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Dissertation on

A CLINICAL STUDY ON

CHARACTERISTICS OF AMBLYOPIA PRESENTING IN A TERTIARY EYE

CARE CENTRE

Submitted in partial fulfillment of requirements of

M. S. OPHTHALMOLOGY BRANCH III

Of

REGIONAL INSTITUTE OF OPHTHALMOLOGY MADRAS MEDICAL COLLEGE

CHENNAI – 600 003

THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY CHENNAI-600 003

MAY - 2018

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CERTIFICATE

This is to certify that this dissertation titled “A Clinical Study on Characteristics of Amblyopia presenting in a tertiary eye care centre” is a bonafide record of the research work done by Dr.P.SUCHIETA JENNIL.., Post graduate in Regional Institute of Ophthalmology, Madras Medical College and Research Institute, Government General Hospital,Chennai-03, in partial fulfillment of the regulations laid down by The Tamil Nadu Dr.M.G.R. Medical University for the award of M.S.Ophthalmology Branch III, under my guidance and supervision during the academic years 2015-2018.

Prof. Dr.M.V.S. PRAKASH,MS.DO., Department of Squint, Paediatric ophthalmology and Neurophthalmology services,

Regional Institute of Ophthalmology Madras Medical College & Research Institute,

Govt. General Hospital, Chennai – 600 008

Prof.Dr.P.S.MAHESWARI M.S. D.O., Director and Superintendent

,

Regional Institute of Ophthalmology

Madras Medical College & Research Institute,

Govt. General Hospital, Chennai – 600 008

Prof. DR.R.NARAYANABABU.,M.D.,DCH Dean,

Madras Medical College,

Government General Hospital & Research Institute, Chennai-600003

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ACKNOWLEDGEMENT

I would like to thank Prof.DR.R.NARAYANABABU., M.D.,DCH, Dean, Madras Medical College and Research Institute for giving me permission to conduct the study in this Institution.

With due respect and gratitude, I thank Prof.Dr.P.S.MAHESWARI, M.S.,D.O., Director and superintendent, Regional Institute of Ophthalmology and Govt. Ophthalmic Hospital, Chennai for permitting me to conduct this study.

Prof.Dr.M.V.S.PRAKASH, M.S.,D.O., Unit Chief, Squint, Paediatric ophthalmology and neurophthalmology services, and my guide for assigning me this topic for study and guiding me throughout my Post graduate course. I wish to express my sincere thanks for the valuable help, encouragement and guidance at various stages of the study.

My sincere thanks to my Assisstant Professors Dr. T.G. Uma Maheswari, MS, Dr.P.Geetha MS.DO, Dr.S.Sheela MS., for their timely help and guidance in conducting this study.

I wish to express my sincere thanks to my family, friends and all my colleagues who helped me in bringing out this study.

Last but not the least, my heartful gratitude and sincere thanks to all

my patients without whom this endeavor would not have been possible.

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DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled, “A CLINICAL STUDY ON CHARACTERISTICS OF AMBLYOPIA PRESENTING IN A TERTIARY EYE CARE CENTRE” is a bonafide and genuine research work conducted by me under the guidance of Prof. Dr.M.V.S.PRAKASH, M.S., D.O., Head of Department of Squint, Paediatric ophthalmology and neurophthalmology services, Regional institute of ophthalmology & Government Ophthalmic hospital.

Chennai-600008.

Dr. P.SUCHIETA JENNIL Place: Chennai

Date:

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CERTIFICATE

This is to certify that this dissertation work titled “A CLINICAL STUDY ON CHARACTERISTICS OF AMBLYOPIA PRESENTING IN A TERTIARY EYE CARE CENTRE” of the candidate DR.SUCHIETA JENNIL.P with registration number 221513005 for the award of MS in the branch of OPHTHALMOLOGY.

I personally verified the urkund.com website for the purpose of plagiarism Check. I found that the uploaded thesis file contains from introduction to conclusion pages and result shows 0% percentage of plagiarism in the dissertation.

Guide & Supervisor sign with Seal

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CONTENTS

Serial No. Title Page No.

PART 1

1

INTRODUCTION

1

2

REVIEW OF LITERATURE

2

3

REFRACTIVE APPARATUS OF THE EYE

5

4

DEVELOPMENT OF BINOCULAR VISION

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5

CLASSIFICATION OF AMBLYOPIA

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6

PATHOGENESIS OF AMBLYOPIA

18

7

FEATURES OF AMBLYOPIA

20

8

EVALUATION OF A CASE OF AMBLYOPIA

31

9

MANAGEMENT OF AMBLYOPIA

46

PART 2

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AIM OF THE STUDY

56

11

MATERIALS AND METHODS

56

12

RESULTS AND ANALYSIS

59

13

DISCUSSION

86

14

SUMMARY

88

15

CONCLUSION

90

PART 3

16

BIBLIOGRAPHY

i

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PROFORMA

v

18

KEY TO MASTER CHART

vi

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MASTER CHART

ix

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PART 1

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1

INTRODUCTION

Amblyopia is characterized by decrease in best corrected visual acuity which can be unilateral or bilateral with no identifiable cause in the eye and visual pathway.

The meaning of the word amblyopia is ‘dullness of vision’, ‘ambly’ means dull and

‘ops’ means vision.

Prevalence of amblyopia is 2.0% to 2.5% in the general population.

Amblyopia is an important socioeconomic problem as it is a disabling condition for a person who needs high standards of visual acuity for his career. It also poses a problem when the fellow normal eye suffers loss of vision. Hence it is important in identifying the condition promptly and instituting treatment without delay.

Early diagnosis of amblyopia is very essential as the chance of improvement in visual acuity to standard levels is high when treatment is instituted early in childhood. The retinocortical connections in an amblyopic eye is not irrevocably damaged, rather it is dormant. Hence reactivation of these dormant connections through proper treatment will help regain standard visual acuity in the amblyopic eye.

Screening of children at basic health camps helps to detect amblyogenic conditions such as corneal opacities, ptosis, cataracts, refractive errors and strabismus.

This plays a vital role in early diagnosis.

Once diagnosed, treatment requires high compliance. Hence proper education about the disease, the need for compliance to treatment and regular follow up, should be imparted to patients and family.

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2

REVIEW OF LITERATURE

Packwood and coworkers studied the psychosocial difficulties associated with amblyopia. A questionnaire with 20 questions was used for the study, to assess the education, history and treatment of amblyopia, self-image and the effects of amblyopia on school, work and friendships. They concluded that amblyopia affects an individual’s school, work, self image and friendships. Hence proper screening, prevention and treatment should be instituted in the amblyogenic years1.

Vereecken EP and Brabant P studied the improvement in visual acuity in an amblyopic eye after the loss of vision in the good eye. Two hundred three cases were analysed by them and they concluded that foveal fixation is an important prognostic factor which determines the visual improvement in the amblyopic eye after the loss of vision in good eye2.

