Journal
SCHIZOPHRENIA BULLETIN
Volume 35, Issue 6, Pages 1065-1077Publisher
OXFORD UNIV PRESS
DOI: 10.1093/schbul/sbp091
Keywords
entrainment; EEG; neural synchrony; schizophrenia; steady state
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Funding
- Indiana University College of Arts and Sciences
- National Institutes of Mental Health [1 RO1 MH62150, R01 MH074983]
- National Alliance for Research on Schizophrenia and Depression
- Indiana Clinical and Translational Sciences Institute Predoctoral Training Award [TL1RR02575]
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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 T-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.
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