Quantitative magnetic resonance analysis in vascular dementia.

The potential role of magnetic resonance imaging (MRI) in differentiating between specific causes of cognitive decline in patients with vascular dementia (VD) has not yet been fully established. We therefore decided to assess the supratentorial cerebral contents in 24 patients with a diagnosis of probable VD and in 24 normal subjects, matched for age and education level, using MRI volumetric parameters obtained by means of a quantitative method. The volumes of subarachnoid and ventricular spaces, cerebral tissue, and hyperintense areas on T2-weighted images were calculated. In order to reduce interindividual variability caused by differences in intracranial size, each absolute measurement was normalized to the relative size of the intracranial volume. In addition, we calculated the ratio between the areas of the corpus callosum (CC) and supratentorial brain at the same level on the T1-weighted image midsagittal plane. The MRI data were correlated with the deterioration of cognitive functions. Patients with VD showed significantly lower cerebral tissue volume and CC area, and higher ventricular space volume than normal subjects. Furthermore, the total volume of the T2 signal alterations was higher in VD patients than in normal subjects. In VD patients, this volume was found to be proportional to the increase in the volume of the ventricular space. On the other hand, no correlation was found between the volume of the T2 signal alterations and the area of the CC. The degree of global cognitive dysfunction and the score of each neuropsychological test did not show any correlation with the MRI data. Our results suggest that ventricular enlargement in VD patients is correlated with the increase in volume of the T2 signal abnormalities, but that the degree of global cognitive dysfunction is not influenced by the volume of these T2 signal abnormalities. Furthermore, the CC atrophy does not influence the score of any neuropsychological test or the degree of global cognitive dysfunction.