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It has been reported that secondary mania may be caused by various solitary brain lesions. We present a case of a 59-year-old man with mania probably caused by a lacunar infarct in the red nucleus.

A 59-year-old man, who had no history of psychiatric disorders, was admitted to the psychiatric ward for irritable mood and hyperactivity. Twenty-one days prior to admission, he had a mild headache in the morning and suddenly fainted. Eighteen days after this fainting episode, he began to be too elated, with continuous singing and hyperactivity with walking and sleeplessness, with only 2–3 h of sleep each night. At admission, comprehensive physical examination, neurological examination and laboratory testing were normal. However, on brain magnetic resonance imaging there was evidence of a solitary subacute infarct in the right red nucleus. He was treated with valproic acid for the manic symptoms. After 11 days, the dose was increased to 1250 mg/day. Manic symptoms began to improve after 3 weeks’ treatment. His serum valproic acid level was 83.9 μg/ml (normal range = 60–125). When he was discharged 5 weeks after admission, he showed no manic symptoms. Two-week, 1-month and 2-month follow ups after discharge revealed no signs of mania and 1250 mg/day valproic acid continuation treatment was advised.

Frontal subcortical (FSC) circuits have been generally known to play a major role in the affective, motor and cognitive symptoms of a bipolar disorder.[1, 2] Many studies showed that solitary lesion in FSC circuits could be related to secondary mania.[1, 2] However, the present case report showed that secondary mania can be caused by solitary lesion in red nucleus which does not belong to the frontal subcortical circuit. Recently, some studies have suggested that red nucleus is associated with emotional processing, although red nucleus is not directly included in the frontal subcortical circuit.[3-6] Nioche et al.[3] reported that emotional connectivity was found between the red nucleus and subcortical loci (hypothalamus, substantia nigra, mesencephalic tegmentum) via the cerebello-rubro-olivo-cerebellar loop. Therefore, lack of modulatory effect of the red nucleus on the cerebellum via cerebello-rubro-olivo-cerebellar loop may lead to secondary mania in patients with rubral infarct.[5, 6]

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