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Elife. 2014 Nov 28;3:e04499. doi: 10.7554/eLife.04499.

Disruption of thalamic functional connectivity is a neural correlate of dexmedetomidine-induced unconsciousness.

Author information

1
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, United States.
2
MGH/MIT/HMS Athinoula A Martinos Center for Biomedical Imaging, Charlestown, United States.
3
Clinical Research Center, Massachusetts General Hospital, Boston, United States.

Abstract

Understanding the neural basis of consciousness is fundamental to neuroscience research. Disruptions in cortico-cortical connectivity have been suggested as a primary mechanism of unconsciousness. By using a novel combination of positron emission tomography and functional magnetic resonance imaging, we studied anesthesia-induced unconsciousness and recovery using the α₂-agonist dexmedetomidine. During unconsciousness, cerebral metabolic rate of glucose and cerebral blood flow were preferentially decreased in the thalamus, the Default Mode Network (DMN), and the bilateral Frontoparietal Networks (FPNs). Cortico-cortical functional connectivity within the DMN and FPNs was preserved. However, DMN thalamo-cortical functional connectivity was disrupted. Recovery from this state was associated with sustained reduction in cerebral blood flow and restored DMN thalamo-cortical functional connectivity. We report that loss of thalamo-cortical functional connectivity is sufficient to produce unconsciousness.

KEYWORDS:

consciousness; cortico-cortical; default mode network; dexmedetomidine; functional connectivity; human; neuroscience; thalamo-cortical

PMID:
25432022
PMCID:
PMC4280551
DOI:
10.7554/eLife.04499
[Indexed for MEDLINE]
Free PMC Article

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