Eva M Müller-Oehring

Whether disruption of neural communication between cerebellar and cortical brain regions exerts an influence on ataxia in alcohol use disorder (AUD) was the focus of this study.  

We tested the hypothesis that alcoholic patients would demonstrate compromised dorsal anterior cingulate cortex (dACC) -cerebellar functional connectivity when adjusting their strategies to accommodate uncertain conditions and would recruit compensatory brain regions to overcome ineffective response patterns.

We tested whether microstructural fiber changes relate to resting-state functional connectivity changes in alcoholics who have maintained sobriety during a one-year interval, and whether these changes are beyond those potentially exhibited by controls.

Here, we investigated change in CC microstructural fiber integrity over one year in 12 (7w, 5m) alcoholics (ALC) and 13 (7w, 6m) age-matched controls (CTL). ALC and CTL did not differ in years of education (mean=15 years for both groups) or verbal IQ (CTL=107, ALC=104).

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.

Using an fMRI paradigm, we investigated whether memory performance by alcoholics on a face–name association test previously observed to be problematic for alcoholics could be explained by desynchronous activity between nodes of these specific networks.

We tested whether previously published functional magnetic resonance imaging data acquired in 15 recovering alcoholics and 15 controls at rest and while performing a spatial working memory task would fulfill criteria defining functional compensation.