Treatment of GBS has included the use of corticosteroids, plasmapheresis, immunoglobulins, physical therapy, and occupational therapy.3 Until now, the literature has lacked description of orthoptic intervention for the ocular motor sequelae of GBS. We report the successful orthoptic management of a patient with GBS who had severe residual divergence insufficiency and esotropia after complete bilateral ophthalmoplegia.

History A 50-year-old ophthalmologist (author KZ) became vertiginous early one morning while conducting clinical rounds. Within a few hours, he developed progressive bilateral dysfunction of all cranial nerves with the exception of I, II, and X. He was unable to chew, swallow or speak. Diplopia evolved as a result of complete external ophthalmoplegia. There was an efferent pupillary defect in both eyes. Prior to the onset of diplopia, there was no known oculomotor anomaly, and distance and near phorias were negligible. Normal (40 sec arc) stereopsis was present. An MRI of the brain was negative. Neurologic evaluation revealed generalized weakness and areflexia. Cerebrospinal fluid and electrophysiological studies were also consistent with a diagnosis of GBS. The patient required hospitalization for four months and extended physical therapy for two years.

An orthoptic evaluation was performed two months after hospital discharge. A 40 pd esotropia at distance and a 35 pd esotropia at near, combined with 6 pd of right hypertropia, were measured. He had been advised to patch one eye to eliminate diplopia. This proved to be unacceptable, since he was unable to work or navigate with the patch. Eventually a 40 pd base out Fresnel prism, split unevenly between the two eyes (30 BO=6BD OD and 10 BO OS), was prescribed. This eliminated the diplopia; however, the optics induced both chromatic aberration and reduced visual acuity. Thus, the Fresnel prisms were too disturbing to allow him to resume a full, active professional life.

Diagnostic examination and therapeutic regimen He was examined by one of us (JC) three months after his initial orthoptic evaluation. After removing the prismatic glasses, the cover test revealed a 40 pd alternating esotropia at distance and a 35’ pd alternating esotropia at near. There was an associated 4 pd of right hypertropia with degrees of right excyclotorsion at both test distances. Extraocular movements were full. There was no observable nystagmus. Pupillary responses were brisk in each eye without evidence of a Marcus-Gunn pupil. There was incomplete closure of both the right and left eyelids; however, slit-lamp examination was negative for exposure keratitis. With a modified Hess screen, the esodeviation was found to be concomitant, except for a small right hyperdeviation which increased on right head tilt and adduction. This was consistent with the diagnosis of a mild right superior oblique paresis with overaction of the ipsilateral inferior oblique. Dilated fundus examination was unremarkable.

Distance fusional divergence amplitudes were x/-30/-36 (blur. with fusion/disruption of fusion/recovery of fusion), and near fusional divergence amplitudes were x/-25/-36; blur was not reported, and the negative values indicated grossly abnormal binocular fusion. With a corrective prism in place, he was able to detect 40 sec arc of horizontal retinal disparity (Titmus stereo test). The patient was given the following prescription: OD — 1.50