Harwerth RS et al studied the characteristics of the amblyopic eye after the enucleation of the fixating eye in monkeys. Strabismic amblyopia was surgically induced in one eye and then the fixating eye was enucleated. The measures of visual function assessed were photic increment threshold spectral sensitivity, spatial modulation sensitivity, scotopic spectral sensitivity and temporal modulation sensitivity. All the measures were assessed for both the eyes before enucleation and for the deviating eye after enucleation of the fixating eye. They concluded that the visual capacity of the strabismic amblyopic eye increased significantly after the enucleation of the fixating eye3.

Von Noorden GK and Middleditch PR studied the histology of the lateral geniculate body in monkeys after experimental strabismus and unilateral lid closure.

They concluded that animal with unilateral lid closure had the maximum cell

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shrinkage. Monkeys with esotropic amblyopia had lesser shrinkage and the monkeys with exotropia without amblyopia had the least severe changes4.

The paediatric eye disease investigator group (PEDIG) did a randomized control study comparing atropinization and patching as treatment modalities for children less than seven years of age with moderate amblyopia – Amblyopia treatment study 1. They concluded that the visual improvement with both patching and atropine are of similar magnitude and both can be used as the initial mode of treatment in children less than 7 years of age with moderate amblyopia5.

Amblyopia treatment study -2A done by Holmes JM, Kraker RT,et al- paediatric eye disease investigator group concluded that full time patching of normal eye and patching for 6 hours was equally effective in severe amblyopia6. Amblyopia treatment study- 2B done by Repka MX, Beck RW,et al- paediatric eye disease investigator group concluded that for children with moderate amblyopia, patching of sound eye for 6 hours is equally effective as patching for 2 hours when combined with near visual activities for one hour7. In Amblyopia treatment study -2C done by Holmes JM, Beck RW,et al- paediatric eye disease investigator group, the risk of recurrence of amblyopia after cessation of treatment was analysed. It concluded that around one fourth of the children who were successfully treated with patching or atropine had recurrence within one year. For patients who were treated with patching for 6 hours, tapering it to 2 hours of patching per day before cessation had reduced recurrence than abrupt stopping8.

Scheiman MM, Hertle RW et al - PEDIG conducted a randomized trial to analyse the effectiveness of amblyopia treatment in children aged 7 to 17 years. They concluded that for children of age 7 to 12, two to six hours of patching per day along

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with near vision activities causes improvement in visual acuity even though amblyopia was treated previously. For children aged 13 to 17 years, patching and near vision activities are helpful in visual improvement if there is no prior amblyopia treatment9.

A randomized pilot study was done by PEDIG to assess the effect of near activities and non near activities during patching for treatment of amblyopia and to assess the compliance of the children when instructed to do near and non near activities. It was concluded that children who were advised patching and near activities complied to do so and performing near vision activities during patching benefited visual improvement10.

David Wallace, Danielle L. Chandler, PEDIG studied the binocular visual acuity improvement in cases of bilateral refractive amblyopia during treatment in children aged 3 to 10 years. They concluded that vision can be improved in bilateral refractive amblyopia by the use of spectacles alone and most children improved to 20/25 or more within one year11.

Holmes JM, Manh VM, et al – PEDIG did a randomized control study to compare the effects of patching versus a binocular iPad game in amblyopic children of age 5 to 12 years. The amblyopic children were randomized to binocular game one hour per day for 16 weeks or patching for 2 hours per day. In children aged 5 to less than 13 years, the visual acuity in the amblyopic eye improved with both binocular iPad game and patching, especially in children of age 5 to 7 years with no previous amblyopia treatment. The primary noninferiority analysis of the study was indeterminate but a post hoc analysis showed that the improvement in visual acuity is not as effective as 2 hours of patching12.

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REFRACTIVE APPARATUS OF THE EYE

The refractive apparatus of the eye consists of the cornea and the crystalline lens which acts as the focusing system, iris and the pupil which regulates the amount of light that enters the eye, retina which is the light sensitive receptive layer and the aqueous and vitreous which acts as an optically clear medium.

The total dioptric power of the eye is +58 Dioptre. The crystalline lens contributes +15 Dioptres and the cornea contributes +43 Dioptres.

CORNEA

The cornea is a transparent structure. It is more curved vertically than horizontally. The vertical diameter is 10.6mm and the horizontal diameter is 11.7mm.

The thickness is 0.5mm at the center and 0.7mm at the periphery. The anterior radius of curvature is 7.7mm and posterior radius of curvature is 6.9mm. The refractive index of the cornea is 1.376.

ANTERIOR CHAMBER AND POSTERIOR CHAMBER

It is a small cavity bounded anteriorly by the cornea and posteriorly by the iris.

Its volume is 0.2 ml.

It is bound anteriorly by iris and ciliary processes and posteriorly by lens and zonules. Its volume is 0.06ml.

AQUEOUS

It fills the anterior and posterior chamber. It is formed from ciliary process by diffusion, ultrafiltration and active secretion at the rate of 2 to 3 microlitre per minute.

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It provides glucose and other nutrients to cornea and lens, removes metabolic wastes and provides a optically clear medium. The refractive index of the aqueous is 1.336

LENS

The diameter of the crystalline lens is 6.5 mm at birth and 10 mm in an adult.

It is biconvex and covered by a capsule. The central portion is the nucleus and it is surrounded by the cortex. The refractive index of the cortex is 1.386 and that of the nucleus is 1.406. The mean refractive index is 1.39.

VITREOUS

It is a transparent gel which fills the posterior segment of the eye. The refractive index of the vitreous is 1.336.

RETINA

It is the innermost layer of the eyeball. It is very highly developed layer of the eye. It has three important regions. They are the macula, the optic disc and the peripheral retina.

The optic disc is pink in colour, 1.5 x 1.1 mm in size. The centre of the disc has the physiological cup through which the central retinal vessels arise. The macula lutea is present at the posterior pole of the eye, temporal to the disc. The macula represents the central 15º of the field. The central part of the macula which is depressed is called fovea centralis. It measures about 1.85mm in diameter. It represents the central 5º of the field. Foveola is 0.35mm in diameter and is situated in the floor of the fovea. The umbo is a very small depression in the centre of the foveola. It corresponds to the foveolar reflex. The parafoveal area is of 0.5 mm in

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diameter and the perifoveal area is 1.5mm in diameter. The area around macula to ora serrata is the peripheral retina.

