|
 |
| ARTICLES |
|
| Year : 1982 | Volume
: 30
| Issue : 6 | Page : 531-538 |
|
Ocular motility in amblyopic and the fellow eye
Prem Prakash, AK Grover, PK Khosla, DK Gahlot
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India
Correspondence Address:
Prem Prakash
Dr. Rajendra Prasad Centre for Ophthalmic Sciences All India Institute of Medical Sciences, New Delhi
India
 Source of Support: None, Conflict of Interest: None  | Check |
How to cite this article:
Prakash P, Grover A K, Khosla P K, Gahlot D K. Ocular motility in amblyopic and the fellow eye. Indian J Ophthalmol 1982;30:531-8 |
Studies on ocular motility in amblyopes have evinced a great deal of interest during the past three decades. A possible clinical significance of ocular motor abnormalities, as parameters for full functional cure of amblyos pia, has been suggested. A number of workers have studied the ocular motor abnormalities, sometimes with contradictory[2],[3] results.
| Materials and methods | |  |
The study was carried out on 10 normal subjects, 10 strabismic amblyopes and 10 anisometropic amblyopes; taken from the ocular motility and amblyopia clinic of Dr. Rajendra Prasad Centre for Opthalmic Sciences. A full orthoptic work-up was carried out in all subjects. Suppression scotoma was charted by using foveal fusion slides on the synoptophore. Fixation was recorded according to classification by Agarwal et al.[4]
Ocular motility was recorded electro-oculographically on a multichannel recorder Mingograf-800. Fixation, saccades and pursuit movements were recorded both in dark and light adapted states for each eye.
Fixation was recorded while patient looked at a target straight ahead of him. Saccadic movements were recorded as patient looked from one fixation light to the other-an excursion of 30°. Pursuit movements were recorded with the help of an instrument fabricated for the purpose. [Figure - 1] A, B, C outlines the essential components of the instrument.
For the analysis of the results grading of fixation saccades and pursuit movements was done as pointed out in [Figure - 2][Figure - 3][Figure - 4]. Two other parameters - critical frequency (CF) and frequency of disintegration (FD)-as described by von Noorden and Mackenson 5 were utilised to evaluate the pursuit movements, which allowed statistical evaluation of the ocular motor abnormalities to be made.
| Observations | | |
The amblyopes were observed to be having ocular motor abnormalities in fixation, saccadic and pursuit movements as detailed below.
(A) Fixation
The abnormalities observed in fixation were saccadic intrusions (tremors), drifts and superimposition with large saccades [Figure - 5](F), [Figure - 6](F) [Figure - 7](F), [Figure - 8] M. [Table - 1], illustrates thefiequency of abnormalities in the strabismic and anisometropic amblyopes in comparison to the normal subjects. It is apparent that abnormalities in fixation are more frequent in the strabismic amblyopes and are usually severer than in the anisometropic amblyopes.
(B) Saccades
Abnormalities in saccades were infrequent both in the strabismic and anisometropic amblyopes, as is evident from [Table - 2]. The abnormalities observed in saccadic movements were irregular saccadic movements, breaking up of the saccade into multiple small saccades, static overshooting and glissadic undershooting [Figure - 5](S), [Figure - 7](S)). The adnormalities in saccadic movements were usually mild in nature.
(C) Pursuit movements
Abnormalities in pursuit movements were almost invariably present in the amblyopesboth strabismic and anisometropic. The abnormalities observed were saccadic intrusions in the pursuit, abnormal saccadic substitution, cog wheeling of pursuit, early break up of pursuit and asymmetry of pursuit in nasal and temporalward directions [Figure - 5](P),[Figure - 6](P),[Figure - 7](P),[Figure - 8](P). As is evident from [Table - 3] the abnormalities in the strabismic amblyopes tended to be somewhat severer than in the anisometropic amblyopes.
