Extracranial distal aneurysm of posterior inferior cerebellar artery

1997 ◽  
Vol 39 (5) ◽  
pp. 344-347 ◽  
Author(s):  
C. J. Chen ◽  
S. T. Chen
2020 ◽  
Author(s):  
Fabio Frisoli ◽  
Joshua S. Catapano ◽  
Stefan Koester ◽  
Gabriella Paisan ◽  
Michael Lang ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
pp. e238120
Author(s):  
Christopher Houle ◽  
Varun Reddy

This report describes a patient who developed intraprocedural vascular stasis immediately following elective endovascular coil emboliation. Urgent antiplatelet treatment with the GpIIb/IIIa agent tirofiban was used. It was infused intra-arterially during the procedure, followed by a fixed rate intravenous continuous infusion, and successfully restored normal circulation. There were no reports of further bleeding or haemodynamic compromise during the hospital stay. The patient’s condition returned to baseline and he was discharged the following day with no neurological deficits.


2010 ◽  
Vol 19 (5) ◽  
pp. 420-424
Author(s):  
Kenta Aso ◽  
Yoshitaka Kubo ◽  
Shunsuke Kakino ◽  
Hiroshi Kashimura ◽  
Atsushi Sugawara ◽  
...  

1997 ◽  
Vol 117 (4) ◽  
pp. 308-314 ◽  
Author(s):  
J. Magnan ◽  
F. Caces ◽  
P. Locatelli ◽  
A. Chays

Sixty patients with primitive hemifacial spasm were treated by means of a minimally invasive retrosigmoid approach in which endoscopic and microsurgical procedures were combined. Intraoperative endoscopic examination of the cerebellopontine angle showed that for 56 of the patients vessel-nerve conflict was the cause of hemifacial spasm. The most common offending vessel was the posterior inferior cerebellar artery (39 patients), next was the vertebral artery (23 patients), and last was the anterior inferior cerebellar artery (16 patients). Nineteen of the patients had multiple offending vascular loops. In one patient, another cause of hemifacial spasm was an epidermoid tumor of the cerebellopontine angle. For three patients, it was not possible to determine the exact cause of the facial disorder. Follow-up information was reviewed for 54 of 60 patients; the mean follow-up period was 14 months. Fifty of the patients were in the vessel-nerve conflict group. Forty of the 50 were free of symptoms, and four had marked improvement. The overall success rate was 88%, and there was minimal morbidity (no facial palsy, two cases of severe hearing loss).


1993 ◽  
Vol 33 (9) ◽  
pp. 634-637 ◽  
Author(s):  
Shoichiro KAWAGUCHI ◽  
Toshisuke SAKAKI ◽  
Kitaro KAMADA ◽  
Hideaki IWANAGA ◽  
Katsushige TAKEHASHI ◽  
...  

Neurosurgery ◽  
1990 ◽  
Vol 26 (3) ◽  
pp. 465-471 ◽  
Author(s):  
James I. Ausman ◽  
Fernando G. Diaz ◽  
Balaji Sadasivan ◽  
Manuel Dujovny

Abstract Intracranial vertebral endarterectomy was performed on six patients with vertebrobasilar insufficiency in whom medical therapy failed. The patients underwent operations for stenotic plaque in the intracranial vertebral artery with the opposite vertebral artery being occluded, hypoplastic, or severely stenosed. In four of the patients, the stenosis was mainly proximal to the posterior inferior cerebellar artery (PICA). In this group, after endarterectomy, the vertebral artery was patent in two patients, and their symptoms resolved: in one patient the endarterectomy occluded, but the patient's symptoms improved; and in one patient the endarterectomy was unsuccessful, and he continued to have symptoms. In one patient, the plaque was at the origin of the PICA. The operation appeared technically to be successful, but the patient developed a cerebellar infarction and died. In one patient the stenosis was distal to the PICA. During endarterectomy, the plaque was found to invade the posterior wall of the vertebral artery. The vertebral artery was ligated, and the patient developed a Wallenburg syndrome. The results of superficial temporal artery to superior cerebellar artery anastomosis are better than those for intracranial vertebral endarterectomy for patients with symptomatic intracranial vertebral artery stenosis. The use of intracranial vertebral endarterectomy should be limited to patients who have disabling symptoms despite medical therapy, a focal lesion proximal to the PICA, and a patent posterior circulation collateral or bypass.


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