Antiphospholipid Antibodies and Neuro-Ophthalmology

During the past decade, the antiphospholipid antibody (aPL) syndrome has been delineated as a distinct clinical entity. These antibodies occur in association with systemic lupus erythematosus (SLE) or other autoimmune diseases and in isolation from any associated systemic disease as a primary aPL syndrome. Production of aPL may also be seen secondary to infection and certain drugs. Antiphospholipid antibodies are a heterogeneous group of immunoglobulins of the IgG, IgM, or IgA class that are directed against any negatively charged phospholipid, though cardiolipin is the antigen most frequently used for detection indirect tests. The presence of aPL may also be uncovered indirectly by their ability to prolong phospholipid dependent coagulation tests and when discovered in this manner are referred to as lupus anticoagulants (LA). The pathogenic affect of aPL appears to occur primarily upon phospholipid ! membranes of platelets or endothelium resulting in immune- : mediated thrombosis. Several recent reviews have overed the historical development and features of this syndrome to ! include its clinical manifestations of arterial and venous thrombosis, thrombocytopenia, fetal loss, neurologic disorders, valvular heart disease and livedo reticularis. In this review, the current literature of the aPL syndrome will be discussed with a focus upon the clinical manifestations pertinent to neuro-ophthalmology.