Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005
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Fenestration of optic nerve sheath too has not shown good results.
The children with non improvable vision should be given low vision aids and treated as partially visioned children. They should be encouraged to stay in schools with normal children and encouraged to learn profession that is compatible with low vision.
Kjers juvenile optic neuropathy. This condition is less common than Leber’s optic neuropathy but commonly diagnosed as Leber’s because of its bilaterality and persistent visual loss. There is a strong family history. The disorder starts between 4 to 8 years. Vision is never less than 6/60. Never goes to loss of perception of light. There is acquired blue yellow dyschromatopsia. There is a central or centrocecal scotoma. Peripheral fields are normal. The optic nerve shows mostly temporal pallor with mild excavation of cup. There is no nystagmus.
No treatment is effective. Low vision aid may help the child.
Behr’s recessive optic neuropathy. There are two types of recessive optic neuropathy, one is called simple and the other complicated.
The simple starts in neonates hence also wrongly called congenital neuropathy. Though the disease starts in infancy, it is missed unless the eyes are examined with special reference to vision and changes in the disc. Generally the children are brought for examination round about school going age i.e. 3-4 years. Visual loss is severe that may be as low as H.M.Nystagmus is common which is generally associated with achromatopsia otherwise severe dyschromatopsia is common. However vision remains stationary. Consanguinity is common.38 There is no known treatment.
Complicated. Commonest age of presentation is between one to nine years. Loss of vision is moderate. Children never go blind. In about half the children there is nystagmus and strabismus, there is moderate loss of colour vision. Disc shows temporal pallor. The vision is generally stable at 6/60-6/36. No treatment is known.
Optic neuropathy in juvenile diabetics. This has a recessive form of inheritance. There is severe loss of vision that may be as low as counting fingers. It is a progressive condition. There is severe colour defect. Nystagmus is absent, there may be hearing loss. The disc has marked pallor. No treatment is available for optic neuropathy.
Congenital optic atrophy42, 43. These rare conditions are generally confused with heredo-familial degeneration of optic neuropathy. The heredo familial neuropathies are not present at birth. There are two types of congenital optic atrophy i.e. dominant and recessive. The loss of vision is not severe and stable in spite of dead white colour of disc, and excavation. The whole of the disc is involved. Nystagmus is common. There may be other members of the family who have uncorrected visual defect from childhood. There may be dyschromatopsia mostly for blue colour.
Gray (grey) pseudo optic atrophy37. This rare condition is seen in premature children, who are born with very poor vision that improves with in few months to normal level. On examination, the pupil are dilated and fixed. The colour of the disc is grey. The condition is thought to be delayed myelination of the disc.42
Tumours of Optic Nerve44, 49
Tumours of optic nerve are far less common than that of retina. The tumours of optic nerve can be seen any where from optic nerve head to chiasma.
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They can be grouped broadly into two groups45
1.Ectodermal—Anterior visual pathway gliomas
2.Mesodermal—Meningioma.
The former is mostly seen in children and rarely in adults while glioma of the optic nerve is a benign or marginally malignant tumour in children. Its counterpart in adults is highly malignant.
Meningiomas are not met with in children.
The optic nerve glioma. It is a slow progressing mostly unilateral painless growth of substance of optic nerve. On rare occasions it can be bilateral. It can be divided into two types according to its clinical presentation i.e. glioma of the optic nerve and glioma of the chiasma. Glioma of optic nerve can arise anywhere in its orbital part. Posteriorly located tumours are more common than anteriorly located tumours. Occasionally the tumour may start in the anterior part and spread like a fusiform growth all along its length. Posteriorly placed gliomas are more likely to invade the optic canal. Similarly a glioma of chiasma may spread towards the orbit.
The tumour is said to be congenital hamartoma, which does not manifest before 4 years of age. Its association along with neurofibromatosis is seen in 20-30% of cases. Hence in all cases of neurofibromatosis the optic nerve function should be evaluated that should include, vision, pupillary reaction, fundus examination, CT and MRI. A child with café au lait spot anywhere on the body with diminished vision should be examined for presence of proptosis and visual function. Neurofibromatosis type I46 is more likely to be associated with glioma of optic nerve.
