第48回日本神経学会総会
＜シンポジウム3-3＞神経疾患と自己抗体
脳炎における抗GluR抗体の意義
高橋 幸利1）2）, 山崎 悦子1）, 久保田 裕子1）, 西村 成子1）, 角替 央野1）, 池田 浩子1）, 高橋 宏佳1）, 美根 潤1）, 大谷 早苗1）, 藤原 建樹1）
1）国立病院機構 静岡てんかん・神経医療センター〔〒420-8688 静岡市葵区漆山886〕
2）岐阜大学医学部小児病態学
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.
(臨床神経, 47：848−851, 2007)
key words：急性脳炎, 急性脳症, 辺縁系脳炎, グルタミン酸受容体, 自己抗体
（受付日：2007年5月16日）
