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| ARTICLES |
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| Year : 1971 | Volume
: 19
| Issue : 4 | Page : 172-176 |
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Optic atrophy (Review of 100 cases)
MR Chaddah, KK Khanna, GD Chawla
Department of Ophthalmology, Medical College, Amritsar, India
Correspondence Address:
M R Chaddah
Department of Ophthalmology, Medical College, Amritsar
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 15745415 
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 |
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 | |  |
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 | | |
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 | | |
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 | | |
100 cases of optic atrophy involving 172 eyes have been studied. Incidence of varying etiology and the pathogenesis have been discussed.
| References | | |
| 1. | 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.  |
| 2. | AGARWAL, L. P., BATTA, R. K. and KHOSLA, P. K. (1965) Primary Optic Atrophy. Orient. Arch. Ophth. 3½ 221. |
| 3. | HIERONS, R. and LYLE, T. K. (1954) Quoted by AGARWAL, L. P. et, al. (1965). primary Optic Atrophy. Orient. Arch. Ophth. 3: 19. |
| 4. | IQUI. H., INOMATA, H. and HAYASHI, J. (1966)-The Pathogenesis of Haemorrhage in the Optic Nerve Sheath. Acta. Soc. Ophthal. Jap., 70: 2196. |
| 5. | LUMSDEN, C. E. (1961) Cons deration of Multiple Sclerosis in relation to the Auto-Immunity Process. proc. R. Soc. Med. 54: 11. |
| 6. | MOONEY, A. J. (1959). Further Observations on the Ocular Complications of Tuberculous Meningitis. Amer. J. Ophthal., 48: 297. |
| 7. | SCOTT. G. I. (1952) Neuromyelitis Optica. Amer. J. Ophthal. 35: 755. |
| 8. | STANSBURY. F. C. (1949) Quoted by Scott. F. C. (1949) Neuromyelitis Optica. Amer. J. Ophthal. 35: 755. |
[Table - 1], [Table - 2], [Table - 3]
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