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Review
. 2008 Feb;50(2):161-70.
doi: 10.1007/s00234-007-0315-0. Epub 2007 Oct 23.

Idiopathic aneurysms of distal cerebellar arteries: endovascular treatment after rupture

Affiliations
Review

Idiopathic aneurysms of distal cerebellar arteries: endovascular treatment after rupture

A P Mitsos et al. Neuroradiology. 2008 Feb.

Abstract

Introduction: Idiopathic ruptured aneurysms of distal cerebellar arteries (DCAAs) are rare, and their endovascular therapy (EVT) has as yet not been extensively reported. They are usually assumed to result from local arterial wall disruption rather than infection, unlike distal supratentorial artery aneurysms. This study was performed to audit their frequency, potential aetiology and results of EVT.

Patients and methods: Using strict inclusion criteria and a database of 1715 EVT patients, we identified ten idiopathic ruptured DCAAs (0.6%) over a 13-year period (1993-2006). The series comprised six males and four females with mean age of 64 years and solitary aneurysms located on posterior inferior cerebellar artery (five patients), anterior inferior cerebellar artery (three patients) and superior cerebellar artery (two patients). Nine aneurysms were fusiform and were treated by endovascular parent artery occlusion, and one was saccular and treated by endosaccular packing. Endovascular therapy was performed with coils in seven cases, n-butyl-2-cyanoacrylate (NBCA) in two cases and with both in one case.

Results: Primary EVT was successful in eight patients. One patient died following a procedure-related re-bleeding and one patient required re-treatment after failed endosaccular packing. Nine patients made good or excellent clinical recoveries (modified Rankin Scale 2 or less). Focal cerebellar infarctions were seen on computed tomography images after EVT in three patients, only one of whom was symptomatic with transient dysmetria, which resolved completely during follow up. No aneurysm recanalisation was detected on late follow-up imaging up to 24 months.

Conclusion: Ruptured DCAAs are rare. The majority are fusiform in shape and their aetiology remains uncertain. Endovascular treatment is feasible and effective. It usually requires parent artery occlusion.

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