|Year : 1995 | Volume
| Issue : 2 | Page : 78-79
Optic neuropathy secondary to herpes zoster ophthalmicus
Vimala Menon1, Gautam Kumar1, Radhika Tandon2
1 From Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India
2 From Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhivv, India
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110 029
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Menon V, Kumar G, Tandon R. Optic neuropathy secondary to herpes zoster ophthalmicus. Indian J Ophthalmol 1995;43:78-9
|How to cite this URL:|
Menon V, Kumar G, Tandon R. Optic neuropathy secondary to herpes zoster ophthalmicus. Indian J Ophthalmol [serial online] 1995 [cited 2021 May 14];43:78-9. Available from: https://www.ijo.in/text.asp?1995/43/2/78/25264
Ophthalmologic manifestations occur in approximately 17% of the cases of herpes zoster. In a few cases, the external manifestations of herpes zoster ophthalmicus may be associated with a granulomatous artertis and an ocular syndrome including ophthalmoplegia, ischemic optic neuropathy, hypotony, phthisis bulbi and contralateral hemiplegia. Optic neuritis, a rare but serious complication of herpes zoster, was first described by Hutchinson in 1866. In view of its rarity, we present a case of herpes zoster ophthalmicus with optic neuropathy developing after cicatrization of the skin lesions.
| Case report|| |
A 48-year-old, otherwise healthy, female presented with sudden loss of vision in the left eye one month after an attack of herpes zoster ophthalmicus. There was no history of pain, redness or trauma to the eye. She had dark pigmented patches on the left half of the forehead in the region of frontal branch of the ophthalmic division of the trigeminal nerve.
Her best-corrected visual acuity was 6/6 in the right eye and perception of light with accurate projection in the left eye. Ocular examination revealed normal ocular movements in both eyes. There was anisocoria with the left pupil being larger than the right. There was a relative afferent pupillary defect present in the left eye. The rest of the anterior segment including corneal sensations was normal in both eyes. The intraocular pressure was 14 mm Hg in both eyes. Fundus examination in both eyes did not show any abnormality. The general physical and neurological evaluations were unremarkable. Goldmann perimetry was normal in the right eye. The VER pattern response was extinguished in the left eye and normal in the right eye. The haematological and roentological evaluations were normal and a computed tomography scan of the head did not show any lesion.
The patient was started on oral prednisolone, 1 mg/kg of body weight, along with vitamin B complex. At the end of three months, the patient had a best-corrected visual acuity of perception of light with accurate projection in the left eye. Fundus examination of the left eye showed a temporal pallor of the optic disc (Figure).
| Discussion|| |
Herpes zoster is caused by the varicella-zoster virus and is produced by inflammation of the sensory neurons in the posterior root ganglia and the ganglia of certain cranial nerves, such as the Gasserian ganglion. The inflammation extends from this ganglion to the ophthalmic division of the trigeminal nerve.
The development of optic neuritis as a sequel to herpes zoster ophthalmicus is rare. It may occur during the acute stage of the vesicular eruption or more commonly as post-herpetic complication even 10 weeks after the onset of the disease. It may be monocular or binocular; intraocular and retrobulbar., The clinical course is often variable but the final outcome in majority of patients is loss of perception of light.
The exact mechanism of optic neuropathy in herpes zoster ophthalmicus is not known. Naumann et al discussed the pathological findings of 21 enucleated eyes with herpes zoster ophthalmicus and found extensive inflammation around the posterior ciliary nerves and vessels; and in association with patchy necrosis of the iris, suggests a generalised ocular ischemia. In addition, local extension into the meninges and brain tissue may lead to mild meningoencephalitis which may damage the optic nerve. A third mechanism proposed is a direct invasion of the nerves, muscles and optic nerve by the virus through the sinus cavernosus. Reports of herpes zoster ophthalmicus associated with optic neuropathy and central retinal artery occlusion lend further credibility to the ischemic mechanism.,
Our patient presented as a retrobulbar neuritis late in the course of the disease after cicatrization of the skin lesions. The anisocoria in presence of a normal anterior segment and full ocular movements possibly reflects viral ciliary ganglionitis. The ultimate outcome was a visual acuity of light perception with accurate projection along with optic atrophy.
Through this report, we intend to highlight the fact that herpes zoster ophthalmicus in addition to the known usual complications, could also cause optic neuropathy. For this reason, the patients should be put on long-term follow-up.
| References|| |
Harrison EQ. Complications of herpes zoster ophthalmicus. Am J Ophthalmol 60:1111, 1965.
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Naumann G, Glass JDM, Font RL. Histopathology of herpes zoster ophthalmicus. Am J Ophthalmol 65:533, 1968.
Kattah JC, Kennerdell JS. Orbital apex syndrome secondary to herpes zoster ophthalmicus. Am J Ophthalmol 85:378, 1978.
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