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Year : 1971  |  Volume : 19  |  Issue : 4  |  Page : 172-176

Optic atrophy (Review of 100 cases)

Department of Ophthalmology, Medical College, Amritsar, India

Correspondence Address:
M R Chaddah
Department of Ophthalmology, Medical College, Amritsar
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Source of Support: None, Conflict of Interest: None

PMID: 15745415

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How to cite this article:
Chaddah M R, Khanna K K, Chawla G D. Optic atrophy (Review of 100 cases). Indian J Ophthalmol 1971;19:172-6

How to cite this URL:
Chaddah M R, Khanna K K, Chawla G D. Optic atrophy (Review of 100 cases). Indian J Ophthalmol [serial online] 1971 [cited 2022 May 17];19:172-6. Available from: https://www.ijo.in/text.asp?1971/19/4/172/34971

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Table 1

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Table 1

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Optic Atrophy is the end result of various lesions of the visual pathways from ganglion cell layer to the lateral geniculate body. Clinically, optic atrophy is diag­nosed from the well known triad of pallor of the optic disc, dimi­nution in the visual acuity and visual field defects. Depending upon the histology, etiology and ophthalmoscopic picture, different classifications of optic atrophy have been in vogue. In Western countries, besides the specific in­fections, demyelinating diseases are held responsible for most of the cases of optic atrophy of un­known etiology. It has been gene­rally felt that demyelinating dise­ases are not common in tropical and sub-tropical countries like India and Africa. Hence in most of the cases of optic atrophy in this country, the etiology remains unknown inspite of the battery of investigations employed. This study of 100 cases of non-glauco­matous optic atrophy involving 172 eyes presents the incidence of varying pathologies responsible for optic atrophy in Northern India.

  Method and Material Top

All the patients comprising this series of 100 cases of optic atrophy were admitted in the Ram Lal Eye Hospital and other hospitals attached to the Medical College, Amritsar (Punjab) for diagnostic study and determination of etio­logy.

Besides the detailed history of present complaints, with parti­cular reference to neurological complaints the study included ophthalmological check up con­sisting of external examination of the eyes, recording of visual acuity, refraction, ophthalmosco­pic examination, perimetery and slit lamp examination. Medical check up including general physi­cal neurological, respiratory and cardio-vascular examination and E.N.T. check up were carried out in each case. Clinical investiga­tions comprised of total and diffe­rential leucocyte count, erythro­cyte sedimentation rate, haemo­globin estimation, Mantoux test, serological test for syphilis and complete urine and stools exami­nation. In addition complete cere­brospinal fluid examination, skia­grams of skull and nasal sinuses and chest screening were done where indicated.

The atrophy was classified ac­cording to the ophthalmoscopic picture as under:­

1. Primary Optic Atrophy: These patients had pallor of the disc involving the entire disc or temporal pallor extending upto the disc margin, with well defined borders of the papilla; normal calibre or slight constriction of the bigger vessels and disappearance of the vessels of small cali­bre. Physiological cup was slight­ly deeper than normal and lamina cribrosa were seen more clearly.

2. Secondary Optic Atrophy: Ophthalmoscopic examination showed pallor of the disc with evidence of present or preceding exudation, including obstruction of the physiological cup, irregu­larity and distortion of the neuro-retinal outlines, veiling of the lamina cribrosa with fibrous or glial tissues which may extend along the retinal vessels. Such a picture may be due to papilloe­dema or papillitis.

Secondary Optic Atrophy was attributed to papilloedema when there were other evidences of raised intra-cranial tension, histo­ry of slow gradual progressive loss of vision, and to papillitis when history of sudden loss of vision and no evidence of raised intracranial tension were evident.

3. Consecutive Optic Atrophy: Waxy looking disc with evidence of inflammatory and degenerative changes in the chorio-retinal tissues.

  Observations Top

Out of 100 cases 66 were males and 34 females. In both the sexes the incidence of the disease was more in the first four decades of life [Table - 1]. The disease was bilateral in 72 patients whereas 28 patients presented with uni­lateral manifestations. In unilate­ral cases, right and left eyes were involved in an equal number, [Table - 2].

The disease manifested as pri­mary optic atrophy in 48 patients, as secondary optic atrophy due to papilloedema in 15 cases and due to papillitis in 26 cases. 11 cases had consecutive optic atrophy.

In 27 cases no cause could be detected. Of the established causes, meningitis topped the list involving 16 cases. Other common pathology detected was syphilis and intra-cranial space occupying lesions 10 cases each, demyelinat­ing process 7 cases, trauma 7 cases, choroidal sclerosis 5 cases, pigmentary degeneration of re­tina 4 cases [Table - 3].

  Discussion Top

The literature shows marked variations in the incidence of various etiological factors in optic atrophy. This seems to depend on the prevelance of a particular disease in a particular era and area. Our series of 100 cases shows a marked preponderance of optic atrophy in the first four decades. In 27 % of the cases no cause could be found while in the rest of 73% cases definite etiolo­gical factor was present. Some of the causes like intra-cranial space occupying lesions, craniostenosis, retinal degeneration and tumours of the optic nerve are self expla­natory whereas in others, more comon causes like syphilis, tuber­culosis and demyelinating disea­ses, atrophy of the optic nerve en­sues differently.

In children, the most important cause of bilateral optic atrophy is tubercular meningitis, and men­ingo-enephalitis whereas unilate­ral atrophy is mostly of trauma­tic nature.

