They may exhibit increased anti-GQ1b antibodies in Miller Fisher syndrome, Guillain-Barre syndrome with ophthalmoplegia, Bickerstaff Rhombencephalitis, and Acute Ophthalmoplegia without ataxia , the so called "anti-GQ1b syndromes". We report a 72 years old man who was admitted because of diplopia, acute onset ophthalmoplegia and retro-ocular pain. He had a similar episode fi ve years ago, fully recovered. At admission he showed complete bilateral ophthalmoplegia without ptosis, miosis and slight enophthalmos of the right eye. Preserved muscle strength, deep tendon arefl exia, without sensory or cerebellar commitment. CSF and electromyography were normal. Brain MRI showed uptake and T2 hyperintensity of the third and sixth cranial nerves. Spinal cord MRI showed no change in the spinal roots. Serum anti-GQ1b increase of 46.2 / 25. He improved without treatment. Thirty days later, paresis was only the sixth pair. The anti-GQ1b is a marker that identifi es neuropathies with oculomotor commitment. The acute ophthalmoplegia without ataxia have normal refl ex, 30% had arefl exia. There are only Guillain-Barré and Miller-Fisher syndromes recurrent case reports with anti-GQ1b. It would be the fi rst case of recurrent anti-GQ1b-positive acute ophthalmoplegia without ataxia.
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