Rinsho Shinkeigaku (Clinical Neurology)

The 48th Annual Meeting of the Japanese Society of Neurology

Autoantibodies against Glutamate receptors in patients with encephalitis

Yukitoshi Takahashi, M.D.1)2), Etsuko Yamasaki, M.D.1), Yuko Kubota, M.D.1), Shigeko Nishimura, M.D.1), Hisano Tsunogae, M.D.1), Hiroko Ikeda, M.D.1), Hiroka Takahashi, M.D.1), Jyun Mine, M.D.1), Sanae Otani, M.D.1) and Tateki Fujiwara, M.D.1)

1)National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders
2)Department of Pediatrics, Gifu University School of Medicine

We examined autoantibodies against GluRε2 in patients with acute encephalitis, who were categorized into localized encephalitis and widespread encephalitis. Patients with localized encephalitis are defined as patients showing psychic symptoms (illusions, anxiety and distraction etc.), solitary seizures and/or very mild impairment of consciousness in the initial stage. Patients with widespread encephalitis are defined as patients showing a profound loss of consciousness and or convulsive status in the initial stage.
In 24 patients with localized encephalitis, immunoglobulin (Ig) M autoantibodies against GluRε2 tended to appear in CSF in the acute stage (0-20 days after onset of neurological symptoms) or recovery stage (21-60 days after onset of neurological symptoms) of encephalitis. In 22 patients with widespread encephalitis, IgM autoantibodies against GluRε2 in CSF tended to appear in the recovery stage (21-60 days after onset of neurological symptoms) or chronic stage (>60 days after onset of neurological symptoms) of encephalitis. All patients with localized encephalitis had autoantibodies to the extracellular N epitope. However, no patients with widespread encephalitis had autoantibodies to the extracellular N epitope in acute stages.
These data may suggest that GluR autoimmunity contributes to the onset of localized encephalitis.

(CLINICA NEUROL, 47: 848|851, 2007)
key words: acute encephalitis, acute encephalopathy, limbic encephalitis, glutamate receptor, autoantibodies

(Received: 16-May-07)