This article includes discussion of hypercoagulable states and cerebrovascular disease, hypercoagulability, thrombophilia, and prothrombotic. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
In this update, the author discusses advances in the epidemiology, diagnosis, treatment, and prognosis of patients with ischemic stroke and cerebral venous thrombosis associated with genetic and acquired thrombophilia.
• Genetic and acquired hypercoagulable states, such as factor V Leiden deficiency and antiphospholipid syndrome, are associated with cerebrovascular events, including cerebral venous thrombosis and ischemic stroke.
• Understanding the pathophysiology of the hypercoagulable state is essential to understand the associated stroke syndromes and appropriate treatments.
• Study of the epidemiology, pathophysiology, and treatment of many recently described hypercoagulable states is an active and important area of research in neurology.
Historical note and terminology
Rudolf Virchow proposed in 1862 that the pathophysiology of thrombosis involved a triad of interrelated factors: damage to blood vessel endothelium, stasis of blood flow, and disorders in blood coagulability.Activated protein C resistance due to factor V Leiden mutation, prothrombin 20210A gene mutation, protein C deficiency, protein S deficiency, and antithrombin III deficiency are the most frequently seen causes of a hereditary hypercoagulable state; antiphospholipid antibody syndrome is the most common acquired disorder.
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