked to end his treatment, stating that he had stopped taking his medications a few months ago. The clinicians were concerned about discharging him because he appeared mildly disinhibited, overly enthusiastic, and slightly socially inappropriate. However, his wife insisted that this was close to his pre-TBI baseline. After long discussions about the risks and benefits of not being in treatment, he was discharged.
One month later, the patient’s wife called to make an urgent appointment. She reported that her husband had been unusually cheerful, talking "nonstop," and spending excessive amounts of time in karaoke bars, and that he had become uncharacteristically preoccupied with Internet pornography. He was evaluated immediately. His mental status examination revealed elevated mood, expansive self-attitude, and energized vital sense. His diagnosis was reformulated to Bipolar Disorder, Manic, and lithium carbonate was started. However, the patient developed bilateral lower-extremity edema, with a negative medical work-up. Lithium was discontinued; the edema resolved, and he was started on sodium valproate. As the valproate dose was titrated upward, his mood symptoms gradually improved, and he was more efficient in his cognitive functioning, with better impulse-control.
He has continued to attend follow-ups regularly in the Brain Injury Clinic. His mood and behavioral symptoms have stabilized, with no further episodes of depression or mania, but he has remained mildly irritable, disinhibited, flirtatious, and impulsive, and has limited insight into his socially inappropriate behavior. Because these symptoms have been persistent, not associated with a primary change in mood, and neither episodic nor intermittent, "Personality Changes Associated With TBI" was diagnosed. Adjustment of valproate and the addition of escitalopram oxalate did not help these symptoms. However, he has benefited from regular cognitive-behavioral psychotherapy with a focus on maintaining structure and routine in his daily activities. His wife states that this new baseline is on a continuum with "an exaggeration" of his premorbid personality, but with much poorer social judgment. She has needed frequent education about mood disorders and personality changes associated with TBI. Mr. K has been unable to maintain steady employment but has been successful in a voluntary capacity.
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Discussion
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This case illustrates several important clinical points and raises an important research question. First, patients may not seek an early evaluation of psychiatric symptoms because the physical, emotional, and cognitive symptoms are often misattributed solely to the presence of TBI. In the case presented, treatment was sought months after the onset of increasingly severe symptoms, when his wife realized that the change in mood, beliefs, and behavior could no longer be explained as exclusively situational.
Second, major depression is very common after TBI, with a prevalence rate of about 25%–40%.4,5 Although syndromes such as major depression are sometimes influenced and altered by underlying brain pathology, classic presentations are common, with hopelessness, worthlessness, and difficulty enjoying activities being the most characteristic of the diagnosis.5,6 When he presented to our clinic, Mr. K had several classic symptoms, including depressed mood, anhedonia, decreased self-esteem, and mood-congruent delusions. Research also suggests that post-TBI depression is a complex, heterogeneous syndrome, with subtypes based on the clinical presentation, time at onset of symptoms, and brain pathology.7 Depression occurring soon after TBI is associated with lesions in the left dorsolateral prefrontal cortex and/or left basal ganglia regions, but this relationship is absent in delayed-onset depression.4,8 Although the functional deficits may be numerous and varied, the most consistent finding on neuropsychological testing is poor performance on tests of frontal-lobe functions.4 Mr. K clearly had both neuroimaging and neuropsychological evidence of frontal-lobe dysfunction.
Third, Mr. K’s positive response to a combination of pharmacotherapy and psychotherapy (mainly supportive and cognitive-behavioral), is also common.5,9 Unfortunately, his opting to discontinue treatment is also not unusual in people with brain injury, because psychiatric symptoms are often considered a natural reaction to the trauma. The desire to return to some sense of normalcy can override the recognition that maintenance treatment can prevent further exacerbations and consequences. This report highlights the need for ongoing follow-up to continue a process of adaptation and acceptance that will return patients to productive activities and foster the achievement of their full potential.
Although the initial elevation in his mood was thought to be a return to euthymia, the continued and increased elevation was clearly pathological, resulting in the diagnosis of Bipolar Disorder, Mania. Secondary mania has been described in a variety of settings involving brain damage and stimulation.10 The clinical features of episodic elevated mood; increase in goal-directed activity; rapid, pressured speech; and increased energy are diagnostic of mania.11 This aspect of his illness made diagnosis challenging and required reformulation and changes in treatment from antidepressants to mood-stabilizers such as lithium and divalproex. Some studies suggest that valproate is more effective and better tolerated than lithium.10–13 Anticonvulsants improve the affective lability associated with TBI and may suppress the subcortical kindling due to denervation hypersensitivity in limbic structures that results from orbitofrontal damage.8,12,14
Finally, as his affective disorder entered remission, he began to exhibit personality changes commonly seen after TBI: disinhibition, impulsivity, and inadequate self-monitoring of interpersonal behavior.15 The manifestation of these emotional and behavioral difficulties is generally multifactorial and involves contributions from brain, premorbid personality, and environmental variables.16 Management of such symptoms often requires setting limits, maintaining structure, redirecting negative behavior, and reinforcing positive behavior,17 as well as pharmacologic approaches. Personality changes associated with TBI can be difficult to differentiate from mania or hypomania; regular follow-up and history from family regarding premorbid personality and the nature, frequency, and duration of symptoms helps to establish the diagnosis.
Treatment of the TBI patient should be proactively expanded to include an important, and often neglected, component: the caregiver. The caregiver should be given the opportunity to discuss problems and be encouraged with progressive education. The stresses of caregiving should also be emphasized, and caregivers may be given instructions or "prescriptions" about how to find support, relief for their own distress, and periodic respite from the demands of the patient.
Finally, there is limited literature on the risk factors and treatment of mood disorders and personality changes after TBI. Research on possible biopsychosocial risk factors and screening tools may lead to earlier identification of at-risk patients and more rapid diagnosis after TBI. Early appropriate treatment of these at-risk patients may improve outcome and prevent future adverse consequences.
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Conclusion
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Mr. K. experienced a broad set of psychiatric symptoms and disorders that were to be expected, given the results of his neuropsychological testing and neuroimaging studies, but which responded well to specific treatment of each, resulting in improved quality of life. Our clinical experience with other patients who have sustained a TBI suggests that his experiences are not the exception, but rather, the rule. Thus, we recommend that patients with TBI who have a change in mood and behavior undergo a thorough psychiatric evaluation for specific diagnoses; that they receive individualized treatment plans; and that they remain in active follow-up in order to refine treatment and monitor for the emergence of new disorders.
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ACKNOWLEDGMENTS
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The authors thank Dr. Peter Rabins for his guidance in preparing this manuscript.
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REFERENCES
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INTRODUCTION
Case Report
