EPSTEIN-BARR VIRUS ENCEPHALITIS AND NEUROLOGIC SEQUELAE

Abstract

IN REPLY: Dr. Joncas points out two important risk factors for the development of neurologic sequelae following encephalitis: preexisting neuropsychiatric illness; and anoxic central nervous system lesions as a result of delays in treatment, or suboptimal intensive care. Although none of the patients we reported had a formal neuropsychiatric history, Patient 4 had repeated a grade, and Patient 7 was considered "emotionally disturbed" as a result of possible sexual abuse. Neither of these patients developed neurologic sequelae. All 11 patients described were hospitalized at the time of presentation. Nine were admitted directly to our pediatric intensive care unit, one to the general pediatric ward (Case 9) and one to the psychiatric ward (Case 10). Intensive supportive therapy was available to all of the patients admitted to the pediatric intensive care unit, although only one had evidence of diffuse cerebral edema (Case 5). Despite aggressive attempts to manage the cerebral edema in that patient, it is probable that cerebral hypoxia/anoxia from the underlying edema contributed to her stormy course. Specific risk factors were not readily identified for any of the other cases of neurologic sequelae after primary Epstein-Barr virus encephalitis in our series. Finally Dr. Joncas raises the possibility that the encephalitis may have been caused by a separate and distinct infection coinciding with the acute Epstein-Barr virus infection. Indeed, we maintain a high index of suspicion for this possibility and perform extensive laboratory evaluations of the serum and cerebrospinal fluid from such patients. Unfortunately archived aliquots of the cerebrospinal fluid samples are unavailable to confirm the presence of Epstein-Barr viral DNA using PCR. Joseph B. Domachowske, M.D. Leonard B. Weiner, M.D. Department of Pediatrics; State University of New York; Health Science Center of Syracuse; Syracuse, NY