| Literature DB >> 11806116 |
M Honda1, N Yagi, H Baba, M Yonekura.
Abstract
We analyzed the clinical course of eight female patients of oculomotor nerve palsy due to unruptured internal artery posterior (IC-PC) communicating artery aneurysm in order to speculate on the mechanism of aneurysmal rupture. Seven of the eight patients had preceding headache or ophthalmalgia, three of them deteriorated oculomotor nerve palsy and one showed worsening of ophthalmalgia. These deteriorations occurred between three to seven days after the first clinical symptom appeared. Neck clipping of aneurysm was performed for all eight patients. These aneurysms were profiled except for one patient whose aneurysm ruptured before operation. None of these seven patients had subarachnoid hemorrhage in the operative field. The patients who showed clinical deterioration had fragile aneurysm wall, wall with bleb, and one aneurysm showed minor blood leakage during operative manipulation. In the four patients who did not show clinical deterioration, aneurysm attached oculomotor nerve, these aneurysm walls were arteriosclerotic and we could not find the fragile portion during operation. Repeated minor bleeding near the oculomotor nerve or direct aneurysmal compression are the main causes of oculomotor nerve palsy with unruptured IC-PC aneurysm. Adhesion or stimulation of aneurysm on the upper border of cavernous sinus cause the headache or ophthalmalgia and these deteriorations are thought to occur gradually. However, these deteriorations occur more rapidly than ever thought and reflect acute aneurysmal growth and its direct affect on the oculomotor nerve. IC-PC aneurysm is the only aneurysm we can observe its aneurysmal growth by its unique clinical presentation. From this study, we conclude that the deterioration of oculomotor nerve palsy, preceding headache or ophthalmalgia reflects rapid growth of unruptured IC-PC aneurysm. We neurosurgeons consider it to be an urgent rupture period and should introduce surgical management to prevent its rupture and the devastating consequence of subarachnoid hemorrhage.Entities:
Mesh:
Year: 2001 PMID: 11806116
Source DB: PubMed Journal: No To Shinkei ISSN: 0006-8969