Abstract TP377: Posterior Cerebral Artery Stenosis and Thalamic Periventricular Anastomosis in Moyamoya Disease

Introduction: Moyamoya disease is defined by progressive stenosis of intracranial carotid arteries and compensatory collateral formation. Studies show that periventricular anastomoses (PA)—including lenticulostriate, thalamic, and choroidal subtypes—help maintain cerebral perfusion and autoregulation, but are fragile and prone to rupture or clotting. Identifying drivers of PA formation is therefore critical. Since the posterior cerebral artery (PCA) supplies deep perforators to the thalamus and periventricular regions, we examined whether PCA stenosis serves as a vascular marker for specific PA subtypes. Methods: We retrospectively analyzed 191 patients with bilateral moyamoya disease treated at Stanford Medicine from 2015 to 2024 (159F/32M; age 18–50). All underwent MRA using 3T MRI systems. PCA stenosis was scored as absent (0) or present (1) per hemisphere, with a composite variable set to 1 if stenosis was present on either side. PA was classified as lenticulostriate, thalamic, or choroidal, and graded 0–2 per hemisphere (0 = absent, 1 = mild, 2 = prominent). For modeling, grades 1–2 were combined as present. Logistic regression tested associations between PCA stenosis and PA presence, with odds ratios, 95% confidence intervals, and Fisher’s exact test performed in parallel. Results: Patients with PCA stenosis were over twelve times more likely to display thalamic PA (OR 12.06, 95% CI 4.56–31.91, p < 0.001), as shown in the bar plot ( Figure 1 ) and forest plot ( Figure 2) . By contrast, choroidal PA showed a weaker association (OR 2.80, 95% CI 1.23–6.37, p = 0.014), while lenticulostriate PA showed none (OR 1.30, 95% Cl 0.58–2.89, p = 0.53). Illustrative MRAs are shown in Figure 3 , where Patient A (39M; no stenosis) displayed no PA, whereas Patient B (36F; right stenosis) demonstrated prominent thalamic PA in the right hemisphere. Together, these findings establish PCA stenosis as a vascular marker of thalamic PA, with weaker or absent links to other subtypes. Conclusion: We evaluated PCA stenosis as a predictor of thalamic PA in moyamoya disease. Our findings establish a novel imaging marker for risk stratification and surgical planning. Incorporating PCA stenosis into routine evaluation could guide timely intervention for patients most likely to develop thalamic collaterals. Predicting treatment outcomes using pre-surgical periventricular anastomosis may further enhance the clinical utility of this marker, which is an area of our ongoing investigation.