Neurocognitive dysfunction associated with alcohol and substance use disorders (SUDs) has been well-established and is the topic of most chapters in this book. However, neurocognitive changes occurring during abstinence from alcohol and substances have been less frequently described. This chapter first summarizes the main neurocognitive and neurobiological abnormalities associated with alcohol and SUDs, before reviewing more extensively the neurocognitive and neurobiological changes that occur with abstinence from alcohol and other substances. As a recent review focused on findings from functional magnetic resonance imaging (fMRI) and positron emission tomography studies during abstinence from alcohol (Charlet et al., 2018), the neurobiological descriptions here focus on brain morphological and spectroscopic MR studies of individuals with alcohol and/or SUDs. While the neurocognitive and neurobiological abnormalities associated with addiction increase mortality and morbidity for the afflicted individual and the society, there is also clear evidence of adaptive and variable recovery from these abnormalities. A better understanding of the specific changes associated with abstinence, their trajectories over time, and of their potential mechanisms will inform more efficacious interventions for alcohol and SUDs in future. Additionally, a better understanding of the course of neurobiological changes associated with abstinence can ultimately serve as powerful psychoeducational information for those considering and seeking treatment for alcohol and SUDs.
NEUROCOGNITIVE DEFICITS IN ADDICTIONAlcohol and SUDs in general (cocaine, methamphetamine, cannabis, or tobacco) are associated with dysfunction, primarily in the domains of learning/memory, working memory, and other executive-based skills, including cognitive/inhibitory control (extensively reviewed in previous chapters). Persons with alcohol use disorder (AUD) have been studied most, with the nature and level of impairment showing considerable variability (for recent reviews, see Stavro et al., 2013;Bernardin et al., 2014;Oscar-Berman et al., 2014;Le Berre, Fama et al., 2017). Approximately 55% of AUD manifest clinically significant neurocognitive deficits after acute detoxification (i.e., >1.5 standard deviations below the level in healthy controls), but some degree of recovery from these deficits is apparent with short-term (i.e., ≤1 month), intermediate-term (i.e., 1-12 months), and long-term (i.e., >1 year) abstinence from alcohol (Rourke and Grant, 2009;Durazzo et al., 2014b). Some dysfunction has been reported to persist into long-term abstinence from alcohol, particularly in the domains of executive and visuospatial skills, learning and memory, and postural stability (