VISUAL PATHWAY

Figure 1: Visual pathway

The optic nerve extends from the optic disc to the optic chiasma. It is made up of the continuation of the retinal nerve fibre layer. The two optic nerves meet at the chiasma. At the chiasma decussation of the nerve fibres arising from the nasal half of the retina occurs. The optic tracts run from the optic chiasma to the lateral geniculate body. Each optic tract is made up of nerve fibres from temporal half of the ipsilateral eye and nasal half of the contralateral eye. The lateral geniculate body is an oval structure present at the termination of the optic tracts. It consists of six layers of grey matter or neurons which alternate with white matter made up of optic fibres. Laminae 1,4,6 receive the crossed fibres and laminae 2,3 and 5 receive the uncrossed fibres.

Optic radiations arise from the lateral geniculate body and extend upto the visual cortex. The optic radiations are called as geniculocalcarine pathway. The inferior

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fibres of the radiations pass through the temporal lobe and superior fibres pass through the parietal lobe to reach the visual cortex. The visual cortex is present on the occipital lobe on its medial aspect. It is divided into visuosensory area which is area 17 and visuopsychic area which is peristriate area 18 and parastriate area 19.

DEVELOPMENT OF BINOCULAR VISION

Most of the visual functions are present at the time of birth but their maturation occurs during postnatal period. The early postnatal period is critical in the development of refined visual functions. Hence any obstacle in this critical period of visual development may result in abnormal development of binocular vision.

The anatomy of the eyes and orbits are not developed completely at the time of birth. The orbits continue to develop until teenage. The interpupillary distance is 45mm at birth and increases to 66mm in adult. The axial length of the globe increases from 17.5mm of birth to 24mm in adult. The extraocular muscles are not of adult size at birth but functionally developed completely.

At birth there is no bifoveal fixation and coordinated eye movements. There is poor fixation at birth because awareness of the presence of the object and attention towards the object is necessary for conscious fixation which is not present in a new born infant. Initially the fixation develops monoocularly around 3 weeks of age and sustained by 5 weeks. Around 6 weeks of age there is rapid alternate fixation and then the child begins to fixate binocularly. Later conjugate movements develop to follow large near objects. Convergence is developed fully by 6 months.

At birth the basic visual functions are present but complex functions like binocular cooperation are developed later to establish bifoveal single vision. At birth

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the eyes act as two independent sense organs. The foveas are not fully developed until third month of life after which the child learns that the image details are most clear when brought to focus by both the foveas simultaneously. After this the child develops space perception. Any obstacle which prevents the association of both the fovea will result in failure of development of binocular single vision.

NEUROPHYSIOLOGY OF DEVELOPMENT

The M and P pathways arise from different populations of retinal ganglion cells. The lateral geniculate nucleus has small cells or P cells and large cells or M cells. The Parvocellular pathway is related to colour perception, high spatial frequencies and fine stereopsis. Magnocellular pathway is sensitive to speed, motion, direction and gross stereopsis. Parvocellular neurons project to areas of central visual field and fovea. Magnocellular neurons project to peripheral retina. The properties of these neurons like binocularity, orientation specificity are highly influenced by the child’s visual experience during the first few postnatal months. The neonatal visual system is highly plastic during the maturation stage. Patterned visual stimuli acts as a stimulant for development and refinement of the neuronal connections in the visual cortex. Any disruption occurring during the maturation stage like congenital cataract, strabismus or refractive error will prevent the development of binocular single vision.

THEORY OF BINOCULAR VISION CORRESPONDENCE AND DISPARITY

Each retinal element in one retina shares a common visual direction with the retinal element in the other retina. These retinal elements are called corresponding points. These corresponding points form the framework or zero system of binocular

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vision. When these corresponding points are stimulated by one object point, a single visual impression is transmitted without depth perception. When two objects which differ in character stimulate the corresponding points retinal rivalry occurs. When one object point stimulates disparate retinal elements, diplopia occurs. But if the horizontal disparity is within the limits of the Panum’s area, a single visual impression with stereopsis is elicited.

NEUROPHYSIOLOGIC BASIS OF CORRESPONDENCE

The work of Hubel and Wiesel has given physiologic evidence for the correspondence theory. 80% of the neurons can be stimulated by either eye. But only 25% of these binocularly driven cells are equally stimulated by each eye. The remaining 75% of the neurons have graded degrees of influence from either eye. 10%

of the neurons are stimulated exclusively by either right or left eye. The receptive field of a visual neuron is the part of the visual field that can influence the stimulation of that neuron. Visual neurons that are driven by either eye have receptive fields which are nearly equal in size and in corresponding positions in the visual field.

Summation or inhibition of the neuronal response occurs depending on the alignment or misalignment of the stimulus on the receptive field. Whenever the corresponding points of the receptive field are stimulated, summation of the neuronal response occurs.

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ABNORMALITIES IN DEVELOPMENT OF BINOCULAR VISION

The time at which a lesion occurs in the visual system is an important factor which determines the effect it will have on the disruption of the existing visual function and further development of the complex visual functions.

DIPLOPIA

Diplopia occurs when there is a misalignment of the visual axes which cause an image to fall on the fovea of one eye and a non-foveal point on the other eye.

When these images fall on non corresponding points outside Panum’s area, diplopia occurs. The patient will see the same object in two different locations in the subjective space. The foveal image will be clearer than the non foveal image.

CONFUSION

Confusion occurs because of ocular misalignment but it is much less common than diplopia. In confusion, the patient will see two different images which are superimposed on each other. This occurs because two dissimilar objects fall on each fovea.

SUPPRESSION

Active cortical inhibition of one eye to avoid diplopia or confusion causes suppression. The scotoma which develops because of suppression is functional and not organic. Hence when the suppressed eye is made to take up fixation by occluding the other eye, the scotoma disappears. In an alternating strabismus, the suppression is facultative. However if the strabismus is constant and the other eye remains the

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fixating eye, the suppression becomes deep and constant. In such a condition even if the deviating eye is forced to take up fixation, the suppression will remain and the visual acuity will be defective. This is obligatory suppression.

AMBLYOPIA

A child with strabismus or anisometropia or stimulus derivation develops facultative suppression initially. Age is an important factor which decides the development of facultative suppression or amblyopia. Young infants who develop strabismus early in life before the maturation of the visual system have deep amblyopia when compared to older children who develop strabismus. Hence if suppression inhibits the development of the fovea even before maturation, the visual acuity cannot be improved to standard levels even after treatment. The visual improvement will be only upto the level it was before the development of amblyopia.

ABNORMAL RETINAL CORRESPONDENCE

In abnormal retinal correspondence the fovea of one eye acquires a common visual direction with a non foveal point in the other eye. It is an active cortical adjustment that occurs in a young child with strabismus. This adaptation is developed to gain some form of binocular vision and to prevent diplopia and confusion.

AMBLYOPIA

Amblyopia is a decrease in the best correct visual acuity of an eye without any identifiable pathology in the eye or the visual pathway13. It may occur due to foveal pattern deprivation or abnormal binocular interaction or both14.

