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   Table of Contents      
ORIGINAL ARTICLE
Year : 2001  |  Volume : 49  |  Issue : 4  |  Page : 261-3

The effect of anisometropia on binocular visual function.


Guru Nanak Eye Centre, Maulana Azad Medical College, New Delhi, India

Correspondence Address:
S Dadeya
Guru Nanak Eye Centre, Maulana Azad Medical College, New Delhi
India
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Source of Support: None, Conflict of Interest: None


PMID: 12930119

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  Abstract 

PURPOSE: To investigate the effects of anisometropia on binocular vision. METHODS: One to three dioptres of unilateral hyperopia, myopia or astigmatism was induced in 30 normal adults. The effect on binocularity was assessed with the Worth-four dot test, Titmus stereo test and Bagolini's lenses. RESULTS: Binocular vision deteriorated with increasing anisometropia. Spherical anisometropia was more deleterious than astigmatic anisometropia. CONCLUSION: In addition to amblyopia, the potential effect of anisometropia on binocular vision should be considered while prescribing spectacles in young children during the sensitive period.

Keywords: Adult, Anisometropia, complications, physiopathology, Astigmatism, complications, Depth Perception, Humans, Vision, Binocular, Visual Acuity,


How to cite this article:
Dadeya S, Kamlesh, Shibal F. The effect of anisometropia on binocular visual function. Indian J Ophthalmol 2001;49:261

How to cite this URL:
Dadeya S, Kamlesh, Shibal F. The effect of anisometropia on binocular visual function. Indian J Ophthalmol [serial online] 2001 [cited 2019 May 25];49:261. Available from: http://www.ijo.in/text.asp?2001/49/4/261/14691

Anisometropia is considered to be a causative factor in the pathogenesis of amblyopia and strabismus. While the exact prevalence of anisometropia in the general population is not known, a prevalence of 4 - 4.7% has been described in the literature.[1] The conventional recommendation is that anisometropic refractive error be corrected in patients with established amblyopia or strabismus to ensure optimal visual development and maturation. However, the exact level of anisometropia and the age at which correction should be undertaken in healthy children remains to be determined.

It has been recommended that anisometropic refractive errors, that is, astigmatism >1.5 D, hyperopia >1.5 D and myopia >3 D should be corrected.[2] However, there is not much published literature to support these recommendations. In this prospective study stereoacuity was measured following experimentally induced anisometropia in healthy adults. The sensory blurring achieved experimentally mimics that experienced by an anisometropic child with an equivalent amount of monocular blur. Although this population is different, this approach might yield insight into the relationship between anisometropia and stereopsis, and identify the level of possible stereopsis in individuals affected by various degrees of anisometropia.


  Materials and Methods Top


This study was conducted in 30 normal adult patients aged 20-30 years at a tertiary eye-care center. Written informed consent of patients was taken prior to their inclusion in this study. The inclusion criteria were: best corrected visual acuity of 6/6; absence of manifest squint on cover, test; absence of stereopsis of 40 arc seconds or better; no previous therapy for amblyopia; no other ocular pathology; normal binocular response with Bagolini lenses; and normal fusion response with Worth-four-dot at 33 cm and 6m. Patients with more than 4 PD of hetrophoria on cover test while wearing full refractive correction were excluded from the study.

Refraction of all patients was done by one of the investigators under 1% cyclopentolate. Fogging technique was used to ensure that patients did not have excessive minus power. A trial frame was used to create the anisometropia with the experimental lens placed over the right eye. Four different types of anisometropia were induced, in random order, by placing trial lenses of 1-3 D over the right eye [1-3 D of hypermetropia, 1-3 D of myopia, unilateral against-the-rule (ATR) astigmatism +1 to + 3 D axis 90 and +1 to +3 D of astigmatism axis 45]. Normal room lighting was used for all sensory testing. Worth-four dot test for distance and near was used to measure if the patient had suppression scotoma. The stereoacuity was measured by using the Titmus stereo test. Bagolini lenses were used at reading distance to assess fusion. Chi-square test was used for statistical analysis.


