Myanesin was first investigated in animal experiments by Berger and Bradley (1946) and found to have a curare-like muscle relaxing effect. This they thought was mainly due to action on the spinal cord, because strychnine convulsions were inhibited by the drug. Smaller doses were more effective for this than for the reduction of Metrazol convulsions. Hunter and Waterfall (1948) reported an immediate disappearance of epileptic seizures in man after intravenous administration of.4-1 gm. of Myanesin. Gammon and Churchill (1948) found that the spike and dome pattern of the E.E.G. in cases of petit mal disappears following Myanesin, whereas E.E.G. alterations associated with grand mal seizures were uninfluenced. Higher doses might, however, abolish these changes. Geer (1949) used the drug (in doses up to 3 1/2 gm.) in conjunction with electric convulsive therapy (E.C.T.) for mental disorders and found it of no demonstrable value because it apparently tended to make convulsions more severe, although it slightly increased the voltage time stimulus necessary to produce a convulsion. Unna and Kaplan (1949) examined the anticonvulsive properties of Myanesin in mice. Metrazol seizures of mice treated with Myanesin were seen to be at least as severe as controls and often prolonged. The tonic extensor phase was, however, eliminated. The death in Myanesin-treated animals was delayed as compared with controls. Electroshock also caused a seizure in 89 per cent. of the Myanesin treated mice, but no deaths occurred, whereas controls without Myanesin had a mortality of 33 per cent. Here, again, Myanesin appeared to abolish the tonic phase of the fit and only more violent clonic convulsions occurred. Schlau and Unna (1949) reported that the pattern and duration of seizures in E.C.T. in man were not changed following 2 gm. of Myanesin four times daily by mouth. They did, however, observe a shortening of the period of apnoea following the convulsion.