Letters to the Editor
Response of Catatonic Schizophrenia to Amisulpride: A Case Report
Catatonia is a neuropsychiatric syndrome in which an abnormal mental state is associated with cataleptic phenomena; namely, akinesia, posturing, and mannerisms (1). Despite its emerging link to affective disorders, catatonia is still classified in DSM-IV as a subtype of schizophrenia. The prevalence is as high as 10% of all schizophrenia cases (2). Catatonia can be acute or chronic; therefore, treatment varies accordingly (3). Acute presentations are most effectively treated with high dosages of benzodiazepenes or with ECT (4,5). Case reports of treatment with antipsychotics exist (6,7). Chronic presentations prove more challenging to treat and have shown poor response to these standard therapies (3). We report a case of an individual with chronic catatonic schizophrenia who responded to amisulpride. To our knowledge, this is the first reported case of its kind in the literature.
Mr D, a 24-year-old white man, was hospitalized for catatonic schizophrenia at age 21 years. His symptoms included mutism, facial grimacing, posturing, and periods of catatonic excitement and stupor. Extensive laboratory evaluations and diagnostic imaging were all unremarkable. Scores on the Bush-Francis Catatonia Rating Scale (BFCRS) varied throughout his illness, with a high of 18. Adequate trials of lorazepam, ECT, loxapine, and olanzapine yielded minimal response. A trial of clozapine was undertaken with some symptom reduction and later augmented with lamotrigine. Subsequent neutropenia developed, leading to discontinuation of both drugs. The patient was started on risperidone and titrated to 6 mg daily in conjunction with lorazepam 6 mg daily. This combination produced moderate improvement after 2 months; however, for unclear reasons, the patient began refusing lorazepam. Significant extrapyramidal side effects (EPSE) developed, which necessitated a reduction in risperidone dosage, and subsequent clinical deterioration ensued. Augmentation with gabapentin and quetiapine proved ineffective. Amisulpride was then added to risperidone and titrated to 600 mg daily. After 2 months on this combination therapy, the patient began to engage in nonverbal communication. He achieved complete resolution of mutism after another 3 weeks. By the third month of amisulpride, all catatonic symptoms had resolved. The patient was discharged 6 months later on amisulpride 300 mg twice daily and risperidone 1.75 mg daily. His BFCRS score on discharge was 0.
Catatonia is thought to result from a hypodopaminergic state (8) but may also involve dysfunction in neurotransmission of GABA and glutamine (4). The use of antipsychotics in treating catatonic schizophrenia is controversial, because the therapeutic effectiveness is exerted through dopamine antagonism. In fact, catatonia is cited as a risk factor for developing neuroleptic malignant syndrome (NMS) (5). The acute catatonia in this individual did not respond to first-line agents (benzodiazepenes and ECT), leading to untreated illness and chronicity. Chronic catatonia may involve a different pathophysiologic mechanism of action than the acute counterpart (3), advocating for the use of antipsychotics to target the underlying psychotic illness. In our case, risperidone provided partial response and was maintained for this reason. Adding amisulpride alleviated Mr D’s catatonic symptoms dramatically. It remains to be determined, however, whether symptom resolution was attributable to amisulpride alone or to the combined therapy. Because receptor profiles in the 2 drugs differ, a degree of synergy may be in operation (9,10). This result may allow for further elucidation of the pathophysiologic mechanism of chronic catatonic schizophrenia and promote the judicious use of atypical antipsychotics in its treatment.
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Kelly French, MD
Diane Eastwood, MD
Halifax, Nova Scotia