Magnetization transfer ratio of white matter hyperintensities in subcortical ischemic vascular dementia

Citation
Jl. Tanabe et al., Magnetization transfer ratio of white matter hyperintensities in subcortical ischemic vascular dementia, AM J NEUROR, 20(5), 1999, pp. 839-844
Citations number
32
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging","Neurosciences & Behavoir
Journal title
AMERICAN JOURNAL OF NEURORADIOLOGY
ISSN journal
01956108 → ACNP
Volume
20
Issue
5
Year of publication
1999
Pages
839 - 844
Database
ISI
SICI code
0195-6108(199905)20:5<839:MTROWM>2.0.ZU;2-X
Abstract
BACKGROUND AND PURPOSE: In subjects with subcortical ischemic vascular deme ntia (SIVD), tissue vacuolization, myelin pallor, and demyelination have be en found on pathologic examination of white matter signal hyperintensities (WMSH). Magnetization transfer ratio (MTR) values provide a potential measu re of compromised white matter integrity. The purpose of this study was to determine if there were differences in MTR of WMSH between subjects with SI VD and cognitively normal healthy control subjects, METHODS: Fifteen subjects with SIVD and 16 control subjects of comparable a ge and sex were studied, MTR images were coregistered to MR images segmente d into tissue classes (gray matter, white matter, CSF, WMSH, and lacunar in farcts), MTR of WMSH was compared across groups and examined by WMSH locati on, size, and total burden, RESULTS: WMSH burden was greater in SIVD patients than in control subjects (2.4% vs 0.67%), MTR of WMSH did not differ between groups, but MTR of peri ventricular WMSH was lower in SIVD patients than in control subjects (37.6% vs 39.4%). Even after accounting for covariant effects of lesion burden, t here was still a trend toward reduced periventricular WMSH MTR in the group with dementia. There was no correlation between WMSH MTR and WMSH lesion s ize. CONCLUSION: These findings are consistent with observations that pathologic changes in vascular dementia are most severe in the periventricular white matter and suggest that insight into the pathophysiology of SIVD might be g leaned from studies of the periventricular region.