Visual sensory processing deficits in Schizophrenia and their relationship to disease state

Abstract

peer-reviewedContext: Visual Evoked Potential (VEP) abnormalities have been a fairly consistent finding in patients with schizophrenia, and it has been suggested that electrophysiological markers of early sensory processing may be useful as trait markers for the illness, and for development as potential diagnostic measures. Objective: Clear amplitude reductions in the occipital P1 component of the VEP (~100 ms), have been repeatedly demonstrated in patients with schizophrenia. Here, we investigated whether the extent of this deficit was related to age, clinical symptoms, medication status and length of illness, in a large cohort of ethnically homogenous patients. Design, setting and participants: VEP responses to simple isolated-check stimuli were examined in 52 DSM-IV diagnosed patients with schizophrenia, and compared with responses from 26 healthy age-matched control subjects. Using high-density electrical scalp recordings, we assessed the integrity of the visual P1 component across the two groups. This study was conducted at St.Vincent?s Psychiatric Hospital in Fairview, Dublin, Ireland. Results: Substantially reduced P1 amplitude was demonstrated in the patient group compared to controls. The deficit was not linked to age, length of illness or medication status. A small positive correlation, accounting for about 11% of the variance, was found between P1 amplitude and clinical symptoms scales (BPRS and SANS). In addition, we found that a slightly later (~110 ms) fronto-central component was relatively increased in the patient group, and was inversely correlated with the occipital P1 amplitude in the patients, but not in the healthy control subjects. Conclusions: Our findings clearly demonstrate a deficit in early visual processing in patients with schizophrenia (with a large effect size; Cohen?s d = 0.7) that is unrelated to chronicity. The results are consistent with recent findings showing that the P1 deficit is endophenotypic of the disorder and related to genetic risk factors rather than the disease process itself