Cerebral venous sinus thrombosis overview
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Cerebral venous sinus thrombosis Microchapters |
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Differentiating Cerebral venous sinus thrombosis from other Diseases |
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Diagnosis |
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Cerebral venous sinus thrombosis overview On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Sharmi Biswas, M.B.B.S
Overview
Cerebral venous thrombosis(CVT)is thrombosis of cerebral veins, a rare form of stroke which is different from arterial strokes. CVT incidence is 1.3 in per 1,00,000/year in developed countries. Young children and women especially pregnant/puerperium have a higher frequency of CVT. Due to the wide spectrum of clinical features, CVT frequently gets misdiagnosed as other strokes. Commonly known risk factors and causes of cerebral venous thrombosis are venous thromboembolism, thrombophilia (especially antithrombin deficiency, protein C and S deficiency and factor V Leiden mutation), pregnancy, oestrogen therapy/oral contraceptives, hypercoagulability as part of inflammatory disease, head trauma, local infections and underlying cancer. Pathophysiology of CVT includes two mechanisms including thrombosis of cerebral veins creating local edema and venous infarction; intracranial hypertension created by increased venous pressure and decreased absorption of CSF. Clinical presentations of CVT can be categorized into 4 categories as isolated intracranial hypertension, neurological deficits, encephalopathy and seizure. Symptoms related to increased intracranial hypertension are headache, diplopia, papilledema, sixth nerve palsy and decreased consciousness; focal neurological deficits present as motor and sensory impairments, aphasia. Though in 90% of patients with CVT , headache is the most common symptom, followed by seizures in 40% patients and 20 % patients with seizure. Superior sagittal sinus is the most commonly involved sinus approximately 62% of patients and transverse sinus is the next common site (40-45%). Internal cerebral vein and straight sinus are less commonly involved in CVT but associated with worse outcomes. Diagnosis of CVT is based on clinical findings and neuroimaging. D-dimer level is more than 500 μg/L in most of the patients with CVT. Per recommendation of American Heart Association (AMA) and the European Federation of Neurological Societies (EFNS), MRI/MRV is preferred for brain imaging. But CT can be considered if MRI is unavailable. Treatment of CVT includes early initiation of anticoagulant therapy and treatment of other underlying causes as sepsis, dehydration, discontinuation of prothrombotic medications; seizure and intracranial hypertension management.