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13 CLASSIFICATION OF AMBLYOPIA

Amblyopia can be classified as

FUNCTIONAL OR REVERSIBLE AMBLYOPIA ORGANIC OR IRREVERSIBLE AMBLYOPIA

Functional or reversible amblyopia occurs due to deprivation of form vision or abnormal binocular interaction. It is reversible and the extent of reversibility depends on the age at which treatment was started and the duration of amblyopia. It includes anisometropic amblyopia, strabismic amblyopia, meridional amblyopia, stimulus deprivation amblyopia.

Organic or irreversible amblyopia occurs due to subtle retinal damage which cannot be detected on ophthalmoscopic examination.

Chavasse classified amblyopia as

AMBLYOPIA OF ARREST AMBLYOPIA OF EXTINCTION

Amblyopia of arrest occurs due to hindrance in the normal visual development in infancy. This occurs before 6 months of age before the complete maturation of visual development.

Amblyopia of extinction occurs after the visual development is complete. This arises in a situation where the visual impulses from an eye has to be suppressed to avoid abnormal binocular interaction.

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CAUSES OF AMBLYOPIA STRABISMIC AMBLYOPIA

Strabismic amblyopia occurs due to inhibition of visual impulses arising from the deviating eye. It is unilateral and amblyopia occurs in the deviating eye.

Strabismic patients with alternation of fixation have a lesser chance of developing amblyopia than patients who have a fixation preference for one eye.

Patients with esotropia have a higher chance of developing amblyopia than patients with exotropia. This is because in esotropia there is competition between foveal impulses of the deviating eye with the temporal field of the normal eye which is stronger, whereas in exotropia competition of foveal impulses is with the weaker nasal field of the other eye15. Hence amblyopia in strabismus is caused due to suppression of the foveal impulses of the deviating eye in the retinocortical pathways.

Another cause for development of amblyopia in the deviating eye is insufficient stimulation of the fovea16. Few characteristics of strabismic amblyopia are better grating acuity and improvement of visual acuity with a neutral density filter, which is contrary to organic ambyopia.

Figure 2: Strabismic amblyopia

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ANISOMETROPIC AMBLYOPIA

Anisometropic amblyopia occurs when the two eyes have a different refractive error. The eye with the higher refractive error receives a blurred image than the eye with the lesser refractive error. Hence to overcome the problem of a blurred image over a focused image the impulses from the eye with the higher refractive error are suppressed leading to the development of amblyopia. Another cause for amblyopia in anisometropia is the presence of aniseikonia after refractive correction. Hence the amblyogenic factors are defective form vision and competitive suppression. Also visual acuity will be better when the eyes are tested monocularly than the visual acuity in binocular conditions.

A hypermetrope with anisometropia has a higher chance of developing amblyopia than a myope with anisometropia. Also the depth of amblyopia is higher in a hypermetrope with anisometropia than a myope with anisometropia. This is because the hypermetropic eye never receives a focused image while in myopes the lesser myopic eye is used for distance vision and the more myopic eye is used for near vision. Hence an anisometropia of even +1 Dioptre can cause amblyopia in hypermetropes while in myopes ambylopia occurs when there is an anisometropia of - 3 Dioptres.

MERIDIONAL AMBLYOPIA

Meridional amblyopia occurs in patients with astigmatic error which is uncorrected. It is because of the blurred image formed in one meridian that causes pattern vision deprivation. Astigmatism of 1.5 Dioptre can cause amblyopia.

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BILATERAL AMETROPIC AMBLYOPIA

Bilateral ametropic amblyopia occurs in patients with high refractive errors in both eyes which is uncorrected. This type of amblyopia is of a lesser degree than anisometropic amblyopia because deprivation of form vision is the only amblyogenic factor and there is no competitive inhibition of one eye. It occurs more commonly in hypermetropes. Uncorrected hypermetropes of more than +5 Dioptres and uncorrected myopes of more than -10 Dioptres have a chance of higher degree of amblyopia.

STIMULUS DEPRIVATION AMBLYOPIA

Stimulus deprivation amblyopia is also called as AMBLYOPIA OF DISUSE or AMBLYOPIA EX ANOPSIA. The primary cause of this type of amblyopia is inadequate stimulation of the retina. Causes of stimulus deprivation amblyopia include media opacities like congenital cataracts, traumatic cataracts, surgical lid closure, unilateral ptosis17.

Figure 3: Congenital cataract operated- both eyes pseudophakia

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Figure 4: Left eye ptosis OCCLUSION AMBLYOPIA

Occlusion amblyopia is iatrogenically induced stimulus deprivation amblyopia which occurs after unilateral prolonged patching or atropinization for a long duration18.

AMBLYOPIA FOLLOWING NYSTAGMUS

In this condition there occurs both nystagmus and amblyopia and it is quite difficult to conclude if the nystagmus has caused the reduced vision or the reduced vision has caused the nystagmus. Fixation should be determined in all patients with amblyopia with a visuoscope or a direct ophthalmoscope. This is important because micronystagmus may be the cause of reduced vision in a patient who has no other causes for amblyopia.

IDIOPATHIC AMBLYOPIA

Idiopathic amblyopia is characterized by unilateral reduction of vision without any amblyogenic causes like strabismus, visual deprivation, uncorrected refractive errors19. It is due to transient anisometropia or astigmatism that occurs during infancy

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which causes foveal inhibition in one eye during visual development. The amblyogenic anisometropia or astigmatism disappears with advancing age but ambylopia persists. Recurrence of amblyopia following cessation of occlusion therapy is common in this type of amblyopia.

ORGANIC AMBLYOPIA

Organic amblyopia is an irreversible amblyopia caused due to subtle retinal damages which cannot be detected on ophthalmoscopic examination.

In certain types of amblyopia, treatment may improve the visual acuity but cannot restore the visual acuity to normalcy. It is called as RELATIVE AMBLYOPIA OF BANGERTER. This occurs because of occurrence of reversible amblyopia superimposed over irreversible amblyopia.

PATHOGENESIS OF AMBLYOPIA

A great amount of research is ongoing to elucidate the pathogenesis of amblyopia yet it is still not fully understood. There are differences in the pathogenesis of various types of amblyopia. Deprivation of form vision, deprivation of light, abnormal binocular interaction, cortical inhibition and the development of retina and visual pathway are the most important factors in the pathogenesis of amblyopia.

The amblyogenic factors responsible for the development of amblyopia are deprivation of form vision, deprivation of light and abnormal binocular interaction.

