Abstracts

RATIONALE:_Sensory gating deficits contribute to the development of psychotic symptoms. These deficits can be studied by recording the P50, a positive evoked potential peaking around 50 ms following auditory stimulation. Normally, the P50 is reduced in amplitude with repetition. However, this attenuation is deficient in schizophrenia patients and 50% of their relatives. Up to now, it has not been shown which brain structures mediate sensory gating in humans. METHODS: We recorded evoked potentials to acoustic stimuli from hippocampal depth and subdural strip electrodes in 26 patients undergoing invasive presurgical evaluation for epilepsy surgery. 20 patients had bilateral hippocampal depth electrodes; 12 had additional strip electrodes, and in 6 further patients grid electrodes were implanted. In a paired click paradigm we used headphones to present two identical stimuli (S1 and S2) with a short interstimulus interval of 500 ms and a longer interpair interval of 8 s. RESULTS: With depth electrodes we recorded pronounced negative field potentials peaking around 250 ms following S1 within the hippocampus proper on both the focal and the non-focal side. By contrast, neural responses to S2 were very small in amplitude - if present at all. However, they were significantly more negative-going on the focal side thus indicating that the epileptogenic process reduces sensory gating processes within the epileptic hippocampus. Well-defined P50 potentials which were attenuated in amplitude with repetition were only present in temporo-parietal areas bordering the Sylvian fissure but not in the frontal lobes. CONCLUSIONS: Our data indicate that the human temporo-parietal cortex contributes to early pre-attentive sensory gating processes. By contrast, the human hippocampus seems to be more involved in later attentive sensory gating, and this hippocampal function can be impaired by the epileptogenic process. Future studies will have to address the question whether these deficits are associated with psychiatric complications in epilepsy patients and whether lesions of the temporo-parietal sensory gating area may contribute to the development of post-operative de-novo psychoses.