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緒言
実験的アレルギー性脳脊髄炎(EAE)に関しては,内外に多数の業跡があり,今日ではこれが,狂犬病ワクチン接種後脳脊髄炎と共に免疫学的操作に基づくものであることは疑いのないところである。1955年Waksrnan Adamsは末梢神経を材料とし,FreundのAdjuvantを加えて家兎に多発性神経炎(EAN)を惹起せしめることに成功し,ヒトのGuillain-Barré症候群を主徴とする急性多発性神経炎との類似性を指摘した。翌年更に海獏,白鼡を用いてのこれらの種族間の比較病理の実験において,前者には中枢神経にも病変を認めた。その後Petteらによる実験以外この種の仕事はほとんど行なわれていない。
我々は海獏を用いてEAN実験を行ない,やはりその半数に中枢神経にも病変を認めた。このことは狂犬病ワクチン接種後に,広汎な弛緩性麻痺を呈する報告例6)や,多発性神経炎に際し,中枢神経にも同一性格の病変の認められること2)15)と考え合せて意義の深いものといわざるを得ない。
EAN was produced by intramuscular injectionof human brachial nerve along with adjuvantsin guinea pigs. Clinically ataxia was predominant and paralysis of the lower extremity andvesicorectal incontinence were noticed only insevere cases especially cases associated withinvolvement of CNS. The early lesion consistedof mononuclear cell infiltration in or adjecentperineurium to the dorsal or semilunar gangliasor it's capsule. Granular disintegration of myelin in the schwann cell seemed to follow. Disseminated lesions then appeared to extend toperipherally or centrally from ganglias whichare site of initial damage. Subsequent lesions wereoften severe enough to undergo necrosis associated with infiltration of polymorphonuclearleucocytes and plasmic imbibition. Wanderingmononuclear cells disintegrated early and plasma cells appeared. Myelin droplets were subsided leaving Schwann cell proliferation withinone week. In two weeks secondary degenerationbecame appearent and simulatanously notedremyelination which was still incomplete in theganglia in 29 days case and completed in 129days case. 14 out of 27 cases were associatedwith CNS lesions. 15 cases showed focal histiocytic accumulation in the chorioid of eye.
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