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Updated: Jun 11, 2025

Microsurgical Clip Obliteration of Middle Cerebral Aneurysm Using Intraoperative Flow Assessment
Published on: September 25, 2009
Convexity subarachnoid hemorrhage revealed contralateral internal carotid artery dissection due to Eagle syndrome: a
Kazuki Obara1,2,3, Takahiro Furuta4,5, Chikako Yagi4,6
1Department of Neurology, TOYOTA Memorial Hospital, Toyota, Aichi, Japan. obara.kazuki.a0@f.mail.nagoya-u.ac.jp.
Background:
Atraumatic localized convexity subarachnoid hemorrhage (cSAH) is an uncommon form of nonaneurysmal subarachnoid hemorrhage characterized by bleeding limited to the cerebral convexities. Ipsilateral cSAH can result from a variety of causes, such as internal carotid artery stenosis, obstruction, and dissection, although concomitant contralateral cSAH is exceptionally rare. In this case, the initial findings of cSAH led us to discovering contralateral internal carotid artery dissection (ICAD) and an elongated styloid process (ESP). ESP is recognized as a risk factor for ICAD, which is a hallmark of Eagle syndrome. This sequence of findings led to the diagnosis of Eagle syndrome, illustrating a complex and intriguing interplay between cerebrovascular conditions and anatomical variations.
Case Presentation:
A 47-year-old Japanese woman experienced acute onset of headache radiating to her neck, reaching its zenith approximately two hours after onset. Given the intractable nature of the headache and its persistence for three days, she presented to the emergency department. Neurological examination revealed no abnormalities, and the coagulation screening parameters were within normal ranges. Brain computed tomography (CT) revealed right parietal cSAH, while CT angiography (CTA) revealed ICAD and an ESP measuring 30.1 mm on the left side, positioned only 1.4 mm from the dissected artery. The unusual occurrence of contralateral cSAH prompted extensive and repeated imaging reviews that excluded reversible cerebral vasoconstriction syndrome (RCVS), leading to a diagnosis of left ICAD secondary to Eagle syndrome. The patient underwent conservative management, and the dissected ICA spontaneously resolved. The patient has remained recurrence-free for two and a half years.
Conclusions:
Managing cSAH requires diligent investigation for ICAD, extending beyond its identification to explore underlying causes. Recognizing Eagle syndrome, though rare, as a potential etiology of ICAD necessitates the importance of evaluating ESPs. The method for preventing recurrent cervical artery dissection due to Eagle syndrome is controversial; however, conservative management is a viable option.
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