When there is monocular deprivation of form vision during the sensitive period of visual system maturation, the eye that is deprived of form vision is dominated by the sound eye leading to the development of amblyopia. Here both

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deprivation of form vision and abnormal binocular interaction are amblyogenic factors. This occurs in strabismic amblyopia, unilateral stimulus deprivation amblyopia and anisometropic amblyopia. When there is binocular deprivation of form vision, there is no domination of one eye over the other. This occurs in bilateral ametropic amblyopia and bilateral stimulus deprivation amblyopia like bilateral cataracts. There is no competition between the two eyes the amblyopia is not as severe like that of monocular deprivation.

Deprivation of light causes amblyopia in cases of congenital and developmental cataracts. It may be unilateral or bilateral. When it is unilateral there is both deprivation and abnormal binocular interaction. When it is bilateral only light deprivation acts as an amblyogenic factor.

Abnormal binocular interaction is a strong amblyogenic factor. It causes amblyopia of a severe degree because of competition. This occurs in strabismic amblyopia, anisometropic amblyopia and unilateral stimulus deprivation amblyopia.

Active cortical inhibition is an important factor in the pathogenesis of amblyopia. Experimental studies have been done by inducing unilateral deprivation amblyopia in monkeys and enucleating the normal eye in one group and enucleating the amblyopic eye in the other group. It was found that more number of visual cortical neurons were driven by the amblyopic eye in the group in which the normal eye was enucleated than the other group in which the amblyopic eye was enucleated. There are also evidences that the vision in the amblyopic eye improves following loss of function of the good eye. Hence cortical inhibition driven by the normal eye is responsible for development of amblyopia in the other eye.

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20 SENSITIVE PERIOD

Amblyopia develops in a period when the visual system and retinocortical connections are immature and not after complete maturation of the visual system.

This period is called as sensitive period or critical period or susceptible period. The sensitive period for different types of amblyopia are not identical. Sensitive period also has interindividual variability because of different rate of maturation of the visual system. Usually the tendency for strabismic amblyopia to occur extends upto seventh year of life. Beyond this is it unlikely and even when it occurs, only a milder form of amblyopia develops.

FEATURES OF AMBLYOPIA VISUAL ACUITY AND FIXATION

Any difference in visual acuity of two lines between the two eyes is considered as amblyopia. In patients who are old enough to be tested for visual acuity, the diagnosis of amblyopia is easy. However in infants and younger children other methods like grating acuity, preferential looking tests, visually evoked responses and fixation preference assessment are used to assess the difference in visual acuity between the two eyes.

If there is free alteration of fixation there is very less probability that the child may have amblyopia. If the child has a strong preference to fixation of one eye, the probability of amblyopia is high. Such a child will not resist occlusion of the amblyopic eye but will strongly resist occlusion of the normal eye. Amblyopia should be suspected when there is roving searching movements of one eye when the other eye is occluded. The time taken for the deviated eye to take up fixation when the

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normal eye is occluded also gives a clue to the presence of amblyopia. The maintenance of fixation is important, if the child is maintaining fixation with an eye even after a blink, there is no amblyopia in that eye usually. Amblyopia can also be detected by allowing the eye to follow a fixation target from adducted position to abducted position. The point at which fixation changes from one eye to the other is noted. If the change occurs at primary position there is no amblyopia. If the eye continues to follow the target beyond primary position into abduction it means the other eye may be amblyopic.

EFFECT OF NEUTRAL DENSITY FILTERS ON VISUAL ACUITY

Figure 5: Neutral density filter

Ammann found that in eyes with central retinal lesions and glaucoma there was a great reduction in visual acuity when a neutral density filter is used, while in amblyopia the use of neutral density filters did not reduce vision and in some cases the vision improves. This is known as the AMMANN PHENOMENON. This is more so in strabismic amblyopia where there is increase in visual acuity of the eye in mesopic conditions and at certain times the visual acuity even matches that of the

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normal eye. The neutral density filter test can be used to differentiate organic amblyopia from reversible amblyopia20. This also indicates that the amblyopic eye does not work best in photopic conditions.

CROWDING PHENOMENON

In amblyopia visual acuity measured with single optotype in a uniform background is better than visual acuity measured with a row of characters in a line.

This is known as CROWDING PHENOMENON or SEPARATION DIFFICULTIES.

Hence the amblyopic eye will have two different visual acuities, a line acuity when tested with Snellen’s chart and a single E acuity. The discrepancy between the line acuity and single E acuity is more when the visual acuity is poorer in the amblyopic eye.

Crowding phenomenon occurs because of contour interaction and there is reduced lateral inhibition of foveal cones in amblyopic eyes. The reduced lateral inhibition leads to disinhibition of the monosynaptic foveal cone system. Hence a physiological blur is created and a fuzzy image would be transmitted to the cortical visual centers.

Crowding phenomenon is important while treating amblyopia as visual acuity with single optotype improves prior to line acuity21. Treatment should not be stopped once single optotype acuity reaches standard acuity level. Treatment should be continued until the line acuity reaches the standard level. Premature cessation of treatment before line acuity reaches the standard level may lead to recurrence of amblyopia. So a patient with amblyopia should never be assessed with single optotype acuity alone as it overestimates the vision, but it provides the true visual potential of the eye which is masked by amblyopic process.

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ACCOMMODATION

Accommodation will be defective in patients with amblyopia. This defective accommodation is due to the abnormal visual experience in early life and sensory loss of the foveal region.

COLOUR VISION

Colour vision is affected in amblyopia only when the visual acuity is poor.

Abnormal colour vision in dense amblyopia is due to eccentric fixation where the peripheral retina is used for fixation.

TYPES OF FIXATION

Amblyopic patients may have a central or eccentric fixation. Usually patients with strabismic amblyopia have eccentric fixation.

BANGERTER’S CLASSIFICATION of fixation patterns include 1. Central fixation

2. Eccentric fixation 3. No fixation Eccentric fixation may be

a. Parafoveolar fixation- adjacent to foveola

b. Parafoveal fixation- outside fovea but close to foveal wall

c. Peripheral eccentric- between edge of the fovea and rarely beyond disc

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24 Figure 6: Types of fixation

Generally in esodeviations the fixation is nasal and in exodeviations the fixation is temporal. There may be few exceptions. When esodeviations have temporal fixation and exodeviations have nasal fixations, it is known as paradoxical fixation behavior. This usually occurs in consecutive deviations following surgery.

Further the fixation both central and eccentric may be a steady fixation or wandering fixation. Wandering fixation may occur in the amblyopic eye on occluding the normal eye. It must be differentiated from spontaneous monocular pendular oscillations occurring in dense amblyopia. This is known as HEIMANN BEILSCHOWSKY PHENOMENON22.

Haidinger’s brushes or Maxwell spots are used to diagnose eccentric fixation, they have therapeutic uses also. Haidinger brushes are yellow in colour and has a brush like pattern. The center of the brush corresponds to the point of fixation. If the patient has central fixation, the center of the brush will be superimposed over the point of fixation. If the patient has eccentric fixation the center of the brush will be away from the point of fixation. Maxwell’s spots is another method using entoptic

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phenomenon in which the macula appears as dark spot when viewed through a blue filter.