Pathologically glioma arises from neuroglia of the optic nerve. Histopathologically the tumour is an astrocytoma. It is generally called juvenile pilocytic astrocytoma47, 49 due to thread like appearance of astrocytes in the tumour. There are two known patterns of the tumour :
1.Tumour related to neurofibroma are circumferential, perineural tumour, proliferating in subarachnoid space.
2.Intraneural tumour is not related to neurofibroma.48
Presentation. Common age is between 4 to 8 years. It may be diagnosed as late as end of second decade if the growth is small and slowly progressively.
There are two modes of presentation :
1.Proptosis with diminished vision.
2.Strabismus with diminished vision.
The later happens when diminished unilateral vision has not been noticed because of its gradual painless nature. Such children are brought mainly for squint and found to have glioma.
Proptosis in case of glioma of optic nerve is axial, of gradual progress. Degree of proptosis depends upon position of growth, a smaller growth near the orbital apex causes more proptosis than a larger growth just behind the globe. The growth is always intraconal. It takes one to three months for a growth to cause proptosis in younger patients50. The proptosis is non tender, non pulsative and non compressible, there is no bruit present and the proptosis does
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not increase either by lowering the head or Valselva procedure. Generally examiners finger can be insinuated all round the globe and the orbit. The movements are normal or may be minimally reduced.
Strabismus is due to loss of vision.
Occasionally there is rapid progression of proptosis due to mucinous degeneration in the tumour and not true increase in number of cells.
There is slow and uniform enlargement of orbit.
Rarely in extreme degree of unattended proptosis, cornea may be abraded and develop
ulcer.
Vision. Loss of vision is a common feature of optic nerve glioma and is variable ranging between loss of few lines on Snellen’s chart to loss of perception depending upon number of visual fibres involved.
Generally visual loss is early that deteriorates slowly, proptosis follows visual loss. Generally there is central or centrocecal field defect.
Loss of vision is due to resultant optic atrophy. Anteriorly placed tumour cause post papilledematous optic atrophy while posteriorly placed and chiasmal lesions produce primary optic atrophy.
Pupillary reaction also depends upon involvement of afferent pupillary fibres. Poor vision is associated with afferent pupillary reaction.
Diagnosis of optic nerve glioma is not difficult in cases of moderate glioma which cause unilateral loss of vision with proptosis in a child under ten years of age.
Investigation 1. X-ray :
(a) X-ray of orbit shows uniform enlargement of orbit behind the orbital rim without any intraocular or intra orbital calcification.
(b) X-ray optic foramen (Rhese view) shows circular enlargement of optic foramen with intact margin due to slow growth of the tumour. If the posterior end of the glioma has not extended in to the optic canal the x-ray of the foramen is unaltered and equal on both sides. In early cases X ray of both the foramen should be taken for comparison.
When the growth extends in the optic canal, it too is enlarged most of the time in a funnel shape i.e. wider anteriorly. Size of the foramen is reduced following removal of growth.
2.Ultrasonography of orbit shows uniform fusiform or secular growth inside the cone of the eye.
3.CT and MRI are useful in early cases.
4.Fine needle biopsy has not proved to be more useful than CT, MRI or X-ray.
Management. Management of optic nerve glioma is controversial. There is no medical treatment available. The main argument revolves round the question if the growth should be left as such or be surgically removed.
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Points against surgical intervention are :
1.It is slow progressive benign growth that is self limiting and after some time stops growing.
2.By removing the growth, the vision can not be restored.
3.The growth has to be removed either by a lateral orbitotomy, craniotomy or endoscopically via trans nasal, trans ethmoidal route that requires help of neurosurgeon and ENT surgeon.
Only point in favour of surgical intervention is cosmetic. To a growing child, a large proptosed strabismic eye is not cosmetically acceptable.
Surgical options available are :
1.Tarsorrhaphy if cornea is compromised before definitive surgical procedure.
2.Removal of the growth along with the eye if the exposed cornea has sloughed and perforated.
3.Removal of the growth leaving blood vessels either via orbitotomy, craniotomy or by transnasal and trans ethmoidal endoscopic surgery.
Radio therapy is not of much use unless the growth is malignant, which is rare in chil-
dren.
Chiasmal glioma50, 51. Chiasmal gliomas are more common than isolated orbital glioma but are not diagnosed as early as orbital glioma for obvious reason that there is no proptosis which is a hallmark of optic nerve glioma and unilateral loss of vision in child may go unnoticed unless the child develops squint or nystagmus.
