Persons with schizophrenia experience subjective sensory anomalies and objective deficits on assessment of sensory function. Such deficits could be produced by abnormal signaling in the sensory pathways and sensory cortex or later stage disturbances in cognitive processing of such inputs. Steady state responses (SSRs) provide a noninvasive method to test the integrity of sensory pathways and oscillatory responses in schizophrenia with minimal task demands. SSRs are electrophysiological responses entrained to the frequency and phase of a periodic stimulus. Patients with schizophrenia exhibit pronounced auditory SSR deficits within the gamma frequency range (35-50 Hz) in response to click trains and amplitude-modulated tones. Visual SSR deficits are also observed, most prominently in the alpha and beta frequency ranges (7-30 Hz) in response to high-contrast, high-luminance stimuli. Visual SSR studies that have used the psychophysical properties of a stimulus to target specific visual pathways predominantly report magnocellular-based deficits in those with schizophrenia. Disruption of both auditory and visual SSRs in schizophrenia are consistent with neuropathological and magnetic resonance imaging evidence of anatomic abnormalities affecting the auditory and visual cortices. Computational models suggest that auditory SSR abnormalities at gamma frequencies could be secondary to gamma-aminobutyric acid-mediated or N-methyl-D-aspartic acid dysregulation. The pathophysiological process in schizophrenia encompasses sensory processing that probably contributes to alterations in subsequent encoding and cognitive processing. The developmental evolution of these abnormalities remains to be characterized.

An oral loading dose was combined with intravenous infusion of 6% alcohol at rates adjusted on-line to close the gap between measurements of breath alcohol concentration (BrAC) and a target of 50 mg%. The goal was to minimize the deviation from a prescribed course of BrAC over time. In a pilot study of 10 young men, subjects underwent three experimental sessions: twice at 50 mg% and once in a 0 mg% control condition. The pilot study assessed the performance of the BrAC clamp, its potential utility in studies of acute tolerance to alcohol, and the retest reliability of directly measuring the alcohol elimination rate (AER) calculated from the steady-state infusion rate. Reduced variance was demonstrated in 4 of 5 experimental parameters, compared with results of an earlier approach using a split-dose oral administration procedure. Subjects' perceptions about alcohol effects were measured in one BrAC clamping session, using Schuckit's Subjective High Assessment Scale: 3 of 15 Schuckit's items demonstrated statistically significant indices of acute tolerance to alcohol. Within-subject AERs calculated in the steady-state had a coefficient of variation of 6.5%. Details of the BrAC clamping procedure are provided. The pilot study demonstrated the ability to prescribe experimental parameters of the brain's exposure to alcohol while preserving experimental flexibility in studies of acute tolerance to alcohol and AER.

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Subjective response to alcohol is heritable, and genetic effects on subjective intoxication are partly shared with genetic effects on personality.