An open-label trial of buspirone in the treatment of tardive dyskinesia

An open-label trial of buspirone in the treatment of tardive dyskinesia

Schizophrenia 48 BIOL PSYCHIATRY 199| ~ng:43A-| 85A 65A PERFORMANCE OF SCHIZOPHRENIA SPECTRUM MEMBERS ON CONTINUOUS PERFORMANCE TESTS Jackie Mosko...

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Schizophrenia

48

BIOL PSYCHIATRY 199| ~ng:43A-| 85A

65A

PERFORMANCE OF SCHIZOPHRENIA SPECTRUM MEMBERS ON CONTINUOUS PERFORMANCE TESTS Jackie Moskowitz, M.A., Richard S.E. Keefe, Ph.D., Philip D. Harvey, Ph.D., Jeremy Silverman, Ph.D., Larry J. Siever, M.D., Richard C. Mohs, Ph.D. Bronx VA Medical Center and Mount Sinai School of Medicine, New York, NY 10029. Unmedicated schizophrenic patients (n = |81, patients w i ~ schizotypal personality disorder ¢n = I7L first-degree relatives of schizophrenics (n = 19L and an ~fective control group ~n = 15) were compared on two versions of the Continuous Performance Test (CPTt: a 3-7 ve~ion and a V ~ a b l e Continues Performance Test (VCPT), a single digit identical pairs version. For both the affec,tive and schiz~ypal group, performance on the two tasks was not significantly different. For both schizophrenic sample and the sample of first-degree relatives, the number of errors on the VCPT was significantly (p < 0.05t increased relative to the standard version. The initial impression might be that the VCPT is an improvemer~t over the standard version, in that there is increased ,~ariation in the performance of the relatives. However, the correlation between errors on the VCPT and the number of schizotypat symptoms in the relatives was nonsignificant (r = - 0.18), whereas the correlation between errors on the standard CPT and the number of schizotypai in relatives was .52 (p < 0.05). The data suggest the need to carefully monitor ~ e concurrent validity of different potential vulnerability markers and suggest that manipulations ~at increase marker task variability will not always lead to increases in valid identificatioa of vulnerabiliD' factors.

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AN OPEN-LABEL TRIAL OF BUSPIRONE IN THE TREATMENT OF TARDIVE DYSKINESIA Samuel Brown, M.D., William O. Faustman, Ph.D., Robert Mone, M.A., Kyungtak Minn, M.D., Debra Harris, M.D., John W. Newcomer, M.D., Paul B. Hicks, M.D., John G. Csernansky, M.D. Napc State Hospital Biological Ps)'chiato" Treatment and Research Unit and Stanford/VA Mental Health Clinical Research Center Collaborative Project; Program 2, Napa State Hospital, Napa, CA 94558. In animal models Buspirone can reverse neuroleptic-ioduced increases in striatal dopamine receptor binding and reverse neuroleptic-induced catalepsy. We evaluated the ability of Buspirone to reduce abnormal movements in 10 patients with tardive dysklnesia. Patients had a global rating of at least moderate on the Gerlach Abnormal Movements Rating Scale at entry. Patients were maintained on a stable medication regime. Following a 2-week baseline, Buspirone was increased to 40 rag/day (10 mg QID) over a 2-week pefit~d. Patients were maintained at this dose for 6 weeks and were rated weekly by two independent ra~rs using the Gerlach. BPRS. and CGI. Compare.son of endpoint ratings (8 weeks of Buspirone tx) to baseline ratings revealed no clinically significant (:> 50%) change in global item ratings of tardive dyskinesia in group or individual data. Though some patients showed mild improvements Luring Buspirone treatmeat. nonparametric comparisons of baseline to endpoint symptoms were not statistically significant for the sum of squared hyperkinesia items, the sum of raw hyperkinesia items, or the global item. (Supported by MH 30854 and The State of California.)