The chiasmal gliomas have same pathological features as optic nerve glioma except that they are more likely to be invasive than optic nerve glioma.
Chiasmal gliomas may produce bilateral loss of vision due to spread to the contra lateral side of the midline.
Chiasmal glioma may extend :
1.In the optic canal and become intraorbital that results in proptosis.
2.Extend into the third ventricle and cause internal hydrocephalus, raised intracranial pressure, and hypothalamic signs and symptoms of precocious puberty, obesity, somnolence, dwarfism and diabetes insipidus. There may be involvement of pituitary as well.
The presenting features are :
Loss of vision, initially unilateral that may become bilateral. Vision may vary between mild to severe. In late cases there may be loss of perception as well.
Squint and nystagmus are common.
Afferent pupillary reaction is seen in unilateral involvement. In bilateral involvement both pupil are large and sluggish.
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Field changes of chiasmal glioma are variable, so long the growth has not crossed the mid line, the field changes are same as in optic nerve glioma. The other eye may also show unilateral field change of optic nerve type i.e. central or centrocecal scotoma.
Bi-temporal hemianopia, which is expected in chiasmal lesion is absent in chiasmal glioma.
X-ray—Optic canal : Widening of optic canal means intra orbital extension.
X-ray skull lateral view shows change in sella that appears either as Jor W shaped sella without supra sellar calcification.
Management of chiasmal glioma is difficult more so when there is extension in the surrounding structure. Palliative radio therapy may arrest the growth.
Tumours of optic nerve head :
Growth of optic nerve head may be benign or malignant.
Benign growths are : Drusen of optic nerve that may be intra neural and non visible ophthalmoscopy or may protrude in the vitreous as irregular grey mass. Other such growths are : neurofibromatosis and tuberous sclerosis.
Another rare growth is benign melanocytoma which is not common in children.
Remnants of hyaloid system may be mistaken as tumours arising from the disc. A malignant tumour that invades optic nerve head in children commonly is retinoblastoma. It is always associated with visible retinoblastoma and means extra ocular spread. Similarly neuroblastoma may occasionally invade the optic nerve head45 so can leukaemia.
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2.Duke Elder S. ; Optic nerve in System of ophthalmology. Vol. II. p-273–294, Henry Kimpton, London, 1961.
3.Banumathy S.P. ; Optic nerve in Anatomy of the eye. p-68–73, Edited by Natchair G. Arvind Eye Hospital, Maduari.
4.Nema H.V. ; The optic nerve in Anatomy of the eye and its adnexa. Second edition. p-85–90, Jay Pee Brothers, New Delhi, 1991.
5.Shields M.B. ; Optic nerve head and peripapillary retina in Text Book of glaucoma. Fourth edition, p-72–77, Williams and Wilkins, Philadelphia, 1997.
6.Anderson D.R., Braveman S. ; Re-evaluation of the optic disc vasculature. Am.J.Op. 82:165, 1976.
7.Nancy Anderson Hamming and Apple D. ; Anatomy and embryology of the eye in Principles and practice of ophthalmology. Vol. I. p-13–14, Edited by Peyman G.A., Sanders D.R. and Goldberg M.F. Jay Pee Brothers, New Delhi, 1987.
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8.Duke Elder S. and Cook C. ; Embryology of the eye in System of ophthalmology. Vol. III, part I. p-109–118. Henry Kimpton, London, 1963.
9.Dutta L.C. ; Congenital anomalies of the retina in Ophthalmology principles and practice. First edition. p-151–153, Current Book International, Calcutta, 1995.
10.Kanski J.J. ; Congenital optic disc anomalies in Clinical ophthalmology. Second edition. p-451–455, Butterworth, London, 1989.
11.Duke Elder S. ; Anomalies of optic disc and nerve in System of ophthalmology. Vol. II. p-668–687, Henry Kimpton, London, 1964.
12.Shirly H. Wray ; Congenital optic disc anomalies in Manual of ocular diagnosis and therapeutics. Third edition. Edited by Deborah Pavan Langston, p-341–342, Littlebrown.
13.Duke Elder S. ; Medulated nerve fibres in System of ophthalmology. Vol. II. p-646– 650, Henry Kimpton, London, 1964.
