Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome

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

Research output: Contribution to journalArticle

56 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)277-293
Number of pages17
JournalJournal of Cognitive Neuroscience
Volume9
Issue number2
StatePublished - 1997

Fingerprint

Alcohol Amnestic Disorder
Functional Neuroimaging
Glucose
Positron-Emission Tomography
Parietal Lobe
Gyrus Cinguli
Short-Term Memory
Neuroimaging
Cerebral Cortex
Brain

ASJC Scopus subject areas

  • Behavioral Neuroscience
  • Experimental and Cognitive Psychology
  • Cognitive Neuroscience

Cite this

Paller, K. A., Acharya, A., Richardson, B. C., Plaisant, O., Shimamura, A. P., Reed, B. R., & Jagust, W. J. (1997). Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome. Journal of Cognitive Neuroscience, 9(2), 277-293.

Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome. / Paller, Ken A.; Acharya, Ananth; Richardson, Brian C.; Plaisant, Odile; Shimamura, Arthur P.; Reed, Bruce R; Jagust, William J.

In: Journal of Cognitive Neuroscience, Vol. 9, No. 2, 1997, p. 277-293.

Research output: Contribution to journalArticle

Paller, KA, Acharya, A, Richardson, BC, Plaisant, O, Shimamura, AP, Reed, BR & Jagust, WJ 1997, 'Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome', Journal of Cognitive Neuroscience, vol. 9, no. 2, pp. 277-293.
Paller KA, Acharya A, Richardson BC, Plaisant O, Shimamura AP, Reed BR et al. Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome. Journal of Cognitive Neuroscience. 1997;9(2):277-293.
Paller, Ken A. ; Acharya, Ananth ; Richardson, Brian C. ; Plaisant, Odile ; Shimamura, Arthur P. ; Reed, Bruce R ; Jagust, William J. / Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome. In: Journal of Cognitive Neuroscience. 1997 ; Vol. 9, No. 2. pp. 277-293.
@article{9d431fa0eb8e4507ab2e34315dbdd041,
title = "Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome",
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.",
author = "Paller, {Ken A.} and Ananth Acharya and Richardson, {Brian C.} and Odile Plaisant and Shimamura, {Arthur P.} and Reed, {Bruce R} and Jagust, {William J.}",
year = "1997",
language = "English (US)",
volume = "9",
pages = "277--293",
journal = "Journal of Cognitive Neuroscience",
issn = "0898-929X",
publisher = "MIT Press Journals",
number = "2",

}

TY - JOUR

T1 - Functional neuroimaging of cortical dysfunction in alcoholic Korsakoff's syndrome

AU - Paller, Ken A.

AU - Acharya, Ananth

AU - Richardson, Brian C.

AU - Plaisant, Odile

AU - Shimamura, Arthur P.

AU - Reed, Bruce R

AU - Jagust, William J.

PY - 1997

Y1 - 1997

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0030899907&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030899907&partnerID=8YFLogxK

M3 - Article

VL - 9

SP - 277

EP - 293

JO - Journal of Cognitive Neuroscience

JF - Journal of Cognitive Neuroscience

SN - 0898-929X

IS - 2

ER -