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Year : 1983  |  Volume : 31  |  Issue : 6  |  Page : 709-711

Classification, etiology and pathology of myopia


Correspondence Address:
T N Ursekar

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Source of Support: None, Conflict of Interest: None

PMID: 6676248

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How to cite this article:
Ursekar T N. Classification, etiology and pathology of myopia. Indian J Ophthalmol 1983;31:709-11

How to cite this URL:
Ursekar T N. Classification, etiology and pathology of myopia. Indian J Ophthalmol [serial online] 1983 [cited 2023 Dec 10];31:709-11. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1983/31/6/709/29306

Classification of refractive errors in general involves a lot of problems. It is possible to clas­sify any single eye from its refraction alone. The problem is biological and not optical. Thus to classify myopia there are a number of practical defects. It is necessary to study the entire clinical appearance of the eye and the individual. Not only dioptric elements and the state of the fundus are to be considered but herediatary and clinical behavious have to be studied.

Myopia is classified in a simple manner as

i) simple

ii) pathological

Simple Myopia is not progresive beyond the amount included within normal development; is associated with good vision and requires no treatment except optical correction.

Pathological Myopia on the other hand is a degenerative myopia accompanied by changes in the posterior segment of the eyeball with lengthening of AP axis of the globe. Besides, the axial pathological myopia,there are other types of myopia due to defects in the curvature of cornea and lens and due to drauma. Today, I will confine my remarks only to pathological axial Myopia.

The pathological myopia shows degenera­tive changes in the posterior pole. Thus it can be named as degenerative myopia (Duke Elder). It may occur as an independent de­velopmental (congenital) condition or in as­sociation with other occular diseases or gen­eral disease.

Von Jeager first described congenital myopia in 1855. Since then a number of cases have been reported. Majority of congenital myuopias remain stationary. Some progress further leading to detachment of the retina. Vision is good in somecases, while in others it is subnormal.

Many congenital anomalies are associated with myopia e.g. microphthalmos, mic­rocornea, microphakia, ectopia lentis. Vari­ous tapeto-retinal dystrophies are accom­panied by high myopia.

Etiology of Myopia is as diverse and con­troversial as one can imagine. Everything in medicine has been blamed as a cause of Myopia. Two types of theories are put foward:

1) Mechanical and Environmental

2) Biological

Mechanical theories explained the develop­ment of high myopia by distension of normal sclera. This is caused byseveral factors. In­creased intra-ocular pressure caused by the ac­tion of extraocular muscles or intra-ocular muscles or by insidious chronic glaucoma.

Others put forward the theory of weakening of the sclera by various causes like venous con­gestion, inflammation or dietary deficiency.

Among these theories two factors were prominently discussed - excessive close work and general debility. Incidence of High Myopia: among school going children was at­tributed to excessive close work. However, this was disapproved when high myopia was reported among illiterate population.

Secondly, malnutrition, calcium and vitamin deficiency were attributed as factrors causing high myopia. However, this has also been dis­proved when we see high myopia among well­nourished children and in high socio-economic groups. Thus the cause of myuopia is still un­known. However, twofactors stand out clearly:

1. Hereditary. 2. General Growth

The exact knowledge of genetics in the prog­ression of myopia is still unknown.

As regards the development of myopia to processes of growth, it is said that the lengthening of the posterior segment of the eye commences only during the period of ac­tive growth. The eye and the brain show pre­cocious growth at the age of 4 years; the brain is 84% and the eye 78% and the rest of the body 21%. After this, both the eye and the brain increase slowly while the body grows more rapidly. However, when axial myopia continues to progress, it is interpretted as a precocious growth which has failed to get ar­rested. We do not as yet know what this influ­ence is.

Pathology: The highly myopic eye is en­larged and egg shaped. However, the elonga­tion of the eye is entirely confined to the post­erior pole and the anterior half of the eyeball is usually normal.

The sclera becomes thin in the posterior pole. Donders postulated that the thinning oc­curs following mechanical stretching, but this view was not accepted. Heine's postulation that scleral atrophyas a cause of thinning is now generally accepted, although the cause of atrophy is not clear.

The choroidal changes are essentially at­rophic innature. However, in juvenile myopia, choroidal atrophy is not common. Secondly, atropy occurs very late and is not proportion­ate to the degree of myopia. The main changes in the choroid are generalised thinning and at­rophy of choriocapillaries exposing large choroidal vessels. At the same time, there is less pigment and the elastic elements.

Atrophic changes in the retina progress coin­cidentally with those in the ehoroid. There is marked alteration in the pigment apithelium and atrophy of rods and cones leading to chorioretinal fusion. The normal hexagonal pattern of pigment cells is altered. There is proliferation of pigment leading to branched pigment figures or conglomerate masses (Forster-Fuchs spot) at the macula on account of clumping of the pigment in this area.

Changes in the optic disc: The optic disc is large in myopic eyes. The myopic crescent usually occurs at the temporal half of the disc. The choroid terminates some distance from the margin of the disc and is absent in the area of the crescent. The outer retinal layers and pigmentary epithelium may be absent in the area of the crescent and only inner layers con­tinue. The course of the crescent is though to bestretching, the choroid being dragged back into the ectasia, at the posterior pole. The supertraction of the retina occurs at the nasal border of the optic disc. The choroid stops at the disc margin and the retina overlaps it. The optic disc itself shows changes of lacunar at­rophy resembling glaucomatous optic at­rophy.

The changes at the macula are characteristic. i) Lacquer cracks and ii) Forster Fuchs Spot.

Lacquer cracks are seen in the early course of the disease. They have poor prognostic sign because they lead to chorioretinal atrophy in the later stage of the disease.

The Fuchs Spot is invariably an accumula­tion of pigment proliferation. It is associated with serious leaks or haemorrhages from sub­retinal neovascular lesion in the central area.

Peripheral retinochoroidal atrophy is characterised by numerous small patches of at­rophy and pigment proliferation near the area, but is not peculiar to high myopia. Scleral ec­tasias are relatively frequent in higher degrees of myopia. In majority of cases, it involves the posterior pole of the eye signifying poor prog­nosis in adult life.

Changes in the Vitreous in myopia are characterised by liquefaction of the jelly and posterior detachment. The liquefaction takes place at first at the posterior pole and the area immediately behind the lens. There is micro­fibrillar degeneration leading to opacities in the vitreous.


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