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| ARTICLES |
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| Year : 1970 | Volume
: 18
| Issue : 4 | Page : 176-179 |
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Nylidrin hydrochloride in optic atrophy
JS Mathur, HV Nema, JN Char, KS Mehra
Department of Ophthalmology, College of Medical Sciences, Banaras Hindu University, Varanasi-5, India
Correspondence Address:
J S Mathur
Department of Ophthalmology, College of Medical Sciences, Banaras Hindu University, Varanasi-5
India
 Source of Support: None, Conflict of Interest: None  | Check |
How to cite this article:
Mathur J S, Nema H V, Char J N, Mehra K S. Nylidrin hydrochloride in optic atrophy. Indian J Ophthalmol 1970;18:176-9 |
The subject of optic atrophy poses a great challenge to the ophthalmologist as we know little about its exact etiology and management in good percentage of cases. It is an established fact that the optic nerve fibres lack neurilemnal sheath. It is, therefore, incapable of regeneration which contributes for tie poor prognosis in bulk of the cases despite treatment. However, there remains a group of cases with incomplete degeneration where the nerve fibres remain in a state of ischaemia. This group may recover to some extent if proper and prompt therapy with vasodilators is instituted. With this end in view, several vasodilators like Acetyl choline (Dastoor [1] ), Priscoline and Isox-suprine Hydrochloride have been tried. The results obtained with these drugs were not consistent and encouraging. Hence, there is a constant search for an ideal, potent and safe vasodilator which could be used in these desperate cases.
Nylidrin hydrochloride is a new vasodilator with a structural formula as in [Figure - 1]. It is related chemically to the epinephrine - ephedrine series. Claims have been made that it is an excellent drug in the management of peripheral vasoconstrictive diseases, (Stein [5] ) Considering these merits, an attempt has been made in the present communication to evaluate the drug in cases of optic atrophy.
| Material and Methods | |  |
Between January, 1967 and December, 1968, 39 cases of optic atrophy were selected for this study. Optic atrophy in these cases was consequent upon tubercular meningitis, viral encephalitis, arachnoiditis and methyl alcohol poisoning. Criterion of diagnosis of optic atrophy was loss or marked deterioration of vision, pallor of the optic disc and marked visual field defects (wherever charting was possible). A proper record regarding the visual acuity, fundus changes (color and vascularity of the optic disc, appearance of macula, calibre of blood vessels and details of periphery) and visual fields was maintained. The cases were divided at random into two groups of 25 and 14. 49 eyes of the first group were taken as test while 28 eyes of the second group were kept as control.
In the test group, Nylidrin hydrochloride 1 ml. (0.5 ml. in children below 6 years of age) was injected retrobulbarly every 4th day for consecutive 32 days. It was supplemented with intramuscular injection of B, 100 mgm. and B 12 5oo ugm. on alternate days for 2o days and oral Nicotinic acid 50 mgm. thrice daily for one month. The control cases received only systemic therapy. Each case was re-examined soon after the termination of the scheduled therapy and findings were recorded.
Visual improvement was graded as marked (++++), good (+++), moderate (++), slight (+), no (O) and deterioration (-). Follow-up examination was done at an interval of 3o days for 6 months after which the response was evaluated.
| Observations | | |
It has been noted that retrobulbar administration of Nylidrin hydrochloride resulted in improvement in the visual acuity in 19 (38.78%) out of 49 test eyes. It was marked, good and moderate in 2, 2 and 5 eyes, respectively. Slight improvement was recorded in 10 eyes. Only one eye showed further deterioration of vision despite treatment. In the control group 6 (21.43%) of the 28 eyes showed visual improvement. Improvement was moderate in 2 eyes and slight in 4 eyes. 2 eyes in this group showed further visual deterioration. 59.18% of the test eyes did not show any improvement in spite of retrobulbar injection as compared to 71.43% of the eyes in the control group [Table - 1].
