title: Synchrony of corticostriatal-midbrain activation enables normal inhibitory control and conflict processing in recovering alcoholic men.
abstract: BACKGROUND
  Alcohol dependence is associated with inhibitory control deficits, possibly related to abnormalities in frontoparietal cortical and midbrain function and connectivity.
  
  
  METHODS
  We examined functional connectivity and microstructural fiber integrity between frontoparietal and midbrain structures using a Stroop Match-to-Sample task with functional magnetic resonance imaging and diffusion tensor imaging in 18 alcoholic and 17 control subjects. Manipulation of color cues and response repetition sequences modulated cognitive demands during Stroop conflict.
  
  
  RESULTS
  Despite similar lateral frontoparietal activity and functional connectivity in alcoholic and control subjects when processing conflict, control subjects deactivated the posterior cingulate cortex (PCC), whereas alcoholic subjects did not. Posterior cingulum fiber integrity predicted the degree of PCC deactivation in control but not alcoholic subjects. Also, PCC activity was modulated by executive control demands: activated during response switching and deactivated during response repetition. Alcoholics showed the opposite pattern: activation during repetition and deactivation during switching. Here, in alcoholic subjects, greater deviations from the normal PCC activity correlated with higher amounts of lifetime alcohol consumption. A functional dissociation of brain network connectivity between the groups further showed that control subjects exhibited greater corticocortical connectivity among middle cingulate, posterior cingulate, and medial prefrontal cortices than alcoholic subjects. In contrast, alcoholic subjects exhibited greater midbrain-orbitofrontal cortical network connectivity than control subjects. Degree of microstructural fiber integrity predicted robustness of functional connectivity.
  
  
  CONCLUSIONS
  Thus, even subtle compromise of microstructural connectivity in alcoholism can influence modulation of functional connectivity and underlie alcohol-related cognitive impairment.
authors.affiliation: Neuroscience Program, SRI International, Menlo Park, California 94025-3493, USA. tilman.schulte@sri.com
authors.forename: Tilman
authors.initials: T
authors.lastname: Schulte
authors.forename: Eva M
authors.initials: EM
authors.lastname: Müller-Oehring
authors.forename: Edith V
authors.initials: EV
authors.lastname: Sullivan
authors.forename: Adolf
authors.initials: A
authors.lastname: Pfefferbaum
mesh_terms: D000437:Alcoholism / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology*; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology*; D003220:Conflict, Psychological; D056324:Diffusion Tensor Imaging; D056344:Executive Function / Q000502:physiology; D059907:Functional Neuroimaging / Q000379:methods / Q000523:psychology / Q000706:statistics & numerical data; D006179:Gyrus Cinguli / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D007266:Inhibition, Psychological; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008636:Mesencephalon / Q000473:pathology / Q000503:physiopathology*; D008875:Middle Aged; D009413:Nerve Fibers, Myelinated / Q000473:pathology / Q000502:physiology; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology; D017397:Prefrontal Cortex / Q000473:pathology / Q000503:physiopathology*; D057190:Stroop Test / Q000706:statistics & numerical data