Basilar extension and posterior inferior cerebellar artery involvement as risk factors for progression of the unruptured spontaneous intradural vertebral artery dissection.
OBJECTIVE
Spontaneous intradural vertebral artery dissection (siVAD) primarily causes stroke in young and middle-aged individuals; however, data on the relationship between vertebrobasilar morphology and the progression of siVAD are limited.


METHODS
We retrospectively reviewed the data of 77 adult patients who were diagnosed with unruptured siVAD and treated conservatively. We analysed the clinical characteristics, vertebrobasilar morphologies and progression. Progression was defined as siVAD-induced stroke or morphological worsening of the siVAD.


RESULTS
Twenty patients experienced progression. Recurrent ischaemic events that occurred in the vertebrobasilar territory were seen in three patients (3.9%). Two of these three patients and other 17 patients showed morphological worsening. None of the patients presented with subarachnoid haemorrhage. The log-rank test showed male sex, migraine, basilar extension and the posterior inferior cerebellar artery involvement were associated with the progression. Multivariate analysis using the Cox proportional hazards model showed that only basilar extension and the posterior inferior cerebellar artery involvement were significantly related to the progression (p=0.012 and 0.019). In addition, patients with these two vertebrobasilar morphologies had a significantly shorter period of progression of siVAD than those without these morphologies (both, median 242 days; one of two, median 1292 days; none, median 2445 days).


CONCLUSIONS
Thus, some vertebrobasilar morphologies might be markers of the progression of unruptured siVAD. Although all unruptured siVAD patients should be closely monitored, those with basilar extension and posterior inferior cerebellar artery involvement should perhaps be more carefully followed than those without such morphologies.
Department of Neurosurgery, St. Luke's International Hospital, Tokyo, Japan.
Hidetoshi
H
Matsukawa
Department of Neurosurgery, St. Luke's International Hospital, Tokyo, Japan.
Masaki
M
Shinoda
Department of Neurosurgery, St. Luke's International Hospital, Tokyo, Japan.
Motoharu
M
Fujii
Division of General Internal Medicine, Department of Medicine, St. Luke's International Hospital, Tokyo, Japan.
Osamu
O
Takahashi
Department of Neuroendovascular therapy, St. Luke's International Hospital, Tokyo, Japan.
Akihiro
A
Uemura
Department of Neuroendovascular therapy, St. Luke's International Hospital, Tokyo, Japan.
Yasunari
Y
Niimi
D001488:Basilar Artery / Q000473:pathology*; D002531:Cerebellum / Q000098:blood supply / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D006801:Humans; D018810:Magnetic Resonance Angiography; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D020521:Stroke / Q000150:complications / Q000175:diagnosis / Q000473:pathology; D020217:Vertebral Artery Dissection / Q000150:complications / Q000175:diagnosis / Q000473:pathology*
Cerebrovascular Disease; Stroke