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Parietal Gray Matter Volume Loss Is Related to Spatial Processing Deficits in Long-Term Abstinent Alcoholic Men

Authors

  • George Fein,

    1. From the Neurobehavioral Research, Inc. (GF, RS, RC), Honolulu, Hawaii; and California Pacific Medical Center (JB), San Francisco, California.
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  • Ryan Shimotsu,

    1. From the Neurobehavioral Research, Inc. (GF, RS, RC), Honolulu, Hawaii; and California Pacific Medical Center (JB), San Francisco, California.
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  • Russell Chu,

    1. From the Neurobehavioral Research, Inc. (GF, RS, RC), Honolulu, Hawaii; and California Pacific Medical Center (JB), San Francisco, California.
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  • Jerome Barakos

    1. From the Neurobehavioral Research, Inc. (GF, RS, RC), Honolulu, Hawaii; and California Pacific Medical Center (JB), San Francisco, California.
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Reprint requests: Dr. George Fein, Neurobehavioral Research, Inc. 1585 Kapiolani Blvd, Ste 1030, Honolulu, HI 96814; Fax: 808-442-1156; E-mail: george@nbresearch.com

Abstract

Background:  We previously demonstrated relatively intact cognitive function (with the exception of suggestive evidence for persistent deficits in spatial information processing) in middle-aged long-term abstinent alcoholics (LTAA, abstinent for 6 months or more) compared to age and gender comparable nonalcoholic controls (NAC) (Fein et al., 2006).

Methods:  In the current study, we examine cortical gray matter volumes in the same samples to determine whether gray matter volumes in LTAA are consistent with the cognitive results – i.e., exhibiting gray matter volumes comparable to NAC in most brain regions, except for possible indications of persistent shrinkage in the parietal lobe subserving spatial information processing.

Results:  We found gray matter shrinkage in LTAA in the parietal lobe consistent with the spatial processing deficits in this same sample. More compelling, in LTAA, the magnitude of parietal gray matter shrinkage was negatively associated with spatial processing domain performance and positively associated with alcohol dose. Gray matter volume deficits were present in the occipital and other cortical tissue, but poorer visuospatial test performance correlated significantly with smaller volumes in the parietal cortex only.

Conclusions:  Taken together, the cognitive and structural imaging data provide compelling evidence that chronic alcohol abuse results in shrinkage of the parietal cortex with associated deficits in spatial information processing.

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