Literature DB >> 20410871

Dual tasking and working memory in alcoholism: relation to frontocerebellar circuitry.

Sandra Chanraud1, Anne-Lise Pitel, Torsten Rohlfing, Adolf Pfefferbaum, Edith V Sullivan.   

Abstract

Controversy exists regarding the role of cerebellar systems in cognition and whether working memory compromise commonly marking alcoholism can be explained by compromise of nodes of corticocerebellar circuitry. We tested 17 alcoholics and 31 age-matched controls with dual-task, working memory paradigms. Interference tasks competed with verbal and spatial working memory tasks using low (three item) or high (six item) memory loads. Participants also underwent structural MRI to obtain volumes of nodes of the frontocerebellar system. On the verbal working memory task, both groups performed equally. On the spatial working memory with the high-load task, the alcoholic group was disproportionately more affected by the arithmetic distractor than were controls. In alcoholics, volumes of the left thalamus and left cerebellar Crus I volumes were more robust predictors of performance in the spatial working memory task with the arithmetic distractor than the left frontal superior cortex. In controls, volumes of the right middle frontal gyrus and right cerebellar Crus I were independent predictors over the left cerebellar Crus I, left thalamus, right superior parietal cortex, or left middle frontal gyrus of spatial working memory performance with tracking interference. The brain-behavior correlations suggest that alcoholics and controls relied on the integrity of certain nodes of corticocerebellar systems to perform these verbal and spatial working memory tasks, but that the specific pattern of relationships differed by group. The resulting brain structure-function patterns provide correlational support that components of this corticocerebellar system not typically related to normal performance in dual-task conditions may be available to augment otherwise dampened performance by alcoholics.

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Year:  2010        PMID: 20410871      PMCID: PMC2919220          DOI: 10.1038/npp.2010.56

Source DB:  PubMed          Journal:  Neuropsychopharmacology        ISSN: 0893-133X            Impact factor:   7.853


  61 in total

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4.  fMRI measurement of brain dysfunction in alcohol-dependent young women.

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Journal:  Alcohol Clin Exp Res       Date:  2001-02       Impact factor: 3.455

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6.  The SRI24 multichannel atlas of normal adult human brain structure.

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7.  The human basal forebrain integrates the old and the new.

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8.  Patterns of neuronal loss in the cerebral cortex in chronic alcoholic patients.

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  35 in total

1.  Remapping the brain to compensate for impairment in recovering alcoholics.

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2.  Cerebral blood flow in posterior cortical nodes of the default mode network decreases with task engagement but remains higher than in most brain regions.

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3.  Integrity of white matter microstructure in alcoholics with and without Korsakoff's syndrome.

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Review 4.  The cerebellum and addiction: insights gained from neuroimaging research.

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Review 5.  Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications.

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6.  Disruption of functional connectivity of the default-mode network in alcoholism.

Authors:  Sandra Chanraud; Anne-Lise Pitel; Adolf Pfefferbaum; Edith V Sullivan
Journal:  Cereb Cortex       Date:  2011-03-02       Impact factor: 5.357

7.  A selective insular perfusion deficit contributes to compromised salience network connectivity in recovering alcoholic men.

Authors:  Edith V Sullivan; Eva Müller-Oehring; Anne-Lise Pitel; Sandra Chanraud; Ajit Shankaranarayanan; David C Alsop; Torsten Rohlfing; Adolf Pfefferbaum
Journal:  Biol Psychiatry       Date:  2013-04-12       Impact factor: 13.382

Review 8.  Anosognosia for Memory Impairment in Addiction: Insights from Neuroimaging and Neuropsychological Assessment of Metamemory.

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9.  Atypical spatial working memory and task-general brain activity in adolescents with a family history of alcoholism.

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10.  White matter microstructure, alcohol exposure, and familial risk for alcohol dependence.

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