Abstract
OBJECTIVE: To investigate the features of local collateral vessel formation at the site of intracranial atherosclerotic stenosis (ICAS) and its relationship with cerebral infarction events. METHODS: Retrospectively analyzed patients diagnosed with ICAS or moyamoya disease (MMD) who underwent three-dimensional T1-weighted turbo-spin-echo (3D T1W-TSE), 3D time-of-flight magnetic resonance angiography (TOF-MRA), and DSA between June 2018 and March 2025. Key imaging features, including ICAS with local collateral vessels (ICAS-lcv), hyperintense vessel sign score, degree and location of M1-MCA stenosis, plaque enhancement grade, and posterior cerebral artery (PCA) diameter, were independently quantified by two neuroradiologists blinded to clinical data. Subgroup and logistic-regression analyses were then performed. RESULTS: A total of 149 cases with atherosclerotic stenosis in the middle cerebral artery (MCA) and 41 cases with MMD were enrolled. Among them, 29 cases with ICAS-lcv, and 59 MMD lesions exhibited moyamoya vessels. More ICAS-lcv cases were observed in individuals with severe stenosis or occlusion. Multivariable logistic regression identified the degree of stenosis as an independent risk factor for collateral formation in non-infarcted ICAS. Inter-group and subgroup analyses revealed that the infarct group had a lower incidence of ICAS-lcv than the non-infarct group. After adjustment for confounders, multivariable logistic regression showed that the presence of ICAS-lcv (OR, 0.24; 95%CI [0.08–0.70]; p = 0.009) was independently associated with infarction. Moreover, the diameter of the PCA distinguished ICAS-lcv from MMD with an area under the curve (AUC) of 0.87. CONCLUSION: The evidence of local collateral vessels on TOF-MRA contributes to managing the risk of cerebral infarction in ICAS, whereas the caliber of the PCA serves as a potential imaging marker to differentiate ICAS-lcv from MMD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12880-026-02218-1.