Abstract
To clarify the etiology of periventricular hyperintensity (PVH) seen on MRI, PVH were studied in 103 patients with first-ever cerebral thrombosis (thrombosis group), compared with 2 groups of agematched controls, which consisted of 37 patients with hypertension/diabetes (risk group) and 78 patients with neither stroke nor any risk factors. MRI (T2-weighted) and angiography, examined within 3 months after the onset of stroke, were analyzed with regard to causative lesions, angiographic findings, risk factors for cerebrovascular accidents, and PVH. Causative lesions, compatible with neurological manifestations, were subdivided into 4 types; infarction involving the cerebral cortex (COR type), infarction located in the centrum semiovale (CSO type), small infarction in the internal capsule/corona radiata (IC-CR type), and infarction of brainstem/cerebellum (BS type). PVH was classified into 4 grades; none, rims/caps, patchy, and diffuse. Smooth PVH, adjoining the anterior/posterior angles and the margins of lateral ventricles, were defined as caps and rims, respectively. Irregular PVHs, confluent with each other, were defined as patchy, while diffuse PVHs extending below the cortex beyond the level of corpus callosum were defined as diffuse. Angiographic findings, obtained from 47 patients, were divided into 3 types; occlusion, stenosis (more than 75% of the lumen), and sclerotic/normal. There were 46 of the IC-CR type, 25 of the COR type, 22 of the BS type, and 10 of the CSO type. Both the COR and BS types were frequently associated with none/rims/caps PVHs, whereas diffuse PVH was seen in 60% of the CSO type and patchy PVH in 54% of the IC-CR type. On angiogram, diffuse PVH was prominent in patients with stenotic change, but none/rims/caps and patchy PHVs were accompanied by variable angiographic findings. Irregular, large PVHs (patchy and diffuse) were so frequent in the thrombosis group and hypertensive patients that these PVHs were considered to be pathologic changes due to vasculopathy. Moreover, diffuse PVH coexisted with stenotic changes and the CSO type infarction, which was caused hemodynamically by occlusive lesion of the major cerebral artery. In contrast, patchy PVH was mainly correlated with the IC-CR type infarction, which was based on the lesion of the perforating artery. These findings suggested that hemodynamic changes caused by large vessel diseases could result in diffuse PVH, while patchy PVH was confluented with multiple lesions induced by small vessel diseases.
