Sensory-gating deficit of the N100 mid-latency auditory evoked potential in medicated schizophrenia patients.

The clinical and neuro-cognitive correlates of the P50 and N100 auditory evoked responses gating deficits in schizophrenia have thus far eluded identification. Based on our prior results, we hypothesized that, in addition to the P50, gating of the N100 is significantly decreased in schizophrenia and that this deficit correlates with the negative symptoms dimension of schizophrenia. Amplitudes and gating measures of the P50 and N100 were compared between stable out-patients (N=45) (mainly on atypical antipsychotics) with chronic schizophrenia and age- and gender-matched healthy controls (N=49) and the clinical correlates examined. All subjects underwent the paired-stimulus paradigm in 3 or 4 different days. Data from day one and the mean of all days (MOAD) were examined. P50 and N100 amplitudes and gating measures were correlated with PANSS and Wisconsin Card Sorting Test data. Utilizing day one data, no amplitude or gating measures were significantly different between the groups. Utilizing MOAD data, both P50 and N100 gating were significantly decreased in schizophrenia patients. The N100 gating deficit correlated with the negative-symptoms cluster and measures of frontal lobe dysfunction. The data suggest a correlation between N100 gating deficit and the negative-cognitive deficits dimensions of schizophrenia. Data also suggest that improving the signal to noise ratio (MOAD data) increases the sensitivity for detecting gating abnormalities and assessing their clinical correlates.

Genetic and environmental influences on sensory gating of mid-latency auditory evoked responses: a twin study.

A deficit in sensory gating measured by the suppression of P50 auditory event-related potential (ERP) has been implicated in the biological bases of schizophrenia and some other psychiatric disorders and proposed as a candidate endophenotype for genetic studies. More recently, it has been shown that gating deficits in schizophrenics extend to ERP components reflecting early attentive processing (the N1/P2 complex). However, evidence for heritability of sensory gating in the general population is very limited. Heritability of P50, N1, and P2 amplitudes and gating was estimated in 54 monozygotic and 55 dizygotic twin pairs using a dual-click auditory paradigm. Genetic model-fitting analysis showed high heritability of peak amplitudes of P50, N1, and P2 waves. Genetic influences on P50 gating (S2/S1) were modest, while heritability of N1 and P2 gating was high and significant. The alternative gating measure (S1-S2 difference) showed significant heritability for all three ERP components. Weak genetic influences on P50 gating ratio can be related to its poor test-retest reliability demonstrated in previous studies. These results suggest that gating measures derived from the N1/P2 wave complex may be useful endophenotypes for population-based genetic studies of the sensory gating function and its impairments in psychopathology.