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Corresponding author: Eun Yeon Joo, Department of Neurology, Samsung, Medical Center, Sungkyunkwan, University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul, 135-710, Korea, Tel.
Acute retinal necrosis (ARN), a viral retinal disease with poor visual prognosis, following herpes simplex encephalitis (HSE) are uncommonly seen, and there has been no case yet reported of the reverse situation. A 57-year-old man was referred to Samsung Medical Center with abrupt confusion, fever, and loss of vision in both eyes. His brain magnetic resonance imaging (MRI) showed a hyper-intense lesion in the left medial temporal and bilateral medial occipital areas on T2-weight images, suggestive of HSE (Fig. After administration of intravenous acyclovir for 14 days, his systemic symptoms consistent with encephalitis slowly resolved, but his vision was not restored. Cases with ARN following HSE have been uncommonly reported,5a€“9 and to our knowledge, this is the first report of the reverse situation, HSE following ARN, in even an immune-competent patient. ARN usually presents as retinal necrosis with discrete borders located in the peripheral retina, rapid progression, circumferential spread, occlusive vasculopathy with arterial involvement, and a prominent inflammatory reaction in the vitreous and anterior chamber.3 Our patient was initially diagnosed with retinal vasculitis and treated with a high-dose systemic corticosteroid, which was not effective.
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We herein present the reverse situation, an immune-competent patient with HSE following ARN.
The prevalence of the disease is equal in both genders, and it occurs in the 5tha€“7th decade of life.4 Though the diagnosis of ARN is made clinically in most patients, polymerase chain reaction (PCR) analysis of the aqueous humor or vitreous is known as a confirmative method to detect the causative virus. The patient was in his usual state of health until two weeks prior, when he began to develop sudden loss of vision in his right eye. Fundus examination showed retinal hemorrhage, confluent retinal necrosis affecting almost the whole retina, vascular sheathing involving both arterioles and venules, optic disc swelling, and exudative retinal detachment in both eyes (Fig.
On follow-up examination, retinal necrosis did not progress, but he still suffered from severe bilateral ocular pain with partial improvement of the exudative retinal detachment (Fig. ARN associated with HSE is known to be caused by axonal transmission of a reactivated latent virus from the brain to the retina, and retinitis occasionally occurs after the encephalitis. Fluid-attenuated inversion recovery magnetic image revealed hyperintensity in the left medial temporal (arrow) and bilateral occipital cortices (arrow heads). In children, it occurs primarily on the oral mucous membranes but also may be systemic.Instructions for downloading images.
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A 57-year-old man who had been under steroid therapy for retinal vasculitis the prior two weeks, presented with abrupt confusion and high fever.
As shown by our patient, opposite direct transmission from the retina to the brain seems to be possible. Intraocular or systemic corticosteroids may induce retinal necrosis in patients with viral infection.
Systemic steroid therapy may have exacerbated herpes viral infection in the retina, with subsequent spread to the contralateral eye and brain.
Herpes simplex virus type 2 as a cause of acute retinal necrosis syndrome in young patients. Herpes simplex encephalitis and bilateral acute retinal necrosis syndrome after craniotomy. Three consecutive episodes of acute retinal necrosis due to herpes simplex-1 over twelve years following herpetic encephalitis.


Thus, it is recommended that corticosteroids should be used in combination with antiviral agents or after beginning antiviral therapy.12 In this patient, the contralateral eye became infected, and HSE occurred during initial corticosteroid therapy without antiviral medication. Prompt treatment (within 48 hours) with antiviral medication such as valacyclovir (Valtrex), acyclovir (Zovirax), or famciclovir (Famvir), may reduce the length and severity of an infection. Ophthalmic examination and polymerase chain reaction of the vitreous specimen revealed ARN by herpes simplex virus type 2. Two days after initiation of intravenous methylprednisolone, he complained of decreased vision in his left eye. In cases with an unusual clinical course, especially in retinal vasculitis with arterial involvement, viral uveitis including HSV infection should be suspected. After intravenous acyclovir therapy, retinal necrosis with hemorrhage was decreased, but vascular sheathing (black arrows) and exudative retinal detachment persisted.
One week after initiation of intravenous methylprednisolone, he became drowsy and high fever occurred, and he was then referred to Samsung Medical Center. On the night of admission, the patient experienced a generalized tonic-clonic seizure during sleep.
Bilateral rhegmatogenous retinal detachment with optic atrophy was found six weeks later, thus vitrectomy with silicone oil tamponade was done in the right eye. This case implies that ARN may be a risk factor for HSE and the virus may reach the brain from the eye. Infectious retinitis including acute retinal necrosis was suspected, but in terms of the location of necrosis, his clinical features were not typical of ARN Diagnostic vitrectomy confirmed the presence of HSV-1. Inappropriate administration of a systemic steroid may exacerbate herpes viral infection in the retina, with subsequent spread to the brain.



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