Journal of Pediatric Ophthalmology and Strabismus

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Short Subjects 

A Surgical Option for Antipodean Strabismus: Four Horizontal Muscle Resection

Faye E. Mellington, BMBCh, MA, MRCOphth; Ahmed A. Assaf, FRCS, FRCOphth, MD

Abstract

The authors report a case of symptomatic antipodean strabismus caused by a combination of mechanical restriction of eye movement secondary to thyroid eye disease, longstanding intermittent divergence, and convergence weakness, which was alleviated by simultaneous resection of all four horizontal recti muscles.

Abstract

The authors report a case of symptomatic antipodean strabismus caused by a combination of mechanical restriction of eye movement secondary to thyroid eye disease, longstanding intermittent divergence, and convergence weakness, which was alleviated by simultaneous resection of all four horizontal recti muscles.

From the Ophthalmology Department, Milton Keynes Hospital, Milton Keynes, United Kingdom.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Faye E. Mellington, BMBCh, MA, MRCOphth, Ophthalmology Department, Milton Keynes Hospital, Standing Way, Eaglestone, Milton Keynes, MK6 5LD United Kingdom. E-mail: fayemellington@hotmail.com

Received: January 07, 2010
Accepted: May 12, 2010
Posted Online: August 23, 2010

Introduction

Antipodean strabismus is a rare type of ocular misalignment in which there is exodeviation with one eye fixating and esodeviation with the other eye fixating. We report a case of troublesome diplopia secondary to antipodean strabismus unresponsive to prisms or uniocular occlusion, where resolution occurred after simultaneous resection of all four horizontal recti muscles.

Case Report

A 56-year-old man presented with several years’ history of horizontal diplopia for near that had been getting worse during the past 18 months. He had a history of intermittent decompensating exophoria as a child and had worn glasses since age 8 years for myopia. Medical history included excision of a thyroglossal cyst 10 years prior to presentation, obstructive sleep apnea, and hypertension. There was no history of trauma or previous ocular surgery.

Uncorrected visual acuity was 20/12.5 in both eyes. A 10 prism diopter (PD) alternating exotropia at 1/3 m and a minimal exophoria with good recovery with 1 PD left hypertropia were noted at 6 m. There was horizontal diplopia in all directions of gaze, including in the primary position. Versions showed −1 restriction of abduction in both eyes (5-point scale: 0 = full duction and - 4 = no duction past the midline) and a −1 restriction of elevation and adduction in the right eye. Convergence was to only 28 cm. He had full color vision, no relative afferent pupillary defect, no proptosis, intraocular pressure of 10 mm Hg in both eyes in primary gaze and 12 mm Hg in both eyes on up gaze, and normal optic discs. Thyroid function tests and magnetic resonance imaging of the orbits were normal. He was diagnosed as having longstanding intermittent divergence and convergence weakness. Convergence exercises, a Blenderm occlusion patch (3M, St. Paul, MN), and a 15 PD base-in prism to the right spectacle lens of reading glasses were all tried without success.

Four months later, he was subjectively and objectively worse. He had 14 to 16 PD right exotropia for near and 4 to 6 PD exophoria with good recovery (becoming a right exotropia at times) for distance. Eye movements had become more limited: versions demonstrated bilateral limitation of gaze of between −1 and −3 in all directions except down gaze and left adduction.

Thirty months later (2½ years after initial presentation), he complained of worsening diplopia and eye ache. He still had 14 PD right exotropia for near but had developed 8 PD left esotropia for distance. Ocular movements measured restriction of −2 in all directions bilaterally except for down gaze, which was normal. Convergence was nil. He had developed bilateral upper eyelid retraction and eyelid lag, but there were no signs of optic nerve compromise. Magnetic resonance imaging of the orbits demonstrated moderate bilateral proptosis (right eye more than left eye) and an increased STIR (Short TI Inversion Recovery) signal within several muscles bilaterally (particularly inferior and medial recti) but no extraocular muscle enlargement. He was anti-acetylcholine receptor antibody negative and thyroid function test results remained within the normal range. In addition to ocular lubricants, he began a short course of oral prednisolone (40 mg by mouth once daily for 2 weeks), which failed to alleviate his symptoms.

