OBJECTIVE: P50 gating in schizophrenia has contributed much to our understanding of the pathophysiology of the illness. We examined euthymic bipolar patients to determine if they also have a P50 gating deficit. METHOD: P50 gating was measured in 81 euthymic bipolar patients (50 with a lifetime history of psychotic symptoms), 92 stable schizophrenic patients, and 67 control subjects. RESULTS: P50 gating was significantly lower in control subjects than in bipolar patients with a lifetime history of psychosis (P = 0.001) and schizophrenic patients (P = 0.0001). In all patient groups, the percentage of patients with P50 gating was higher than in the control group (chi(2) = 30.596; P < 0.0001). There was no statistically significant correlation between P50 gating and other clinical variables. CONCLUSION: Our data suggest that P50 gating deficit is a neurobiological marker that is present in stable schizophrenic patients and euthymic bipolar patients.
OBJECTIVE:P50 gating in schizophrenia has contributed much to our understanding of the pathophysiology of the illness. We examined euthymic bipolarpatients to determine if they also have a P50 gating deficit. METHOD:P50 gating was measured in 81 euthymic bipolarpatients (50 with a lifetime history of psychotic symptoms), 92 stable schizophrenicpatients, and 67 control subjects. RESULTS:P50 gating was significantly lower in control subjects than in bipolarpatients with a lifetime history of psychosis (P = 0.001) and schizophrenicpatients (P = 0.0001). In all patient groups, the percentage of patients with P50 gating was higher than in the control group (chi(2) = 30.596; P < 0.0001). There was no statistically significant correlation between P50 gating and other clinical variables. CONCLUSION: Our data suggest that P50 gating deficit is a neurobiological marker that is present in stable schizophrenicpatients and euthymic bipolarpatients.
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