Relations between cognitive and motor deficits and regional brain volumes in individuals with alcoholism

Abstract

Despite the common co-occurrence of cognitive impairment and brain structural deficits in alcoholism, demonstration of relations between regional gray matter volumes and cognitive and motor processes have been relatively elusive. In pursuit of identifying brain structural substrates of impairment in alcoholism, we assessed executive functions (EF), episodic memory (MEM), and static postural balance (BAL) and measured regional brain gray matter volumes of cortical, subcortical, and cerebellar structures commonly affected in individuals with alcohol dependence (ALC) compared with healthy controls (CTRL). ALC scored lower than CTRL on all composite scores (EF, MEM, and BAL) and had smaller frontal, cingulate, insular, parietal, and hippocampal volumes. Within the ALC group, poorer EF scores correlated with smaller frontal and temporal volumes; MEM scores correlated with frontal volume; and BAL scores correlated with frontal, caudate, and pontine volumes. Exploratory analyses investigating relations between subregional frontal volumes and composite scores in ALC yielded different patterns of associations, suggesting that different neural substrates underlie these functional deficits. Of note, orbitofrontal volume was a significant predictor of memory scores, accounting for almost 15% of the variance; however, this relation was evident only in ALC with a history of a non-alcohol substance diagnosis and not in ALC without a non-alcohol substance diagnosis. The brain-behavior relations observed provide evidence that the cognitive and motor deficits in alcoholism are likely a result of different neural systems and support the hypotheses that a number of identifiable neural systems rather than a common or diffuse neural pathway underlies cognitive and motor deficits observed in chronic alcoholism.

Brain-behavior relations and effects of aging and common comorbidities in alcohol use disorder: A review.

“…Regression analysis revealed that the rostral middle frontal and cerebellar cortical volume were significant selective predictors of performance on an executive functions battery and critically not of a test of general cognitive status (Nakamura-Palacios et al, 2014). Relative to controls, alcoholics scored lower on three sets of composite scores and had smaller frontal, cingulate, insular, parietal, and hippocampal volumes; within the alcoholics, executive function scores correlated with frontal and temporal volumes; explicit memory scores correlated with frontal volume; and balance scores correlated with frontal, caudate, and pontine volumes (Fama, Le Berre, Sassoon, et al, in press). A visuospatial processing deficit in long-term abstinent alcoholics was related selectively to parietal volume shrinkage but not to other cortical volume deficits; greater parietal volume shrinkage occurred with greater amount of alcohol consumed over a lifetime (Fein, Shimotsu, Chu, & Barakos, 2009).…”

TRAIL Mediates Neuronal Death in AUD: A Link between Neuroinflammation and Neurodegeneration

“…In AUD, neuronal loss increases with duration of alcohol abuse and is found in regions such as the orbitofrontal cortex (OFC) [ 31 , 32 , 33 ], entorhinal cortex (ENT) [ 19 , 34 ], superior frontal gyrus [ 35 ], and hippocampus [ 36 , 37 , 38 ]. Neuronal loss in the OFC is associated with cognitive impairment to promote increased risk of relapse [ 33 , 39 ], poor decision making [ 32 ], memory deficits [ 36 ], and loss of cognitive control [ 40 , 41 ]. Damage to the ENT involves learning and memory deficits through its regulation of hippocampal function [ 18 , 19 , 38 , 42 , 43 ].…”

Short-term neuropsychological recovery in alcohol use disorder: A retrospective clinical study

“…It is well-known that alcohol use disorder (AUD), characterized by chronic and excessive alcohol consumption, is associated with brain damage and cognitive deficits (Epstein, Pisani, & Fawcett, 1977;Fama et al, 2019;Oscar-Berman, Shagrin, Evert, & Epstein, 1997;Parsons, 1977;Pitel et al, 2011). Indeed, executive functions and episodic memory abilities were repeatedly reported as impaired in recently detoxified AUD patients (Le Berre, Fama, & Sullivan, 2017;Oscar-Berman et al, 2014 for a review).…”