  Results Top


All subjects showed fusion on Worth-four dot test before induction of anisometropia. Unilateral defocus caused suppression scotoma depending on the degree of anisometropia. All 30 patients were able to fuse on Worth-four dot test at 6-m distance under isometropic conditions. Four subjects were able to achieve fusion with 1D of uncorrected myopia (UM) or uncorrected hypermetropia (UH); five subjects were able to achieve fusion with 1D of against-the-rule astigmatism (ATR); and six subjects were able to fuse a2t 6m with 1D of uncorrected oblique astigmatism (UOA). Only one subject was able to fuse with the Worth-four dot test at 6m with 2D of spherical anisometropia and two subjects with ATR and UOA maintained this level of fusion. At 3 D of anisometropia, none of the subjects were able to fuse and one subject with ATR and UOA was able to fuse.

Stereoacuity levels were reduced in proportion to the degree of anisometropia. One dioptre of spherical anisometropia reduced the stereoacuity to an average of 92 arcs of second. However, 10 of the 30 subjects (33%) maintained 40 arc seconds of stereopsis with this level of spherical anisometropia. In contrast, one dioptre of cylindrical anisometropia reduced the stereoacuity to an average of 60 seconds for ATR and 55 seconds for UOA though 12 (40%) suspects with ATR and 15 (50%) subjects with UOA maintained 40 arc seconds stereoacuity. 3D of anisometropia caused marked reduction of stereoacuity in all subjects (Figure) regardless of type. This decrease in stereoacuity, which occurred with each dioptre increment in anisometropia, was statistically significant (p<0.05) for all patients regardless of type. Binocular response (fusion) was demonstrated by Bagolini's striated glasses in all subjects regardless of induced anisometropia.


  Discussion Top


Amblyopia is characterised by a constellation of deficits in spatial vision as induced by visual acuity, spatial contrast sensitivity and other tasks. Anisometropia is one of the leading causes of amblyopia and the mechanism of anisometropic amblyopia is poorly understood. While it is generally agreed that anisometropic refractive errors should be corrected in patients with established amblyopia or strabismus, it is not clear what levels of anisometropia should be empirically corrected in otherwise healthy children and at what age such correction should be made to ensure optimal visual development and maturation. This question is important in preventing and managing amblyopia, because the available data supports the notion that uncorrected anisometropic response during critical periods can alter the binocular response.[3-4]

The clinically acceptable level of 40 arc seconds of stereopsis can be maintained with a 1.0 D blur on Randot test and 0.5 D on the Titmus test.[5] Most of these subjects were able to maintain moderate levels of stereopsis with a 2.00 D monocular blur while approximately 20% subjects maintained gross stereopsis with even 4.00 D of monocular blur. The results of Lovasik differ radically from those of Peters,[6] who reported that 80% of his subjects lost stereopsis with a 1.0 dioptre monocular blur. However Lovasik's results agree with those of Levy and Glick,[7] who reported a stereoacuity level of 50 arc seconds on the Titmus test for subjects with a 2 line interocular difference in Snellen visual acuity.

One dioptre of anisometropia whether UM, UH, ATR or UOA has potential to degrade stereopsis to sub-normal levels in visually mature adults. [5,8] Low levels of anisometropia, both spherical and astigmatic, can have potentially significant adverse effects on high-grade binocular interaction in adults. These data suggest that effects of anisometropia on stereopsis should be considered in empiric correction of anisometropic refractive errors in children.[9] In all these studies considerable variation in susceptibility between individuals was noted. In hypermetropic patients, as the degree of anisometropia increases, the depth of amblyopia becomes greater and the level of binocularity becomes poor.[10] Moreover, Tomac and Birdal concluded that the depth of amblyopia is more effective than the amount of anisometropia in causing deterioration in binocularity.[11] The Titmus stereotest was used due to its ease of presentation, with the understanding that it may not be sensitive enough to make a precise quantitative measurement of stereoacuity sufficient to detect small differences. The test cannot exclude monocular clues.

The precise mechanism by which anisometropia causes a decrease in stereoacuity is not clear. It has been suggested that foveal suppression in the defocused eye is the cause of decreased stereopsis. However, other factors such as contrast and density of fusional details may also play an important role.[12] The results of Worth four dot test in this study clearly support the presence of suppression. It is speculated that anisometropia induced binocular rivalry, which in turn caused suppression. However, this does not clearly explain why this should occur only under conditions of sufficient monocular blur and not in its absence, as rivalry exists in both cases.

