Cortical hypersynchrony predicts breakdown of sensory processing during loss of consciousness.
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Cortical hypersynchrony predicts breakdown of sensory processing during loss of consciousness. / Supp, Gernot; Siegel, Markus; Hipp, Jörg; Engel, Andreas K.
in: CURR BIOL, Jahrgang 21, Nr. 23, 23, 2011, S. 1988-1993.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Cortical hypersynchrony predicts breakdown of sensory processing during loss of consciousness.
AU - Supp, Gernot
AU - Siegel, Markus
AU - Hipp, Jörg
AU - Engel, Andreas K.
PY - 2011
Y1 - 2011
N2 - Intrinsic cortical dynamics modulates the processing of sensory information and therefore may be critical for conscious perception. We tested this hypothesis by electroencephalographic recording of ongoing and stimulus-related brain activity during stepwise drug-induced loss of consciousness in healthy human volunteers. We found that progressive loss of consciousness was tightly linked to the emergence of a hypersynchronous cortical state in the alpha frequency range (8-14 Hz). This drug-induced ongoing alpha activity was widely distributed across the frontal cortex. Stimulus-related responses to median nerve stimulation consisted of early and midlatency response components in primary somatosensory cortex (S1) and a late component also involving temporal and parietal regions. During progressive sedation, the early response was maintained, whereas the midlatency and late responses were reduced and eventually vanished. The antagonistic relation between the late sensory response and ongoing alpha activity held for constant drug levels on the single-trial level. Specifically, the late response component was negatively correlated with the power and long-range coherence of ongoing frontal alpha activity. Our results suggest blocking of intracortical communication by hypersynchronous ongoing activity as a key mechanism for the loss of consciousness.
AB - Intrinsic cortical dynamics modulates the processing of sensory information and therefore may be critical for conscious perception. We tested this hypothesis by electroencephalographic recording of ongoing and stimulus-related brain activity during stepwise drug-induced loss of consciousness in healthy human volunteers. We found that progressive loss of consciousness was tightly linked to the emergence of a hypersynchronous cortical state in the alpha frequency range (8-14 Hz). This drug-induced ongoing alpha activity was widely distributed across the frontal cortex. Stimulus-related responses to median nerve stimulation consisted of early and midlatency response components in primary somatosensory cortex (S1) and a late component also involving temporal and parietal regions. During progressive sedation, the early response was maintained, whereas the midlatency and late responses were reduced and eventually vanished. The antagonistic relation between the late sensory response and ongoing alpha activity held for constant drug levels on the single-trial level. Specifically, the late response component was negatively correlated with the power and long-range coherence of ongoing frontal alpha activity. Our results suggest blocking of intracortical communication by hypersynchronous ongoing activity as a key mechanism for the loss of consciousness.
KW - Humans
KW - Male
KW - Electroencephalography
KW - Brain Mapping
KW - Perception/physiology
KW - Alpha Rhythm/drug effects/physiology
KW - Cerebral Cortex/physiology
KW - Electroencephalography Phase Synchronization/drug effects/physiology
KW - Propofol/pharmacology
KW - Unconsciousness/chemically induced/physiopathology
KW - Humans
KW - Male
KW - Electroencephalography
KW - Brain Mapping
KW - Perception/physiology
KW - Alpha Rhythm/drug effects/physiology
KW - Cerebral Cortex/physiology
KW - Electroencephalography Phase Synchronization/drug effects/physiology
KW - Propofol/pharmacology
KW - Unconsciousness/chemically induced/physiopathology
M3 - SCORING: Journal article
VL - 21
SP - 1988
EP - 1993
JO - CURR BIOL
JF - CURR BIOL
SN - 0960-9822
IS - 23
M1 - 23
ER -