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Gender differences in neuroleptic-refractory chronic schizophrenic disorder patients were examined to determine whether a superior or equivalent antipsychotic response in women vs. men existed similar to that of the general schizophrenic population. Sixty-nine DSM-III schizophrenic patients (47 males and 22 females) were treated with clozapine using a standardized medication regime. The gender differences in these neuroleptic-nonresponsive chronic schizophrenic disorder patients differed from those previously observed in the general schizophrenic population in that an equivalent antipsychotic treatment response in females versus males was not found. These treatment-refractory women appear to be a severely ill subgroup of female schizophrenics with distinct onset of illness, course and treatment response characteristics.

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BACKGROUND: Current hypotheses about the neuroanatomical structures involved in obsessive-compulsive disorder (OCD) suggest abnormalities in cortical-striatal-thalamic-cortical circuits. This study examined selected brain regions within or adjacent to these circuits. METHODS: Magnetic resonance imaging scans from 26 patients with OCD and 26 healthy controls were analyzed to determine the volumes of the following structures: prefrontal cortex (cortex anterior to the genu of the corpus callosum), caudate nucleus, lateral and third ventricles, and whole brain. RESULTS: Patients with OCD had significantly smaller caudate nucleus volumes than controls (F[1,48] = 9.4, P = .004) but did not differ in prefrontal cortex size or in volumes of the lateral or third ventricles. Structural volumes were not significantly correlated with the duration or severity of OCD symptoms. CONCLUSION: Our findings provide additional evidence for pathological involvement of the caudate in OCD.

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OBJECTIVE: The purpose of this study was to determine if plasma clozapine levels were associated with treatment response. METHOD: To examine this question, neuroleptic nonresponsive patients with schizophrenia or schizoaffective disorder were given clozapine, which was titrated to 500 mg/day by day 14 of treatment, and the dose was held fixed at least through day 21. Subsequently, clozapine doses were adjusted as clinically indicated, up to a maximum of 900 mg/day. Plasma clozapine levels were obtained at weeks 3 and 6, and standard clinical ratings (Brief Psychiatric Rating Scale [BPRS] and Clinical Global Impression) were done at baseline and at weeks 3 and 6. RESULTS: Data from 45 subjects were analyzed. There were no correlations between plasma clozapine levels and change in BPRS scores at treatment weeks 3 and 6. However, when the subjects were classified as responders or nonresponders, therapeutic response was associated with clozapine blood levels above 350 ng/ml. CONCLUSIONS: This study suggest that clozapine blood levels are correlated with clinical response.

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BACKGROUND: We compared three doses of a neuroleptic as a treatment for mania. METHOD: Forty-seven newly admitted in-patients with mania were randomised to receive 10, 30, or 80 mg a day of oral haloperidol, under double-blind conditions for up to six weeks. All subjects received prophylactic benztropine. RESULTS: Repeated-measures analysis of variance and survival analysis showed no difference in outcome by the different doses. Excluding drop-outs (38%), most of whom left the study during the first two weeks, 72% of the subjects responded. Side-effects were minimal; there were no differences among the three doses. Non-responders received more adjunctive lorazepam than responders. CONCLUSIONS: The limited data suggest that more than 10 mg a day of haloperidol offers no advantage in mania.

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The relative efficacy of conventional treatment alternatives that are routinely used to treat acutely relapsed schizophrenic patients who have failed an initial course of standard neuroleptic therapy has not been adequately studied, nor have predictors of poor treatment response been reliably identified. We have recently reported preliminary findings that suggest that these patients may subsequently fail to respond to such conventional alternative treatments as (1) maintaining the same dose of the neuroleptic over an extended trial, (2) significantly increasing the dose of the same neuroleptic, or (3) switching to a different class of neuroleptic. Negative symptoms and acute extrapyramidal side effects (EPS) evident during the initial treatment trial were associated with a less favorable clinical response to neuroleptic treatment. We now report on the association between clinical response and negative symptoms and acute EPS. Present findings suggest that a particular degree of negative symptoms apparent prior to treatment may be associated with a poor subsequent treatment response and that negative symptom scores and EPS ratings demonstrate a significant correlation with severity of psychiatric ratings during the treatment trial. The relationship among neuroleptic resistance, negative symptoms, and acute EPS requires further study.

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The effects of clozapine on the dopamine and serotonin systems may underlie its atypical pharmacologic and clinical profile. To examine this hypothesis, we measured dopamine and serotonin plasma and cerebrospinal (CSF) metabolites and the relationship of these values to treatment response in 19 neuroleptic refractory and intolerant schizophrenic patients. Only a small change in the CSF and plasma homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5HIAA) levels was found. However, the pretreatment CSF HVA/5HIAA ratio and, to a lesser extent, the CSF HVA level predicted treatment response. These results suggest that the modest relationship between HVA and 5-HIAA and treatment response supports the involvement of both neurotransmitters in the pathophysiology of schizophrenia.

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