[Neurological aspects in antiphospholipid syndrome]

Area of Science:

• Cardiovascular Medicine
• Immunology
• Neurology

Background:

• Antiphospholipid syndrome (APS) is linked to acquired hypercoagulable states, causing stroke and transient ischemic attacks.
• Antiphospholipid antibodies (aPL) are a diverse group, with lupus anticoagulant (LA) and beta 2-glycoprotein I dependent anticardiolipin antibodies (β2GPI aCL) being significant markers.
• LA is increasingly associated with phosphatidylserine anti-prothrombin antibodies.

Observation:

• aPL is an independent risk factor for initial ischemic strokes and a prognostic marker for recurrent strokes.
• Stroke occurrence in aPL patients is precipitated by β2GPI-dependent aCL, GPL aCL levels >40, and concurrent LA.
• Impaired protein C activation and aPL's role in accelerating atherosclerosis, as seen in LDL receptor-deficient mice immunized with β2GPI, are implicated mechanisms.

Findings:

• Therapeutic strategies for preventing ischemic stroke in aPL patients include antiplatelet, anticoagulant, and immunosuppressive therapies.
• Combination antiplatelet and anticoagulation therapy demonstrated lower recurrence rates compared to other treatments.
• The WARSS-APASS study found no significant difference in recurrence rates between monotherapy with antiplatelets or anticoagulants.

Implications:

• aPL is investigated for roles in neurological disorders like multiple sclerosis, chorea, migraine, and convulsions.
• While aPL's contribution to convulsions is suggested, its link to multiple sclerosis remains uncertain, and it's not associated with migraines.