126 



molecular mechanism of myotonia unsolved. It supports the as- 

 sumption that energy transmissions may be disturbed in this dis- 

 ease, possibly owing to labilization of the triplet state and the con- 

 secutive shortened lifetime of triplet excitations. Such an effect 

 may be due to the shortage of stabilizing agents as glutathione, or 

 to the presence of labilizing agents, analogous to 2,4D. In any 

 case, the experiments quoted need to be extended and suggest fur- 

 ther experimentation. They suggest, for instance, the search for 

 substances rendering triplets more stable and transition into the 

 triplet state more probable. There are substances which act this 

 way. Some of them have been mentioned before: iodide, or iodine 

 in its organically bound form. There are other such substances, 

 even among normal cell constituents. As has been shown, sero- 

 tonine is one of them, lysergic acid another. Extensive experimen- 

 tal work is possible on these lines and this work may eventually 

 lead not only to a better understanding of the degenerative dis- 

 eases of muscle but also may reveal ways of curing them. Thoughts 

 on this line may find encouragement also in the experience that 

 amphetamin and ephedrine were found to produce changes in the 

 excitation of riboflavine similar to those produced by 2,4D. One 

 of these, ephedrine, is known to have a beneficial eflfect on myas- 

 thenia, which may be found to be true even to a higher degree in 

 other drugs, having a similar but stronger action in £*. 



Symptoms of myotonia can be relieved in man by quinidine. It 

 seems worth noting that S. L. Baird (unpublished) found the 

 drug equally active in myotonia, induced in mice by 2,4D. It may 

 be more than a coincidence that while 2,4D shortens the lifetime 

 of excitations, quinidine has a strong tendency to undergo a long- 

 lived excitation in presence of a great variety of substances. 



