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| ARTICLES |
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| Year : 1975 | Volume
: 23
| Issue : 2 | Page : 15-17 |
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Internal ophthalmolplegia in a young child suffering from Herpes zoster
Hamida Buch1, RL Vaid1, Vijaya Wali1, Daljit Singh2
1 Department of Ophthalmology, Govt. Medical College, Srinagar, India
2 Department of Paediatrics, Govt. Medical College, Srinagar, India
Correspondence Address:
Hamida Buch
Department of Ophthalmology, Govt. Medical College, Srinagar.
India
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 1236445 
How to cite this article:
Buch H, Vaid R L, Wali V, Singh D. Internal ophthalmolplegia in a young child suffering from Herpes zoster. Indian J Ophthalmol 1975;23:15-7 |
Herpes zoster, caused by a virus very akin to vericella is known to occur in all ages but ocular involvement in young children is rare, very few cases have been reported so far, where the children were involved [1],[2][4],[5],[9],[10],[11],[12],[22]. Fewer cases are known where, internal ophthalmoplegia was associated with the ophthalmic involvement [3],[17],[24] . The present case is of interest, as there was isolated internal ophthalmoplegia without recovery, in a case herpes zoster ophthalmicus.
| Case report | |  |
H, a muslim female child of six years reported in the paediatric out-patient department with severe pain in the left eye and left half of the forehead, with chemosis of lids and diminution of vision. The child was diagnosed as a case of Herpes zoster ophthalmicus and was referred to ophthalmology department of SMHS Hospital [Figure - 1].
On examination of the left eye, the lids were red, swollen and covered with vesicles which were present over the left half of forehead and scalp also. A few round superficial infiltrations were found on the cornea, conjunctiva was congested and corneal sensations were absent. Pupil was dilated and both direct and consensual light reactions were absent. Reaction to accommodation was also absent. No medicine had been used inside the eye, except some indigenous medicine which had been applied over the scalp which could not be removed at the time of examination, [Figure - 1]. Ocular movements were normal. Fundus was also normal. Visual acuity was 6/24.
Right eye was normal, with 6/6 visual acuity.
Treatment : The patient was put on local antibiotic ointment in left eye. Lotio calamine was applied over the vesicles. Systemically neurovitamins and analgesics were given.
Follow-up of the left eye
After one week : Lids were still red, swollen and covered with vesicles, cornea was insensitive and keratitis was still there. Pupil was dilated and fixed, reaction to light and accommodation was absent.
After four weeks : Skin eruptions had disappeared and were replaced by pitted scars. Cornea was clear but insensitive. Pupil-semidilated and fixed. Visual acuity was 6/24. Reaction to accommodation and light still absent.
After eight weeks: Corneal sensation was dull. Pupil was still semi-dilated and fixed. Visual acuity was 6/24 but it improved to 6/6 with+1.OOD Sph. and N8 with +2.00 D Sph.
After 12 weeks : Same condition.
After 16 weeks : Same condition.
| Comments | | |
Herpes zoster ophthalmicus occurs mostly in old people and is due to the infection of gassarian ganglion by the zoster virus. How the virus reaches the ganglion is not known, it may be that the virus is lying dormant in human tissues, becomes activated due to certain ill understood lesions or environmental factors [7] . The viruses of zoster and varicella are very akin to each other and it is very likely that one confers immunity against the other. The varicella infection most commonly affects the children in. epidemic form giving immunity against the zoster virus [7] , which may explain a rare occurance of herpes zoster ophthalmicus in young children.
In addition to the typical extra-ocular involvement, 50 per cent of the cases show ocular involvement in the eruptive or the post eruptive stage [6],[7],[18],[19] . The commonest are the keratitis [21] (40 per cent) and conjunctivitis, while uveitis and scleritis may also occur. The optic neuritis does occur occasionally while palsies of intra and extra-ocular muscles are rare [3],[13],[17],[24]. Amongst the oculomotor nerves involved third cranial nerve involvement is most common [17] . Deformities of the pupil and the accommodation as isolated
defects, are very rare [3],[9],[17],[24] . How this defect is brought about is still conjectural. Naquin [16] feels that it is peripheral in origin while Godtfredsen [8] feels that there is involvement of upper cranial nerves in radiculomeningitis in the region of cavernous sinus where these nerves share the brainstem encephalitis. Naquin [16] explains it on the basis of proximity of pupillomotar, sympathetic and parasympathetic, fibres to the afferant fibres of the trigeminal ganglion from the eye. On the other hand it is felt by Gogi [9] that ciliary and accessory ciliary ganglion may be involved in the same way as the gassarian ganglion and result in internal ophthalmoplegia of isolated type. The explanations are interesting but do not conclusively prove the site of the lesion.
In our case the corneal sensations did not reappear so far and internal ophthalmoplegia persisted even after a lapse of three months which was rather unusual and does not corroborate the belief held so far that recovery is nearly complete within six weeks
| Summary | | |
A young girl of 6 years with herpes zoster ophthalmicus has been reported where in addition to other lesions, she had isolated internal ophthalmoplegia which has not recovered so far even after the lapse of 4 months.
| References | | |
| 1. | Ahmed, M. 1969, Orient. Arch. Ophthal; 7 :38. 
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| 2. | Aubertein, Pesme and Rivere 1950. Cited by Duke Elder, (7) 340. |
| 3. | Baranov, M 1922, Trans. Ophthal. Soc, U.K. 42 : 176. |
| 4. | Birks, D.A. 1963, Brit. J. Ophthal. 47 :60. |
| 5. | Counter and Corn 1950. Cited by Duke Elder, (7).340. |
| 6. | Doggart, J.H. 1933, Brit. J. Ophthal., 17 :513.
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| 7. | Duke Elder 1965 System of ophthalmology. 8, part I, 337 : Henry Kimpton. |
| 8. | Godifredesca, 1948. Cited by Duke Elder (7) 342. London, U.K. |
| 9. | Gogi, R; Sood, AX; Goel, B.S. and Vaid. R.L. 1972. Orient Arch. Ophthal., 10 : 270. |
| 10. | Gavrett 1958. Cited by Duke Elder, (7) 342. |
| 11. | Kolab 1909 cited by Poulsen 1955. |
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| 13. | Leunberger, 1961. Cited by Duke Elder (7) 342. London, U.K. |
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| 15. | Malik, S.R.K; Sood, G.C; Gupta, D.K. 1966 Orient. Arch, Ophthal., 4 : 241. |
| 16. | Naquin, H.A. 1954. Amer. Jr. Ophthal., 10: 305. |
| 17. | Niramkari, M.S., and Singha, S.S; 1967. Orient. Arch. Ophthal. 5 : 287. |
| 18. | Parkinson 1948. Cited by Duke Elder. (7). 342. |
| 19. | Pincus, M.H. 1949. Amer. J. Ophthal. 32: 130. |
| 20. | Poulsen 1955. Acta., Medical Scand 151 : 131. |
| 21. | Pritkin and Duchon 1951. cited by Duke Elder, (7).343. |
| 22. | Saxena, G.S. 1964. J. All Ind. Ophthal. Soc, 12: 132. |
| 23. | Safar, 1949. Cited by Duke Elder. (7), 340. |
| 24. | Walsh, F.B. 1957. Clinical Neurophthalmology., Ed. II, 459, Baltimore, Williams and Wilkins company. |
[Figure - 1]
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