Figure 7: Haidinger’s brushes

Visuoscope can be used to determine the point of fixation. It projects a star as a fixation target. The position of the star on the retina determines the fixation.

Determination of eccentric fixation in an amblyopic patient is important because as the point of fixation moves away from the foveola the visual acuity decreases. Hence in a patient greater the eccentricity of the point of fixation poorer is the visual acuity. Visual acuity and fixation also depends on the position of the eye and extraocular movements. In an esotropic eye the eccentricity of fixation is more in abduction than in adduction.

Fixation is also an important prognostic factor while treating an amblyopic patient. An amblyopic eye with steady eccentric fixation has a poorer prognosis than an unsteady wandering fixation.

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26 THEORIES OF ECCENTRIC FIXATION CUPPERS THEORY

Cuppers theory is also known as anomalous correspondence theory. According to Cuppers theory the ‘straight ahead’ sensation is transmitted by some eccentric retinal area instead of the fovea. This concept also differentiates eccentric fixation from eccentric viewing. In eccentric fixation the patient subjectively feels he is looking straight ahead but the image falls in a nonfoveolar area. This is true eccentric fixation. Whereas in eccentric viewing the patient tells that he is looking past the target object.

SCOTOMA THEORY

According to this theory in an amblyopic eye the area near the scotoma has highest resolving power and the amblyopic eye fixates with this area.

VON NOORDEN’S explanation for mechanism of eccentric fixation is abnormal fixation reflex23. Fovea is the retinomotor center or retinomotor zero. When an image falls on the retina away from the fovea, a fixation reflex is elicited which moves the eye in such a way that the image falls on the fovea. In eccentric fixation an abnormal fixation reflex is adjusted to a peripheral retinal area because of decrease in foveal visual acuity. Hence the fovea is no longer the retinomotor zero.

LIGHT SENSE AND THRESHOLD IN AMBLYOPIA

The simple light perception of the amblyopic eye is normal at fovea and periphery. But there is a dissociation between light sense which is normal and acuity function which is abnormal. In dark adapted state the fixation is more steady and central. Therefore the amblyopic eye functions best at mesopic conditions and it

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works worst at photopic conditions as the amblyopic effect is more at higher levels luminance.

SPATIAL SUMMATION

Normally the coefficient of summation is low and receptive fields are smaller in retinal center. The coefficient of summation is high and receptive fields are larger in retinal periphery. But in amblyopia the receptive fields of the retinal center are enlarged similar to retinal periphery. The lateral inhibition of the cones at the fovea are also reduced.

CONTRAST SENSITIVITY

At photopic conditions the amblyopic eye needs high contrast requirement with high background illumination. But in low illumination the requirements of amblyopic eye are similar to that of a normal eye.

In strabismic amblyopia the contrast sensitivity of the foveal region is similar to the contrast sensitivity of the peripheral retina in the normal eye. At low luminance levels, the contrast sensitivity of strabismic amblyopia improves and becomes normal but the deficit in contrast sensitivity persisted in anisometropic amblyopia.

MOVEMENT PERCEPTION

The P system or the parvocellular cortical areas process high spatial frequency stimuli and is associated with visual resolution. The M system or the magnocellular cortical areas process low spatial frequency stimuli and is associated with movement perception. In amblyopia there is dissociation between the parvocellular and the

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magnocellular system. The deficit is more in the P system while the M system may actually perform better than the P system.

Oscillatory movement displacement threshold is the smallest movement in a stimuli that will give rise to a perception of movement. It is a form of hyperacuity. In amblyopic patients with stereopsis there is no deficits in oscillatory movement displacement threshold. But amblyopic patients without stereopsis have deficits in oscillatory movement displacement threshold.

ERRORS OF LOCALIZATION AND SPATIAL DISTORTION

Spatial uncertainty or imprecision is a feature of amblyopic eyes. Amblyopic patients have distortion and fragmentation of optotypes. There is distortion and fading of grating pattern in contrast sensitivity testing. They also have defects in relative localization.

CRITICAL FLICKER FREQUENCY

The frequency of a light stimulus determines if the stimulus is perceived as a flicker or a continuous sensation. The frequency at which the flicker just disappears is called critical flicker frequency. The critical flicker frequency is faster in the amblyopic eyes with eccentric fixation than amblyopic eyes with foveal fixation as more number of magnocellular retinal ganglion cells are stimulated in the retinal periphery.

PUPILLARY RESPONSES

The pupil of the amblyopic eye has an increased latency of contraction and dilatation. There is a decrease in time of contraction of the pupil but there is no

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decrease in speed of contraction when compared with the normal eye. This is confirmed by infrared electropupillography. There is no correlation between the pupillary response and the visual acuity in the amblyopic eye24.

INTEROCULAR INHIBITORY EFFECTS

For normal binocular single vision, the functioning of one eye is influenced by the functioning of the other eye. When visual stimulus is presented to one eye and in quick succession a visual stimulus is presented to the corresponding retinal elements in the other eye, the second stimulus extinguishes the perception of the first stimuli.

This is known as EXTINCTION PHENOMENON. This affects corresponding retinal elements and also an an area around it. The farther the stimulation is from the fovea larger is the area of extinction. In amblyopia, the area of extinction is larger in the amblyopic eye than the normal eye.

Interocular inhibitory effects is cause for decreased visual acuity in the amblyopic eye in binocular conditions. In most cases of amblyopia the visual acuity in the amblyopic eye improves on occluding the normal eye. The decrease in visual acuity in binocular conditions is more common in esotropia and hypermetropic anisometropia.

The inhibitory effect of the normal eye on the amblyopic eye continues even after the monocular visual acuity in the amblyopic eye has improved to standard levels. It is important in therapeutic point of view, because treatment should continue until visual acuity in amblyopic eye reaches standard levels in binocular conditions.

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The importance of the interocular inhibitory factors is shown by the findings that visual acuity in the amblyopic eye recovers after the functional loss of the normal eye in adults or after enucleation of the normal eye in amblyopic monkeys.

EYE MOVEMENTS

The amblyopic eye has a tendency to drift away while fixing a stationary visual target. The amblyopic eye has exaggerated unsteadiness in fixation. There is improvement in this unsteadiness of fixation in a dark adapted state of the amblyopic eye.

Amblyopic eyes have an increased latency of saccadic movements. The reaction time is made up of two phases namely sensation time and motor response time. The sensation time has interindividual variability but the motor response time is stable. In amblyopic eyes the reaction time is increased because of increased sensation time.

ELECTRORETINOGRAPHY AND ELECTRO-OCULOGRAPHY IN AMBLYOPIA

It is unclear whether amblyopia affects electroretinography as the subtle changes in amblyopia cannot be reliably detected. Electro-oculography is affected due to unsteadiness of fixation.

