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Updated: May 8, 2026
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Disruption of Frontal Lobe Neural Synchrony During Cognitive Control by Alcohol Intoxication
Published on: February 6, 2019
Functional Neuroimaging of Cortical Dysfunction in Alcoholic Korsakoff's Syndrome
K A Paller1, A Acharya, B C Richardson
1Lawrence Berkeley National Laboratory and Northwestern University.
Journal of Cognitive Neuroscience
|August 22, 2013
Summary
Alcoholic Korsakoff's syndrome impairs delayed memory due to widespread brain metabolism decline, not just diencephalic damage. This suggests disrupted thalamocortical interactions contribute to memory loss in these patients.
Area of Science:
- Neuropsychology
- Neuroimaging
- Cognitive Neuroscience
Background:
- Alcoholic Korsakoff's syndrome is characterized by amnesic deficits.
- Structural neuroimaging implicates midline diencephalic damage, but functional deficits remain unclear.
Purpose of the Study:
- To investigate regional cerebral metabolic rates for glucose utilization in alcoholic Korsakoff patients using PET.
- To explore the neuropathology contributing to cognitive dysfunction in Korsakoff's syndrome.
Main Methods:
- High-resolution positron emission tomography (PET) was employed.
- Regional cerebral metabolic rates for glucose utilization were measured.
- Subjects included five alcoholic Korsakoff patients and nine alcoholic controls.
Main Results:
- Korsakoff patients showed normal immediate memory but impaired delayed recognition.
- PET revealed widespread glucose metabolism decline in frontal, parietal, and cingulate regions in Korsakoff patients.
- Hippocampal glucose metabolism did not differ between groups.
Conclusions:
- The findings suggest widespread cerebral cortical dysfunction contributes to memory impairment in Korsakoff's syndrome.
- Evidence does not support parallel brain dysfunctions after hippocampal and diencephalic damage.
- A disruption of thalamocortical interactions is hypothesized to underlie Korsakoff's syndrome amnesia.
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