Neuroleptic effects on P50 sensory gating in patients with first-episode never-medicated schizophrenia
ABSTRACT 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=24], 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, never-medicated schizophrenia and that treatment with typical and atypical antipsychotics has no significant impact on such gating in this illness.
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ABSTRACT: Impaired inhibition of P50 cerebral evoked response is one of the best validated endophenotypes in schizophrenia. There are controversial data on the relationship between P50 evoked potential deficit and measures of cognitive function in schizophrenia. A comprehensive clinical and neurocognitive assessment plus an evaluation of P50 sensory gating was performed in 160 schizophrenia patients and 64 controls. Neurocognitive scores from each cognitive domain were converted to demographically-adjusted T-scores (age, gender, and years of education) for all study participants. The relationship between P50 and neurocognitive variables was assessed via parametric and nonparametric correlations and categorical strategies: we compared neuropsychological test scores in patients and controls in the lowest P50 quartile vs. the highest. Controls had better performance than schizophrenia patients in all cognitive domains. Schizophrenia patients had significantly higher P50 ratios than controls, and no significant correlation was found between P50 gating measures and neuropsychological test scores in schizophrenia patients or healthy controls. Moreover, no differences in neurocognitive performance were found between subjects in the lowest P50 ratio quartile vs. the highest in healthy controls or patients with schizophrenia. We concluded that there is no evidence of an association between P50 ratio and cognitive measures in schizophrenia patients, and this seems to be also the case in healthy controls.Schizophrenia Research 11/2012; 143(1). DOI:10.1016/j.schres.2012.10.017 · 4.43 Impact Factor
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ABSTRACT: Categorization of psychotic illnesses into schizophrenic and affective psychoses remains an ongoing controversy. Although Kraepelinian subtyping of psychosis was historically beneficial, modern genetic and neurophysiological studies do not support dichotomous conceptualization of psychosis. Evidence suggests that schizophrenia and bipolar disorder rather present a clinical continuum with partially overlapping symptom dimensions, neurophysiology, genetics and treatment responses. Recent large scale genetic studies have produced inconsistent findings and exposed an urgent need for re-thinking phenomenology-based approach in psychiatric research. Epidemiological, linkage and molecular genetic studies, as well as studies in intermediate phenotypes (neurocognitive, neurophysiological and anatomical imaging) in schizophrenia and bipolar disorders are reviewed in order to support a dimensional conceptualization of psychosis. Overlapping and unique genetic and intermediate phenotypic signatures of the two psychoses are comprehensively recapitulated. Alternative strategies which may be implicated into genetic research are discussed.Neuroscience & Biobehavioral Reviews 11/2009; 34(6):897-921. DOI:10.1016/j.neubiorev.2009.11.022 · 10.28 Impact Factor
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ABSTRACT: P50 sensory gating deficit has repeatedly been demonstrated in schizophrenia. Studies have produced inconsistent findings with respect to normalization of P50 gating in patients with schizophrenia receiving treatment with different antipsychotics. The current study was designed to determine whether there is a difference in P50 gating in schizophrenia patients treated with first-generation antipsychotics (FGAs) and second-generation antipsychotics (SGAs), including clozapine. P50 evoked potential recordings were obtained from 160 patients with schizophrenia and 77 healthy comparison subjects. Forty-three patients were being treated with clozapine, sixty-eight were taking SGAs (33 risperidone, 21 olanzapine, 11 aripiprazole, and 3 combinations of SGAs) and 49 were being treated with FGAs. Schizophrenia patients exhibited significantly higher P50 ratios than healthy subjects. When patients treated with different antipsychotics were compared, there were no differences in any of the neurophysiological findings. Second-generation antipsychotics were not related to more normal sensory gating in this population of patients with chronic schizophrenia.European neuropsychopharmacology: the journal of the European College of Neuropsychopharmacology 12/2009; 19(12):905-9. DOI:10.1016/j.euroneuro.2009.09.001 · 5.40 Impact Factor