A Stroke Without a Source? Unmasking Vasospasm and Arterial Embolization in ICAD

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Chest

Abstract

INTRODUCTION: Embolic stroke is traditionally attributed to cardioembolic or extracranial large-vessel disease, while cerebral vasospasm is most commonly associated with aneurysmal subarachnoid hemorrhage (aSAH). However, vasospasm can occur without hemorrhage, and its role in stroke pathogenesis is poorly understood. This case presents an atypical mechanism of embolic stroke, wherein diffuse intracranial atherosclerosis led to endothelial injury, triggering cerebral vasospasm and subsequent shower embolization in the absence of a conventional embolic source. CASE PRESENTATION: A 65-year-old woman with a history of hypertension, type 2 diabetes Mellitus, and ovarian cancer was found unresponsive at home with foaming at the mouth and urinary incontinence. On presentation, her Glasgow Coma Scale (GCS) was 11, and non-contrast head computed tomography (CT) showed no acute pathology. Shortly after, she experienced a generalized tonic-clonic seizure. She subsequently deteriorated neurologically, necessitating intubation. Following clinical stabilization, A computed tomography angiography (CTA) of the brain showed diffuse, smooth, long-segment narrowing of medium-to-small caliber vessels throughout the ACA, MCA, and PCA distributions, with distal extension into penetrating branches. These luminal changes were inconsistent with primary atherosclerosis and instead suggestive of a superimposed vasospastic process. Nimodipine was initiated for suspected vasospasm. Magnetic resonance imaging (MRI) demonstrated multiple acute to subacute ischemic infarcts in the centrum semiovale, bilateral frontal lobes, occipital lobes, and posterior left temporal lobe, consistent with embolic infarctions. Magnetic resonance angiography (MRA) revealed significant intracranial atherosclerosis, affecting segments of the right middle cerebral artery (MCA), segments bilaterally, left anterior cerebral artery (ACA), and posterior circulation, including the distal left vertebral artery, upper half of the basilar artery, and bilateral posterior cerebral arteries (PCA).Extensive embolic workup revealed no definitive cardioembolic source. Transesophageal echocardiography confirmed a left ventricular ejection fraction of 55%, with no left atrial thrombus, or patent foramen ovale. Carotid ultrasound demonstrated only mild atherosclerotic disease with normal flows bilaterally. A loop recorder placed postdischarge showed no atrial fibrillation. Given the extensive intracranial atherosclerosis, concurrent vasospasm, and absence of a conventional embolic source, we believe the diffuse vasospasm was secondary to arthroemoblic stroke from the diffuse intracranial atherosclerosis which had precipitated vasospasm, The patient was subsequently initiated on dual antiplatelet therapy (aspirin and clopidogrel) and a high-intensity statin. DISCUSSION: This case highlights an atypical yet clinically relevant stroke mechanism: shower emboli from intracranial atherosclerosis. While vasospasm is well-described in aSAH, its occurrence in the absence of hemorrhage is uncommon and remains poorly characterized. Cerebral vasospasm has been reported in conditions such as reversible cerebral vasoconstriction syndrome, traumatic brain injury, and systemic infections, but its role as a secondary consequence of intracranial atherosclerosis has not been extensively documented. The absence of a cardioembolic source, lack of extracranial large-vessel disease, and radiographic evidence of vasospasm suggest a novel stroke mechanism wherein intracranial arthroemoblic stroke from the diffuse intracranial atherosclerosis had precipitated vasospasm. CONCLUSIONS: This case challenges conventional stroke paradigms, demonstrating that diffuse cerebral vasospasm can occur secondary to intracranial atherosclerosis and serve as a trigger for embolic stroke. Recognizing this mechanism is crucial for optimizing treatment strategies and improving patient outcomes.

Volume

168

Issue

4S

First Page

2934A

Comments

American College of Chest Physicians CHEST Annual Meeting, October 19-22, 2025, Chicago, IL

Last Page

2935A

DOI

10.1016/j.chest.2025.07.1669

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