Stroke in patients with fusiform vertebrobasilar aneurysms

Abstract

We studied seven patients with brainstem infarction and large fusiform vertebrobasilar (VB) aneurysms to clarify the clinical, radiologic, and pathologic features. All presented with pontine infarcts; one also had a cerebellar infarct. VB TIAs preceded brainstem infarction in four patients. Angiography and CT documented VB fusiform aneurysmal dilatation. Four had intraluminal thrombi and one had severe basilar artery stenosis. Two distinct clinical pictures emerged: unilateral pontine infarcts with favorable outcome, presumably related to obstruction of a pontine penetrating artery at its origin from the posterior wall of the aneurysmal basilar artery, and major fatal bilateral pontine infarcts from basilar artery occlusion. Two patients came to autopsy. One had thrombus in the dilated basilar artery and a posterior cerebral artery branch embolus with hemorrhagic occipital infarction; the other had basilar artery thrombus with aneurysmal rupture and subarachnoid hemorrhage. Fusiform VB aneurysms caused brainstem stroke by intraluminal thrombus, local embolism, atherostenosis, and obstruction of paramedian penetrating arteries. Subarachnoid hemorrhage is an uncommon complication.

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.…”

Intracranial Bleeding in Patients With Vertebrobasilar Dolichoectasia

“…[7][8][9][10][11][12][13] However, pathological changes in the arterial wall, consisting primarily in defects in the internal elastic lamina with thinning of the media secondary to smooth muscle atrophy, 14 -16 may predispose patients to intracranial bleeding of various kinds. Knowledge of hemorrhagic stroke as a clinical feature of VBD has come from case reports involving a small number of patients.…”

Progressive cervicocranial arteriopathy with dilatations and stenoses: case report

“…The last two terms seem to designate different degrees of progression of the same disease. Etiopathogenic heterogeneity is suggested by descriptions of a number of wall abnormalities 1,[6][7][8][9][10][11] . The most frequent findings in affected arteries have been loss of medial layer components, collagen fiber degeneration, fibrosis, atherosclerotic changes and parietal thrombosis 7,8,10,11 .…”

“…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 .…”