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The article you requested is

An Integrated Analysis of Acute Treatment-Emergent Extrapyramidal Syndrome in Patients With Schizophrenia During Olanzapine Clinical Trials: Comparisons With Placebo, Haloperidol, Risperidone, or Clozapine.

J Clin Psychiatry 2003;64:898-906
Copyright 2003 Physicians Postgraduate Press, Inc.

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Background: The frequency and severity of extrapyramidal syndrome (EPS) were evaluated in patients with DSM-III or DSM-IV schizophrenia in the acute phase (<= 8 weeks) of randomized, double-blind, controlled trials from the integrated olanzapine clinical trial database.

Method: This retrospective analysis included 23 clinical trials and 4611 patients from November 11, 1991, through July 31, 2001. Incidences of dystonic, parkinsonian, and akathisia events were compared using treatment-emergent adverse-event data. Categorical analyses of Simpson-Angus Scale and Barnes Akathisia Scale (BAS) scores, use of anticholinergic medications, and baseline-to-endpoint changes in Simpson-Angus Scale and BAS scores were compared.

Results: A significantly smaller percentage of olanzapine-treated patients experienced dystonic events than did haloperidol- (p < .001) or risperidone-treated patients (p = .047). A significantly greater percentage of haloperidol-treated patients experienced parkinsonian (p < .001) and akathisia (p < .001) events than did olanzapine-treated patients. Categorical analysis of Simpson-Angus Scale scores showed significantly more haloperidol- (p < .001) or risperidone-treated patients (p = .004) developed parkinsonism than did olanzapine-treated patients. Olanzapine-treated patients experienced significantly greater reductions in Simpson-Angus Scale scores than did haloperidol- (p < .001), risperidone- (p < .001), or clozapine-treated (p = .032) patients. Categorical analysis of BAS scores showed significantly more haloperidol-treated patients experienced treatment-emergent akathisia versus olanzapine-treated patients (p < .001). Significantly greater reductions in BAS scores were experienced during olanzapine treatment versus placebo (p = .007), haloperidol (p < .001), and risperidone (p = .004) treatments. A significantly smaller percentage of olanzapine-treated patients received anticholinergic medications compared with that of haloperidol- (p < .001) or risperidone-treated patients (p = .018). Compared with that in olanzapine-treated patients, the duration of anticholinergic cotreatment was significantly longer among haloperidol- (p < .001) or risperidone-treated patients (p = .040) and significantly shorter among clozapine-treated patients (p = .021).

Conclusion: This analysis of available data from olanzapine clinical trials lends additional support to olanzapine's favorable EPS profile.