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August 1995

Cortical Abnormalities Associated With Subcortical Lesions in Vascular Dementia: Clinical and Positron Emission Tomographic Findings

Author Affiliations

From the Departments of Psychiatry and Biobehavioral Sciences (Drs Sultzer, Cummings, Van Gorp, and Hinkin) and Neurology (Drs Mahler and Cummings), University of California—Los Angeles School of Medicine; and Psychiatry Service (Drs Sultzer, Mahler, and Cummings), Psychology Service (Drs Van Gorp and Hinkin), and Nuclear Medicine Service (Dr Brown), Veterans Affairs Medical Center, West Los Angeles.

Arch Neurol. 1995;52(8):773-780. doi:10.1001/archneur.1995.00540320049012

Objective:  To examine the effects of subcortical lesions on cortical metabolic rate and clinical symptoms in patients with vascular dementia.

Method:  Eleven elderly patients with vascular dementia who demonstrated no lesion involving the cerebral cortex on magnetic resonance imaging underwent 18F-fluorodeoxyglucose positron emission tomography to assess global cortical metabolism and metabolic activity in each cortical lobe. Subcortical lesions on magnetic resonance imaging (periventricular hyperintensities, deep white matter hyperintensities, and subcortical lacunar infarcts) were measured using a graded scale of severity. Cognitive and noncognitive symptoms were assessed with the Neurobehavioral Rating Scale.

Results:  Reduced cortical metabolism was generally associated with the severity of subcortical pathologic changes, but there was substantial heterogeneity in the relationship between subcortical lesions and cortical metabolic activity. Mean global cortical metabolism was lower in patients with periventricular hyperintensities in anterior subcortical regions than in those without such lesions. The metabolic rate in the frontal cortex was lower in patients with a lacunar infarct of the basal ganglia or thalamus than in those without. Neurobehavioral Rating Scale total score, the Verbal Output Disturbance factor score, and the Anxiety/Depression factor score were correlated with the severity of white matter lesions.

Conclusions:  Cortical metabolic dysfunction is related to ischemic subcortical lesions in patients with vascular dementia. Metabolism in the frontal cortex may be particularly dependent on pathologic alterations of subcortical nuclei. Anxiety, depression, and the overall severity of neuropsychiatric symptoms in vascular dementia are associated with the extent of white matter ischemia.

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