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In April, 2007, a 42-year-old woman was admitted to hospital with periorbital swelling, double vision, hyper osmia, and dizziness. Recent history included a gastro intest inal in fection (February, 2007), bilateral ear pain, and a sore throat. Systolic blood pressure was 150 mm Hg, heart rate was 80 beats per min, and temperature was 37∙4°C. Laboratory tests showed a low concentration of thyroidstimulating hormone (0∙04 mU/L, normal value 0∙27–4∙2 mU/L) and raised values of free T3 (12∙1 pmol/L; 3∙1–6∙8 pmol/L) and free T4 (36∙1 pmol/L; 12∙0–22∙0 pmol/L). TSH-receptor antibodies (1∙9 U/L; normal 15 000 U)— suggesting the presence of Miller-Fisher syndrome. Our patient continued treatment with carbimazole and prednisolone; her Miller-Fisher syndrome was managed supportively. 4 months later all her symptoms had disappeared. Carbimazole and prednisolone were gradually reduced and then stopped completely. Miller-Fisher syndrome is a rare variant of the GuillainBarre syndrome and is characterised by combined ophthalmoplegia, ataxia, and hyporefl exia. Antibodies to GQ1b, which are present in 85–90% of patients, are highly sensitive for this syndrome, indicating that peripheral nerve myelin is the target of an immune attack. The binding of anti bodies to oculomotor nerves causes ophthalmoplegia. The diff erential diagnosis encompasses Guillain-Barre syn drome, acute ophthalmoplegia without ataxia, and Bickerstaff ’s brainstem encephalitis, but not other neuropathic disorders. Molecular mimicry may have a signifi cant role in the onset of the Miller-Fisher syndrome, since the GQ1b epitope has been found in lipopoly sac charides of Campylobacter jejuni. Therapeutic regimens for the Miller-Fisher syndrome include treatment with intravenous immuno globulin and plasmapheresis to remove the anti bodies to GQ1b, although the rate of spon tan eous recovery is high. Our patient had a mild form of Graves’ disease—the thickened eye muscles visible on MRI were compatible with the presence of an endocrine ophthalmopathy, but the pattern of limited eye movement was atypical and is better explained by the coinciding presence of Miller-Fisher syndrome.