Authors: Dr. Gina Rami Salama Ibrahim Abdelmesih

Abstract

Introduction: Miller Fisher Syndrome (MFS) is a rare, immune-mediated variant of Guillain-Barré Syndrome (GBS), classically presenting with the triad of ophthalmoplegia, ataxia, and areflexia.  A viral or gastrointestinal illness usually precede MFS

MFS incidence is 0.09 per 100,000 annually and accounts for roughly 1–5% of GBS cases in Western populations. It predominantly affects males and typically presents in middle age. Although the initial presentation can mimic other serious neurological conditions such as brainstem stroke, MFS usually has a benign course with good recovery if treated early and appropriately.

Case description : A 59-year-old previously healthy man presented to the Emergency Department (ED) with the sudden onset of tongue heaviness and difficulty speaking while at work, which began one hour prior to arrival. His symptoms were accompanied by blurry vision, unsteadiness, and dizziness. He denied any limb weakness, headache, chest pain, or vomiting. His vital signs were stable. Based on the initial neurological assessment, a stroke was suspected, and the patient was transferred to the nearest hospital with a designated stroke unit for urgent neuroimaging and evaluation.

Brain imaging, including a non-contrast CT and MRI of the brain, showed no evidence of acute ischemia or hemorrhage. After being cleared of stroke, the patient was transferred back to our ED for further evaluation due to persistent neurological deficits. On examination by the intensivist and neurologist, the patient demonstrated complete ophthalmoplegia, bilateral ptosis, dysphagia, ataxia, dynamic dysarthria, and generalized areflexia, while motor strength remained fully preserved in all four limbs.

Laboratory investigations were unremarkable. The patient was admitted to the intensive care unit for close neurological monitoring and respiratory observation, including serial forced vital capacity (FVC) assessments, due to the risk of respiratory compromise.

On further history, the patient recalled having a febrile upper respiratory tract illness one week prior to symptom onset. An extensive diagnostic workup was performed, including lumbar puncture (which showed normal opening pressure and mild protein elevation), nerve conduction studies, CT of the chest, abdomen, and neck, and MRI of the orbits, all of which were either normal or revealed nonspecific findings initially.

Given the clinical presentation and after ruling out structural and infectious causes, the patient was started empirically on intravenous immunoglobulin (IVIG) and corticosteroids to cover for the possible differential diagnosis. Over the following days, he demonstrated marked clinical improvement in his ocular movements and gait.

Ganglioside antibody testing returned later and revealed elevated levels of GD1a, GD1b, GT1a, and GQ1b antibodies, confirming the diagnosis of Miller Fisher Syndrome. The patient continued to improve and was transitioned to ward-level care with a favorable prognosis.

Conclusion : Miller Fisher Syndrome, though rare, must be recognized by ED physicians as a potential cause of acute neurological deficit. Its presentation can mimic stroke, vasculitis, or intoxication/ Wernicke’s encephalopathy, leading to misdiagnosis or delayed care. Early identification in the emergency setting enables appropriate neurology referral, and initiation of management. Awareness of MFS in the ED is essential—not only to prevent unnecessary interventions (Intubation, investigations) but also to reassure patients of its typically favorable prognosis when accurately diagnosed

Keywords: MILLER FISHER SYNDROME, stroke, diplopia, ataxia, Guillain-Barré Syndrome, Brain imaging