1998 Volume 29 Issue 3 Pages 331-336
A 32-year-old woman developed diplopia and dizziness several days after an upper respiratory tract infection. On admission, bilateral blepharoptosis, disturbance of ocular movements mimicking bilateral internuclear ophthalmoplegia, ataxia and areflexia were noted. CSF protein level was normal. Serum virus titers did not show any significant changes. Anti-GQ1b and anti-GT1b ganglioside antibodies were positive. Brain CT and MRI were normal. H wave was not elicited in nerve conduction study. She was diagnosed as suffering from Fisher's syndrome. Although her ocular motility dysfunction closely resembled internuclear ophthalmolegia, no proof of damage to the medial longitudinal fasciculus was obtained as shown by the normal findings in MRI. Meanwhile, disappearance and subsequent re-appearance of H wave during the clinical course rather suggested the peripheral origin of her ocular disturbance. Pseudo-internnuclear ophthalmoplegia has been reported in myasthenia gravis, Guillain-Barre syndrome and surgical pare is of the medial rectus muscle, indicating that lesions of the peripheral nerve and muscle simulate what has previously been considered a specific brainstem sign. Dissociated nystagmus in this ophthalmoplegia can also be explained by an adaptiveprocess theory. Namely, any attempt to increase the innervation to a weakened muscle in one eye is thought to be accompanied by a commensurate increase in innervation to the yoke muscle in the other eye, giving rise to saccadic overshoot followed by backward postsaccadic drift.
