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Herpes simplex virus type 1 (HSV) causes approximately 10% of encephalitis cases among humans worldwide, corresponding to an incidence of 1 per 500,000 persons.1 Prior to the development of effective antiviral therapy, which consisted first of vidarabine and later the more effective drug acyclovir, as many as 70% of individuals with HSV encephalitis (HSE) died, and the vast majority of survivors had severe neurologic sequelae. As greater numbers of patients survived HSE, astute clinicians recognized that some survivors, as many as 10%–25%, experienced relapses or recrudescence of neurologic symptoms despite appropriate antiviral treatment. Numerous cases have been reported during the past 3 decades.2,3 Common to most cases has been an inability to detect replicating virus in brain tissue or viral DNA in CSF, observations that led many authors to speculate that immune-mediated mechanisms accounted for the recurrences of neurologic symptoms.2 Some authors suggested that relapse among children with HSE may mimic acute disseminated encephalomyelitis, a potential complication of many different viral infections of childhood, and suggested that corticosteroids be used, in addition to acyclovir, when such relapses occurred.4 Within the past 4 years, immunoglobulin G antibodies against the GluN1 subunit NMDA receptor (NMDAR) have been detected in patients with HSE and have been implicated as a key factor in the pathogenesis of neurologic symptoms following recovery from the initial episode of HSE.5,6
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See page 1736
- © 2015 American Academy of Neurology
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