"Central Pontine Myelinolysis"を呈した慢性アルコール中毒の1例

A CASE OF CHRONIC ALCOHOLISM WITH CENTRAL PONTINE MYELINOLYSIS

緒言

　R．D．Adams，M．Victor, E．L．Mancall^1）（1959）は3例のアルコール中毒患者，1例の鞏皮症患者において，橋底中心部の1つの大きな左右対称性の脱髄病巣を見出し，central pontine myelinolysisとして報告した。その後，central pontine myelinolysisの報告例は30例以上におよんでいるが，その病因については，現在まだ不明のままである。

　日本では，安芸ら^2）（1961）の髄膜腫の1例以来，11例の報告があり，白木ら^3）（1964）は6例を報告し，その病変はvascular originであろうと述べているが，いづれもアルコール中毒性のものではない。

A case of chronic alcoholism with central pontine myelinolysis has been presented.

1) A 62 year-old man, who has drunken much sake for many years, was treated for hypertension about 2 months before admission. He admitted to Hospital of Moriyama-Sou with visual hallucination and abnormal behavior. After admission, he became delirious and restless, and soon, was temporarily comatous. After impairment of consciousness, de-mentia, speech-disturbance and gait disturbance were outstanding. Abnormal speech and action, aggression and violence to nurses and uncleanly behavior were sometimes observed, also. About 2 months after admission, he was found follen down under uncon-sciousness, and then, the physical and neurological examination revealed nuchal rigidity, positive Ker-nig's sign, anisocoria (r >1), positive bilateral Ba-binski's sign, high blood pressure and high fever. But, soon he recovered again. Since about 6 months after admission, he was apathy and abulic, and then continued to lie down on bed till death. Emaciation progressed relatively rapidly. High fever, decubitas and edema appeared in the terminal stage and died about 10 months after his onset.

2) Autopsy was restricted to brain. Macroscpoical-ly, no specific change was found. Microscopically, central pontine myelinolysis was revealed, but in this lesion, demyelination was relatively slight, oli-godendroglia was relatively preserved, and, no gitter cell and gliosis were seen. Another specific change of this region was the local lesion which consisted of destruction of tissure and collection of gitter cells. The other main changes were demyelination in cere-bellar white matter, a few desolating foci in frontal cortex, incomplete softening focus of right external capsule, a local focus of perivasculer cuffing of lym-phocytes and collection of mesenchimal cells in oc-cipital lobe, and sclerotic changes of nerve cells in cerebral cortex.

3) This case was discussed comparing with other references.