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Neurology ; 98(18 SUPPL), 2022.
Article in English | EMBASE | ID: covidwho-1925357

ABSTRACT

Objective: To increase the awareness of neurological complications of arteriovenous malformation (AVM) due to obstruction of the venous drainage despite being on anticoagulants. Background: Cerebral AVMs are high-flow intracranial vascular malformation comprised of feeding arteries, a nidus of vessels with intervening brain parenchyma through which arteriovenous shunting occurs and dilated draining veins allowing significant hemodynamic gradient without an interposed resistance. Venous drainage stenosis or occlusion will increase the hemodynamic pressure gradient within the AVM compartments and potentially lead to redistribution of flow resulting in cerebral venous sinus thrombosis or hemorrhagic stroke from nidus rupture. This effect might be worsened in the presence of a generalized hypercoagulable state causing microvascular injury and thrombosis;despite adequate anticoagulation therapy. Design/Methods: N/A Results: 66-year-old obese woman with history of atrial fibrillation, coronary artery disease, diabetes, hypertension, hyperlipidemia, prior stroke, small left frontal AVM diagnosed on conventional angiogram and recent COVID-19 infection presented to our comprehensive stroke center with seizures and right hemiparesis. MRI brain showed T2/FLAIR hyperintense lesion in the left frontal/parasagittal region with an extensive vasogenic edema, heterogeneous diffusion restriction, and gyriform contrast enhancement. Conventional angiogram showed AVM without nidus opacification but with an associated mass effect correlating with parenchyma edema and early venous shunting. Patient was initially misdiagnosed as low-grade neoplasm although accurate diagnosis of left parasagittal frontal venous infarct in the setting of spontaneous venous thrombosis of left frontal AVM was made with conventional angiogram. Conclusions: Venous infarct due to CVST is a devastating complication of AVM. The hemodynamic pressure gradient within the AVM might play a larger role in contributing to hypercoagulable state within the venous system leading to cerebral venous sinus thrombosis despite patient being on therapeutic anticoagulation.

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