Posterior Circulation Infarcts in Patients With Vertebrobasilar Dolichoectasia

Abstract

Background and Purpose-Vertebrobasilar dolichoectasia (VBD) may produce symptoms by direct compression of cranial nerves or the brain stem, by obstructive hydrocephalus, or by ischemia in the vertebrobasilar arterial territory. This study was undertaken to examine and characterize clinical and imaging findings in patients with stroke associated with VBD and compare these data with those for patients with VBD who did not have a stroke. Methods-We studied 40 consecutive stroke patients with associated VBD. All were evaluated by CT scan (nϭ9), MRI (nϭ6), or both (nϭ25). The diameter of the basilar artery (BA), height of bifurcation, and transverse position were evaluated. Clinical and imaging findings were compared with those found in a group of 40 VBD patients without stroke. Results-More than half of the patients (24 of 40) had infratentorial infarcts, located mainly in the midpons. Sixteen patients had supratentorial lesions localized in the thalamus (nϭ8) or in the superficial arterial territory of the posterior cerebral artery (PCA; nϭ8). The diameter and height of the bifurcation of the BA were correlated with the location of the lesion (PCA territory versus BA territory), in that severe ectasia and vertical elongation of the BA were significantly more often observed in patients with infarcts in PCA territory than in patients with infarcts in territories supplied by branches of the BA. Comparison of VBD patients with and without stroke showed that the incidence of arterial hypertension and the degree of ectasia and lateral displacement of the BA were not significantly different in the two groups. Patients with stroke more often had atherosclerotic changes of the posterior circulation (Pϭ.0006) and a higher degree of vertical elongation of the BA (Pϭ.025). Conclusions-In patients with VBD, superimposed atheromatous changes of the posterior circulation may have an important role in precipitating ischemia. However, other factors related to the severity of the dolichoectasia also favor ischemia and in some cases are the only factors responsible. (Stroke. 1998;29:653-659.)

The Pipeline Embolization Device for the treatment of posterior circulation fusiform aneurysms: lessons learned at a single institution

“…VFAs most commonly manifest as posterior circulation ischemic strokes, but they may also cause cranial nerve palsies, brainstem compression, obstructive hydrocephalus, and intraparenchymal or subarachnoid hemorrhage (SAH). 5,14,[18][19][20][21][22]29 VFAs have an ominous natural history with a reported mortality up to 30%. 3,24,29 Passero and Rossi reported that 43% of patients without treatment experienced anatomical progression and 60% experienced new symptoms.…”

Progressive cervicocranial arteriopathy with dilatations and stenoses: case report

“…The presence of dilatations in cervical or cranial arteries is a phenomenon that has received diverse and somewhat imprecise denominations, such as dilatative arteriopathy 1 , arterial dysplasia 2 , dolichoectasia 3 and fusiform aneurysms (FAs) [4][5][6] . The last two terms seem to designate different degrees of progression of the same disease.…”

“…FAs may be asymptomatic or cause brain stem and cranial nerve compression, subarachnoid hemorrhage (SAH) or infarction. The latter is more commonly caused by thrombosis of small collateral branches or embolism to distal arteries 3,9 . Complete occlusion of the affected vessel appears to be rare 12 .…”

Brainstem compression syndrome caused by vertebrobasilar dolichoectasia: microvascular repositioning technique

“…Some authors suggest that VBD may be a congenital vasculopathy of the elastic layer of the arterial wall, and may be cause of posterior circulation dysfunction independent of atherosclerosis disease affecting the intimal layer 1,3,10 . Others suggest a hypothesis that try to explain the posterior circulation ischaemia by the induced atherosclerosis in dolichoectatic arteries at the regions of maximum angulation [10][11][12] .…”

“…Others suggest a hypothesis that try to explain the posterior circulation ischaemia by the induced atherosclerosis in dolichoectatic arteries at the regions of maximum angulation [10][11][12] . Some still believe in the correlation between prolonged systemic arterial hypertension and the marked thinning of the internal elastic lamina and media of the abnormal vessel 2 .…”