
| ID | 31864 |
| JaLCDOI | |
| フルテキストURL | |
| 著者 |
Jinnai, Dennosuke
Okayama University
|
| 抄録 | In such animals not having any organic changes in their brains during the initial stage showed a descendence of convulsive threshold. abnormal findings in their electroencephalogram and ascending activity of ChE. But what is the cause of these functional changes? First, from the fact that though there was no organic changes, they were sensitized and reiniected by a known antigen, which is obviously an antigen-antibody reaction. Second, from the fact that we got a histological.change, which was acknowledged as C.L.A. changes by increasing the concentration of these solution and the number of injections, it could be thought that these functional changes were caused by what I called latent C.L.A.. That is, it seems it could be thought that it would give functionally a permanent hypersensitivity, which is called convulsive arrangement. Furthermore, a similar histological findings as seen in old epileptics were made experimentally after prolonged and repeated injections of very diluted antigens. I believe it can be said, also from this histological point that they are experimental epileptics. But I am not trying to say that idiopathic epilepsy is the same allergic disease as asthma. If it was so, it should offer clinically a problem of eosinophilia in the blood of epileptics. But actually there is no eosinophilia in epileptics. Also, in adult epileptics, convulsive attacks is not often seen soon after introduction of antigens. Consequently, my theory that epilepsy is allergic, does not mean that allergy is the direct cause of epileptic attacks. What I mean is, the causal genesis of idiopathic epilepsy is hypersensitivity of nerve cells in the brain. This hypersensitivity was attained as a tissue reaction by some allergic mechanism without any organic changes. This functional change gives the nerve cell a hypersensitive state, which becomes the base of the beginnihg of convulsion. Its inducement of attack could be water stagnation in the body, anemic state of the brain, alkalosis, or introduction of allergens. In short, the cause of attack does not always come from allergic reactions. |
| Amo Type | Article
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| 出版物タイトル |
Acta Medicinae Okayama
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| 発行日 | 1954-03
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| 巻 | 8巻
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| 号 | 4号
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| 出版者 | Okayama University Medical School
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| 開始ページ | 423
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| 終了ページ | 450
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| NCID | AA00041342
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| 資料タイプ |
学術雑誌論文
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| 言語 |
英語
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| 論文のバージョン | publisher
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| 査読 |
有り
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| NAID |