Cerebral venous sinus thrombosis overview
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Differentiating Cerebral venous sinus thrombosis from other Diseases |
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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.
CVT has good prognosis in 75% of patients with full functional recovery while in 15% of patients die or become dependent. Male sex, older age, confusion or coma, intracranial hemorrhage, deep vein involvement, infection and malignancy are the risk factors for poor outcomes.
Historical Perspective
Cerebral venous sinus thrombosis (CVT) as first described by a French physician Ribes in 1825. But till the second half of 20th century, CVT was a diagnosis after death as it was frequently misdiagnosed due to overlapping of clinical symptoms and physical findings overlapping with other strokes. In 1951, introduction of venography made a drastic change in diagnosis of CVT.
Classification
There is no classification of cerebral venous thrombosis (CVT).
Pathophysiology
Imbalance in prothrombotic and fibrinolysis processes are the main pathophysiologic mechanisms leading to cerebral venous sinus thrombosis. Hypercoagulability is the main cause of cerebral venous thrombosis.
Causes
Genetic or acquired conditions causing thrombosis are considered as risk factors for developing cerebral venous sinus thrombosis. Some of the common causes are thrombophilia due to factor V Leiden mutation, protein C and S deficiency, pregnancy, puerperium, oral contraceptive use, Nephrotic syndrome and other related factors.