The treatment of myasthenia gravis has advanced remarkably in the past five years. Changes in therapy have kept pace with a better understanding of the mechanism of the transmission of excitation, with particular reference to the region of the myoneural junction. Our interest in this has been enhanced by the introduction of prostigmin,1 (the dimethylcarbamic ester of 3-hydroxyphenyltrimethylammonium methylsulfate), an analog of physostigmine. Walker2 in 1934 first described a case of myasthenia gravis in which the use of physostigmine resulted in definite improvement. In the following year she3 demonstrated the dramatic temporary relief of symptoms in two patients with myasthenia gravis to whom prostigmin was administered. Since Walker's original observations, others4 have given testimony to the efficacy and mode of action of prostigmin in the treatment of myasthenia gravis.
In a study of the chemical processes which accompany activity and recovery in the myasthenic muscle, Nevin
WINKELMAN NW, MOORE MT. PROSTIGMIN IN THE TREATMENT OF MYASTHENIA GRAVIS AND MUSCULAR DYSTROPHY: RESULTS OBTAINED WITH DIVIDED DOSES. Arch NeurPsych. 1937;37(2):237–252. doi:10.1001/archneurpsyc.1937.02260140023002
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