Neurological manifestations of antiphospholipid antibody syndrome

• Published in: Lupus 1998-01, Vol.7 (2_suppl), p.67-74
• Main Authors: Brey, R.L., Escalante, A
• Format: Article
• Language: English
• Subjects: Adult; Antibodies, Antiphospholipid - immunology; Anticoagulants - therapeutic use; Antiphospholipid Syndrome - complications; Antiphospholipid Syndrome - immunology; Autoimmune Diseases - complications; Autoimmune Diseases - immunology; Blood Coagulation - immunology; Brain - immunology; Brain - pathology; Brain Ischemia - etiology; Case-Control Studies; Child; Chorea - etiology; Depression - etiology; Fibrinolytic Agents - therapeutic use; Hearing Loss, Sensorineural - etiology; Humans; Magnetic Resonance Imaging; Middle Aged; Migraine Disorders - epidemiology; Myelitis, Transverse - etiology; Nervous System Diseases - etiology; Nervous System Diseases - immunology; Nervous System Diseases - prevention & control; Neurocognitive Disorders - etiology; Platelet Aggregation Inhibitors - therapeutic use; Polyradiculoneuropathy - etiology; Seizures - etiology; Sinus Thrombosis, Intracranial - etiology; Thrombophilia - etiology
• ISSN: 0961-2033; 1477-0962
• DOI: 10.1177/096120339800700216

Thrombosis, thrombocytopenia, recurrent fetal loss and a variety of non-thrombotic neurological disorders have all been associated with antiphospholipid antibodies (aPL). Cerebral ischemia associated with aPL is the most common arterial thrombotic manifestation. Depression, cognitive dysfunction, depression and psychosis have all been associated with aPL. The presumed pathophysiologic mechanism underlying these manifestations is thought to be a result of cerebral ischemia in some, but not all cases. Seizures, chorea and transverse myelitis all appear to be associated with aPL. An interaction between aPL and central nervous system cellular elements rather than aPL-associated thrombosis seems to be a more plausible mechanism for these clinical manifestations. Migraine on the other hand, does not appear to be associated with aPL in either lupus or non-lupus populations. Neuroimaging studies show an increased frequency of brain abnormalities in patients with aPL, but none appear to be specific. The best treatment strategy for preventing neurological manifestations of aPL is not fully defined. For thrombotic manifestations, both antiplatelet and anticoagulant therapies have been suggested. In some patients, immunosuppressant therapy has been used. For non-thrombotic manifestations, some combination of immunosuppressant therapy and symptomatic treatment may be warranted.