Anterior communicating artery aneurysm clinical features

• High-resolution vessel wall imaging-driven radiomic analysis for the precision prediction of intracranial aneurysm rupture risk: a promising approach
• Predictive models for assessing the risk of brain aneurysm rupture
• Evaluation of FeMnN alloy bioresorbable flow diverting stents in the rabbit abdominal aorta
• AI-Driven Prediction of Glasgow Coma Scale Outcomes in Anterior Communicating Artery Aneurysms
• The FRED-X Flow Diverter-An Australian Experience
• Investigating the role of blood models in predicting rupture status of intracranial aneurysms
• Microsurgical clipping of ruptured basilar artery perforator aneurysms in the endovascular era: A single-center experience
• A Review of the Current Literature on Cerebral Aneurysms

Anterior communicating artery aneurysms are usually silent until they rupture.

Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnesia, or hypothalamic dysfunction.

Neurologic deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), brain hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe signs (20%).

May also present with diabetes insipidus (DI) or other hypothalamic dysfunction.

see Anterior Communicating Artery Aneurysm Visual Symptoms

Sayama et al. studied the incidence and timing of hyponatremia (Na < 135 mEq l-1) after subarachnoid hemorrhage (SAH) with special reference to ruptured anterior communicating artery (A-com) aneurysms. Hunt and Kosnik (HK) grading, symptomatic vasospasm in A-com aneurysm, and hydrocephalus were analyzed for connections to hyponatremia in 55 patients with ruptured A-com aneurysms, 65 with ruptured internal cerebral artery (ICA) aneurysms, and 49 with ruptured middle cerebral artery (MCA) aneurysms. Hyponatremia occurred in 28 (51%) of 55 patients with A-com aneurysms and in nine (18%) of 49 patients with MCA aneurysms. Severe hyponatremia (Na < 130 mEq l-1) occurred in 16 patients (29%) in the A-com group, four patients (6%) in the ICA group, and three patients (6%) in the MCA group. The A-com aneurysm group had a significantly higher incidence of mild hyponatremia (p < 0.01) and severe hyponatremia (p < 0.001) than other groups. Among A-com cases, hyponatremia occurred significantly more often in HK grade III and IV cases (p < 0.05), in cases with vasospasm (p < 0.001), and in cases with hydrocephalus (p < 0.01). Respective days of onset for symptomatic vasospasm and for hyponatremia were day 7.6 +/- 4.4 and day 10.6 +/- 5.8 following SAH, representing a 3-day delay for hyponatremia (p < 0.05). In most patients hyponatremia resolved within 28 days following SAH. Hyponatremia occurred more often with A-com aneurysms, possibly because of vasospasm around the A-com or hydrocephalus causing hypothalamic dysfunction. Since hypervolemic therapy can cause hyponatremia, particularly careful observation is required during such therapy in patients with A-com aneurysm ¹⁾.

Talland et al reported in 1967 a amnesic syndrome with anterior communicating artery aneurysm ²⁾.