The relation of cerebral magnetic resonance signal hyperintensities to Alzheimer's disease

• Published in: Journal of the neurological sciences 1996-10, Vol.142 (1-2), p.121-125
• Main Authors: FAZEKAS, F, KAPELLER, P, SCHMIDT, R, OFFENBACHER, H, PAYER, F, FAZEKAS, G
• Format: Article
• Language: English
• Subjects: Aged; Alzheimer Disease - diagnosis; Alzheimer Disease - pathology; Atrophy; Biological and medical sciences; Corpus Callosum - pathology; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Humans; Magnetic Resonance Imaging; Male; Matched-Pair Analysis; Medical sciences; Middle Aged; Nerve Fibers - pathology; Neurology; Predictive Value of Tests
• ISSN: 0022-510X; 1878-5883
• DOI: 10.1016/0022-510X(96)00169-4

To further elucidate the relation of cerebral magnetic resonance signal hyperintensities to Alzheimer's disease (AD) we performed a case-control comparison between 30 consecutive patients with probable AD (age range 49-76, mean 65 years) and 60 asymptomatic volunteers matched for age, sex, and major cerebrovascular risk factors. We used a 1.5T magnet and determined the extent of morphologic abnormalities both by visual grading and measurement. AD patients showed comparable grades of deep/subcortical white matter hyperintensities (WMH) and a similar extent of the total WMH area as controls (3.3 cm2 +/- 8.8 vs. 2.0 cm2 +/- 4.6). They had significantly more often a "halo' of periventricular hyperintensity (PVH) (p < 0.0005) and an increased mean PVH thickness (3.0 mm +/- 1.9 vs. 1.3 mm +/- 1.2; p < 0.001). This PVH thickness correlated significantly with measures of ventricular enlargement. While univariate logistic regression also suggested a significant association of PVH thickness with a diagnosis of AD this association was lost against atrophy measures in a multivariate analysis. Our results confirm a significantly greater extent of PVH in AD patients than controls even when matched for cerebrovascular risk factors. However, this abnormality was not independently related to the disease but rather appears to be an epiphenomenon of brain atrophy.