Letters to the Editor
Risperidone Treatment of Periodic Catatonia
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, gegenhalten, 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 tachypnea. 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, Mr A 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. He was discharged on risperidone (3 mg daily) on the 11th day. He scored 0 on the BFCRS at the time of discharge. The diagnosis at discharge was brief psychotic disorder.
Discussion
Substance-induced catatonia is a differential that cannot be entirely excluded in this presentation, as the patient’s drug screen might not have detected all substances. Another differential is nonconvulsive status epilepticus, but the EEG did not support this diagnosis. This patient experienced previous episodes of catatonia alternating with clearing of catatonic symptoms, which clinically defines periodic catatonia (1). Periodic catatonia therefore seems the likely diagnosis for this patient. Further, coexistence of both akinetic and hyperkinetic symptoms, with one pole predominating, is typical of periodic catatonia as manifested by this patient (4). The DSM-IV does not recognize the diagnosis of periodic catatonia, and most cases are diagnosed as catatonic schizophrenia. The periodic nature of this illness, coupled with the prompt resolution of symptoms and a negative organic work-up, might have led the internists in the medical ED to misdiagnose him as suffering from conversion disorder. This case calls for greater awareness among medical ED staff of catatonia generally and, specifically, of its periodic nature in some patients.
Psychotic symptoms (classified by Leonard under “unsystematic schizophrenia”) have been described in patients with periodic catatonia, which may partly explain risperidone’s effectiveness in treating this patient’s catatonia (1). Antipsychotic medications may alter the illness course in periodic catatonia and may have the potential to limit catatonic phases (1). A recent report describes the successful treatment of periodic catatonia with ziprasidone (5). Other reports describe the use of atypical antipsychotics such as risperidone and olanzapine for treating catatonia in general (3). However, the use of antipsychotics in catatonia treatment is a contentious issue, given reports that high potency antipsychotics precipitated or exacerbated catatonia or neuroleptic malignant syndrome (NMS), a variant of malignant catatonia (3). In this regard, some authors suggest adjunctive use of a benzodiazepine while the antipsychotic drugs are being introduced, in the hope that a benzodiazepine may reduce the risk of NMS (6). We cannot ascertain whether this patient would have responded to higher dosages of lorazepam. However, the dosage this patient received is in the range used by other investigators to treat catatonia (2). While benzodiazepines, ECT, or atypical antipsychotics have been used to treat the acute phase of periodic catatonia, more research is needed on the duration of treating the acute phase with these modalities, as well as on the treatment of interepisode residual symptoms.
References
1. Beld JT, Philbrick K, Rummans T. Periodic catatonia. In: Caroff SN, Mann SC, Francis A, Fricchione GL. Catatonia: from psychopathology to neurobiology. Washington (DC): American Psychiatric Publishing Inc; 2004. p 93–104.
2. Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia. II. Treatment with lorazepam and electroconvulsive therapy. Acta Psychiatr Scand 1996;3:137–43.
3. Fink M, Taylor MA. Catatonia. Cambridge (UK): Cambridge University Press; 2003.
4. Pfuhlmann B, Stöber G. The difference conceptions of catatonia: historical overview and critical discussion. Eur Arch Psychiatry Clin Neurosci 2001;251(Suppl 1):4–7.
5. Levy WO, Nunez CY. Use of ziprasidone to treat bipolar-associated catatonia. Bipolar Disord 2004;6:166–7.
6. Rosebush PI, Mazurek MF. Pharmacotherapy. In: Caroff SN, Mann SC, Francis A, Fricchione GL. Catatonia: from psychopathology to neurobiology. Washington (DC): American Psychiatric Publishing Inc; 2004. p 141–50.
Harpreet S Duggal, MD, DPM
Gaurav Gandotra, MD
Pittsburgh, Pennsylvania
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