Despite important new diagnostic laboratory and imaging technologies, the cause of
brain infarction remains unexplained in 20% to 40% of subjects. Most
stroke patients do not require extensive evaluations of coagulation, but
hypercoagulability may account for a significant proportion of unexplained
strokes.
Hemostatic abnormalities associated with
stroke may be broadly classified as familial or acquired. Principal among the familial thrombotic coagulopathies are deficiencies in concentration or function in
protein-C,
protein-S, and
antithrombin III, but other hereditary abnormalities include
sickle cell disease,
homocystinuria, and dysfibrinogenemia. The acquired disorders of hemostasis associated with
stroke probably constitute a larger proportion of the important
stroke-related coagulopathies. In particular, the aPL antibody syndrome is now strongly associated with thrombotic events including
stroke, although neither the mechanism of
thrombosis nor effective
therapies for this syndrome have been clearly elucidated. Many of the acquired
hemostatic abnormalities exist within a special clinical setting such as with
malignancy or with myeloproliferative diseases,
nephrotic syndrome, and
liver disease. Presumably many of these share common pathways of coagulation activation or dysfunction with the inherited disorders. Most of the
hemostatic disorders in
stroke are associated with dysfunction of vascular endothelium and abnormalities of or interference with the natural
anticoagulant proteins:
protein-C,
protein-S, and
antithrombin III. Improved understanding of these relationships should lead to better diagnosis and treatment for people at risk of
stroke.