14.Radhika Tandon, Verma L. ; Optic disc pit in Clinical practice in ophthalmology. First edition. Edited by Saxena S., p-494, Jay Pee Brothers, New Delhi, 2003.
15.Shields J.A., Stephen R.E. and Sarin L.K. ; Morning glory syndrome in Pediatric ophthalmology. Vol. II. Second edition. Edited by Harley R.D., p-1152, WB Saunders Company, Philadelphia, 1983.
16.Mukherjee P.K. ; Congenital pit of the optic nerve in Current ocular therapy. Fifth edition. Edited by Fraunsfelder F.T. and Roy F.H., p-558, WB Sanuders Company, Philadelphia, 2000.
17.Glaser J.S. ; Optic disc - congenital anomalies of shape and size in Neuro ophthalmology. p-73–74, Harper and Row, London, 1978.
18.Martyn L.J. ; Optic nerve hypoplasia in Pediatric ophthalmology. Vol. II. Second edition. Edited by Harley R.H. p-831, WB Saunders Company, Philadelphia, 1983.
19.Levine R.A., Rosenberg, M.A. and Rabb M.A. ; Drusen in Principle and practice of ophthalmology. Vol. III. Edited by Peyman G.A., Sanders D.R. and Goldberg M.P. p-2130–2132, Jay Pee Brothers, New Delhi, 1987.
20.Dutta L.C. ; Papilledema in Modern ophthalmology. Vol. II. Second edition. p-977- 981, Jay Pee Brothers, New Delhi, 2000.
21.Shirley H. Wray ; Papilledema in Manual of ocular diagnosis and therapy. Third edition. Edited by Deborah Pavan Langston. p-343, Little Brown.
22.Kuhn F., Halda, T. ; Optic nerve in Optic differential diagnosis. Edited by Roy, H. p-618–619, Williams and Wilkins. Baltimore, 1996.
23.Manikavasagan T. ; Pathogenesis of papilledema. Recent concept in Neuro ophthalmology. Edited by Natchiar G. p-11–01 to 11-04, Arvind Eye Hospital, Maduri.
24.Kanski J.J. ; Papilledema in Clinical ophthalmology. Second edition. p-447–448, Butterworth, London, 1989.
25.Badrinath S.S. ; Papilledema in Sankar Netralaya Clinical practice and pattern in ophthalmology. First edition. p-288-289, Jay Pee Brothers, New Delhi, 2004.
26.Sundarajan S. ; Optic neuritis in Neuro ophthalmology. Edited by Natchiar G. p-12.1–12.8, Arvind Eye Hospital, Maduri.
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27.Horton J.C. ; Disorders of the eye in Harisson’s principles of internal medicine. 14th edition. Vol. I. p-159–172, McGraw Hill Book Company, 1988.
28.Brain W.R. ; Lesion of optic nerve in Diseases of nervous system. 6th edition, p-125– 132, Oxford University Press, London, 1962.
29.Bajandas F.J. and Kline L.B. ; Pale optic disc in Neuro ophthalmology review manual. Third edition. p-135–140, Jay Pee Brothers, New Delhi, 1989.
30.Miller S.J.H. ; Degeneration of the optic nerve : optic atrophy in Parson’s diseases of the eye. Seventh edition. p-229–230, Churchill Livingstone, 1984.
31.Lois J. Marthyn ; Opticatrophy in Pediatric ophthlmology. Vol. II. Second edition. Edited by Harley RD. p-817–820, W.B. Saunders Company, Philadelphia, 1983.
32.Levine R.A., Rosenberg M.A., Rabb M.F. ; Optic atrophy in Principles and practice of ophthalmology. Vol. III. p-2125–2129, First edition. Jay Pee Brothers, New Delhi, 1989.
33.Hebber K.G. ; Optic atrophy in Neuro ophthalmology. Ist edition. Edited by Natchair. p-13.1–13.12, Arvind Eye Hospital, Maduri.
34.Dutta L.C. ; Optic neuritis : Optic neuropathy in Modern ophthalmology. Vol. II. Second edition. p-956–962, Jay Pee Brothers, New Delhi, 2000.
35.Miller M.R. ; Traumatic optic neuropathy in Current ocular therapy. Edition V. p-567–568, Edited by Fraunfelder F.T. and Hampton Roy F., WB Saunders Company, Philadelphia, 2002.