In his study of ocular aspect of tuberculosis, Mooney [6] found three types of lesions giving rise to optic atrophy.

(a) Edema of brain and meninges leading to obstruction of the ven­tricular foramina in the posterior cranial fossa producing internal hydrocephalus and manifesting as papilloedema.

(b) Granulation tissue or fibrous bands around the chiasma and op­tic nerve causing strangulation of nerve fibres manifesting as primary optic atrophy

(c) Interstitial perineuritis ex­tending upto the disc manifesting as papillitis and neuro-retinitis.

In our series 9 cases of tuber­cular meningitis (all children be­low the age of 10 years) presented with papilloedema, papillitis and primary optic atrophy in equal distribution. Incidentally, none of these cases developed choroidal tubercles during any stage of the disease.

In 12 cases syphilis was responsi­ble for the optic atrophy which was primary in 10 cases and post neuritic following papillitis in 2 cases. Out of these 12 cases 41.6% were above 50 years of age.

Syphilitic peri-neuritis is res­ponsible for the post neuritic type of picture whereas primary type of optic atrophy is due to paren­chymatous lesions of the nerve fibres generally seen in the terti­ary stage of the disease. Syphi­litic meningitis can lead to papi­lloedema but in none of our cases it was responsible for optic atro­phy.

In 7 % of our cases, atrophy was due to trauma to the temporal region. In none of these cases any fracture could be detected on the base of skull and the optic canal. Trauma was generally of minor to moderate intensity producing sud­den loss of vision followed by primary type of atrophic changes within a period of 3 weeks. This is believed to be due to haemorr­hange in the sheath of the optic nerve, haematoma pressing the nerve fibres producing pressure atrophy. Our findings are in agreement with those of Iqui [3] .

In choroidal sclerosis, optic atrophy is due to progressive dimi­nution of blood supply. The more highly differentiated tissues in the optic nerve fibres disappear but there is no reactive formation of scar tissue.

The incidence of demyelinating disease is believed to be low in our country. In 7 % of cases the optic atrophy was thought to be due to demyelinating diseases on clinical grounds. Recently, more stress has been laid on the demy­elinating diseases as the cause of unilateral or bilateral optic atro­phy. Hierons [2] suggested a localiz­ed form of encephalomyelitis res­ponsible for optic atrophy where­as Scott [7] and Stansbury [8] reported neuromyelitis optica responsible for bilateral retrobulbar neuritis and papillitis with or without transverse myelitis. Thus isolated primary or secondary optic atrc­phy can occur due to demyelinat­ing pathology.

Aneamia and nutritional neu­ropathies have also been blamed to be the cause of optic atrophy in tropics and under developed countries. Our cases, however, revealed no such deficiency. Only in 1 case microcytic hypochromic anaemia could be accounted for the causation of optic atrophy.

The baffling problem posed by the present series is the fact that no etiological factor could be detected in 27 cases; 12 cases of primary and 15 cases of secondry optic atrophy. Agarwal Goswami and Khosla in their series of 120 cases of primary optic atrophy reported 86 cases (70%) in whom no cause could be detected.

Lumsden [4] postulated localized involvement of optic pathways in the demyelinating disease due to a particular field factor increasing the susceptibility of particular area of the nervous system to dernye­linating process. Agarwal et al [1] explained that the optic atrophy of unknown etiology is due to high incidence of the so called field factor in the optic nerve pro­ducing localized auto-immune re­action initiated by some obscure nutritional element or some neu­rotropic virus. We are inclined to agree with Agarwal et al [1] that the incidence of optic atrophy of un­known etiology in tropics and sub­tropics may be a localized demy­elinating disorder initiated by nutritional deficiency or neuro­tropic virus.

  Summary Top

100 cases of optic atrophy in­volving 172 eyes have been stu­died. Incidence of varying etio­logy and the pathogenesis have been discussed.

  References Top

AGARWAL, L. P., GOSWAMY, S. and KHOSLA, P. K. (1965) proteins in C.S.F. following traumatic dege­neration of Optic Nerve. Orient. Arch. Ophth. 3: 19.  Back to cited text no. 1
AGARWAL, L. P., BATTA, R. K. and KHOSLA, P. K. (1965) Primary Optic Atrophy. Orient. Arch. Ophth. 3½ 221.  Back to cited text no. 2
HIERONS, R. and LYLE, T. K. (1954) Quoted by AGARWAL, L. P. et, al. (1965). primary Optic Atro­phy. Orient. Arch. Ophth. 3: 19.  Back to cited text no. 3
IQUI. H., INOMATA, H. and HAYASHI, J. (1966)-The Patho­genesis of Haemorrhage in the Optic Nerve Sheath. Acta. Soc. Ophthal. Jap., 70: 2196.  Back to cited text no. 4
LUMSDEN, C. E. (1961) Cons dera­tion of Multiple Sclerosis in rela­tion to the Auto-Immunity Process. proc. R. Soc. Med. 54: 11.  Back to cited text no. 5
MOONEY, A. J. (1959). Further Observations on the Ocular Com­plications of Tuberculous Meningi­tis. Amer. J. Ophthal., 48: 297.  Back to cited text no. 6
SCOTT. G. I. (1952) Neuromyelitis Optica. Amer. J. Ophthal. 35: 755.  Back to cited text no. 7
STANSBURY. F. C. (1949) Quoted by Scott. F. C. (1949) Neuromyelitis Optica. Amer. J. Ophthal. 35: 755.  Back to cited text no. 8


  [Table - 1], [Table - 2], [Table - 3]


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