In 1925 while clinically testing ephedrine sulphate for the most suitable dosage in the treatment of hay fever and asthma, one of us observed that a number of our patients who were taking large doses of ephedrine complained that they had little or no desire to pass urine and encountered some difficulty in relaxation of the sphincter ani. A study of the vegetative nervous supply to the bladder, vesical sphincter and trigon impressed us with the possibility that an extensive use of the drug might produce urinary retention. We at once reported these untoward clinical observations to the manufacturers of the drug and advised that they mention them in their literature.
In 1926, in a discussion of the physiologic action of ephedrine, we1 attempted to explain the mechanism of the phenomenon described. In 1928, Boston2 reported six cases of urinary retention, requiring catheterization, due entirely to the continuous