A four-year-old healthy boy presented with bilateral poor visual acuity (VA) which was worse in the left eye (LE). His mother complained of the LE gradually becoming divergent.
On examination VA was 20/30 and 10/200 (Snellen's) in the right eye (RE) and LE respectively improving only in the LE to 20/20 with -10 diopter sphere (DS). Cover test revealed left exotropia with hypotropia measuring 16 prism diopter (PD) base in (BI) with 10PD R/L at distance and 45 PD BI with 6PD R/L at near fixation [Fig. 1]. Ocular movements showed a V pattern with increased divergence on upgaze. The LE had 2 mm pseudoptosis. Both eyes had equal central lamellar cataracts with good red reflex. He was prescribed total light occlusion for the RE six hours daily for 12 months and glasses for the LE. Biometry (IOL Master, Carl ZeissTM) confirmed axial lengths to be 20.89 mm (RE) and 24.31 mm (LE) with a difference of 9 diopter (D) in the intraocular lens (IOL) power (RE: 27D; LE: 18D). He underwent phacoaspiration, posterior capsulorrhexis, anterior vitrectomy and IOL implantation in the LE followed by similar surgery in RE 12 weeks later. Best corrected VA at two-year postoperative follow-up was 20/20 (-1 DCyl at 55°) and 20/40 (-1.50 DS / -1 DCyl at 130°) in RE and LE respectively. Cover test showed improvement of exotropia (12PD BI at distance and 30PD BI at near fixation) and the appearance was cosmetically good in primary position [Fig. 2].
Bagshaw reported vertical deviation in anisometropic myopic eye which was fitted with a contact lens, the eye being hypotropic and exotropic. She named it the 'heavy eye phenomenon'.1 Subsequent studies mentioned coexistent features like reduced VA from unilateral high myopia, amblyopia, exotropia, hypotropia, reduced upgaze, ptosis, pseudoptosis and increased axial length all under the same entity.
In our patient lamellar cataract was an additional association. We blame it partially for the amblyopia and secondary exotropia in addition to anisometropic myopia which is rarely reported to cause ocular malalignment by dissociation.2 The V pattern could be explained by inferior oblique overaction due to an abnormal posterior insertion.3 Increased axial length can cause mechanical restriction as the center of gravity moves forward in the orbit anterior to the supporting ligament of Lockwood making the eye hypotropic.3 Muscle path shift of lateral rectus inferiorly (reduced abduction and increased infraduction) and superior rectus nasally (reduced supraduction) due to superotemporal eyeball prolapse in acquired esotropia with high myopia could be recalled here although the present case developed secondary exotropia.4 Large myopic eyes showed mechanical restriction due to contact between elongated posterior aspects of the globe and bones of the orbital apices.5
In conclusion, understanding this phenomenon could prevent undue intervention for strabismus. Eye and lid positions could give a false impression of third cranial nerve paresis and ptosis versus pseudoptosis should be evaluated. Endocrine ophthalmopathy in unilateral high myopes with restrictive motility should be considered after excluding the 'heavy eye'. Younger patients benefit from refraction, contact lenses and occlusion therapy. Horizontal muscle surgery should be reserved for patients who are symptomatic with diplopia or cosmetically unacceptable.
1. Bagshaw J. Vertical deviations of anisometropia Transactions of first international orthoptic congress. 1968 London Kimpton:277–86
2. Shippman S, Schampel P. The heavy eye phenomenon Am Orthopt J. 1996;46:150–4
3. Taylor R, Whale K, Raines M. The heavy eye phenomenon: orthoptic and ophthalmic characteristics Ger J Ophthalmol. 1995;4:252–5
4. Aoki Y, Nishida Y, Hayashi O, Nakamura J, Oda S, Yamade S, et al Magnetic resonance imaging measurements of extraocular muscle path shift and posterior eyeball prolapse from muscle cone in acquired esotropia with high myopia Am J Ophthalmol. 2003;136:482–9
5. Demer JL, Von Noorden GK. High myopia as an unusual cause of restrictive motility disturbance Surv Ophthalmol. 1989;33:281–4