نقش اختلالات کارکردهای اجرایی برای اختلال در حافظه اپیزودیک در افراد مبتلا به اعتیاد به الکل

Individuals with alcoholism commonly exhibit impaired performance on episodic memory tasks. However, the contribution of their impaired executive functioning to poor episodic memory remains to be clarified. Thirty-six recently detoxified and sober asymptomatic alcoholic men and 36 matched non-alcoholic participants were tested for processing speed, prepotent response inhibition, mental flexibility, coordination of dual-task and a verbal episodic memory task. Compared with non-alcoholic individuals, the alcoholic patients showed impaired executive functions combined with below normal performance on both free and delayed recall. In contrast, processing speed, cued recall and recognition were preserved. Regression analyses revealed that 47% of alcoholics' episodic memory's free recall performance was predicted by mental flexibility and that 49% of their delayed recall performance was predicted by mental flexibility, manipulation of dual-task and prepotent response inhibition. Regarding participants' executive predictors of episodic memory performance, the slopes of β coefficients were significantly different between the two groups, with alcoholics requiring more their executive system than non-alcoholics. Once detoxified, alcoholic patients showed episodic memory deficits mainly characterized by impaired effortful (executive) processes. Compared with controls, patients used effortful learning strategies, which are nonetheless less efficient.

Alcohol dependence, characterized by compulsive preoccupation with alcohol consumption despite the devastating consequences, which affects social and occupational functioning (e.g. in the area of employment, family, education and health) (American Psychiatric Association, 1994), is a widespread psychiatric disorder with a reported prevalence of approximately 8–10% in many Western countries (World Health Organization, 2004). In agreement with other addictive disorders, individuals with alcoholism are very vulnerable to relapse after cessation of drinking (Anton et al., 2006). Long-term abuse of alcohol, in association with nutritional deficits (thiamin deficiency), can lead to classical neurological illnesses, i.e. Wernicke-Korsakoff syndrome (for a review, see Kopelman, 1995). However, during the last three decades, evidence for brain abnormalities in ’non-Korsakoff’ chronic alcoholics has been presented which includes electrophysiological (for a review, see Campanella et al., 2009), morphological and functional metabolism (for a review, see Sullivan and Pfefferbaum, 2005) as well as a wide range of neuropsychological deficits (for a review, see Bates et al., 2002). Typical cognitive deficits which charaterise a state of alcohol dependence include impaired episodic memory (e.g., Glenn and Parsons, 1992, Schwartz et al., 2002, D'Argembeau et al., 2006 and Pitel et al., 2007a) and executive functions (e.g., Joyce and Robbins, 1991, Tivis et al., 1995, Moselhy et al., 2001 and Brokate et al., 2003) which are likely to be predominant. By definition, episodic memory (EM) refers to a neurocognitive system that enables conscious recollection of personal happenings and events from one's personal past as well as the mental projection of anticipated events into one's subjective future (Wheeler et al., 1997). Importantly, executive functioning is of the greatest importance in EM functioning (Shallice et al., 1994, Tulving et al., 1994, Fletcher et al., 1995 and Davidson et al., 2006), in that it facilitates both encoding and retrieval in this memory system (Kapur et al., 1994), maintaining a fixed sequence, and integrating diverse types of information (factual, temporal, spatial) into a meaningful representation (Baddeley, 2000). In the broadest sense, executive function is an umbrella term for all processes recruited for managing and controlling cognition in situations where the routine selection of actions is unsatisfactory and is involved in the genesis of plans and willed actions (Norman and Shallice, 1986 and Miyake et al., 2000). As explained by Moscovitch and Winocur (1992), executive functions are involved in the conscious and strategic aspects of memory performance which may operate at both encoding and retrieval phases; this can be considered as “working-with-memory processes”, which improve memory functioning through the use of efficient strategies. Our hypothesis therefore relates to the fact that a decline in executive functioning, which is a hallmark of alcoholism, is involved in frequently reported impairments of episodic memory (EM). In individuals with alcoholism (and abstinent for a period ranging from several days (Pitel et al., 2007), to several months (Munro et al., 2000) and even years (Brandt et al., 1983)), EM disorders have been identified with the help of psychometric tasks such as the Wechsler Memory Scale (e.g., Glenn and Parsons, 1992 and Fama et al., 2004), the learning of face-name associations (e.g., Beatty et al., 1995 and Tivis and Parsons, 1995), lists of words (e.g., Brokate et al., 2003 and Hildebrandt et al., 2004), and even addresses and stories (Fama et al., 2009). However, the underlying processes for this EM impairment and related brain structures remain unclear (see the critical view by Pitel et al., 2007a). Some findings suggest that effortful retrieval and encoding processes are impaired in chronic alcoholism (Weingartner et al., 1996, Schwartz et al., 2002 and Pitel et al., 2007a; Chanraudet al., 2009). For example, memory tasks, which measure accuracy in judging the source of what is remembered and require reflective processes (i.e., self-monitoring performance and suppress cognitive responses), showed that a subsample of alcoholics made errors in acurately identifying the source of correctly remembered knowledge (Weingartner et al., 1996). Such findings suggest that cognitive processes underlying alcoholics' episodic memory disorders are worthy of further clarification. In addition to EM abnormalities in non-amnesic alcoholics who are recently detoxified, disturbances in the executive system are one of the most consistent and predominant impairments in sober alcoholics (e.g., Joyce and Robbins, 1991, Dao-Castellana et al., 1998, Noël et al., 2001b, Brokate et al., 2003 and Oscar-Berman et al., 2004). Indeed, such patients are generally less efficient than comparison subjects controls in carrying out two tasks simultaneously; for example, to inhibit prepotent response, to detect rules, to shift between multiple sets of responses and to plan and to generate concepts. One interesting study showed that alcoholics had reduced mental flexibility, when assessed by verbal fluency tasks, which accounts for approximately 40% of diminished free recall performance (Pitel et al., 2007a). However, some issues remained to be addressed. Firstly, the impact of a general slowing down of processing speed which was not assessed in this study. Secondly, patients were tested only at the start of alcohol detoxification whereas the neuropsychological profile of alcoholic subjects receiving treatment evolves rapidly during the first 3 weeks (e.g., Carlen and Wilkinson, 1983 and Bartsch et al., 2007). Thirdly, this study (Pitel et al., 2007a) did not include important aspects of executive functioning that may impact on effortful aspects of both encoding and retrieval of episodic memory. This includes suppression (inhibition) of pre-potent response or the capacity to realize two tasks simultaneously (Repovs and Baddeley, 2006 and Clarys et al., 2009). Finally, in the present study, we tested inpatient alcoholic subjects who had been sober for 3 week on average and 1 week after stopping all detoxification medication. This period corresponds to the moment when patients are usually discharged from the alcohol detoxification program, which increases the clinical interest of this article. We hypothesized that poor mental flexibility, prepotent response inhibition and difficulty in the coordination of dual tasks would be responsible for poor verbal recollection in sober alcoholics’ episodic memory.