1999 Volume 36 Issue 11 Pages 803-810
This study was conducted to clarify brain and carotid lesions in patients with asymptomatic carotid bruits and their characteristics. We studied 37 patients with carotid bruits, who had various diseases other than stroke and were all neurologically normal, using by brain computerized tomography (CT) and ultrasonography (US). On CT, localized low density areas (LDAs) and their distribution were assessed, as well as the grade of periventricular lucency (PVL). Carotid lesions on US were classified into 3 categories; plaque (locally thickened intima-media complex of 2.1mm or more in thickness), stenosis (narrowed lumen between 50% and 90% of the linearly measured diameter), and occlusion (severely narrowed lumen more than 90%). Ankle pressure index (API) less than 0.9 was defined as low. Mean age was 73.2 years-old and 28 of them were men. Bruits were heard bilaterally in 15 patients. CT findings showed LDA in 13 patients (35%) and severe PVL in 12 patients (32%). Twenty-three LDAs (13 in the left hemisphere and 10 in the right hemisphere) were seen and all were considered to be infarctions. Nineteen LDAs, 13 of them seen in the basal ganglia, were lacunae. Another 3 LDAs were seen in the watershed zone between the middle and posterior cerebral arteries, whereas the remaining one was a small cortical infarction in the left premotor area in the middle cerebral artery territory. Ultrasonography showed carotid lesions in 65 of 74 carotid arteries (plaque in 28, stenosis in 26, and occlusion in 11) and low API in 18 of 37 patients. Compared with patients with normal CT finding, the frequency of hypertension (92% vs 50%) and ischemic heart disease (69% vs 29%) was significantly high in 13 patients with silent infarction, although there was no difference in US findings. In the hemisphere ipsilateral to the carotid with bruits, which was frequently stenotic, the frequency of infarction was similar to that in the hemisphere ipsilateral to the carotid with no bruit. Regression analysis revealed that hypertension significantly correlated with the presence of cerebral infarction. These findings indicated that incidence of infarction in the elderly patients with asymptomatic carotid bruits was high and was associated with hypertension and advanced atherosclerosis in many organs, including the carotid and peripheral arteries. The reason for the lack of symptoms was considered to be that most of the infarctions were lacunae and located in the basal ganglia, although infarction did not significantly correlate with bruits or carotid lesions.
