The mechanism of ischemic stroke in patients with dolichoectatic basilar artery

Abstract

Basilar artery dolichoectesia (BD) may cause brainstem ischemia by multiple mechanisms, including thrombosis, embolism, occlusion of deep penetrating arteries. The objective of this study was to determine and characterize clinical, imaging findings and hemodynamic mechanisms in patients with cerebrovascular event associated with BD and compare these data with those for patients with BD who did not have stroke. We studied 29 consecutive stroke, two transient ischemic attack (TIA) patients with BD who have been admitted to our stroke unit. We sought the diameter of ectasia, height of the bifurcation, lateral displacement, shape deformities, and blood flow velocity of the basilar artery (BA) by transcranial Doppler. Imaging and hemodynamic findings were compared with those found in a group of 18 patients without stroke or TIA. The main infarct localization was pons, eight (28%) with restricted single lesion, 10 (32%) with multiple lesions involving thalamus, midbrain, posterior cerebral artery (PCA) territory. Patients with BD were more probably to have had stroke fitting a clinical and imaging patterns of multiple infarcts than those with restricted infarct in territories supplied by branches of the BA (60% vs. 40%). Hypertension and atherosclerotic changes of the posterior circulation were more frequent in patients with stroke than those without (P = 0.004 and P = 0.028, respectively), whilst the incidence of other vascular risk factors were not significantly different in two groups. Patients with stroke/TIA had more often low blood flow velocity but not significant in the BA when compared with those for BD patients without cerebrovascular event (71% vs. 39%; P = 0.1). Reduced blood flow velocity in the BA was correlated significantly with distal lesions involving thalamus, midbrain and PCA territory rather than those located in the territory supplied by branches of the BA (P = 0.02). In conclusion, it seems probably that BD may cause vertebrobasilar system ischemia by multiple mechanisms, especially reduced blood flow in the BA and atheromatous changes in the vertebrobasilar system may precipitate thromboembolic stroke.