36.Sorsby A. ; Maldevelopment defects—Leber’s disease in Modern Ophthalmology. Vol. III. First edition. p-311–319, Butterworth, London, 1964.
37.Lois Martyn ; Leber’s hereditary optic atrophy in Pediatric ophthalmology. Vol. II. Second edition. p-818–820, W.B. Saunders Company, Philadelphia, 1983.
38.Glasers J.S. ; Heredo degenerative optic atrophies in Neuro ophthalmology. p-93– 100, Harperz Row, New York, 1977.
39.Bajandas F.J. and Kline L.B. ; Pale optic disc - optic atrophy in Neuro ophthalmology. Review manual. Third edition. p-139, Jay Pee Brothers, New Delhi, 1989.
40.Gittinger J.W. ; Leber’s optic atrophy in Manual of clinical problems in ophthalmology. First edition. p-167–168, Edited by Gittinger J. and Asdourian G.K. Little Brown and Co., Boston, 1998.
41.Seal S.K. ; Retrobulbar neuritis in G.N. Seal’s Text Book of Ophthalmology. Fifth edition. p-340–341, Current Book International, Kolkota, 2002.
42.Duke Elder S. ; Congenital optic atrophy in System of ophthalmology. Vol. III, part II. p-683–684, Henry Kimpton, London, 1964.
43.Sorsby A. ; Congenital optic atrophy in Modern ophthalmology. Vol. III. p-264-265, Butterworth, London, 1964.
44.Green C.H. ; Orbital gliomas in Ocular pathology. First edition. p-181-183, Blackwell. Scientific publication, Oxford, 1963.
45.S.J.H. Miller ; Primary tumours of optic nerve and its sheath in Parson’s diseases of the eye. Seventh edition. p-335–337, Churchill Livingstone, London, 1984.
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46.Hoyt W.F., Baghdassarian S.A. ; Optic glioma of childhood; natural history and rationale of conservative treatment. BJO 53:793-798, 1969.
47.Levine R.A., Rosenberg M.A., Rabb M.F. ; Glioma in Principles and practice of ophthalmology. Vol. III. p-2136–2142, Edited by Peyman G.A., Sander D.R. and Goldberg M.F. First Indian edition. Jay Pee Brothers, New Delhi, 1987.
48.Lois J. Martyn ; Optic glioma in Pediatric ophthalmology. Vol. II, Second edition. Edited by Harley R.D. p-839–841, W.B. Saunders Company, Philadelphia, 1983.
49.Nicholson D.H. and Green W.R. ; Glioma in Pediatric ophthalmology. Vol. II. Second edition. Edited by Harley R.D. p-1259–1262, W.B. Saunders Company, Philadelphia, 1983.
50.Natrajan M. ; Tumours of the optic nerve inNeuro ophthalmology. Edited by Natchiar. p-14.1–14.10, Arvind Eye Hospital, Maduri.
51.Glaser J.S. ; Optic gliomas in Neuro ophthalmology. p-116–120, Harper and Row, London.
52.Radhika Tandon and Verma L. ; Optic neuritis in children in Clinical practice in ophthalmology. First edition. p-480, Edited by Saxena S. Jay Pee Brothers, New Delhi, 2003.
53.Scheie H.G., Albert D.M. ; Optic neuritis in Text Book of ophthalmology. 9th edition. p-39, W.B. Saunders Company, Philadelphia, 1977.
54.Dutta L.C. ; Multiple sclerosis in Modern ophthalmology. Vol. II. Edition II. p-958– 960, Jay Pee Brothers, New Delhi, 2000.
55.Radhika Tandon and Verma L. ; Optic nerve disorders in Clinical practice in ophthalmology. Edited by Saxena. S., First edition. p-477–495, Jay Pee Brothers, New Delhi, 2003.
56.Levine R.A., Rosenberg, M.A. and Rabb M.F. ; Degenerative optic neuritis in Principles and practice of ophthalmology. Vol. III. First Indian edition. p-2115–2129, Edited by Peyman G.A., Sanders D.R., Goldberg M.F. Jay Pee Brothers, New Delhi, 1987.