Asymmetry of Pursuit
Gross asymmetry of pursuit was evident in 3 of the 10 strabismic amblyopes and 11 anisometropic amblyopes [Figure - 5](P), [Figure - 6](P)). One of the subjects was an esotrope and demonstrated a worse temporalward movement while two exotropes demonstrated a worse nasalward movement. The asymmetric pursuit could not be correlated to the presence of asymmetric suppression scotomas, as only one of the three patients had an asymmetric suppression scotoma and several patients with asymmetric suppression scotomas showed no asymmetry of pursuit.
| Effect of dark adaptation on ocular motility | | |
(i) Strabismic amblyopes
A slight trend for improvement of fixation in the dark adapted state was evident. [Table - 1] Saccades and pursuit movement, however, showed no trend for improvement in the dark adapted states. Mean CF and FD in the dark adapted states were not significantly different from the value in light adapted states.
(ii) Anisometropic amblyopes
Fixation and saccadic movement [Table - 1][Table - 2] showed no marked difference in the frequency or severity of ocular motor abnormalities. Pursuit movements [Table - 3], similarly, showed no significant improvement in the dark adapted states. Mean CF and FD in the dark and light adapted states were not significantly different from each other.
| Correlation of different parameters with extent of ocular motor abnormalities | | |
Both in strabismic and anisometropic amblyopes no direct relationship was observed between the extent of ocular motor abnormalities and certain parameters like.
(i) Visual acuity
(ii) Site of fixation
(iii) Suppression scotoma
| Discussion | | |
The existence of ocular motor abnormalities in the amblyopic eyes reported earlier by many workers has been amply confirmed. However, the frequency with which these abnormalities were observed differs from the observations made by some earlier workers.
There was little or no improvement of fixation and saccades in the dark in the amblyopic eyes. This is in marked contrast to the total improvement in dark adapted state reported by von Noorden and Burian[3]. Similarly the pursuit movements of amblyopic eyes have not shown a marked improvements in the dark adapted state.
The presence of abnormalities of ocular motility in strabismic and anisometropic amblyopes, as well as in patients with the alternating squint[6] suggested the probability that the common factor operating in these conditions is the presence of sensory adaptations, either facultative or obligatory. The exact mechanism by which the primary sensory anomaly leads to ocular motor abnormalities is not clear. The results suggest that the ocular motor abnormalities may be a result of the abnormalities in the binocularly driven cells of the visual cortex. These binocular cells are coordinating afferent stimuli to the occipital and probably the frontal oculomotor system. An abnormal input to the occipital oculomotor system could affect the `Position Maintenance System' and the `pursuit system'. The observations made in the present study that the defect in fixation and pursuit movements is very frequent while the defect in saccadic movements is markedly less frequent suggests that the occipital oculomotor system is affected to a greater extent than the frontal oculomotor system.
This hypothesis is supported by the experimental evidence that the abnormal binocular stimuli in the critical period result in decrease in the number of binocularly driven cells in the striate cortex ; shown by mono ocular occulusion[7] and by producing artificial strabismus or alternate occlusion[8],[3].
The presence of asymmetry of pursuit with nasalward movements being worse in the exotropes and temporalward movements in the esotropes is not correlatable to existence of asymmetric suppression scotoma. Selective greater involvement of binocular cells subserving certain receptive fields in particular areas of retina based on deviational characteristics may possibly be responsible for the presence of asymmetry.
| References | | |
| 1. | Ciuffreda, M.J.. Kenyon, R.V., and Stark, L. (1979); Inv. Ophthal. Vis. Sci., 18/5 : 506.  |
| 2. | Mackenson, G. (1957) : Elfin. Mbl. Augenheilk, 131/5: 640. |
| 3. | Von Noorden, G.K., and Burian, H.M. (1958) Amer. J. Ophth3i., 46 (No. 1, Part II) : 68. |
| 4. | Agarwal, L.P., Parkash, P., Malik, S.R.K., and Mohan M. (1963) : Orient. Arch. Ophthal., 1 :39. |
| 5. | Von Noorden, G.K, and Dowling, J.E. (1970) : A.M.A. Arch. Ophthal., 84 :215. |
| 6. | Parkash P., Grover A.K. Khosla P.K. and Gahlot D.K. (under publication). |
| 7. | Von Noorden, G.K. and Mackenson, G. (1962) Amer. J. Ophthal. 53 : 477. |
| 8. | Hubei, D.H. and Wissel, T.N. (1965): J. Neurophysiol., 28 : 1041. |
[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8]
[Table - 1], [Table - 2], [Table - 3]
|
Search Pubmed for