Longitudinal structural MRI studies demonstrate that some brain morphological changes are reversible upon discontinuation of alcohol consumption. After periods of abstinence, previously enlarged ventricles decrease in size (Schroth, Naegele, Klose, Mann, & Petersen, 1988; Shear, Jernigan, & Butters, 1994) and a number of brain areas increase in volume including the temporal, insular, and anterior cingulate cortices; amygdala; thalamus; hippocampus; brainstem; and cerebellar cortex (Cardenas, Studholme, Gazdzinski, Durazzo, & Meyerhoff, 2007; Demirakca et al., 2011; Liu, Lemieux, Shorvon, Sisodiya, & Duncan, 2000; van Eijk et al., 2013; Wrase et al., 2008). Whether complete recovery occurs is difficult to conclude because older age contributes to alcoholism-related brain compromise: for example, older relative to younger alcoholics have significantly reduced capacity for recovery (Munro, Saxton, & Butters, 2000). Furthermore, brain differences may predate alcohol exposure: prior to alcohol exposure, children with at least one AUD-diagnosed parent demonstrate increased impulsivity and poor spatial memory and morphological changes to medial and lateral orbital and superior parietal cortices (Henderson et al., 2018). Similarly, sons from high-density AUD families have altered cortical thickness (middle frontal gyrus and inferior parietal lobule), which correlates with perturbed emotional processing and problems with executive functioning (Holla, Bharath, Venkatasubramanian, & Benegal, 2018).
