Miller Fisher syndrome(MFS) isaclinicalcondition first reported in 1956 byMiller Fisherat Harvard MedicalSchool. It ischaracterized by total external ophthalmoplegia,ataxia,and reduced orabsent deep tendon reflexes.[1] MFS is often associated with various other disorders such as infectionscaused byHemophilus influenza, Campylobacter jejuni, Epstein-Barr virus, Salmonellaenteritidis, Cytomegalovirus, Chlamydia pneumoniaand Mycoplasma pneumonia,and Burkitt lymphoma.[2] Though the presentation ofMFS is dramatic, it isa benign, self-limited disease with completerecoverywithinweeks.[3] Both central nervous systemchanges (abnormalitiesat pons, brainstem,cerebellar tract, or posterior column)and peripheral nervous systemchanges have been reported inMFS.[3,4] However,availableevidenceindicate MFS to bea variant of Guillain-Barresyndrome with peripheral nerve demyelination as theclassic pathologic mechanism.[3] AntiGQ1b immunoglobulinG(lgG) antibodies have been found in 80-100%of patients withMFS,especially in cases with ophthalmicinvolvement.[3,5] However,antiGD1b IgG antibodies have not been reported withMFS. Rather, it is used to differentiateataxic variant ofGBS fromMFS in clinical practice. Here, we reportararecase ofrecurrent MFS. To the best of our knowledge, this is thefirstcase ofrecurrent MFS with ophthalmicinvolvementand ataxia associated with antiGQ1b lgGand antiGD1b IgGantibodies.
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