Psychosomatics 48:433-435, September-October 2007
doi: 10.1176/appi.psy.48.5.433
© 2007 Academy of Psychosomatic Medicine
Manic Behavior Resulting From Left Frontal Closed Head Injury in an Adult With Fetal Alcohol Syndrome
Jeremy R. Camden, M.D.S., and
David R. Spiegel, M.D.
Received July 7, 2006; accepted October 5, 2006. From Eastern Virginia Medical School Department of Psychiatry and Behavioral Sciences, Norfolk, VA. Send correspondence and reprint requests to David R. Spiegel, M.D., Eastern Virginia Medical School Department of Psychiatry and Behavioral Sciences, 825 Fairfax Ave., Norfolk, VA 23507. e-mail: spiegedr{at}evms.edu
©2007 The Academy of Psychosomatic Medicine
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ABSTRACT
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Closed head trauma has been associated with various neuropsychiatric sequelae, including mood disturbances such as depression and mania. Although mood disturbances can occur with injury to either hemisphere, mania has been primarily associated with right-side frontal lobe injury. We present a case of manic behavior after a closed head injury to the left hemisphere in an adult with preexisting fetal alcohol syndrome.
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INTRODUCTION
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Closed head injuries are one of the most common reasons for emergency hospital admissions. Development of manic behavior from these head injuries has often been recognized as a rare outcome. Most cases of secondary mania have been associated with right frontal-lobe injury, whereas case reports of similar behavior change with left-side frontal damage are rare.1–4 We report a case of manic behavior after a closed head injury to the left hemisphere in an adult with preexisting fetal alcohol syndrome.
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Case Report
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"Mr. C" is a 19-year-old African American man with a history of fetal alcohol syndrome (low birth weight and learning disability) and one episode of anxiety during high school that was not medically treated. He had no physical health problems, and there was no family history of mental illness. The patient is a high school graduate but was in "special education" classes from kindergarten through 12th grade.
Mr. C. was a pedestrian in a motor vehicle-versus-pedestrian accident while he was attempting to cross the highway. He was taken to a local hospital, where he was found to have a closed head injury with a mild subarachnoid hemorrhage, left tibial fracture, left open dislocation of the elbow and distal humerus, and a right forehand laceration. Computerized tomography (CT) scan of the head without contrast revealed complex fractures involving the floor of the anterior cranial fossa, sphenoid bone, and the left orbit. The fracture extended through the cribiform plate to the left orbital roof with a small bony spicule projecting into the left orbital gyrus frontal lobe, causing parenchymal contusion and subarachnoid bleeding (Figure 1 [A]). Repair of the complex lacerations to the face and open reduction and internal fixation of the left upper- and lower-extremity fractures were performed. Eight days after his initial injury, a repeat head CT without contrast revealed a moderate-sized area of encephalomalacia in the left frontal lobe, measuring 4.4 x 2.5 cm (Figure 1 [B]). His subarachnoid hemorrhage resolved, and he was transferred to our hospital 2 months later for continued physical, occupational, and speech therapy.
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FIGURE 1. Head Computed Tomography (CT) Without Contrast Studies After Closed Head Injury
[A]: Initial injury with a bony orbital roof spicule projecting into the left orbital gyrus frontal lobe, causing subarachnoid hemorrhage. [B]: Evolution of hemorrhagic contusion injury into a large area of encephalomalacia 8 days after initial injury.
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After admission to the inpatient rehabilitation department in our hospital, the patient was noted to have developed rapid, pressured speech, tangential thought process, decreased need for sleep, increased energy, elevated mood, and hyperactivity. He was not hypersexual, hyperreligious, grandiose, or delusional. The patient scored 32 on the Young Mania Rating Scale, indicating moderate mania or hypomania. The patient also was noted to have developed an intermittent, lateral, darting, left eye movement secondary to the injury to his left orbit. He was determined not to have social or occupational impairment, and he was discharged without any psychiatric medication after he completed his rehabilitation.
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Discussion
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Secondary mania later develops in patients mainly after brain lesions that are located in limbic or limbic-related areas (orbitofrontal and basotemporal cortex, head of caudate, and thalamus) that have strong connections with the frontal lobes.1 Most studies have also suggested that brain asymmetries may play an important role in the production of disinhibited behaviors and that the development of a disinhibition syndrome may require both a lesion in a specific brain area and the involvement of the right hemisphere.1,2 However, there have been rare case reports of mania after left-frontal lesions that argue against the suggested association of mania with right-hemisphere lesions.3,4 Although the mechanisms implicated in the pathogenesis of secondary mania have not been established, this case adds to the growing evidence that head injury may be directly causative in affective disorders, and it is premature to conclude that secondary mania is primarily associated with lesions of the right hemisphere.
This patient had a brain lesion localized to the left frontal gyrus. He had no known risk factors for affective disorder. Relevant risk factors for the development of a post-brain injury disinhibition syndrome may include genetic predisposition for affective disorders.2 This patient had no family history of affective disorders; however, he was exposed to alcohol during fetal CNS development.
Fetal alcohol exposure is a serious problem; 1 in 100 live births show fetal alcohol syndrome or alcohol-related neurodevelopmental disorder.5 CNS involvement in fetal alcohol syndrome results in small brain size and brain malformations, with possible functional deficits that include moderate mental retardation, delayed motor development, poor coordination, tremulousness, hyperactivity, and poor attention span. The only published study of psychiatric diagnoses in adults with fetal alcohol syndrome or fetal alcohol effects found a high risk of psychopathological conditions in these adults.6 This case suggests that exposure to alcohol during fetal CNS development may predispose to manifestation of disinhibited behaviors after traumatic brain injury. The relationship between gestational alcohol exposure and subsequent mental illness after brain injury would therefore be an important next step for examination.
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REFERENCES
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- Starkstein SE, Boston JD, Robinson RG: Mechanisms of mania after brain injury. J Nerv Ment Dis 1988; 176:87–100[Medline]
- Starkstein SE, Robinson RG: Mechanism of disinhibition after brain lesions. J Nerv Ment Dis 1997; 185:108–114[CrossRef][Medline]
- Benjamin S, Kirsch D, Visscher T, et al: Hypomania from left frontal AVM resection. Neurology 2000; 54:1389–1390[Free Full Text]
- Lim LC: Mania following left hemisphere injury. Singapore Med J 1996; 37:448–450[Medline]
- Sampson PD, Streissguth AP, Bookstein FL, et al: Incidence of fetal alcohol syndrome and prevalence of alcohol-related neurodevelopmental disorder. Teratology 1997; 56:317–326[CrossRef][Medline]
- Famy C, Streissguth AP, Unis AS: Mental illness in adults with fetal alcohol syndrome or fetal alcohol effects. Am J Psychiatry 1998; 155:552–554[Abstract/Free Full Text]
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ABSTRACT
INTRODUCTION
