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To the Editor: Traumatic brain injury is often associated with psychiatric disorders (1). Impulsivity, affective instability, and disinhibition are the most frequent neuropsychiatric symptoms associated with traumatic brain injury, while depression, mania, and obsessive-compulsive disorder (OCD) are less frequent (2). To our knowledge, there are no reports of successful treatment of posttraumatic OCD.
Mr. A, an 18-year-old man, suffered severe head trauma in a car accident. Ten months after the head trauma, he had normal results on a neurologic examination and seemed to be in a good general state of health, but he reported severe checking compulsions and obsessions and greater impulsivity. Two years after the accident, he was referred to our psychiatric hospital and scored a total of 30 on the Yale-Brown Obsessive Compulsive Scale (3). He had no other psychiatric disorders.
Magnetic resonance imaging showed multiple lesions affecting the right ventral-lateral prefrontal cortex, the orbital-frontal cortex bilaterally, the right anterior temporal lobe, the corpus callosum, and adjacent white matter regions. [123I]β-Carbomethoxy-3-(4-idiophenyl)-tropane ([123I]β-CIT) single photon emission computed tomography (SPECT), which was performed as part of an ongoing study (4), showed lower serotonin transporter density (two standard deviations below that of age-matched comparison subjects) in the midbrain and hypothalamus.
Mr. A was treated with up to 60 mg/day of fluoxetine for 90 days and showed a good clinical response. His compulsions were more dramatically reduced than his obsessions. His score on the Yale-Brown Obsessive Compulsive Scale decreased from 30 to 10, which was associated with great improvement in his quality of life.
OCD has rarely been described after traumatic brain injury (1, 2), and we know of no reports of its successful treatment. The impression to be gotten from case reports and small case series is that the same medications that have been found to be effective in treating primary OCD—namely, selective serotonin reuptake inhibitors (SSRIs) (5)—are effective in treating secondary (organic) OCD (6).
Findings from neuroimaging and neuropsychological studies implicate dysfunctions of the frontal-orbital-striatal circuits in the pathophysiology of idiopathic OCD (7). We suggest that structural damage to the frontal-orbital-striatal circuits is a direct cause of secondary (organic) OCD.
In addition, our patient showed lower serotonin transporter density in [123I]β-CIT SPECT, and his compulsions responded favorably to SSRI treatment. This might be explained by a lower number of serotonin neurons ascending from the raphe nuclei, accompanied by lesions in the orbital-frontal circuits known to be involved in OCD after traumatic brain injury.
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