Cerebral Venous Sinus Thrombosis Presenting as an Acute Stroke Syndrome

TL;DR

This case study describes a rare stroke-like condition caused by blood clots in the brain's veins, emphasizing the importance of early diagnosis and proper treatment.

Contribution

The paper presents a case of cerebral venous sinus thrombosis with extensive clotting but no known clotting disorder, highlighting diagnostic and treatment considerations.

Findings

CVST can mimic arterial stroke but may lack arterial stenosis or occlusion.

Neurologic deficits in CVST can resolve quickly with anticoagulation alone.

Extensive clot burden does not always indicate an underlying thrombophilic disorder.

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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