Functional neuroimaging of cortical dysfunction in alcoholic korsakoff's syndrome

  • Authors:

  • Ken A. Paller;Ananth Acharya;Brian C. Richardson;Odile Plaisant;Arthur P. Shimamura;Bruce R. Reed;William J. Jagust

  • Affiliations:

  • Lawrence Berkeley National Laboratory and Northwestern University;Lawrence Berkeley National Laboratory and University of California, Davis;Lawrence Berkeley National Laboratory and University of California, Davis;University of California, Berkeley;University of California, Berkeley;Lawrence Berkeley National Laboratory and University of California, Davis;Lawrence Berkeley National Laboratory and University of California, Davis

  • Venue:
  • Journal of Cognitive Neuroscience
  • Year:
  • 1997

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Abstract

Many neuropsychological investigations of human memory have focused on the amnesic deficits of alcoholic Korsakoff's syndrome. Structural neuroimaging suggests that the syndrome results from midline diencephalic damage, but functional neuroimaging has the potential to reveal additional neuropathology that may be responsible for cognitive dysfunction. Accordingly, high-resolution positron emission tomography (PET) was used to measure regional cerebral metabolic rates for glucose utilization in five alcoholic Korsakoff patients and nine alcoholic control subjects. Results from a continuous recognition test administered during the radiotracer uptake period indicated that all subjects performed normally with respect to immediate memory, whereas Korsakoff patients demonstrated a marked memory impairment in delayed recognition. PET results from the Korsakoff group showed a widespread decline in glucose metabolism in frontal, parietal, and cingulate regions, suggesting that these functional abnormalities in the cerebral cortex contribute to the memory impairment. Hippocampal glucose metabolism did not differ between the groups. Thus, the evidence did not support the hypothesis that parallel brain dysfunctions are responsible for the similar amnesic symptomatology after hippocampal and diencephalic damage. We hypothesize that the amnesic dysfunction of Korsakoff's syndrome depends on a disruption of thalamocortical interactions that mediate a function critical for normal memory storage.