He was then referred to our adult ocular motility clinic. On first examination, visual acuity was 0.04 logarithm of the minimum angle of resolution (LogMAR) in the right eye and 0.00 LogMAR in the left eye. He had 18 PD right exotropia for near with glasses (16 PD without glasses) and 20 PD left/alternating esotropia for distance (increasing to 30 PD esotropia without glasses). There was bilateral restriction of −2 in up gaze and abduction and −1 restriction of adduction.

He continued to have almost constant diplopia and his measurements stabilized. At preoperative assessment, best-corrected visual acuity was 0.120 LogMAR in the right eye and 0.00 LogMAR in the left eye. He had a 16 to 18 PD right/alternating exotropia for near and 30 PD left/alternating esotropia for distance (with and without glasses). There was −1.5 restriction of up gaze and adduction and −1 restriction of abduction in both eyes. After remaining stable for 8 months, he underwent bilateral lateral rectus resection (4 mm) and bilateral medial resection (3 mm) on non-adjustable sutures (surgery performed by AA).

At 3 months postoperatively, his best-corrected visual acuity was 0.020 LogMAR in the right eye and 0.040 LogMAR in the left eye. His diplopia had resolved and he had only slight exophoria (14 PD near and 8 PD distance with and without glasses) with good recovery. Bilaterally, there was up gaze restriction of −1 and abduction restriction of −0.5. Convergence improved; he was binocular to 14 cm and he had 60 seconds of stereoacuity using TNO. He has been discharged from clinic.

Discussion

First named by Urist in 1976, antipodean strabismus is the term given to an unusual type of ocular misalignment characterized by esodeviation when one eye is fixating and exodeviation when the other eye is fixating.1

It has been described both in children and adults and attributed to a variety of causal mechanisms, including marked uncorrected anisometropia, dissociated strabismus, asymmetric accommodative convergence to accommodation ratios, and combinations of paresis or mechanical restrictions of eye movement.2–4

In reported cases of antipodean strabismus resulting from unusual combinations of paresis and mechanical restrictions, patients typically have a history of previous neurological abnormalities, trauma, or ocular surgery usually involving excessive weakening of one muscle.4 None of these factors applied to our patient, who had a combination of euthyroid eye disease, longstanding intermittent divergence, and convergence weakness.

In keeping with its proposed multifactorial etiology, management strategies for antipodean strabismus are varied and include bifocals, prisms, monocular occlusion, and surgery. Spectacle lens correction with or without bifocal add may be of benefit in cases of antipodean strabismus and associated asymmetric AC/A ratios, which have been described in children. It is not always a static condition: resolution over time with normalization of AC/A ratios has been reported.4 In our patient, after prisms and monocular occlusion with a Blenderm patch failed to alleviate his debilitating diplopia, and after waiting for stabilization of ocular measurements, we believed that a surgical approach was advocated.

To our knowledge, this is the first report of surgical correction of antipodean strabismus by means of simultaneous resection of all four horizontal recti muscles. It provided excellent symptomatic relief and resolution of diplopia and should be considered in similar cases that have proved refractive to less invasive management strategies.

References

  1. Urist MJ. The fusional balancing innervation in heterophoria for control of antipodal deviations at the null point: a previously undescribed type of binocular innervation. J Pediatr Ophthalmol. 1976;13:65–71.
  2. Merriam SJ, Kushner BJ. An investigation into the mechanisms causing antipodean strabismus. J AAPOS. 2007;11:249–253. doi:10.1016/j.jaapos.2006.10.022 [CrossRef]
  3. Shippmann S, Hermann JS. Antipodean squint. J Pediatr Ophthalmol Strabismus. 1978;15:210–212.
  4. Clarke WN, Noel LP. Antipodean strabismus. Am Orthoptic J. 1984;34:104–109.
Authors

From the Ophthalmology Department, Milton Keynes Hospital, Milton Keynes, United Kingdom.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Faye E. Mellington, BMBCh, MA, MRCOphth, Ophthalmology Department, Milton Keynes Hospital, Standing Way, Eaglestone, Milton Keynes, MK6 5LD United Kingdom. E-mail: fayemellington@hotmail.com

10.3928/01913913-20100818-14

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