Recent advances in the physiology of digestion, particularly the work of Cannon,1 Carlson2 and Alvarez,3 add emphasis to the rôle that motor disturbances play in the production of gastro-intestinal symptomatology. Only a few years ago we were primarily concerned about secretory changes, and fine distinctions were drawn in regard to the variations in gastric acidity. Rehfuss and Hawk4 have shown that the highest degree of acidity occurs in healthy young subjects. Finally the researches of Johnson and Hurst,5 confirmed by Carlson and others, demonstrated that the mucosa of the gastro-intestinal tract (except the anal canal) was devoid of pain nerve endings. Thus it appears that the terms hyperacidity, hyperesthesia gastrica and gastralgia are destined to be relegated to the junk heap of medical history.
Most investigators agree with Carlson that the pain in gastric and duodenal ulcer is largely, if not entirely, due to motor