Clinical Insights on My Acute Ischemic Stroke Caused by a Carotid Web

Acute ischemic stroke, a medical emergency caused by reduced cerebral blood flow, results in brain cell damage. While commonly associated with older individuals, strokes can also occur in young and middle-aged adults, posing significant socio-economic and health challenges due to the long-term impact of the condition. This poses significant socio-economic and health challenges because stroke is a leading cause of disability and mortality. A carotid web (CaW), a rare form of fibromuscular dysplasia, is increasingly recognized as a cause of cryptogenic stroke in young adults. Characterized by a fibrous intimal flap in the internal carotid artery, a CaW disrupts blood flow, promoting thrombosis and increasing stroke risk. I am a 46-year-old pediatrician with no significant medical history who experienced an ischemic stroke due to a CaW. The onset occurred during a morning jog when I experienced nausea, malaise, and unsteady movement. Although I exhibited no headache or paralysis, my wife observed slurred speech, prompting emergency consultation three hours after onset. Imaging revealed ischemia in the left middle cerebral artery territory. I underwent thrombolysis and mechanical thrombectomy, with good recovery except for mild aphasia. Pathological examination confirmed a CaW in the left carotid artery, with myxoid intimal changes and fibroblast proliferation. While the initial ultrasound (US) failed to detect a CaW, subsequent detailed US identified the lesion. Routine magnetic resonance angiography (MRA) also missed the CaW, highlighting its limitations in detecting such abnormalities. Diagnostic modalities like digital subtraction angiography (DSA) and computed tomography angiography (CTA) are effective but invasive. Non-invasive alternatives, such as US and MRA, are limited by operator dependency and technical constraints. For instance, B-mode US in experienced hands can detect CaWs in longitudinal views, but its diagnostic accuracy is lower than that of CTA and DSA. Advanced imaging, such as contrast-enhanced US and 3D MRA, offers potential improvements but is not yet standard practice. In my case, CTA provided a definitive diagnosis, while initial US and MRA missed smaller lesions. My recovery included intensive rehabilitation to address residual aphasia. Although I resumed professional duties within three months, minor symptoms, such as mild numbness and occasional speech difficulty, persist. This case highlights the diagnostic challenges of CaWs, particularly pre-stroke. Further research is needed to improve non-invasive detection methods and understand the pathogenesis of CaWs in order to facilitate earlier diagnosis and prevention.