Infarct Patterns in Patients With Symptomatic Carotid Webs

Abstract

Background Carotid webs (CaWs) may explain embolic strokes particularly in young patients with cerebral embolism of otherwise undetermined cause. We aim to describe the radiological patterns of infarction in patients with symptomatic CaWs. Methods Retrospective analysis of a symptomatic CaW database (September 2014–July 2019) from 2 comprehensive stroke centers. Magnetic resonance imaging scans were reviewed independently by 2 blinded raters. Patterns of acute infarction included territorial (involving ≥2 arterial subdivisions), cortical (affecting 1 arterial subdivision), 1or multiple small cortical infarcts, borderzone infarcts (cortical or internal), striatocapsular lacunes (<1.5 cm in size), or ≥1 deep vascular territory (involving subcortical contiguous deep structures). Different concomitant patterns could coexist. Prior strokes and leukoaraiosis severity (modified Fazekas scale) were evaluated. Results Forty symptomatic patients with CaW who had infarction were identified. The median age of patients was 49 years (interquartile range, 41–57 years), 22% were women, and 78% were of Black race. The median National Institute of Health Stroke Scale was 13 (interquartile range, 4–17), noncontrast Alberta Stroke Program Early CT Score was 8 (interquartile range, 7–8), and 13 (33%) patients received intravenous alteplase. Thirty‐four (85%) individuals presented with large vessel occlusion strokes (9% intracranial internal carotid artery, 62% middle cerebral artery M1 segment, 29% M2 segment). Sixty‐three percent of patients had right hemispheric strokes and 85% large vessel occlusion. Most patients (98%) had cortical infarcts: 30% were territorial, 38% affected 1 subdivision, and 63% had ≥1 small cortical infarct. Ten percent of the patients had infarcts involving borderzone areas. Fifteen percent of patients had striatocapsular lacunes, all of which had a concomitant cortical infarction. Five percent of patients had imaging evidence of previous strokes (all cortical and within the CaW vascular territory) and 20% had leukoaraiosis (18% grade 1 and 2% grade 2). Conclusion Acute cerebral infarction attributed to CaW were all compatible with an embolic mechanism. CaW should be considered in the workup of patients with cryptogenic strokes as a potential source of embolism.