Myopathyの筋電図について

Electromyographic Study of Myopathy

はじめに

　ここでmyopathyの筋電図という場合は筋原性の変化，すなわち筋線維の実質の変性または萎縮，さらに機能的な収縮力の低下のためひとつのNMUのスパイク放電の変化をいうわけであるが，実際上はいろいろ不明瞭の多いことが知られている。しかし臨床的には，一応次のごとくまとめられている。①at restに自発放電のないこと（この場合myotonic reactionは例外である）。②voluntary contractionにおいては電位持続時間の短縮（Kugelberg，1947^1），1949^2）および振幅の減少（Denny-Brown，1949）^3），さらに干渉性であつて，波形が多相性となることなどと定義される（Buchtal，1955^4），Isch，1958）^5）。

　しかし，この定義も問題がないわけではない。すなわち，筋線維の変性，萎縮等にしろ，それがある程度進行すれば，神経終末部に病変がおよぶ可能性がある。またたとえ，終末部変性がなくても，たとえばComplex N-MU voltageの出現の可能性も論ぜられており，実際，そのような例が示されている（島津，1956^6））。また逆にneurogenicの明らかな場合の例でも，myogenic lowvoltageの出現をみる場合もある。したがつてmyopathyの筋電図といつてもclearcutにひとつの枠に総べてをおしこめてしまうわけにはゆかない。

　Electromyographic studies were done in muscular disorders: muscular dystrophy, hyperthyroid and hypothyroid myopathy, periodic paralysis, and the other rarecases.

　Especially, the electromyogram of hypothyroid myopathy was studied in relation to the activities of aldolaseand creatine phosphokinase in serum.

　The results obtained were as follows : 1) From the findings of evoked EMG in the threeforms of muscular dystrophy (Walton's classification),it is concluded that the impulse via the centripetal pathway of GIa fiber may be inhibited by unkown causein this disease.

　2) The finding of the repetitive stimuli of α-efferent fiber in chronic thyrotoxic myopathy showed the tendency of waxing pattern in amplitude, but the findingin the many cases of hyperthyroidism without muscular involvement remained in normal pattern. On theother hand, the finding in hypothyroid myopathy showedwaning pattern.

　And thus, it is summarized from these results thatthe deficiency or overproduction of thyroid hormonemay effect on the state of the combination of neuromuscular junction.

　But, in the cases of chronic thyrotoxic myopathy theappearance of waxing pattern may depend upon the presence of an unknown factor in addition to the changeof the state of neuromuscular junction.

　3) Such waning pattern in hypothyroid myopathywas remarkably to the cases with high creatine phosphokinase activities, so one of the causes of the waningpattern may be attributed to the deficiency of the contraction factor of muscle as well as the state of neuromuscular junction.

　4) The occurances of the paralytic state of non familiar periodic paralysis and primary aldosteronism are clue to neurogenic factor as well as myogenic factor. Because the electromyogram of the paralytic state demonstrated the deficiency of Mai voltage and the presence of giant spike. And then, in addition to these findings, the change of H wave shows that the impulsevia the centripetal pathway GIa fiber may be inhibited by the change of Na/K ratio in serum.

　5) Both the electromyograms of non hereditary distal myopathy and dystrophic arthrogryposis syndromewere similar to that of muscular dystrophy. But, in future, such electromyographic study must be done in datil after the accumulation of these cases.