Dear Editor: Periodic catatonia is an enigmatic and underrecognized clinical entity that has mostly been described in European literature (1). Benzodiazepines remain the first-line treatment for catatonia because of their favourable efficacy and side effect profile. Patients failing to respond to benzodiazepines have been shown to respond to electroconvulsive therapy (ECT, 2). The use of atypical antipsychotics to treat catatonia remains anecdotal, owing to concerns that they may worsen catatonic symptoms (3). We report the use of risperidone in a patient with periodic catatonia whose symptoms did not improve with a benzodiazepine trial; we also discuss the role of atypical antipsychotics in treating catatonia. Case Report The morning before he presented, Mr A, aged 28 years, was found by his mother to be acting strange. He was mute, did not respond to any commands, kept staring into empty space, and sat curled up on the floor for hours without changing his posture. He refused to eat or drink anything and was brought to the medical emergency department (ED). He had a normal head CT, EEG, and blood work-up (including electrolytes, liver and renal function tests, and blood counts). His urine drug screen was negative. He was subsequently transferred to the psychiatric ED with a diagnosis of conversion disorder. On examination, Mr A was alert, awake, and fully oriented. He exhibited psychomotor retardation and rigidity. In addition, he exhibited catatonic signs, including mutism, negativism, staring, posturing, waxy flexibility, gcgenhalten, automatic obedience, urinary incontinence, and ambitendecy. Interspersed with these symptoms were stereotypic movements and facial grimacing. He scored 38 (out of a maximum of 69) on the Bush-Francis Catatonia Rating Scale (BFCRS, 2). There were no focal neurological deficits, and vital signs revealed tachycardia and tachypnca. Interestingly, Mr A had experienced 4 prior episodes of catatonia over the past 5 years. These episodes lasted from a few hours to 1 week. His first catatonic episode was successfully treated with risperidone, but neither he nor his family remembered the dosage of the medication or the duration of treatment. During his last catatonic episode 1 month earlier, which lasted a few hours, Mr A had become extremely agitated while in the medical ED and was given 5 mg of parenteral haloperidol. This single dose resulted in a dramatic resolution of his symptoms. The patient was subsequently discharged without any psychiatric referral. There was no history of treatment with ECT, and he had a normal head CT and EEG during these episodes. The family history was unremarkable. During the index episode, MrA had received 2 mg of lorazepm in the medical ED, with minimal response. After admission to psychiatry, he was continued on lorazepam, up to 4 mg daily; however, he showed no change in his symptoms over the next 2 days, and lorazepam was then tapered in another couple of days. ECT was considered as an option, but given the past response of his catatonia to antipsychotics (specifically, risperidone and haloperidol), we decided to treat him again with risperidone. Mr A was started on risperidone at 1 mg daily 3 days after admission, and 3 days after commencing risperidone, the catatonia began to improve. The patient began to communicate more and reported feeling snapped from stress after a recent break-up with his girlfriend. He provided a history of past depressive symptoms but denied having depressive symptoms just preceding the catatonia. He endorsed auditory hallucinations of a male voice but was not sure about the content. There was no evidence of delusions and he denied any recent drug or alcohol use. Risperidone was increased to 3 mg on the sixth day of admission, with improvement in the remaining catatonic signs. Mr A was no longer incontinent and disorganized and was eating properly and maintaining his hygiene. Hc was discharged on risperidone (3 mg daily) on the 11th day. …
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