Neurological and Neuropsychiatric Manifestations of Antiphospholipid-Antibody Syndrome (APS)

Abstract

Antiphospholipid antibody syndrome (APS) is an autoimmune disorder mediated by the presence of a group of autoantibodies, specifically the anticardiolipin antibody (aCL), the beta-2 glycoprotein I (β2GPI), and the lupus anticoagulant (LA). Patients diagnosed with antiphospholipid antibody syndrome (APS) present with many symptoms, the most common being the consequence of thrombotic events that can be catastrophic and lead to mild to severe residual disabilities over a significant amount of time and can impair the quality of life. These events are often present in the younger population. Many times, these thrombotic events are heralded by a spectrum of psychiatric symptoms, which when worked up in the right direction may hint toward an oncoming thrombotic event and may potentially prevent those events by prompting primary prophylaxis treatment by the treating physician. In this review, we aim to comprehensively put forth the many neurological and neuropsychiatric manifestations of APS, their pathology, and management.

Keywords: antiphospholipid antibody syndrome (aps); autoimmune disorder; neuropsychiatric manifestations of aps; psychosis; stroke in young.

Figure 1. Depicting the two-hit hypothesis in the pathogenesis of APS.

aPL: antiphospholipids, β2GPI: beta-2 glycoprotein I, APS: antiphospholipid syndrome, aPI: antiphospholipid.

Figure 2. Representing sequence of changes set in motion due to β2GPI activity.

β2GPI: beta-2 glycoprotein I, GABA: gamma amino-butyric acid, and LDL: low-density lipoprotein.