ArticleCureus2026
Cerebral Venous Sinus Thrombosis Presenting as an Acute Stroke Syndrome.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral venous sinus thrombosis (CVST) is an uncommon cause of stroke and can present in ways that closely resemble arterial transient ischemic attack or ischemic stroke. Early recognition is important because management differs from typical stroke pathways, and initial noncontrast head CT may be normal. We report a 63-year-old male patient with a history of remote pulmonary embolism, pulmonary hypertension, and a family history of venous thromboembolism who presented with several weeks of headache and neck pain followed by acute left-sided weakness. Initial computed tomography (CT) imaging showed no hemorrhage. CT venography revealed extensive dural venous sinus thrombosis involving the superior sagittal sinus, right transverse sinus, right sigmoid sinus, and extension into the distal right internal jugular vein, without arterial stenosis or large vessel occlusion. MRI with contrast confirmed near-complete involvement of the superior sagittal sinus with extension into the bilateral transverse sinuses. His neurologic deficits resolved quickly, thrombolysis was deferred, and anticoagulation was initiated with intravenous heparin followed by rivaroxaban. A comprehensive evaluation for inherited and acquired thrombophilia was negative. This case highlights the need to consider CVST in patients with headache preceding focal neurologic deficits, even when the initial stroke evaluation is unrevealing. It also demonstrates that extensive clot burden may occur in the absence of an identifiable thrombophilic disorder. Anticoagulation remains the primary treatment, and escalation to endovascular therapy should be guided by clinical course and anatomic patterns rather than clot burden alone.
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