DOI: https://doi.org/10.36347/sjmcr.2026.v14i03.020

Pages: 406-410

Miller Fisher syndrome (MFS) is a rare variant of Guillain–Barré syndrome classically characterized by the clinical triad of ophthalmoplegia, ataxia, and areflexia. It is an acute immune-mediated neuropathy that primarily affects the peripheral nervous system and is strongly associated with anti-GQ1b antibodies. The typical presentation involves rapidly progressive bilateral ophthalmoplegia; however, atypical or incomplete forms are increasingly recognized. These may include unilateral cranial nerve involvement or the absence of one or more components of the classical triad, which may complicate the diagnosis, particularly in the early stages. We report the case of a 43-year-old man who presented with acute binocular diplopia evolving over 15 days and associated with gait instability. Neurological examination revealed left-sided ptosis with impaired upward gaze, accompanied by diffuse areflexia and mild ataxia, while motor strength and sensory examination were normal. Brain magnetic resonance imaging demonstrated lesions in the right juxtacortical region and the left mesencephalic sulcus, initially raising suspicion of a central demyelinating disorder. Cerebrospinal fluid analysis showed albuminocytologic dissociation without pleocytosis or oligoclonal bands. Electroneuromyography demonstrated normal motor and sensory conduction studies with abolition of the H reflex. Serological testing revealed the presence of anti-GQ1b IgG antibodies, supporting the diagnosis of Miller Fisher syndrome. The patient was managed conservatively with close neurological monitoring and physiotherapy, leading to gradual clinical improvement and favorable recovery. Although MFS predominantly affects the peripheral nervous system, central nervous system involvement has occasionally been reported. Magnetic resonance imaging abnormalities are uncommon and usually involve the brainstem or cerebellum, whereas cerebral white matter lesions remain exceptionally rare. This case highlights an atyp