Analysis of fundus examination of both the groups after 6 months of follow-up revealed that 14 test eyes (28.57%) showed improved vascularity of the disc, increased calibre of the retinal arteriols and general improvement in the color of the peripheral fundus, although there was no change in the macular picture. The corresponding changes in the control group were noted in only 4 eyes (14.29%). [Table - 2].
Visual fields could be charted out in only 22 eyes of the test group and 8 eyes of the control group. In these cases, there was increase in the field of vision, both central and peripheral. Still, cases of the test group and 3 cases of the control group had residual generalized peripheral field constriction.
| Discussion | | |
Although, the fundamental basis of management of optic atrophy is the treatment of its underlying cause, it has often been seen that in a sizable number of cases, the etiology remains obscure. However, cases with known etiology, for example, tubercular meningitis and viral encephalitis seek ophthalmic consultation at a very late stage. Usually, in these cases the degeneration of the optic nerve is complete and very little can be done to restore any useful vision in these unfortunates. Cases with partial degeneration of optic nerve which remains in a state of ischaemia form an ideal group where vasodilators can be tried with some hope.
Our present experience with Nylidrin hydrochloride indicates that the drug has limited value in the management of optic atrophy as evident from our observations that it produced visual improvement in only 38.78% of the cases as compared to 21.43% in the control group. The difference between these two groups is insignificant (x 2 = 1.72, P 0.10). It was recorded that retrobulbar injection of this drug improved the vascularity of the disc (by increased circulation through the pial vessels). calibre of the arterioles and general colour of the fundus. It has been claimed that Nylidrin hydrochloride has got a direct vasodilatory effect upon the small arteries and arterioles of the skeletal muscles (Fulton[2]; Green [3] ). Probably, similar action might be occurring on pial and retinal arterioles after its retrobulbar use. Such an effect is consistent with the observations made that the drug enhances the retinal blood fow (Jacobson and Basar[4]).
It was observed that there war a variable correlation between the visual improvement and improvement in the vascularity of the disc and retina. It signifies that mere enhancement in the circulation of retina or around the disc may not help in the restoration of vision as the latter is closely related with the integrity of the optic nerve fibre bundles. In all those cases where degeneration of the optic nerve is incomplete and the nerve is in an ischaemic state, the vasodilator therapy helps in relative recovery. At the same time, it has been observed that some of our cases showed visual improvement even without Nylidrin hydrochloride therapy suggesting that in partial optic atrophy, some recovery is spontaneous rather than due to retrobulbar therapy with vasodilators. Therefore, it may be concluded that introduction of this drug has not significantly changed the prognosis of optic atrophy cases. Still there is no specific treatment for the majority of patients suffering from optic atrophy.
| Summary | | |
Retrobulbar Nylidrin hydrochloride was evaluated in 49 eyes having optic atrophy. Another group of 28 eyes with optic atrophy served as control. Visual improvement was recorded in 38.78% and 21-43% of the cases in test and the control group, respectively.
| Acknowledgements | | |
Our thanks are due to Mr. M. Subbanah of U.S. Vitamin & Pharmaceutical Corporation (I) Ltd. for the supply of the drug.
| References | | |
| 1. | Dastoor, H. D.: A study of Optic atrophy - SRINIVASAN ORATIONJ. All India Ophth. Soc., 14; 55-74 (1966).  |
| 2. | Fulton, G. P. (1956)-Cited in Booklet on Arlidin-by U. S. Vitamin and Pharmaceutical Corporation (I) Ltd. |
| 3. | Green, ff. D.: Minn. Med., 41; 241 (1958). |
| 4. | Jacobson. J. H. and Basar, D.: A.M.A Arch. Ophthal., 56; 865 (1956). |
| 5. | Stein, I. D.: Ann. Internal Med , 45; 185 (1956). |
[Figure - 1]
[Table - 1], [Table - 2]
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