Year : 1973 | Volume
: 21 | Issue : 2 | Page : 59--62
Anisometropia and amblyopia in straight eyes
SD Gupta, SC Scood, IS Jain
Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
S D Gupta
Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh
|How to cite this article:|
Gupta S D, Scood S C, Jain I S. Anisometropia and amblyopia in straight eyes.Indian J Ophthalmol 1973;21:59-62
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Gupta S D, Scood S C, Jain I S. Anisometropia and amblyopia in straight eyes. Indian J Ophthalmol [serial online] 1973 [cited 2020 Oct 27 ];21:59-62
Available from: https://www.ijo.in/text.asp?1973/21/2/59/31410
Anisometropia, is known to cause amblyopia by supression of fovea (JACKSON, PHILLIPS, , HELVESTON et al  and NOORDEN  ). It was PHILLIPS  who suggested the term anisometropic amblyopia for the cases showing varying amount of amblyopia in the more ametropic eye, in the absence of eccentric fixation. Although there is a general agreement so far as the amount of anisometropia and incidence of amblyopia are concerned, a considerable controversy exists over the relationship between the depth of amblyopia and the amount of anisometropia.
The present paper deals with the role of anisometropia in straight amblyopia and its relationship with the depth of amblyopia.
Method and Material
One hundred consecutive cases of straight amblyopia were studied. Patients with a vision of 6/9 or less in one or both eyes which could not be improved with any glasses without any organic disease in the refractive media or the fundii or visual pathways to explain the visual deficit, were labelled as amblyopes. Refraction was done in every case and best visual acuity was recorded. A subject was labelled to have anisometropia which indicated a difference of 0.5 D. Sph. or an equivalent cylinder or more in the refractive error of the two eyes. Media and fundii were examined to rule out any pathology which could give rise to defective vision.
Out of 100 cases of straight amblyopia, 78 were unilateral, and 22 bilateral amblyopes. 74 (94.9%) of the unilateral amblyopes had anisometropia while only 9 (40.97c) of the bilateral amblyopes had anisometropia. Whereas, 83% of all straight amblyopes had anisometropia.
It was further seen that upto a difference of 3.00 D, 61.5% of unilateral amblyopes had vision of 6/18 or better among 74 unilateral amblyopes having anisometropia, while 38.46% showed a vision of 6/24 or less. 22.9% had a vision of 6/18 or better and 77.1% a vision of 6/24 or less in cases of amblyopia having anisometropia more than 3.00 D. This relationship was statistically highly significant (P Anisometropia and supression
Anisometropia varying from 0.5 D to 7.50 D was seen in eighty three of the 100 cases. Supression at the fixation point was seen in 79 (95.2%) of these. Out of the 83 cases, 29 cases had foveal fixation and only 4 cases had no supression while the rest 255 cases had supression at the fovea,
GUPTA et al  reported the incidence of anisometropia (a difference of 0.5 or, more) among all the patients attending the Eye OPD to be 8.16%; 41.57% of these anisometropes had varying degree of amblyopia.
Incidence of anisometropia in straight amblyopia as reported is variable (Ainsworth et al  - 61.1%, KRZYSTKOWA et al  - 80%). Our figures of 83% fairly correspond with those of KRZYSTKOWA et al  . AINSWORTH et al considered anisometropia only when the difference in the two eyes is 1.00 D or more, whereas we included all the cases having a difference of 0.5 D or more. This explains the difference. Incidence of Anisometropia is much higher in straight amblyopes than it could be accounted for by its prevalence in general population.
Anisometropia is an important factor in the genesis of unilateral amblyopia as 94.9% of the unilateral amblyopia had anisometropia as against 40.9% in the bilateral amblyopia. These figures support the findings of GUPTA et al  who also found anisometropia in 96.05% of the unilateral amblyopes and 53.07% of the bilateral amblyopes.
Although now there seems a general agreement over the effect of anisoemtropia on the incidence of amblyopia, its effect on the depth of amblyopia is highly controversial. Chavesse  and Copps  mentioned that intensity of amblyopia tended to vary directly with the amount of anisometropia but HELVESTON  could find no relationship between the anisometropia and depth of amblyopia. MALIK et al  stated that, though there was a tendency for the vision to be better in low anisometropia as compared to high anisometropia, no strict relationship between the two could be established. Our observations [Table 1] support the view of MALIK et al  that with anisometropia of less than 3.00 D, the amblyopia tends to be less dense, and vice versa. An anisometropia of 1.00 D is compatible with vision of 6/60 and anisometropia of 4.00 D with vision of 6/9 or 6/12. So in addition to the amount of anisometropia, time of onset of anisometropia may be another factor in deciding the depth of amblyopia.
The amblyopia in straight eyes owing to anisometropia is possibly due to the blurred image on the retina, thereby fusion of images is not possible and the supression is produced in the more of ametropic eyes. This leads to the cerebral supression, initially of facultative type followed by obligatory in nature as suggested by JACKSON  . HELVESTON et al  and NOORDEN  also blamed foveal supression as a cause of amblyopia in an uncorrected anisometropia due to blurring of images and aniseikonia in a corrected anisometropia.
The presence of supression at the fixation-point in the 25 out of 29 foveal fixators having anisometropia supports the view that the anisometropia causes amblyopia because of supression.
It is easy to explain amblyopia with an anisometropia 2.50D or more on the basis of defective fusion faculty leading to supression, but the lowest significant amount of anisometropia which can produce amblyopia is a question which still remains unanswered. It is commonly observed in daily practice that some patients will not tolerate even 0.5 D difference between the two eyes without any discomfort whereas others will tolerate even an anisometropia of 2-3D without any discomfort and with good binocular single vision.
Therefore, individual adaptability to anisometropia and aniseikonia is variable and may be the determining factor as to which patient with anisometropia will develop amblyopia and which one will not. Even in normal isoametropes, aniseikonia upto 2.98% has been demonstrated by PHILLIPS  .
He also quoted Gillot  who found significant aniseikonic error with supression in two of the seventeen emmetropic subjects. PHILLIPS  suggested that two eyes, with unequal axial length but with compensatory differences in lens and cornea to produce equal or nearly equal refraction, could produce enough aniseikonia to interfere with fusion and thereby leading to supression in the more of ametropic eye.
It could also be possible that such patients had enough anisometropia at younger age, which gradually diminished to a considerable extent by the time they visited the hospital. Lastly, there might have been present macular haemorrhage at the time of delivery, in a low anisometropia, which subsequently cleared up, leaving only microscopical change of the retinal receptors.
It is very difficult to decide, which factor or factors are operating in a given case with a low anisometropia or isometropia or emmetropia, until more delicate tests like measuring the aniseikonia, length of the eye-ball and refraction of all the infants and young children is carried out as a routine.
Various grades of anisometropia were noticed in 831/c of straight amblyopes. Anisometropia is an important cause of unilateral amblyopia. As the amount of anisometropia increases, the depth of amblyopia also increases. But, this relationship is not a strict one. Moreover, all anisometropes do not develop amblyopia. Time of onset of anisometropia and the individual adaptability to anisometropia and aniseikonia may be the modifying factors.
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