Background Clozapine remains the cornerstone of treatment for treatment refractory schizophrenia. Clozapine has been shown to improve quality of life and cognitive functioning and to reduce hospital days in psychiatric patients. The impact of clozapine in a forensic population of psychiatric patients has not been studied. Methods This study is a naturalistic, retrospective database analysis of forensic patients hospitalized at the Northwest Missouri Psychiatric Rehabilitation Center from January 1, 1990 to August 1, 1999 who were treated with clozapine or haloperidol. Patients were either court ordered for hospitalization as having been found not guilty by reason of insanity or as incompetent to proceed to trial. Results Data from 84 patients (69 male, 15 female) were included in the analysis. The primary Axis I diagnoses were substance abuse (n = 61) and schizophrenia (n = 46). Patients had been treated with haloperidol (n = 78) and clozapine (n = 21), and some had received each agent as monotherapy during their course of treatment (n = 15). Assault (n = 22), armed criminal action (n = 18), and burglary (n = 18) were the primary forensic reasons for admission. Of those eligible to obtain a conditional release, 33% of haloperidol-treated patients and 38% of clozapine-treated patients obtained their conditional release on those medications. Haloperidol-treated patients were more likely to have their conditional release revoked (58.8%) versus those treated with clozapine (0%). Clozapine-treated patients were also more likely to stay on conditional release for longer periods of time. Global Assessment of Functioning (GAF) scores improved in both treatment groups; however, of 15 patients converted from haloperidol to clozapine, 93% (n = 14) saw improvements in GAP scores. Conclusions Clozapine and haloperidol effectively reduce psychosis and aggression. In our study, clozapine-treated patients were more likely to obtain a conditional release and stayed on conditional release for longer periods of time. Although the need exists to study this patient population more closely from a longitudinal standpoint, one may suspect that these findings represent a potential decrease in healthcare costs for the treatment of forensic psychiatric patients.
We sought to determine whether patients receiving valproate plus an antidepressant had significantly lower serum valproate levels before initiation of the antidepressant than those patients receiving valproate without an antidepressant. We further sought to identify the prevalence of antidepressant-induced mania and to determine if valproate provided a protective effect against antidepressant-induced mania. A computer database search from January 1, 1990-June 30, 1998, identified patients with bipolar or schizoaffective disorder treated with valproate. Patients receiving an antidepressant during valproate therapy were identified as the treatment group (9 patients), and the remaining patients served as the control group (17 patients). Serum valproate levels were recorded just before starting the antidepressant for the treatment group and monthly during a comparable period for the control group. The mean time to antidepressant initiation was 15 +/- 8 weeks. The mean serum valproate level just before antidepressant initiation was significantly lower for the treatment group compared with the mean serum valproate level averaged over 16 +/- 6 weeks for the control group (54 +/- 24 vs 73 +/- 13 microg/ml, p<0.05). Four patients (44%) developed antidepressant-induced mania. Three required discontinuation of the antidepressant; their serum valproate levels were 54, 60, and 71 microg/ml. Patients requiring the addition of an antidepressant had significantly lower valproate serum levels than those who did not require an antidepressant. Further study is necessary to determine whether higher serum valproate levels are needed for prevention of depressive symptoms in bipolar and schizoaffective disorders.
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