Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease

Citation
G. Fein et al., Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease, NEUROLOGY, 55(11), 2000, pp. 1626-1635
Citations number
46
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
55
Issue
11
Year of publication
2000
Pages
1626 - 1635
Database
ISI
SICI code
0028-3878(200012)55:11<1626:HACAPD>2.0.ZU;2-6
Abstract
Background: The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial. Objectives: To determine whether cognitive impairm ent in SIVD 1) correlates with measures of ischemic brain injury or brain a trophy, and/or 2) is due to concomitant AD. Methods: Volumetric MRI of the brain was performed in 1) elderly subjects with lacunes (L) and a spectrum of cognitive impairment-normal cognition (NC+L, n = 32), mild cognitive imp airment (CI+L, n = 26), and dementia (D+L, n = 29); 2) a comparison group w ith probable AD (n = 28); and 3) a control group with normal cognition and no lacunes (NC). The authors examined the relationship between the severity of cognitive impairment and 1) volume, number, and location of lacunes; 2) volume of white matter signal hyperintensities (WMSH); and 3) measures of brain atrophy (i.e., hippocampal, cortical gray matter, and CSF volumes). R esults: Among the three lacune groups, severity of cognitive impairment cor related with atrophy of the hippocampus and cortical gray matter, but not w ith any lacune measure. Although hippocampal atrophy was the best predictor of severity of cognitive impairment, there was evidence for a second, part ially independent, atrophic process associated with ventricular dilation, c ortical gray matter atrophy, and increase in WMSH. Eight autopsied SIVD cas es showed variable severity of ischemic and neurofibrillary degeneration in the hippocampus, but no significant AD pathology in neocortex. The probabl e AD group gave evidence of only one atrophic process, reflected in the sev erity of hippocampal atrophy, Comparison of regional neocortical gray matte r volumes showed sparing of the primary motor and visual cortices in the pr obable AD group, but relatively uniform atrophy in the D+L group. Conclusio ns: Dementia in SIVD, as in AD, correlates best with hippocampal and cortic al atrophy, rather than any measure of lacunes. In SIVD, unlike AD, there i s evidence for partial independence between these two atrophic processes. H ippocampal atrophy may result from a mixture of ischemic and degenerative p athologies. The cause of diffuse cortical atrophy is not known, but may be partially indexed by the severity of WMSH.