A 73-year-old woman presented to the emergency department with sudden onset of left arm weakness that had occurred one hour prior to arrival. The neurological symptoms lasted several minutes and resolved spontaneously. On examination, her National Institutes of Health Stroke Scale (NIHSS) score was 0. One month earlier, she had been diagnosed with diabetes mellitus (DM) but had not taken the prescribed medication. She had no history of prior stroke or transient ischemic attack, was a non-smoker, and had no other conventional vascular risk factors. Laboratory evaluation revealed marked hyperglycemia with a serum glucose level of 424 mg/dL and a glycated hemoglobin level of 12.84%. Low-density lipoprotein cholesterol was 133 mg/dL, and D-dimer was 0.52 μg/mL. Complete blood count as well as renal and liver function tests were within normal limits. No potential cardioembolic source was identified on electrocardiography or transthoracic echocardiography.

Non-contrast brain computed tomography (CT) showed no acute abnormalities. Brain magnetic resonance imaging (MRI) demonstrated acute ischemic lesions in the right frontal region (Fig. 1A). Magnetic resonance angiography (MRA) revealed a shelf-like intraluminal projection arising from the posterior wall of the proximal right internal carotid artery (ICA) and extending into the lumen without causing significant stenosis, consistent with the characteristic imaging appearance of carotid web (Fig. 1B). At the time of treatment decision, the patient had complete resolution of symptoms with no residual neurological deficits (NIHSS score 0). Because the symptoms were no longer present and were considered non-disabling, intravenous thrombolytic therapy was not administered. During hospitalization, glycemic control was initiated with combination oral antidiabetic therapy. The patient was treated with dual antiplatelet therapy consisting of aspirin 100 mg and clopidogrel 75 mg, together with high-intensity statin therapy (atorvastatin 40 mg daily). She was discharged on hospital day 9 without neurological deterioration.

One week after discharge, the patient was readmitted with newly developed left hemiplegia and dysarthria noted upon awakening. On arrival, her NIHSS score was 9, with deficits involving the left upper and lower extremities and dysarthria. Brain MRI demonstrated newly developed acute ischemic lesions in the right frontoparietal region superimposed on the previous infarcts (Fig. 1C). MRA showed progressive enlargement of the shelf-like filling defect at the site of the carotid web in the proximal right ICA, resulting in a more prominent intraluminal projection than on the initial examination, suggestive of evolving thrombus associated with the carotid web (Fig. 1D). As the patient presented with a wake-up stroke, imaging-based eligibility for reperfusion therapy was assessed. CT perfusion imaging did not demonstrate a significant perfusion deficit or substantial salvageable penumbra (Fig. 1E, 1F). Therefore, acute reperfusion therapy was not pursued.

To further characterize the vascular abnormality, digital subtraction angiography (DSA) was performed the following day. Angiography demonstrated a filling defect consistent with CaW, with a superimposed intraluminal thrombus in the distal portion (Fig. 1G). Given the recurrent ischemic events despite dual antiplatelet therapy and high-intensity statin treatment, together with the presence of a superimposed thrombus, surgical intervention was considered. CEA was planned to remove both the thrombus and the underlying web structure in order to prevent further thrombus formation and recurrent embolic events. In preparation for surgery, clopidogrel was discontinued 5 days before the procedure, while aspirin was continued.

After stabilization of the acute neurological deficits and completion of diagnostic evaluation, CEA was performed on hospital day 8. Intraoperatively, a web-like intimal structure projecting into the lumen of the ICA was identified, along with an attached thrombus (Fig. 1H). An intraoperative shunt was used to maintain cerebral blood flow during carotid cross-clamping, and patch angioplasty was performed using bovine pericardium after endarterectomy. Complete removal of the thrombus and CaW was successfully achieved without perioperative complications. Postoperatively, no neurological deterioration was observed. Follow-up CT angiography demonstrated no residual abnormality in the proximal right ICA. After CEA, the patient was maintained on clopidogrel and high-intensity statin therapy, together with continued management of vascular risk factors including DM. The patient’s neurological deficits gradually improved during hospitalization, and she was transferred to a rehabilitation facility on postoperative day 8 with an NIHSS score of 6 and a modified Rankin Scale (mRS) score of 3. At one-year follow-up, she had mild residual neurological deficits with an mRS score of 2 and remained free of recurrent ischemic stroke.

CaW has been increasingly recognized as a potential cause of cryptogenic ischemic stroke. Although traditionally described in younger patients, recent studies suggest that CaW can occur across a broader age range and may remain clinically silent until a thromboembolic event occurs.^3-6 In elderly patients, CaW may be overlooked or misattributed to atherosclerotic disease, potentially leading to underdiagnosis.

The diagnosis of CaW is primarily based on characteristic imaging findings. On brain CT angiography and MRA, CaW typically appears as a thin shelf-like intraluminal projection arising from the posterior wall of the carotid bulb or proximal ICA.^1,7 On DSA, it is visualized as a linear or triangular filling defect projecting into the lumen, often accompanied by delayed contrast clearance distal to the lesion.⁸ These features help distinguish CaW from atherosclerotic plaque, which generally presents as a broader-based lesion associated with calcification, lipid-rich components, or irregular luminal narrowing.

The proposed mechanism of ischemic stroke in CaW involves flow stagnation and disturbed flow distal to the web, creating a prothrombotic environment that promotes thrombus formation and embolization. These pathological flow characteristics appear to be driven by the geometry of the web itself rather than by the degree of luminal stenosis.^9,10 In the present case, serial MRA demonstrated interval enlargement of the intraluminal filling defect before DSA confirmation of thrombus, suggesting ongoing thrombus formation within the flow stagnation zone created by the web. Although the recurrent infarcts involved both external and internal watershed territories, significant cerebral hypoperfusion was not demonstrated on CT perfusion imaging. Together with the progressive enlargement of the filling defect and subsequent thrombus confirmation on DSA, these findings suggest that thromboembolism arising from the carotid web likely contributed to the recurrent ischemic events.

Previous studies have demonstrated a high risk of recurrent stroke in patients with symptomatic CaW treated with medical therapy alone, whereas carotid revascularization substantially reduces recurrence risk.^2,5,7 In the present case, recurrent stroke occurred despite dual antiplatelet therapy, and serial MRA demonstrated progressive enlargement of the intraluminal filling defect with subsequent DSA confirmation of superimposed thrombus. Because ongoing thrombus formation and recurrent embolization were considered likely despite medical therapy, surgical intervention was pursued after neurological stabilization and completion of diagnostic evaluation. CEA was favored over CAS to allow direct removal of both the web and thrombus while avoiding the potential risk of distal embolization during endovascular manipulation. The patient remained free of recurrent stroke during one year of follow-up.

This report has several limitations. Carotid duplex ultrasonography, late venous-phase angiographic images, and histopathological examination of the resected specimen were not available. Nevertheless, the diagnosis was supported by characteristic serial MRA findings, angiographic confirmation of a corresponding filling defect with superimposed thrombus on DSA, and direct intraoperative visualization of a web-like intimal projection with attached thrombus.

Our study highlights that carotid web (CaW) should not be overlooked as a potential cause of recurrent ischemic stroke, even in elderly patients, and that superimposed thrombus formation may contribute to stroke recurrence. Recognition of CaW as a potential embolic source is therefore important regardless of patient age. In selected symptomatic patients who develop recurrent ischemic events despite medical therapy, particularly in the presence of superimposed thrombus, CEA may be considered to reduce the risk of further stroke recurrence.