Neuroleptic effects on P50 sensory gating in patients with first-episode never-medicated schizophrenia

Sensory gating deficit, as reflected by P50 suppression, has been demonstrated in schizophrenia. Despite extensive evidence of the irreversible effects of typical neuroleptics on this deficit, recent studies of atypical neuroleptics have produced inconsistent findings on the reversibility of P50 suppression in schizophrenia. As the majority of these studies were limited by either their cross-sectional design or the recruitment of patients on multiple medications, the current Study was designed to examine the effects of different neuroleptic medications on the P50 sensory gating index in patients with first-episode, never-medicated schizophrenia. P50-evoked potential recordings were obtained from 62 normal controls when they entered the study and from 65 patients with first-episode, never-medicated schizophrenia at baseline and after six weeks of different neuroleptic treatments (sulpiride [n=241, risperidone [n=24] and clozapine [n-17]). The first-episode, never-medicated schizophrenia patients had impaired sensory gating relative to the normal controls (mean-94.19% [SD = 61.31%] versus mean=41.22% [SD-33.82%]). The test amplitude S2 was significantly higher in the schizophrenia patients than in the normal controls. The conditioning amplitude S1 and the positive symptom scores were related to the P50 gating ratios in schizophrenia at baseline. There was no change in P50 sensory gating (P>0.10) and a significant improvement in the clinical ratings (P>0.10) after six-week neuroleptic treatment for schizophrenia. P50 sensory gating was not significant for the patients who received sulpiride, risperidone or clozapine at baseline (F=1,074, df = 2, 62, P=0.348)or at endpoint (F=0.441, df=2,62, p=0.646). Our findings indicate that there is P50 sensory gating impairment in first-episode, nevermedicated schizophrenia and that treatment with typical and atypical antipsychotics has no significant impact on such gating in this illness.Sensory gating deficit, as reflected by P50 suppression, has been demonstrated in schizophrenia. Despite extensive evidence of the irreversible effects of typical neuroleptics on this deficit, recent studies of atypical neuroleptics have produced inconsistent findings on the reversibility of P50 suppression in schizophrenia. As the majority of these studies were limited by either their cross-sectional design or the recruitment of patients on multiple medications, the current Study was designed to examine the effects of different neuroleptic medications on the P50 sensory gating index in patients with first-episode, never-medicated schizophrenia. P50-evoked potential recordings were obtained from 62 normal controls when they entered the study and from 65 patients with first-episode, never-medicated schizophrenia at baseline and after six weeks of different neuroleptic treatments (sulpiride [n=241, risperidone [n=24] and clozapine [n-17]). The first-episode, never-medicated schizophrenia patients had impaired sensory gating relative to the normal controls (mean-94.19% [SD = 61.31%] versus mean=41.22% [SD-33.82%]). The test amplitude S2 was significantly higher in the schizophrenia patients than in the normal controls. The conditioning amplitude S1 and the positive symptom scores were related to the P50 gating ratios in schizophrenia at baseline. There was no change in P50 sensory gating (P>0.10) and a significant improvement in the clinical ratings (P>0.10) after six-week neuroleptic treatment for schizophrenia. P50 sensory gating was not significant for the patients who received sulpiride, risperidone or clozapine at baseline (F=1,074, df = 2, 62, P=0.348)or at endpoint (F=0.441, df=2,62, p=0.646). Our findings indicate that there is P50 sensory gating impairment in first-episode, nevermedicated schizophrenia and that treatment with typical and atypical antipsychotics has no significant impact on such gating in this illness. (C) 2008 Elsevier B.V. All rights reserved