title: A selective insular perfusion deficit contributes to compromised salience network connectivity in recovering alcoholic men.
abstract: BACKGROUND
  Alcoholism can disrupt neural synchrony between nodes of intrinsic functional networks that are maximally active when resting relative to engaging in a task, the default mode network (DMN) pattern. Untested, however, are whether the DMN in alcoholics can rebound normally from the relatively depressed task state to the active resting state and whether local perfusion deficits could disrupt network synchrony when switching from conditions of rest to task to rest, thereby indicating a physiological mechanism of neural network adaptation capability.
  
  
  METHODS
  Whole-brain, three-dimensional pulsed-continuous arterial spin labeling provided measurements of regional cerebral blood flow (CBF) in 12 alcoholics and 12 control subjects under three conditions: pretask rest, spatial working-memory task, and posttask rest.
  
  
  RESULTS
  With practice, alcoholics and control subjects achieved similar task accuracy and reaction times. Both groups exhibited a high-low-high pattern of perfusion levels in DMN regions during the rest-task-rest runs and the opposite pattern in posterior and cerebellar regions known to be associated with spatial working memory. Alcoholics showed selective differences from control subjects in the rest-task-rest CBF pattern in the anterior precuneus and CBF level in the insula, a hub of the salience network. Connectivity analysis identified activation synchrony from an insula seed to salience nodes (parietal, medial frontal, anterior cingulate cortices) in control subjects only.
  
  
  CONCLUSIONS
  We propose that attenuated insular CBF is a mechanism underlying compromised connectivity among salience network nodes. This local perfusion deficit in alcoholics has the potential to impair ability to switch from cognitive states of interoceptive cravings to cognitive control for curbing internal urges.
authors.affiliation: Department of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford. Electronic address: edie@stanford.edu.
authors.forename: Edith V
authors.initials: EV
authors.lastname: Sullivan
authors.forename: Eva
authors.initials: E
authors.lastname: Müller-Oehring
authors.forename: Anne-Lise
authors.initials: AL
authors.lastname: Pitel
authors.forename: Sandra
authors.initials: S
authors.lastname: Chanraud
authors.forename: Ajit
authors.initials: A
authors.lastname: Shankaranarayanan
authors.forename: David C
authors.initials: DC
authors.lastname: Alsop
authors.forename: Torsten
authors.initials: T
authors.lastname: Rohlfing
authors.forename: Adolf
authors.initials: A
authors.lastname: Pfefferbaum
mesh_terms: D000437:Alcoholism / Q000503:physiopathology*; D001288:Attention / Q000502:physiology*; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology*; D006801:Humans; D018810:Magnetic Resonance Angiography; D008297:Male; D008570:Memory, Short-Term / Q000502:physiology; D008875:Middle Aged; D012146:Rest / Q000502:physiology
keywords: Alcohol; MRI; arterial spin labeling; brain; connectivity; perfusion; working memory