Cortical hypersynchrony predicts breakdown of sensory processing during loss of consciousness.

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 -