Impairments in background and event-related alpha-band oscillatory activity in patients with schizophrenia.

PLoS One

Program in Cognitive Neuroscience, Department of Psychology, The City College of the City University of New York, New York, New York, United States of America; The Zanvyl Krieger Mind Brain Institute, The Johns Hopkins University, Baltimore, Maryland, United States of America.

Published: December 2014


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Article Abstract

Studies show that patients with schizophrenia exhibit impaired responses to sensory stimuli, especially at the early stages of neural processing. In particular, patients' alpha-band (8-14 Hz) event-related desynchronization (ERD) and visual P1 event-related potential (ERP) component tend to be significantly reduced, with P1 ERP deficits greater for visual stimuli biased towards the magnocellular system. In healthy controls, studies show that pre-stimulus alpha (background alpha) plays a pivotal role in sensory processing and behavior, largely by shaping the neural responses to incoming stimuli. Here, we address whether patients' ERD and P1 deficits stem from impairments in pre-stimulus alpha mechanisms. To address this question we recorded electrophysiological activity in patients with schizophrenia and healthy controls while they engaged in a visual discrimination task with low, medium, and high contrast stimuli. The results revealed a significant decrease in patients' ERDs, which was largely driven by reductions in pre-stimulus alpha. These reductions were most prominent in right-hemispheric areas. We also observed a systematic relationship between pre-stimulus alpha and the P1 component across different contrast levels. However, this relationship was only observed in healthy controls. Taken together, these findings highlight a substantial anomaly in patients' amplitude-based alpha background activity over visual areas. The results provide further support that pre-stimulus alpha activity plays an active role in perception by modulating the neural responses to incoming sensory inputs, a mechanism that seems to be compromised in schizophrenia.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3960158PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0091720PLOS

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