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Autoantibodies to glutamic acid decarboxylase (GAD-A) have been associated with focal epilepsy.1 GAD catalyzes the conversion of l-glutamic acid to gamma aminobutyric acid (GABA). GABA is an inhibitory neurotransmitter and indirect suppression of GABA via GAD-A, in theory, could favor the development of seizures. Although originally implicated in the pathogenesis of type I diabetes and stiff-person syndrome,2 GAD-A have been identified in 8 of 51 (12%) patients with focal epilepsy due to conditions including hippocampal sclerosis.1 We attempted to further investigate the presence of GAD-A in a sample of patients with medically refractory focal epilepsy with mesial temporal sclerosis (MTS).
Antiphospholipid antibodies (aPL) have been associated with thromboembolic events, although some have found these antibodies in the serum of patients with seizures unrelated to thromboembolic events.3 A lupus anticoagulant associated with late onset epilepsy was reported in four adults,3 …
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