Our data from the Bagolini lenses corroborate the stereoacuity and Worth-four dot data in demonstrating that some binocularity is preserved at least at gross level, even in the presence of up to 3 D of anisometropia. Finally, our data suggest that different optical forms of anisometropia degrade binocular function differently. Binocularity deteriorated more with spherical anisometropia compared to astigmatic anisometropia. Oguz and Oguz[9] speculated that this is due to the global blur induced by spherical lenses compared to meridional blur caused by cylindrical lenses, a view with which we agree. The possible reason for decrease in stereoacuity with monocular defocus is that the resulting monocular magnification produced aniseikonia, due to which the two monocular images were out of phase. Although this explanation might account for some of the changes in stereopsis with optical defocus, it does not explain the similar reduction in binocular performance. The physiological basis of anisometropic suppression remains unclear. The results of this study confirm other findings suggesting that anisometropia interferes with binocular interaction, and the level of interference is directly related to degree of anisometropia, i.e., higher the anisometropia, poorer the binocular function. [5,8-10]

The probable mechanism underlying loss of binocularity is suppression. This has an important implication because the treatment of anisometropic amblyopia in children is an arduous task, with limited success in most cases. Even when such children are treated at an early age, the outcome is not rewarding and when the treatment is initiated at a later stage the success rate is even lower. Moreover, hypermetropic anisometropia >1.5 D appears to be a risk factor for deterioration of visual acuity in the long term, following treatment of amblyopic eyes by occlusion of the fellow eye.[13]

This study was conducted to detect the level of anisometropia that would interfere with binocular vision in adults. Despite the differences in the two study populations, we agree with Oguz and Oguz[9] that anisometropia in adults is optically identical to anisometropia in children and induced anisometropia interferes with the binocular response. We recommended that due consideration should be given to effects of anisometropia on binocularity during empiric correction of anisometropic refractive errors in children.

 
  References Top

1.
Vries de J. Anisometropia in children: analysis of a hospital population. Br J Ophthalmol 1985;69:504-7.  Back to cited text no. 1
    
2.
Goodwin RT, Romano PE. Stereoacuity degradation by experimental and real monocular and binocular amblyopia. Invest Ophthalmol Vis Sci 1985;26:917-23.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.
Harwerth RS, Smith EL III, Duncan GC, Crawford ML, von Noorden GK. Multiple sensitive periods in the development of primate visual system. Science 1986;232:235-38.  Back to cited text no. 3
    
4.
Wiesel TN, Hubel DH. Single cell responses in striate cortex of kittens deprived of vision in one eye. J Neurophysiol 1963;26:1003-17.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.
Lovasik JV, Szymkiw M. Effects of aniseikonia, anisometropia, accommodation, retinal luminance and pupil size on stereopsis. Invest Ophthalmol Vis Sci 1985;26:741-50.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.
Peters HB. The influence of anisometropia on stereo sensitivity. Am J Optom Arch Am Acad Optom 1969;46:120-23.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.
Levy NS, Glick EB. Stereoscopic perception and Snellen visual acuity. Am Ophthalmol 1974;78:722-24.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.
Brooks SE, Johnson D, Fisher N: Anisometropia and binocularity. Ophthalmology 1996;103:1139-43.  Back to cited text no. 8
    
9.
Oguz H, Oguz V. The effects of experimentally induced anisometropia on stereopsis. J Pediatr Ophthalmol Strabismus 2000;37:214-18.  Back to cited text no. 9
[PUBMED]  [FULLTEXT]  
10.
Rrutstein RP, Corliss D. Relationship between anisometropia, amblyopia, and binocularity. Optometry and Vision Science 1999;76:229-33.  Back to cited text no. 10
    
11.
Tomac S, Birdal E. Effects of anisometropia on binocularity. J Pediatr Ophthalmol Strabismus 2001;38:27-33.  Back to cited text no. 11
[PUBMED]  [FULLTEXT]  
12.
Simpson T. The suppression effect of simulated anisometropia. Ophthalmic Physiol Opt 1991;ll:350-58.  Back to cited text no. 12
    
13.
Levartovsky S, Oliver M, Gottesman N, Shimshoni M. Long term effect of hypermetropic anisometropia on the visual acuity of treated amblyopic eyes. Br J Ophthalmol 1998;82:55-58.  Back to cited text no. 13
[PUBMED]  [FULLTEXT]  



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