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      Neurocognitive impairment associated with alcohol use disorders: Implications for treatment.

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      Experimental and Clinical Psychopharmacology
      American Psychological Association (APA)

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          Abstract

          Between 50% and 80% of individuals with alcohol use disorders experience mild to severe neurocognitive impairment. There is a strong clinical rationale that neurocognitive impairment is an important source of individual difference affecting many aspects of addiction treatment, but empirical tests of the direct influence of impairment on treatment outcome have yielded weak and inconsistent results. The authors address the schism between applied-theoretical perspectives and research evidence by suggesting alternative conceptual models of the relationship between neurocognitive impairment and addiction treatment outcome. Methods to promote neurocognitive recovery and ways in which addiction treatments may be modified to improve psychosocial adaptation are suggested. Specific suggestions for future research that may help clarify the complex relations between neurocognitive impairment and addiction treatment are outlined.

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          A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes.

          Contemporary urge models assume that urges are necessary but not sufficient for the production of drug use in ongoing addicts, are responsible for the initiation of relapse in abstinent addicts, and can be indexed across 3 classes of behavior: verbal report, overt behavior, and somatovisceral response. A review of available data does not provide strong support for these assumptions. An alternative cognitive model of drug use and drug urges is proposed that hypothesizes that drug use in the addict is controlled by automatized action schemata. Urges are conceptualized as responses supported by nonautomatic cognitive processes activated in parallel with drug-use action schemata either in support of the schema or in support of attempts to block the execution of the schema. The implications of this model for the assessment of urge responding and drug-use behavior are presented.
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            Brain gray and white matter volume loss accelerates with aging in chronic alcoholics: a quantitative MRI study.

            Magnetic resonance imaging (MRI) was used to study in vivo the brains of 49 patients with chronic alcoholism, 3 to 4 weeks post-withdrawal, and 43 normal healthy controls, all right-handed male veterans between the ages of 23 and 70 years. MRI scans were analyzed using a semi-automated procedure, which allowed the subcortical regions to be segmented into cerebrospinal fluid (CSF) and brain tissue and the cortical regions to be segmented into CSF, gray matter, and white matter. An age regression model was used to examine the effects of alcohol on brain structure, over and above that expected from the normal aging process. The alcoholics exhibited decreased tissue and increased CSF after correcting for aging. In the cortex, there was significant loss of both gray matter and white matter volume. In this sample of alcoholics, no particular cortical region was preferentially affected or spared. Furthermore, brain tissue volume loss increased with advanced age in the alcoholics. In this group of alcoholics there was no relationship between length of illness and age, i.e., the younger alcoholics had as heavy alcohol use histories as did the older alcoholics. Thus, the increased brain tissue loss with advanced age is interpreted as evidence for age-related increase in brain vulnerability to chronic alcohol abuse.
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              Loss of neurons in the nucleus basalis of Meynert in Alzheimer's disease, paralysis agitans and Korsakoff's disease

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                Author and article information

                Journal
                Experimental and Clinical Psychopharmacology
                Experimental and Clinical Psychopharmacology
                American Psychological Association (APA)
                1936-2293
                1064-1297
                August 2002
                August 2002
                : 10
                : 3
                : 193-212
                Article
                10.1037/1064-1297.10.3.193
                12233981
                0e9cb73e-940c-48b6-831b-27bd2c0c5d7f
                © 2002
                History

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