A 64-year-old male patient was referred to the Ophthalmology emergency department for double vision and dizziness, with apparently no other noteworthy symptoms; however, an instability when standing upright was observed that could not be justified by the diplopia alone.
The only history of interest was that the patient reported having been vaccinated against influenza five days earlier.
Visual acuity was 0.7 in both eyes (AO), and both pupils were dilated and areflexic, with no previous contact with mydriatics. There was a limitation in the abduction of the AO, greater in the left eye (OI), in the supraduction of the AO, and difficulty in the rest of the eye movements, reporting horizontal diplopia. The rest of the ophthalmological examination was normal.

In view of the suspected diagnosis of Miller Fisher syndrome, the patient was referred to the neurology department, which detected an ataxic gait, hyporeflexia, and ruled out limb weakness, deciding to admit him for follow-up and a complete study. The results of the blood tests and the computerised axial tomography (CAT) performed in the emergency department were normal.
Twenty-four hours after admission, respiratory distress appeared, requiring oxygen and physiotherapy, and in the following weeks he developed new neurological symptoms: facial paralysis, dysphonia and dysphagia.
During admission, a lumbar puncture was performed, which detected albuminocyte dissociation, and a magnetic resonance imaging (MRI) definitely ruled out space-occupying lesion or demyelination. Electromyographic study did not provide additional information.
The immunological study was positive for anti-GQ-1b antibody, definitively confirming the initial diagnosis.
The patient's symptoms improved two weeks after admission, having received two cycles of immunoglobulins. The clinical evolution was slow and polysymptomatic, with diplopia persisting with prolonged limitation of bilateral abduction.