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<p>Cerebral sinus venous thrombosis (CSVT) is a&#xa0;rare cerebrovascular disorder predominantly affecting young women, with highly variable clinical presentation. The hallmark symptom is progressive headache, present in over 90% of cases, often accompanied by seizures, focal neurological deficits, and signs of increased intracranial pressure such as impaired consciousness. Two key pathophysiological mechanisms underlie the clinical picture: increased intracranial pressure due to impaired venous and cerebral spinal fluid drainage, and focal brain parenchymal injury from venous infarction and hemorrhage. Risk factors include hormonal influences, thrombophilia, malignancy, and infection. Diagnosis relies on computed tomography (CT) with CT venography or magnetic resonance (MR) imaging with MR venography. The cornerstone of treatment is prompt anticoagulation with heparin (preferentially low-molecular-weight heparin) in the acute phase, followed by oral anticoagulation—preferably with direct oral anticoagulants—for 3&#xa0;months to lifelong, guided by the underlying etiology and risk of recurrent (venous) thromboembolic events. Intracerebral hemorrhage is not a&#xa0;contraindication for anticoagulation. Decompressive craniectomy is indicated in cases of impending herniation. The overall prognosis is favorable, with functional independence achieved in 80–90% of patients. However, psychological sequelae such as anxiety and depression, chronic headache as well as the risk of recurrence of thrombotic events, necessitate structured long-term follow-up at a&#xa0;center with neurovascular expertise.</p>

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Zerebrale Sinusvenenthrombose

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月25日

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  • Tamara Gattringer,
  • Natalie Berger,
  • Melanie Haidegger,
  • Thomas Gattringer

摘要

Cerebral sinus venous thrombosis (CSVT) is a rare cerebrovascular disorder predominantly affecting young women, with highly variable clinical presentation. The hallmark symptom is progressive headache, present in over 90% of cases, often accompanied by seizures, focal neurological deficits, and signs of increased intracranial pressure such as impaired consciousness. Two key pathophysiological mechanisms underlie the clinical picture: increased intracranial pressure due to impaired venous and cerebral spinal fluid drainage, and focal brain parenchymal injury from venous infarction and hemorrhage. Risk factors include hormonal influences, thrombophilia, malignancy, and infection. Diagnosis relies on computed tomography (CT) with CT venography or magnetic resonance (MR) imaging with MR venography. The cornerstone of treatment is prompt anticoagulation with heparin (preferentially low-molecular-weight heparin) in the acute phase, followed by oral anticoagulation—preferably with direct oral anticoagulants—for 3 months to lifelong, guided by the underlying etiology and risk of recurrent (venous) thromboembolic events. Intracerebral hemorrhage is not a contraindication for anticoagulation. Decompressive craniectomy is indicated in cases of impending herniation. The overall prognosis is favorable, with functional independence achieved in 80–90% of patients. However, psychological sequelae such as anxiety and depression, chronic headache as well as the risk of recurrence of thrombotic events, necessitate structured long-term follow-up at a center with neurovascular expertise.