ArticleNeuropsychiatric disease and treatment2010
Role of anti-GQ1B antibody in differential diagnosis of acute ophthalmoparesis.
Article in Neuropsychiatric disease and treatment, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Adult Botulism of Unknown Source with Post-Toxin Anti-GQ1b Antibodies: Implications for Molecular Mimicry-A Case Report.Neurology international · 2025Article
- A Perplexing case of isolated abducens nerve palsy in a primigravida woman: A case report.Case reports in women's health · 2023Article
- Pediatric ocular motor cranial nerve palsy: Demographics and etiological profile.Indian journal of ophthalmology · 2021Article
- Amyotrophic lateral sclerosis in a patient who recovered from Miller Fisher Syndrome: The role of GQ1b antibody revisited.Brain, behavior, & immunity - health · 2021Article
- Miller Fisher syndrome mimicking ocular myasthenia gravis.Optometry and vision science : official publication of the American Academy of Optometry · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
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Abstract
Miller Fisher syndrome (MFS) is a triad of total external ophthalmoplegia, ataxia, and areflexia, while botulism has the usual clinical presentation of involvement of cranial muscles and palsies with blurred vision, diplopia, ptosis, dilated pupils, and facial paralysis, caused by a bacterial neurotoxin which attacks proteins involved in presynaptic vesicle release. In this report, we needed to make the differential diagnosis between MFS and botulism in a patient who presented with acute ophthalmoparesis and a history of diarrhea three days before, which started two days after consuming tinned food. Routine laboratory, neurophysiologic, and imaging investigations were normal. A clinical diagnosis of Miller Fisher syndrome was reached by anti-ganglioside GQ1B and GM1 Ig G and M antibody investigations which proved positive. The patient was treated with intravenous immunoglobulin two weeks after (in the late period) the symptoms started and he has recovered completely. Systemic autoimmune diseases should be considered in patients with bilateral ophthalmoparesis. As in the present patient, the evaluation of specific antibodies helps in the diagnosis and thus early effective treatment is possible.
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