This relates to a set of hypotheses that one of a number of autoimmune conditions is triggering the seizures.


We received the suggestion to consider antiphospholipid antibody syndrome given the patients history of two miscarriages, her children being born pre-term with a history of pre-eclampsia, and the subsequent development of seizures. This syndrome is caused by antibodies against cell-membrane phospholipids that provokes blood clots in veins and causes pregnancy-related complications such as miscarriage, stillbirth, preterm delivery and pre-eclampsia. The syndrome occurs due to the autoimmune production of antibodies against phospholipids. Antiphospholipid syndrome is tested for lupus anticoagulant and anti-cardiolipin anti-bodies. The rhythmicity of the seizures can be related to the lowering of the seizure threshold by the cycle increase in estrogen associated with menstruation.

Follow Up:

Our consulting researcher believes that if the patient does have APLS, it would be a quite rare form. He recommended an autoimmune profile.

The patients symptoms are not a good match for APLS, e.g. normal platelet counts, no DVT, no thrombocytopenia.

Lang and Hart (2010) review autoimmune epilepsy, and note that there are seizure related syndromes with established autoimmune associations. They further state that there are new epileptic syndromes identified on an ongoing basis where autoimmunity appears to lay a role. From their review, we have the following list of antibodies to consider: NDMA, VGKC, AMPA (including GluR3), GM1, Cardiolipin, Phospholipids, Gliadin, GAD, α-Enolase.

The sudden onset and focal nature of the seizures could be indicative of autoimmune epilepsy, but the patient has no other symptoms of an autoimmune disorder.


Is autoimmune epilepsy a plausible hypothesis, in the absence of autoimmune symptoms?

Which antibody would be the most likely target?

Action Plan:

We are currently scheduling tests to detect the presence of the antibodies with known associations with epilepsy.

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