ELECTROENCEPHALOGRAPHY IN AMBLYOPIA

Alpha rhythm of electroencephalography is blocked when normal eye is exposed to a light stimulus, but the rhythm continues undisturbed when a light stimulus is given to the amblyopic eye.

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VISUAL EVOKED RESPONSE IN AMBLYOPIA

The amplitude of the visual evoked responseis smaller in amblyopic eye than the normal eye. The latency of visual evoked response is increased and it carries a prognostic value. Latency is increased more in eccentric fixation when compared to central fixation.

PHARMACOLOGICAL EFFECTS IN AMBLYOPIC EYES

Central nervous system depressants reduce retinal rivalry. Duffy and Burchfield studied the effect of Bicuculline25. Bicuculline a gamma amino butyric acid (GABA) receptor blocker produces catecholamine depletion and reverses visual deprivation.

Levodopa administration improves visual acuity and contrast sensitivity in amblyopic eyes26.

Cytidine-5’-diphosphocholine (citicoline) also increases visual acuity, contrast sensitivity and visually evoked potential in amblyopia27. It acts by improving membrane adenosinetriphosphate (ATPase) activity.

EVALUATION OF A CASE OF AMBLYOPIA VISUAL ACUITY

Accurate determination of visual acuity is essential for diagnosis and management of amblyopia. Methods used in determination of the visual acuity depends on the age of the patient. Determination of visual acuity in the early age of a child is important since that is the sensitive period of amblyopia.

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32 Infants < 1 year:

Optokinetic nystagmus, Preferential looking test, Visual evoked response, Catford drum test

Children 1 to 3 years:

Marble game test, Sheridan’s ball test, Boek’s candy test, Worth’s ivory ball test Children 3 to 5 years

Kay picture chart, Tumbling E pad test, Allen picture chart, Sheridan-Gardiner HOTV test

Children above 5 years and adults Snellen’s chart, Landolt’s chart

FIXATION PREFERENCE

Determination of fixation preference is important in amblyopia. Both eyes should be alternatively covered to assess if the child fixates with both eyes. A child with equal vision in both eye will not resist occlusion of either eye. A child with amblyopia in one eye will not resist occlusion of that eye while it will resist occlusion of the normal eye.

Assessment of binocular fixation pattern is also important. If the child has spontaneous alteration of fixation and holds fixation with either eye after a blink the visual acuity is almost equal in both eyes. If fixation changes to the habitual fixating eye after a blink there is a moderate fixation preference. If the child holds fixation

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with one eye only for 2 seconds after which the fixation changes to the habitually fixating eye even before a blink there is strong fixation preference.

25 DIOPTRE BASE IN PRISM TEST

25 dioptre base in prism is kept before one eye. This induces an esotropia, so a child with no fixation preference uses the eye without the prism to fixate. If the child fixates with the eye before which a prism is introduced, the other eye is amblyopic.

NEUTRAL DENSITY FILTER TEST

Neutral density filter is used to test if the vision improves under mesopic condition which is characteristic of amblyopia.

CROWDING PHENOMENON

Line visual acuity and single optotype visual acuity should be determined for both eyes. Single optotype visual acuity is better the line acuity because of crowding phenomenon or separation difficulties.

OCULAR EXAMINATION

ANTERIOR SEGMENT

Thorough anterior segment examination should be done to rule out conditions which may cause stimulus deprivation like eyelid ptosis, corneal opacities and cataractous lens.

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34 POSTERIOR SEGMENT

Detailed fundus examination should be done to rule out vitreous opacities, retinal conditions and optic nerve pathology which may be the cause of decreased visual acuity.

REFRACTION

Cycloplegic refraction should be done to detect refractive errors like myopia, hypermetropia and astigmatism which may be the amblyogenic factor. 1% atropine sulphate ointment is the cycloplegic drug used for children less than 5 years. Its effect lasts for 20 days. 2% Homatropine hydrobromide is uded in children from 5 to 8 years of age. Its effect lasts for 3 days. 1% cyclopentolate should be used for patients aged more than 8 years of age and post mydriatic test should be done after 4 days.

EVALUATION OF FIXATION

Fixation of the amblyopic eye should be determined if is central or eccentric, steady and wandering and whether it is maintained. Methods to determine fixation are VISUOSCOPE

The visuoscope projects a star surrounded by concentric rings into the eye which is tested and the other eye is occluded. If the fixation is central, the star will fall on the foveolar refex. If it does not fall on the foveolar reflex, the fixation is eccentric.

The eccentricity is determined by noting the concentric ring on which the star falls.

The distance between each concentric ring is ½ degree. Fixation can also be determined by an opthalmoscopic variant.

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Figure 8: Fixation SYNOPTOPHORE

Presence of eccentric fixation can be evaluated by measuring the angle kappa in each eye. The synoptophore has a unique slide to determine angle kappa. It has a row of numbers and letters or animals for children and illiterates. The distance between each symbol is 1 degree. The patient is asked to see the 0 mark, if the corneal reflex is nasal to centre of pupil angle kappa is positive. If it is temporal then angle kappa is negative. Now the patient turns one letter at a time until the corneal reflex is central. The degree of deviation gives the angle kappa. This method is less used in clinical practice and viscuoscope is most commonly used to assess fixation clinically.

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Figure 9: Angle Kappa HAIDINGER’S BRUSHES

The patient perceives the entoptic pattern of Haidinger brushes and then tries to touch the center of the brushes with a pointer. If the patient is able to touch the centre of the brushes with the pointer fixation is central. If the patient places the pointer elsewhere, fixation is eccentric.

MAXWELL’S SPOT

The eye is exposed to a homogenous blue light. A central dark round spot is seen which is the Maxwell’s spot. If the fixation target is over the Maxwell’s spot, fixation is central. If it is elsewhere, then fixation is eccentric.

EXAMINATION OF STRABISMUS

TESTS FOR SUPPRESSION AND ABNORMAL RETINAL CORRESPONDENCE

WORTH’S FOUR DOT TEST

It consists of two green lights, one red light and one white light. The patient should wear red green goggles, red before right eye and green before left eye. The

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patient will see red light through the red filter and green light through the green filter.

The results are arrived upon depending on the patient’s observation.

Figure 10: Worth Four Dot test

1. If an orthophoric patient sees four lights- two green, one red and one white or combination of red and green , the patient has binocular single vision.

2. If a patient with manifest squint sees four lights- two green, one red and one white or combination of red and green, then the patient has abnormal retinal correspondence (ARC).

3. If the patient observes only two red lights and no green lights, the patient has left suppression.

4. If the patient observes only three green lights and no red lights, the patient has right suppression.

5. If the patient sees two red lights and three green lights alternatively, then the patient has alternate suppression of left and right eyes.

