To the Editor: Two previous case reports have suggested that hydrocephalus is associated with mood cycles, including manic and depressive episodes. In both cases, mood symptoms were unresponsive to pharmacologic treatment, but resolved after surgical treatment.1,2 Here we report a case of a manic episode associated with normal pressure hydrocephalus. The manic but not the depressive symptoms showed a good response to aripiprazole treatment before surgery. However, because mood symptoms remained after surgery, treatment with aripiprazole was continued at the same dose. Case report: Mr A, a 61-year-old man, suffered from irritability, hypertalkativeness, a decreased need for sleep, grandiosity, and aggression toward his family 1 month previously. According to his family, he was healthy, with good social functioning before admission. Three months ago, a sudden onset of depressive mood, urine incontinence, memory impairment, and ataxia occurred. He was sent to a local hospital and bupropion (150 mg/d) was prescribed. The depressive mood was mildly improved. After admission, Mr A received quetiapine (100 mg/d) to treat manic symptoms (per a DSM-IV diagnosis of mania). However, significant extrapyramidal side effects (EPS) appeared, including tremor, salivation, and akathisia. Meanwhile, urine incontinence and ataxia recurred. Brain magnetic resonance imaging revealed ventricular dilatation, and normal pressure hydrocephalus was diagnosed. After about 1 week, medication was switched to aripiprazole 10 mg/d. The manic symptoms improved significantly within 2 weeks. No EPS were noted. A ventriculoperitoneal (VP) shunt was performed when manic symptoms became stable. Mr A was discharged 6 weeks later in a stable mood condition, but with minor impairments of cognitive function. Studies discussing pharmacologic treatment of manic episodes associated with hydrocephalus are scarce. Contrary to previous reports, our patient showed a good response to aripiprazole (10 mg/d). Aripiprazole is an atypical antipsychotic that has a unique partial agonistic effect at D2 receptors. Its efficacy and safety in the treatment of manic episodes have been demonstrated.3 Interestingly, 2 recent positron emission tomography studies demonstrated that the binding of striatal D2 receptors was reduced in normal pressure hydrocephalus4 and up-regulated after VP shunting.5 Moreover, both studies showed that changes in striatal D2 receptors were correlated with improving emotional and cognitive function. Therefore, our case indicates that antipsychotic agents with partial D2 receptor agonistic effects could stabilize the dopamine neurotransmitter system and help in the treatment of the psychological changes associated with hydrocephalus.
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