Attributing pulsatile tinnitus to carotid artery stenosis: a lesion-level narrative review and five-domain diagnostic framework

Background Carotid artery stenosis is frequently identified during the evaluation of pulsatile tinnitus; however, coexistence alone does not establish that the stenotic lesion is the source of the perceived sound. A practical approach to causal attribution remains lacking. Methods We conducted a structured narrative review and evidence synthesis. Evidence was categorized into reports of atherosclerotic carotid stenosis or occlusion, nonatherosclerotic carotid lesions that informed anatomical localization, and contemporary diagnostic cohorts. Study design and major threats to validity were evaluated. The findings were then used to develop a five-domain clinical framework. This framework was conceptually derived and has not undergone statistical derivation or external validation. Results The stenosis-focused evidence included four direct observational or diagnostic studies and 13 interventional case reports or small case series. Five reports of nonatherosclerotic carotid lesions indicated that tortuosity, focal diaphragms or carotid webs, and dissection may produce pulsatile tinnitus through geometry-dependent disturbed blood flow. In a neuroangiographic cohort of 164 patients, arterial abnormalities accounted for only 6.7% of identified causes, whereas venous and arteriovenous shunting disorders were more frequent. Overall, the degree of stenosis alone was insufficient to establish causal attribution. Five clinically relevant domains emerged from the synthesis: symptom phenotype, physical examination, lesion anatomy, hemodynamic plausibility, and exclusion of alternative causes or symptom reversibility. Conclusions A carotid lesion is most plausibly responsible for pulsatile tinnitus when pulse synchrony and symptom laterality correspond to an anatomically and hemodynamically credible lesion and more common alternative causes have been excluded. Symptom improvement after treatment may strengthen causal attribution only when the intervention was independently clinically indicated. The proposed framework is intended to support structured multidisciplinary reasoning and should not be interpreted as establishing a new indication for carotid revascularization.