Quetiapine treatment for mania secondary to brain injury in 2 patients.

Sir: In the only 2 studies that estimate prevalence of mania secondary to traumatic brain injury (TBI), Jorge et al. diagnosed mania in 9% of 66 consecutive brain-injured patients and Van Reekum et al. found 22% of 18 TBI patients developed a bipolar spectrum disorder after mild or moderate TBI. Both of these estimates are higher than the known lifetime prevalence of bipolar I disorder, which is 0.4% to 1.6%. Several other differences suggest mania secondary to TBI is phenomenologically distinct from primary mania. First, 4% to 24% of first-degree relatives of those with bipolar I disorder also have bipolar I disorder, but none of Jorge and colleagues’ subjects had a first-degree relative with bipolar disorder. Also, the average age at onset of mania is 20 years, but mania secondary to TBI has been reported in subjects aged as young as 10 years to as old as 70 years. Finally, brain injury–related bipolar disorder may result in more rapid cycling or prolonged manic states compared to primary mania. These phenomenological differences account for the controversy over considering these syndromes within the bipolar spectrum, as mood disorders secondary to general medical condition, versus neuropsychiatric sequelae of TBI. Regardless of how these disorders are characterized, medication management of psychiatric symptoms following TBI is commonplace. The pharmacologic management of mania secondary to TBI is complicated by animal studies suggesting some antiepileptics and antipsychotics interfere with cognitive or motor recovery. Rats exposed to diazepam after experimental brain injury had persistent sensorimotor asymmetry. Brain-injured rats treated with phenobarbital had significantly delayed recovery in somatosensory deficits. Phenytoin increases the severity of cortical hemiplegia in rats. Haloperidol impairs cognitive performance after traumatic brain injury in rats, retards motor recovery, and blocks the acceleration in motor recovery caused by amphetamine. No controlled trials of treating mania secondary to TBI have been published, but there are case reports of successfully using chlorpromazine and carbamazepine, haloperidol alone, haloperidol and chlorpromazine, haloperidol and clonezepam, clonidine, lithium alone, lithium and thioridazine, valproate alone, valproate and olanzapine, carbamazepine and lithium, and carbamazepine and chlorpromazine. Others have reported failed treatment with electroconvulsive therapy, carbamazepine, verapamil, neuroleptics, lorazepam, trazodone, alprazolam, phenelzine, valproate, phenytoin and clozapine, carbamazepine, and lithium. In an open-label flexible-dose study, Kim and Bijlani reported quetiapine was effective for treating irritability and aggression following TBI at doses from 25 to 300 mg/day. That study was only of the target symptoms of aggression and irritability, however, not the full syndrome of mania. We report the first 2 cases in the literature of mania secondary to TBI successfully treated with quetiapine.