Disruption of thalamic functional connectivity is a neural correlate of dexmedetomidine-induced unconsciousness Articles uri icon

authors

  • AKEJU, OLUWASEUN
  • LOGGIA, MARCO L.
  • CATANA, CIPRIAN
  • PAVONE, KARA J.
  • VAZQUEZ, RAFAEL
  • RHEE, JAMES
  • CONTRERAS RAMIREZ, VIOLETA
  • CHONDE, DANIEL B.
  • IZQUIERDO GARCÍA, DAVID
  • ARABASZ, GRAE
  • HSU, SHIRLEY
  • HABEEB, KATHLEEN
  • HOOKER, JACOB M.
  • NAPADOWE, VITALY
  • BROWN, MERY N.
  • PURDON, PATRICK L.

published in

publication date

  • November 2014

start page

  • e04499

volume

  • 3

International Standard Serial Number (ISSN)

  • 2050-084X

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 alpha2-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.

subjects

  • Biology and Biomedicine