Respective influence of current alcohol consumption and duration of heavy drinking on brain morphological alterations in alcohol use disorder

Abstract

Numerous studies have explored the morphological differences of the brain between subjects with alcohol use disorder (AUD) and control subjects, but very few have investigated the impact of the duration of alcohol use disorder (DAD) and current level of alcohol consumption (CAC) within AUD subjects using magnetic resonance imaging (MRI). We compared the morphological MRI of 44 controls and 66 AUD subjects, recruited at the end of a detoxification program. Additional analyses within the AUD group determined which specific alterations were respectively associated with DAD and CAC using: (1) Bonferroni-corrected multivariable linear regressions to explore the DAD/CAC impact on brain volumes and (2) a general linear model (GLM module of FreeSurfer's Qdec) and Monte Carlo simulation to correct for multiple comparisons (P < 0.05) to explore the DAD/CAC impact on cortical thickness and volumes. Analyses were adjusted for age and tobacco use. CAC and DAD were significantly correlated (ρ = 0.25, P < 0.0001), and sensitivity analyses were conducted with and without both CAC and DAD included in the same model. While the AUD-control comparisons globally reproduced preexisting findings, within-AUD analyses found that CAC was inversely correlated with cortical thickness and gray matter volume in a bilateral dorsal band of the temporal lobe, including the fusiform and parahippocampal gyri. For DAD, only a left and more ventral temporal band that partially overlapped the CAC-associated area was found in cortical thickness analyses.No significant volumetric result was reached after a Bonferroni correction. CAC and, to a lesser extent, DAD were thus associated with specific, though partially overlapping, temporal surface-based signatures.

Regionally specific gray matter volume is lower in alcohol use disorder: Implications for noninvasive brain stimulation treatment

“…Widespread reductions in GMV have been broadly documented in association with chronic alcohol use. Consistent with much previous literature, we found that, relative to controls, individuals with AUD had lower GMV in the ventromedial and orbitofrontal cortices, the anterior cingulate cortex, the bilateral insula, the DLPFC, and the primary motor cortex (Cardenas et al, 2007; Chanraud et al, 2007, 2009; Demirakca et al, 2011; Durazzo & Meyerhoff, 2020; Harding et al, 1996; Jang et al, 2007; Rolland et al, 2020; Segobin et al, 2014; Yang et al, 2016; Zou et al, 2018). Here, we extend the existing literature by quantifying GMV within three discrete noninvasive brain stimulation treatment targets for AUD: the left frontal pole, the left DLPFC, and the left motor cortex.…”

“…Cortical atrophy following chronic alcohol use is likely one of the most documented and critical features that influences TMS efficacy in these individuals (Cardenas et al, 2007; Durazzo et al, 2011; Rolland et al, 2020; Yang et al, 2016; Zahr & Pfefferbaum, 2017). Focal reductions in gray matter volume (GMV) within the frontal lobe (containing the frontal pole and DLPFC) are consistently reported in association with chronic AUD (Cardenas et al, 2007; Chanraud et al, 2007, 2009; Demirakca et al, 2011; Jang et al, 2007; Segobin et al, 2014; Yang et al, 2016).…”

Considering Motor Excitability During Action Preparation in Gambling Disorder: A Transcranial Magnetic Stimulation Study

“…Chronic alcohol consumption has considerable neurotoxic effects, with the most pronounced damage reported in regions underpinning response inhibition, such as the frontal lobes and basal ganglia ( 21 – 23 ). In addition, the degree of brain atrophy is related to the amount of alcohol previously consumed ( 24 ). Hence, the deficit in preparatory suppression could be a consequence of brain damage induced by chronic alcohol exposure.…”

Augmented tendency to act and altered impulse control in alcohol use disorders

“…Several lines of evidence support this hypothesis. First, chronic alcohol consumption has important neurotoxic effects, with the most pronounced damage reported in regions underpinning impulse control, such as the frontal lobes and the basal ganglia ( Chanraud et al, 2007 , Fritz et al, 2019 ), and the degree of brain atrophy correlates with the amount of alcohol previously consumed ( Rolland et al, 2020 ). Moreover, we have shown that a weaker MEP suppression during action preparation was associated with a lower cortical thickness in medial frontal regions ( Quoilin et al, 2021 ), while patients suffering from a behavioral, substance-free, addiction, had a normal pattern of MEP suppression ( Quoilin et al, 2020 ).…”