Rev Neurol. 2003 Oct 1-15;37(7):654-7. INTRODUCTION AND DEVELOPMENT: Over the last two decades antiphospholipid syndrome (APS) has started to be recognized from the association of apparently anionic phospholipid-specific antibodies with thrombosis, thrombocytopenia and recurrent foetal losses. This syndrome affects patients with systemic lupus erythematosus and is considered to be an important cause of thromboembolic disease. Antiphospholipid antibodies are serum immunoglobulins that react with negatively charged phospholipids, albeit directly or by means of a cofactor, affect the coagulation system, and promote thrombosis. Recent research has been directed towards gaining an understanding of the mechanisms by which these antibodies are able to play a direct role in the pathophysiology of thrombosis, and the extent to which certain risk factors, such as smoking, high blood pressure, lipid disorders and so on, exert an influence over the expression of phospholipids in the cerebral endothelium. CONCLUSION: These antibodies have no single mechanism of action; different authors have described different pathological mechanisms, which help us to understand the heterogeneous clinical manifestations of APS.

Acta Neurol Scand. 1999 Jun;99(6):356-61. CONCLUSION: MES may be related to disease activity in patients with SLE and APS. Their detection may help to assess individual cerebrovascular risk and contribute to therapeutic decision making and therapeutic monitoring.

Am J Med. 1995 Oct;99(4):397-401.

Journal of Clinical Endocrinology & Metabolism 2006, 10.1210/jc.2005-2782. Conclusions: APS, revealed by anti-beta-2-glycoprotein (anti-2-GPI) and anti-prothrombin (anti-PT) antibodies positivity, and moderate HHcy related to heterozygous C677T and A1298C point mutations of the MTHFR gene, were identified as a possible cause of thrombotic disorder responsible for the widespread presence of cutaneous and cerebral lesions.

Mov Disord. 1993 Jul;8(3):383-6. We suggest that PAPS must always be considered when isolated or recurrent focal cerebral ischaemia, and particularly hemidystonia, occur in childhood.

Source: Lupus, Volume 12, Number 2, 1 February 2003, pp. 93-98(6)

South Med J. 2000 Nov;93(11):1115-9.

Rheumatology Advance Access originally published online on September 14, 2004. Rheumatology 2005 44(1):95-99; doi:10.1093/rheumatology/keh408.

Shaharao V, Bartakke S, Muranjan MN, Bavdekar MS, Bavdekar SB, Udani1 VP. Recurrent acute transverse myelopathy: Association with antiphospholipid antibody syndrome. Indian J Pediatr 2004;71:559-561

Folia Neuropathol. 1996;34(2):92-6. Morphological picture of arterial fibromuscular dysplasia (FMD) of carotid and cerebral arteries associated with intracranial aneurysm and thrombotic small vessel vasculopathy in a 34-year-old woman with primary antiphospholipid syndrome (PAPS) is presented. The patient died because of hemorrhage caused by aneurysm rupture. In the walls of the aneurysm and aneurysmal dilatation of middle cerebral artery dysplastic changes of FMD type were found. The case fulfills the clinical and serological criteria of antiphospholipid syndrome (APS). Microscopic examination of the brain showed occlusion of small cerebral vessels, characteristic for antiphospholipid syndrome. It was caused by fibrin thrombi and endothelial proliferation or fibrous webs in the vessel lumen. Neither features of systemic lupus erythematosus (SLE) nor related autoimmune diseases were observed in the morphological examination of the brain, skin and internal organs. Therefore, it was feasible to confirm the diagnosis of PAPS in the patient with FMD of the large cephalic arteries.

Mehndiratta MM, Bhattacharya A, Gupta M, Khawaja GK, Puri V. Antiphospholipid antibodies syndrome in 'Stroke in young'. Neurol India 1999;47:122-6 Promotes an INR of greater than 3.0.

Thromb Res. 2004;114(5-6):489-99. CONCLUSIONS: (1) aPL are a risk factor for incident stroke (Grade A, established as useful for the given condition in the specified population). (2) The evidence to support the role of aPL in recurrent stroke is conflicting and, therefore, inconclusive. (3) Warfarin at moderate-intensity doses is equally effective in preventing a recurrent thrombotic event as warfarin at high-intensity doses in patients with APS (Grade A evidence, established as useful for the given condition in the specified population). (4) Warfarin, at moderate-intensity doses is as effective as aspirin (at a dose of 325 mg/day) in preventing recurrent thrombotic events in patients who are aPL-positive at the time of an initial stroke (Grade B evidence, probably useful for the given condition in the given population). (5) Currently there are no data to support the use of any prophylactic therapy in patients with aPL and no clinical manifestations for the purposes of preventing an incident stroke.