Literature DB >> 21549567

Association of impaired EEG mu wave suppression, negative symptoms and social functioning in biological motion processing in first episode of psychosis.

Fiza Singh1, Jaime Pineda, Kristin S Cadenhead.   

Abstract

BACKGROUND: Event related desynchronization (ERD) of mu waves, or mu suppression, over sensorimotor cortex has been observed in response to self-generated movement, viewing movement, or imaging movement. Mu suppression is especially pronounced when the movement has social relevance and is being generated by a biological entity indicating successful social adaptation. And since social adaptation problems are common in schizophrenia, the authors designed a study to test mu wave suppression in a first episode of psychosis population.
METHODS: A total of 32 subjects (first episode of psychosis patients N=20; healthy comparison subjects N=12) aged 13-34 watched movement videos with and without socially relevant cues, executed by biological or non-biological agents. Scalp electrode EEG recordings of mu rhythm (8-13 Hz) over sensorimotor cortex during the session were used to calculate mu wave suppression. Average mu suppression was compared within and between groups, as well as correlations between mu suppression and clinical measures.
RESULTS: First episode patients showed significantly reduced mu wave suppression over sensorimotor cortex when viewing biological motion, compared to healthy subjects. In addition, negative symptom burden and poor social adjustment correlated with impaired mu wave suppression.
CONCLUSIONS: Our finding provides the first description of impaired event related desynchronization of mu waves in response to biological motion and its correlation with negative symptoms and social adjustment in the first episode of psychosis. Future studies can be conducted to determine if mu wave suppression represents an endophenotype with potential applications in biological treatments of negative symptoms and social functioning deficits in schizophrenia.
Copyright © 2011 Elsevier B.V. All rights reserved.

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Year:  2011        PMID: 21549567      PMCID: PMC3139731          DOI: 10.1016/j.schres.2011.04.004

Source DB:  PubMed          Journal:  Schizophr Res        ISSN: 0920-9964            Impact factor:   4.939


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