Autoantibodies and eye movement disorders

Abstract

AbstractIntroductionNew auto‐antibodies seem to be discovered every month and the field of eye movement disorders is fully part of the game: anti‐GAD, GM1, GQ1b, Hu, Ri, etc. What are their specificity? their practical use at the bedside? where and how to ask for their dosage? what to they tell us of their associated conditions?ObjectiveTo answer these questions in a synthetic way.MethodsLiterature review using Pubmed and Google Scholar; chosen clinical cases.ResultsVarious oculomotor presentations should prompt auto‐antibodies dosage: oculogyric crises associated with tics or chorea; progressive saccadic intrusions with associated ataxia, typically evolving into opsoclonus‐myoclonus syndrome; acquired neurological nystagmus with no obvious explanation, and non‐compressive unexplained ophthalmoparesis, especially when associated with unremarkable MRI ‐ or with MRI showing mild signs of encephalitis. The targets of these antibodies can be: the central nervous system, the peripheral nervous system, the neuromuscular junction or the extraocular muscles. Relevant auto‐antibodies can be classified into: antibodies directed against intracellular neuronal proteins, responsible for paraneoplastic neurological syndromes (Hu, Yo, Ri, CV2, amphiphysin, Ma1, Ma2) and antibodies directed against neural surface or synaptic antigens, responsible for autoimmune encephalitis syndromes, most frequent in children (AMPA, CASPR2, GABAR, GAD, GD1a, GD1b, GM1, GQ1b, GT1a, LGI1, NMDA).ConclusionsAuto‐antibodies are often the clue of ‘impossible’ oculomotor cases. They should be dosed in chosen and rare situations with specific techniques; the results should be interpreted according to the known specificity of each auto‐antibody.