Sensory gating deficit, as reflected by P50 suppression, has been demonstrated in schizophrenia. Despite extensive evidence of the irreversible effects of typical antipsychotics on this deficit, recent studies of atypical antipsychotics have produced inconsistent findings on the reversibility of P50 suppression in schizophrenia. However, most of these studies were limited by either their cross-sectional design or the recruitment of patients on multiple medications. The most recent study jointly conducted by Dr. Raymond Chan (Neuropsychology and Applied Cognitive Neuroscience Laboratory, and the Key Laboratory of Mental Health, Institute of Psychology) and Dr. Xiaohong Hong (Mental Health Centre of Shantou University) has specifically examined the effects of different antipsychotic 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 antipsychotic 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. 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). One of the main strength of this study was the recruitment of first-onset never medicated schizophrenia and to compare the potential effects of atypical antipsychotics on P50. In so doing, we could rigorously study the “true” potential effects of antipyschotics, if any, upon the observed P50 impairments in schizophrenia. That means, we could say the observed impairments in P50 in schizophrenia could be mainly due to the disease process rather than the medication effect on the P50 in schizophrenia. The other strength point of this study was that, we could also determine the differential effects of atypical antipsychotics upon P50, and could pave an ample pointer for clinicians to tell the patients and their family members of the efficacy of the drug treatment on the observed neurophysiological deficits. Taken together, the current 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. The observed impairments of P50 in schizophrenia may be considered to be one of the potential endophenotype markers for this clinical group. Further study adopting a rigorous prospective longitudinal study design and extending the subject recruitment to their non-psychotic relatives will be beneficial to validate this speculation.

This study was supported by a grant from the National “Tenth Five-year” Science and Technology Program (2002BA711A08), the Research Fund (KSCX2-YW-R-131) from The Knowledge Innovation Project of the Chinese Academy of Sciences, the National Science Fund of China (30770723), and the National Basic Research Programme (973 Programme No. 2007CB512302).

Fig1. Grand average for the schizophrenia group (SZ) and the normal control group (NC). Clink onset
is at 0 ms. Black think line: S1 response waveform ;grey line:S2 response waveform.

Hong*, X., Chan, R. C. K*., Zhuang, Z., Jiang, T., Wang, X., Wang, J., Xiao, B., Zhou, H., Jian, L., & Weng, P. (2009). Neuroleptic effects on P50 sensory gating in patients with first-episode never-medicated schizophrenia. Schizophrenia Research, 108 (1-3), 151-157.