The Immunologic Basis, Neurological Manifestations and Management of The Anti Phospholipid Antibody Syndrome

aPL may be present in a small percentage of normal population and most of these may be transient. Their association with clinical thrombotic events characterize the APS. Cerebral vasculature is the commonest site for arterial ischemic events, with cerebral ischemia being the most frequently encountered neurological manifestation. The mechanisms of thrombosis are unclear, but believed to be due to a procoagulant state as well as cardiac source of emboli from a left sided valvulopathy. It is postulated that platelet and endothelium damage due to other stroke risk factors such as cigarette smoking, hyperlipidemias and hypertension may trigger or augment aPL mediated thrombosis. Certain serological profiles as a persistently raised aCL IgG titer and associated LA activity carry a higher risk for a thrombotic event. Treatment is largely empirical with antiplatelet anticoagulants being the mainstay of therapy. Ongoing controlled clinical trials as the APASS Collaborative Study [54] may provide the much needed information on the natural course and better management of this fascinating syndrome with potentially devastating neurological sequelae.