6. If the patient sees two red lights and three green lights, then the patient has diplopia.

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38 4D BASE OUT PRISM TEST

4D base out prism test is used to detect presence of central suppression scotoma.

When bifoveal fixation is present,

The patient fixates a distant target then a base out prism placed in front of right eye, will cause displacement of image away from the fovea temporally, so both eyes will move to the left to make a corrective movement to make the image fall on the fovea of right eye. Then the left eye converges so that fusion occurs.

Figure 11: Bifoveal fixation In microtropia,

Suppose the left eye has a microtropia and hence a central suppression scotoma. When the base out prism is placed in front of the left eye, the image is

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shifted temporally but falls in the central suppression scotoma. Hence there is no corrective movement. When the base out prism is placed in front of the right eye, the image is shifted temporally so both eyes move to the left to make a corrective movement to make the image fall on the fovea of the right eye. In the left eye the image falls on the central suppression scotoma, so there is no re-fixation movement in the left eye.

Figure 12: Left microtropia BAGOLINI’S STRIATED GLASS TEST

This test is used to detect binocular single vision, abnormal retinal correspondence and suppression. The lens consists of fine striations and it converts a point source of light into a line. The lenses are placed at 45º and 135º in front of each eye. The patient fixates a point source of light, this is converted to an oblique line of light perpendicular to that seen by the other eye. Hence the images seen by the two eyes are dissimilar. Based on the patient’s observation, the results are interpreted.

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Figure 13: Bagolini’s striated glass test

1. If the patient sees two streaks intersecting at the centre, the patient has binocular single vision

2. In presence of a manifest squint, if the patient sees two streaks intersecting at the centre, the patient has harmonious abnormal retinal correspondence.

3. If the patient sees two streaks but they are not intersecting, the patient has diplopia.

4. If a small gap is present in one of the streaks, the patient has central suppression scotoma.

SYNOPTOPHORE

Synoptophore can be used to assess simultaneous perception, fusion, stereopsis, suppression and abnormal retinal correspondence.

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The synoptophore allows images to be presented to both eyes simultaneously.

It can be used in children from 3 years of age.The synoptophore consists of two cylindrical tubes with a right angle bend which has a mirror. Each eyepiece has a +6.50 Dioptre lens. This sets the testing distance at 6 metres. The instrument has a slide carrier at the outer end of the tube into which the pictures are inserted. The synoptophore can be used to measure horizontal, vertical and torsional misalignments in different cardinal positions.

FIRST GRADE: SIMULTANEOUS PERCEPTION: For simultaneous perception, two dissimilar but not mutually antagonist images like a bird and a cage are used. The patient is asked to move the pictures in relation to each other by moving the arms of the synoptophore such that the bird is put into the cage. If two pictures are not seen then suppression is present in one eye. If the patient cannot fuse the foveal slides, then larger slides can be used to detect macular and paramacular fusion.

Figure 14: Simultaneous macular perception and fusion

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42 SECOND GRADE: FUSION

To detect fusion, two similar slides which are incomplete in a small detail in a different way, are inserted into the slide carrier. Two horses one without a tail and other without a carrot can be inserted. If the patient has fusion, a horse with a tail and a carrot will be perceived. The range of fusion or motor fusion can also be tested by a synoptophore. The arms of the synoptophore are moved in such a way that the eyes have to converge or diverge to maintain fusion.

THIRD GRADE: STEREOPSIS

Stereopsis is the ability to perceive depth. Depth is perceived when two images of the same object taken from a slightly different angle are superimposed.

ABNORMAL RETINAL CORRESPONDENCE

To determine subjective angle of deviation simultaneous perception slides are used. The angle at which the slides are superimposed gives the subjective angle of deviation. The objective angle is measured by the examiner. A target is presented to both the fovea alternatively and the slide in front of the deviating eye is moved until there is no movement of the eyes. This gives the objective angle.

When subjective angle is equal to the objective angle then he/she has normal retinal correspondence. If both are different it is abnormal retinal correspondence (ARC). The difference between the objective angle and subjective angle is the angle of anomaly. If the objective angle is equal to the angle of anomaly, then ARC is harmonious. When objective angle exceeds angle of anomaly, then ARC is inharmonious.

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EVALUATION OF ANGLE OF DEVIATION IN STRABISMUS

HIRSCHBERG TEST

A pen torch is shone into the patient’s eye from an arm’s distance and the patient is asked to fix the light. Normally the corneal reflex will be centered on the centre of pupil. In squint, the corneal reflex will be decentered. The corneal reflex will be decentered temporally in esotropia and nasally in exotropia. Each millimeter of decentration corresponds to 7º. Roughly by assuming the pupil size as 4mm if the reflex is in the pupillary border, the deviation is 15º and if the reflex is on the limbus deviation is 45º

Figure 15: Hirschberg test KRIMSKY TEST

Prisms of increasing strength are placed before the fixating eye until the corneal reflex is symmetrical in both eyes.

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44 Figure 16: Krimsky test COVER – UNCOVER TEST

COVER TEST

Cover test is used in detection of heterotropias. It is done for distance by asking the patient to fixate a target straight ahead and for near, by fixating an accommodative target. If deviation is suspected in the right eye, left eye is covered by the examiner and the right eye is observed for any fixative movement. If the right eye adducts to take up fixation, it is right exotropia. If the right eye abducts to take fixation, it is right esotropia. Downward movement to take up fixation indicates hypertropia. Upward movement to take up fixation indicates hypotropia. No movement means either eyes are orthophoric or there is left heterotropia and the test should be repeated for the other eye.

UNCOVER TEST

Uncover test is used in detection of heterophorias. It is done for distance by asking the patient to fixate a target straight ahead and for near the patient fixates an

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accommodative target. The examiner should cover right eye for 2 to 3 seconds. Then the cover is removed and the eye under cover is observed. If there is no movement, it is orthophoria. If the right eye has deviated when it was under cover, on removal of the cover, it will take up fixation again. If it adducts to take up fixation, it is right exophoria. If it abducts to take up fixation, it is right esophoria. This test should be repeated for the other eye also.

ALTERNATE COVER TEST

Alternate cover test disrupts the fusion and hence should be done after cover- uncover test. The right eye is covered for few seconds and then the cover is shifted to the other eye, repeatedly back and forth for several times. In the presence of an alternating squint, the eye under cover deviates and the uncovered eye takes up fixation alternatively.

PRISM COVER TEST

Prism cover test is used to measure the angle of deviation. Prisms of increasing strength are placed in front of one eye in such a way that the base of the prism is opposite to the direction the deviation of the eye. Alternate cover test is performed. The prism strength is increased until no movement is seen. This is the end point. A further increase in the strength of the prism will cause a movement in the opposite direction.

References

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