Cerebral venous sinus thrombosis overview: Difference between revisions
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==Overview== | ==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. | [[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]]. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Revision as of 17:37, 25 July 2021
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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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Treatment |
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Case Studies |
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Cerebral venous sinus thrombosis overview On the Web |
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American Roentgen Ray Society Images of Cerebral venous sinus thrombosis overview |
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Directions to Hospitals Treating Cerebral venous sinus thrombosis |
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Risk calculators and risk factors for Cerebral venous sinus thrombosis overview |
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.