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The cause of primary encephalitis is usually direct invasion by one of several viruses (arbovirus, enterovirus, adenovirus, herpes virus, mumps virus).
Within 24 hours of contact, the virus invades the bloodstream, lymph nodes, bone marrow, and most organs. Subclinical cases of encephalitis do occur and are largely asymptomatic or are accompanied by flulike symptoms such as fever and general fatigue. The likelihood of complications is related to the etiologic agent and the person’s general premorbid condition.
Axial CT scan without contrast reveals marked hypodensity representing edema within the frontal and temporal lobes with sparing of the basal ganglia and cerebellum. 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. The study is being published September 14 in Science X-Press, an advanced, online edition of the journal Science. In the study, the scientists suggest that herpes simplex encephalitis may reflect a single gene immunodeficiency that confers susceptibility to herpes simplex virus, an idea that contrasts with the prevailing scientific theory of how genes work to make people vulnerable to infections. In the study, researchers focused on blood cells from two French children with a deficiency for UNC-93B, an endoplasmic reticulum protein involved in the recognition of pathogens. This deficiency resulted in high rates of herpes simplex virus-1 proliferation and cell death.
Herpes simplex virus-1 is a common virus that infects about 80 percent of young adults worldwide. Nonetheless, herpes simplex encephalitis, which was first described in 1941, is the most common type of sporadic viral encephalitis in developed countries, accounting for about 10 to 20 percent of all viral encephalitis cases, as per the University of Maryland Medical Center. Did you know?The study is being published September 14 in Science X-Press, an advanced, online edition of the journal Science.

The mode of transmission is usually a mosquito bite, but ticks and amebae may also transmit the virus.
Common early signs of encephalitis are fever, severe frontal headache, nausea, and vomiting.
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).
Assuming these findings extend to neurons, they provide a plausible mechanism for herpes simplex encephalitis. Herpes simplex encephalitis, a viral infection of the brain that affects otherwise healthy patients, affects an extremely small percentage of those infected with herpes simplex virus-1: the number of annual cases is two per million people, as per the University of Maryland Medical Center. Before the advent of anti-viral drugs vidarabine in 1973 and acyclovir in 1981, mortality rates reached up to 70 percent. By day 4, macrophages have replaced the destroyed lymph nodes, bone marrow is depleted, and the cytoplasm and megakaryocyte nuclei are degenerating. If encephalitis is untreated, neurologic signs that may manifest 6 to 7 days after initial infection are nuchal rigidity, lethargy, confusion, stupor, coma, seizure activity, and extremity paralysis.
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. While the introduction of anti-viral therapy has been a boon to patients, brain damage still poses a substantial risk. A rarer secondary encephalitis may occur as a complication of another primary viral infection such as measles, chicken pox, or rubella.
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. By day 6, there is extensive involvement of the meninges, brain, and spinal cord, with petechial hemorrhages, lymphocytic perivascular cuffing, gliosis, and neuronal necrosis, causing cerebral dysfunction. 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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