Neurocognitive impairments are prevalent in persons seeking treatment for alcohol use disorders (AUDs). These impairments and their physical, social, psychological and occupational consequences vary in severity across persons, much like those resulting from traumatic brain injury; however, due to their slower course of onset, alcohol-related cognitive impairments are often overlooked both within and outside of the treatment setting. Evidence suggests that cognitive impairments can impede treatment goals through their effects on treatment processes. Although some recovery of alcohol-related cognitive impairments often occurs after cessation of drinking (time-dependent recovery), the rate and extent of recovery is variable across cognitive domains and individuals. Following a long hiatus in scientific interest, a new generation of research aims to facilitate treatment process and improve AUD treatment outcomes by directly promoting cognitive recovery (experience-dependent recovery). This review updates knowledge about the nature and course of cognitive and brain impairments associated with AUD, including cognitive effects of adolescent AUD. We summarize current evidence for indirect and moderating relationships of cognitive impairment to treatment outcome, and discuss how advances in conceptual frameworks of brain-behavior relationships are fueling the development of novel AUD interventions that include techniques for cognitive remediation. Emerging evidence suggests that such interventions can be effective in promoting cognitive recovery in persons with AUD and other substance use disorders, and potentially increasing the efficacy of AUD treatments. Finally, translational approaches based on cognitive science, neurophysiology, and neuroscience research are considered as promising future directions for effective treatment development that includes cognitive rehabilitation.
Keywords: Alcoholism, Cognitive impairment, Brain damage, Cognitive recovery, Cognitive enhancement, Cognitive training
IntroductionIn 1987, a prescient overview of research on alcohol-associated impairment of the central nervous system and its potential significance to the efficacy of treatment for alcoholism appeared in Parsons, Butters and Nathan’s edited volume, Neuropsychology of Alcoholism: Implications for diagnosis and treatment(Parsons et al. 1987). Studies using computed tomography scans and electroencephalography had documented impairment to brain structure and function in chronic, heavy drinkers. In parallel, neuropsychological testing approaches documented that many persons with alcohol use disorders (AUD) experienced mild to severe impairment of abstract reasoning, visual-spatial skills, memory, and other information processes. There was evidence that cognitive deficits recovered over time following cessation, or substantially reduced, alcohol drinking, and that recovery of function could be facilitated if relevant tasks were practiced early in the recovery process. International experts in the field raised provocative research questions about the relation of cognitive impairment and recovery to the process and outcome of addiction treatment. Yet, enthusiasm was tempered by the modest and inconsistent relations between cognitive impairment and treatment efficacy that had been documented at that time.
Fifteen years later, the literature on neurocognitive impairment associated with AUD and implications for treatment was revisited (Bates et al. 2002a). Development of new brain imaging technologies and behavioral testing approaches had led to substantial progress in understanding the nature and course of alcohol-related neurocognitive impairments. Applications of this new knowledge to develop more effective treatments, however, had lagged behind. There were likely several reasons for the lack of progress in this area. One was the lack of conceptual models of indirect and moderating roles of neurocognitive impairment to represent the interrelated operation of cognitive factors with multiple other person and environmental factors that in concert contribute to treatment outcomes. In addition, few researchers had applied treatment innovations derived from basic cognitive science, and from other brain injury literatures, to the question of cognitive rehabilitation in AUD.
Fortunately, over the past 10 years, this trend has reversed. There has been a surge of clinical and research interest in the relation of cognitive impairment to addiction treatment outcome, and in developing new ways to intervene in non-adaptive neurocognitive processes that may interfere with recovery. Training of working memory and other executive functions shows potential promise to generalize to additional neurocognitive dispositions (e.g., Bickel et al. 2011) and potentially enhance positive substance use outcomes (e.g., Rupp et al. 2012). Both relatively brief and very time intensive cognitive remediation approaches are being explored in persons with a range of alcohol use behaviors spanning hazardous drinking to alcohol dependence, and a range of cognitive problems from cognitive bias to serious brain damage (e.g., Alfonso et al. 2011; Houben et al. 2011; Wilson et al. 2012). Finally, new conceptual models for intervention strategies that build on the bidirectional feedback streams between the brain and body are starting to emerge (Wiers et al. 2011b; Bates and Buckman in press). These novel interventions, described at the article’s end, use relatively simple muscle movements, rhythmical breathing exercises, aerobic exercise, meditation, or combined mental and physical interventions to train (or retrain) neurophysiological systems that support cognition, affect regulation, motivation, and resilience to stress, all of which are compromised by chronic heavy alcohol use.
Cognitive Impairment in AUDA sizeable proportion of persons (estimated to be ~ 50% – 70%) diagnosed with AUD display some degree of neurocognitive deficit relative to healthy controls (Fein et al. 1990; Martin et al. 1986). Although many alcohol dependent adults fortunately demonstrate only subtle or transient cognitive disruptions (Bates and Convit 1999; Rourke and Loberg 1996), a sizable minority of these individuals display impairments as clinically severe as those seen in persons with traumatic brain injury (Bates 1997; Donovan et al. 2001). Chronic, heavy alcohol use appears to selectively affect cognitive abilities associated with controlled and effortful processing of novel information, and selective and divided attention, while sparing general intelligence, over-learned knowledge, and automatic information processes (summarized in Table 1, for review, see Bates et al. 2008; Oscar-Berman and Marinkovic 2007; Lyu and Lee 2012; Le Berre et al. 2010). Executive functions such as working memory and response inhibition, and the frontal lobe structures typically thought to subserve them, appear to be particularly vulnerable to alcohol-related impairment (Ratti et al. 2002; Oscar-Berman et al. 2004; Zinn et al. 2004; Noel et al. 2007; Lawrence et al. 2009; Loeber et al. 2009; Kopera et al. 2012; Ambrose et al. 2001; Pitel et al. 2007b). Fluid cognitive abilities, such as concept formation, abstraction, problem solving, and visual-spatial abilities are also often affected (Nixon 1995; Parsons 1998; Parsons and Farr 1981; Rourke and Loberg 1996; Weinstein and Shaffer 1993; Rupp et al. 2006).