OBJECT: The authors reviewed their 20-year experience with giant anterior communicating artery aneurysms to correlate aneurysm size with clinical presentation and to analyze treatment methods. METHODS: In 18 patients, visual and cognitive impairment were quantitated and clinical outcome was categorized according to the Rankin scale. Statistical analysis was performed using Fisher's exact test. CONCLUSIONS: At least 3.5 cm of aneurysm mass effect was required to produce dementia in the patient (p = 0.0004). Dementia was usually caused by direct brain compression by the aneurysm rather than by hydrocephalus. Optic apparatus compression occurred with smaller aneurysms (2.7-3.2 cm) when they pointed inferiorly. Aneurysm neck clipping was possible in half of the cases. Special techniques, including temporary clipping, evacuation of intraluminal thrombus, tandem and/or fenestrated clipping, and clip reconstruction were often required. Occlusion of or injury to the anterior cerebral artery (ACA) was the main cause of poor outcome or death. Proximal ACA occlusion, even of dominant A1 segments with small or no contralateral A1 artery, was an effective treatment alternative and was well tolerated as a result of excellent leptomeningeal collateral circulation.
OBJECT: The authors reviewed their 20-year experience with giant anterior communicating artery aneurysms to correlate aneurysm size with clinical presentation and to analyze treatment methods. METHODS: In 18 patients, visual and cognitive impairment were quantitated and clinical outcome was categorized according to the Rankin scale. Statistical analysis was performed using Fisher's exact test. CONCLUSIONS: At least 3.5 cm of aneurysm mass effect was required to produce dementia in the patient (p = 0.0004). Dementia was usually caused by direct brain compression by the aneurysm rather than by hydrocephalus. Optic apparatus compression occurred with smaller aneurysms (2.7-3.2 cm) when they pointed inferiorly. Aneurysm neck clipping was possible in half of the cases. Special techniques, including temporary clipping, evacuation of intraluminal thrombus, tandem and/or fenestrated clipping, and clip reconstruction were often required. Occlusion of or injury to the anterior cerebral artery (ACA) was the main cause of poor outcome or death. Proximal ACA occlusion, even of dominant A1 segments with small or no contralateral A1 artery, was an effective treatment alternative and was well tolerated as a result of excellent leptomeningeal collateral circulation.