Neurologic manifestations of the antiphospholipid syndrome: integrating molecular and clinical lessons

Abstract

The antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by autoantibody production and thrombosis or pregnancy morbidity. The most prevalent neurologic manifestation of APS is cerebrovascular ischemic events due to arterial thromboses. Antiphospholipid antibodies can also cause neurologic impairments unrelated to thrombosis, through antibody-cellular interactions, possibly because of a disrupted blood-brain barrier. Antiplatelet or anticoagulant therapies are currently indicated for APS-related ischemic strokes, but they remain controversial for non-thrombotic neurologic manifestations. Scant literature exists on neurologic manifestations and treatment regimens in childhood APS. Modifiable cardiac risk factors and valvular heart disease may worsen APS cerebrovascular outcomes. Adjunctive therapies (eg, statins, antimalarials, and angiotensin-converting enzyme inhibitors) warrant clinical trials.