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AJNR - American Journal of Neuroradiology

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American Journal of Neuroradiology 24:1200-1207, June-July 2003
© 2003 American Society of Neuroradiology

INTERVENTIONAL

Symptomatic Cavernous Sinus Aneurysms: Management and Outcome After Carotid Occlusion and Selective Cerebral Revascularization

Melvin Field^a, Charles A. Jungreis^b, Nicole Chengelis^a, Holly Kromer^a, Lori Kirby^a and Howard Yonas^a

^a Department of Neurological Surgery, University of Pittsburgh School of Medicine, PA
^b Department of Radiology, University of Pittsburgh School of Medicine, PA

Address reprint requests to Melvin Field, MD, Department of Neurological Surgery, University of Pittsburgh School of Medicine, PUH Suite B-400, 200 Lothrop St, Pittsburgh, PA 15213

BACKGROUND AND PURPOSE: Therapeutic internal carotid artery (ICA) occlusion for symptomatic intracavernous artery aneurysms can result in ischemic infarction despite normal clinical balloon test occlusion (BTO). We evaluated outcomes in patients with symptomatic cavernous sinus aneurysms in whom clinical BTO was normal, who underwent carotid occlusion with selective bypass surgery guided by physiologic BTO using quantitative cerebral blood flow (CBF) analysis by means of stable xenon-enhanced CT.

METHODS: After a normal clinical BTO, 26 consecutive patients with symptomatic cavernous sinus aneurysms underwent a baseline xenon-enhanced CT CBF analysis followed by a second CBF analysis, during which repeat BTO was performed. Patients with a decrease in cortical CBF to below 30 mL/100 g/min were considered moderate risk and those with greater than 30 mL/100 g/min were low risk for developing postocclusion ischemic infarction. Moderate-risk patients underwent cerebral revascularization followed by proximal carotid occlusion. Low-risk patients underwent carotid occlusion alone. Patients were clinically followed up for at least 3 months after carotid occlusion. All patients underwent head CT at least 1 month after carotid occlusion.

RESULTS: Eight patients were moderate risk and 18 low risk. Mean follow-up was 15.3 months. Mean CT follow-up was 10.2 months. No low-risk patient developed a postocclusion ischemic deficit by examination or infarct by CT. One patient in the moderate-risk group developed right hemiparesis and a left posterior middle cerebral artery infarction by CT 2 months after carotid occlusion.

CONCLUSION: In this series, BTO combined with quantitative CBF analysis was a safe and reliable technique for identification of patients at risk for ischemic infarction after carotid occlusion, despite a normal clinical BTO.