Brain glucose metabolism in vascular white matter disease with dementia: differentiation from Alzheimer disease

Abstract

Background and purpose: The boundary between vascular dementia and Alzheimer disease (AD) continues to be unclear. Some posit that gradually progressive vascular dementia, as with small vessel disease, is simply vascular disease plus AD. Because AD presents a characteristic pattern on fluorodeoxyglucose positron emission tomography, we sought to determine whether the fluorodeoxyglucose pattern of vascular dementia resembled more AD or the pattern in nondemented patients with severe microvascular brain disease.

Methods: Vascular disease patients were selected on the basis of confluent white matter lesions on both hemispheres. Among them, with a similar degree of vascular disease on MRI, neuropsychological testing separated groups with dementia and without dementia. Patients with AD and healthy controls were also studied. The 4 groups, with 12 subjects each, were matched by age, gender, and educational level. Fluorodeoxyglucose distribution was analyzed using both voxel-based and volume of interest methods.

Results: The AD group had the characteristic pattern of bilaterally decreased metabolism in parieto-temporal association cortex and precuneus. By contrast, patients with vascular disease and dementia had a similar anatomic pattern to that of the vascular patients without dementia, but with greater metabolic abnormalities, particularly in the frontal lobes and deep nuclei.

Conclusions: The anatomy of metabolic abnormalities in vascular disease with dementia suggests that, at least in some cases, dementia with vascular disease may be independent of AD. The metabolic abnormality involves the thalamus, caudate, and frontal lobe, a pattern concordant with the neuropsychological findings of impaired executive function characteristic of vascular dementia.