Association of Japanese encephalitis virus infection with Guillain-Bark syndrome in endemic areas of South India* Ravi V, Taly AB, Shankar zyxwvutsr SK, Shenoy PK, Desai A, Nagaraja D, Gourie-Devi M, Chandramuki A. Association of Japanese encephalitis virus infection with Guillain-Barre syndrome in endemic areas of South India. Acta Neurol Scand 1994: 90: 67-72. zyxwvut 0 Munksgaard 1994. This study is a report of 34 cases of Guillain-Barre syndrome (GBS) observed in Bangalore (South India), an endemic area for Japanese encephalitis virus (J EV) infection. Virological and immunological findings suggested an antecedent and recent JEV infection in 21/34 patients. Nineteen patients among them showed high levels of JEV-specific IgM antibodies in serum and/or CSF, while the viral antigen could be demonstrated in one case and virus isolation from the CSF was successful in one patient. EMG studies revealed features of predominantly demyelinating neuropathy in 18/25 cases. Comparison of clinical findings, duration of illness and outcome in GBS patients with evidence of JEV infection and those without did not reveal any differences. Pathological findings in one patient corroborated the association of JEV with GBS. We conclude that, JEV infection may predispose to Guillain-Barre syndrome in endemic areas. Japanese encephalitis virus (J EV) belongs to the family of Flaviviruses and is the commonest cause of mosquito borne encephalitis in the world (1). This disease has been recognised in India since 1955 and has become endemic in several parts of the country (2). The southern districts of Karnataka state, South India, have been experiencing periodic outbreaks of Japanese encephalitis since 1979. The detailed de- scription of the clinical features, pathological, im- munological, and virological observations in these patients affected during the epidemics in South India, have been reported by us earlier (3-7). However, involvement of peripheral nerves has not been re- ported following JEV infection. In this paper we present immunological, virological and pathological evidence associating JEV with GBS in 21/34 pa- tients. zyxwvutsrqp Material and methods zyxwvutsrqpon Patierits - Thirty-four patients who fulfilled the NINCDS criteria for GBS (8) were included in this study. All of them were admitted to the neurological services of the National Institute of Mental Health * Presented in part at the XIV World Congress of Neurology held at New Delhi. October 22-27. 1989. V. Ravi’, A. B. Taly’, zyx S. K. Shankar3, P. K. Shenoy ’, A. Desai ’, D. Nagaraja’, M. Gourie-Devi’, A. Chandramuki’ Departments of ’ Neurovirology, * Neurology, Neuropathology, National Institute of Mental Health and Neurosciences, Bangalore, India. zyx Key words: Japanese encephalitis virus; Guillain-Barre syndrome; IgM antibodies; viral antigen. V. Ravi, Department of Neurovirology, NIMHANS, Bangalore 560029, India. Accepted for publication November 14, 1993 and Neurosciences hospital during a period of three years from October 1985 to November 1988. None of them had any clinical features of encephalitis al- though there were small outbreaks of J E temporally associated with the GBS cases in all the three years. Both serum and CSF samples were collected in 23 patients while in 10 either paired serum samples (7/33) or CSF (3/33) alone could be obtained. In one patient, where serum and CSF samples were not available, clinical and histopathological features (post mortem examination) indicative of J EV infec- tion were observed. Hence this case was included in the study but not for the analysis of serological data. Electrophysiological studies were performed on 23 patients shortly after hospitalization. Nerve con- duction studies involved median, common peroneal and sural nerves in all and ulnar nerve in 10 patients. Concentric needle EMG was done in one distal (ex- tensor digitorium brevis/abductor-pollicis brevis) and one proximal muscle (quadriceps/biceps). Nerve conduction parameters beyond +_ 2 S D of control values were considered abnormal. For the purpose of categorizing patients as having demyelination the criteria suggested by Albers et al. (9) were followed i.e. there should be at least one of the following abnormalities in two or more motor nerves. a) con- duction velocity less than 95”/, of lower limit of 67