57.Miller S.J.H. ; Diseases of the optic nerve in Parson’s diseases of the eye. Nineteenth edition. p-224, Churchill Livingstone, London, 1984.
CHAPTER 15
Errors of Refraction in Children
General consideration1, 2, 3, 4
A normally developed eye (by 5 to 6 years of age) acts as a convex lens of +60D. This power is divided into two major components i.e. the corneal and lenticular. The converging power of cornea is +43D. This leaves the lens with +17D of power, normal aqueous and vitreous contribute a negligible converging power.
In an eye with normal refractive (diopteric) power, parallel rays are brought to focus on the retina with accommodation at rest, the parallel rays actually form a circle of least diffusion4. This refractive status is called emmetropia. An emmetropic eye has clear image of a distant object without internal adjustment of its optics.6 In contrast to this, if all parallel rays are not brought to focus on the retina in all the meridian with accommodation at rest, the condition is called ametropia.
Almost all emmetropic eyes have an axial length of 24 mm, any change in its length should produce ametropia. However a larger eye can be emmetropic if its total optical power is stronger.8
An absolutely emmetropic eye is extremely rare, most of the eyes have some degree of ametropia.
A full term normal child at birth is about +2 to +3D hypermetropic. This is due to shorter axial length of the new born’s eyeball. As the child grows, this power is neutralised by corresponding lengthening of the eyeball up to 5-7 years when all eyes should become emmetropic. However, if the increase in length does not stop at this point, the eye becomes myopic and if the eye fails to reach the emmetropic length (24 mm) the eye becomes hypermetropic.
The ametropia eye can be :
1.Myopic
2.Hypermetropic
3.Astigmatic
Anisometropia is a term used when the diopteric power in both eyes are not the same.
Possible causes of ametropia4 are:
1. Axial. In this condition, the retina is either in front or behind the circle of least diffusion. If the focus is behind the retina, the condition is called hypermetropia and if the image is formed in front of the retina, the condition is called myopia. Axial astigmatism is very rare. 1 mm change in axial length leads to ametropia of 3D.
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2. Curvature. If the curvature of the cornea is uniformly less than normal, the eye develops curvature hypermetropia, similarly reduction in lenticular curvature also results in curvature hypermetropia. Increase in corneal or lenticular curvature results in curvature myopia. 1 mm change in corneal curvature leads to 6-7D ametropia.
If the corneal or lenticular curvatures are not equal in all meridian, there will be an ametropia called astigmatism.
3.Index. If the refractive index of optical system is low, it will result in hypermetropia and high refractive index will result in myopia.
4.Relative position of lens. A forward shift of lens causes myopia, backward shift results in hypermetropia. An absence of lens from the pupillary area results in aphakia, which is an example of high hypermetropia. An obliquely placed lens causes astigmatism.
MYOPIA
Myopia is the commonest cause of gradually developing painless diminished vision in pediatric age group. It is equally common among boys and girls. It has strong heredity. Fifty percent of myopic children have myopia in both the parents, about a quarter of myopic children have one parent with myopia, and rest are sporadic. Both the hereditary and sporadic cases can transmit myopia in the next generation. It is common to have history of myopia in grand parents from maternal or paternal side. The first cousins too may be myopes. It is very common to have myopia in all or some of the siblings.
Myopia invariably is a bilateral disorder that manifests simultaneously in both eyes that need not be equal, generally difference in two eyes is not much.
In simple myopia rest of the eye is generally as normal as any non myopic eye.
Myopia is the error of refraction in which rays from far point, real or apparent (myopic far point) are focussed in front of photo sensitive layer of retina when accommodation is at rest.1, 2, 3
Myopia is also known as short sightedness or near sightedness as the patient finds it difficult to see beyond a certain distance that may be very short.8
The word myopia represents the phrase “I shut the eye” in Greek. This is because a myopic child narrows the inter-palpebral fissure so much as to make it like a slit. This gives a pin hole effect that improves vision by few lines on Snellen’s chart.
Loss of vision in myopia is so gradual that the child fails to notice its onset and progress. Sometimes the child considers visual status as normal and is resigned to it.
Classification of myopia. Myopia has been classified in various ways, none of the classifications have universal acceptance.
It could be primary or secondary.
Primary could be congenital or developmental. In secondary myopia some detectable cause other than increased axial length of the eyeball is present.