There is no sphincteric muscular arrangement at the cardiac orifice of the esophagus, so that spasmodic stenosis at this level is not possible and the term cardiospasm is, therefore, a misnomer. It was first demonstrated by the author that in so-called cardiospasm the functional closure of the esophagus occurred at the diaphragmatic level, and that it was due to the "diaphragmatic pinchcock." Anatomical studies have corroborated this finding by demonstrating a definite sphincteric mechanism consisting of muscle bands springing from the crura of the diaphragm and surrounding the esophagus at the under surface of the hiatus. An inspection of the cadaveric diaphragm from below will demonstrate an arrangement like double shears admirably adapted to this "pinchcock" action. Further confirmation is the fact that all dilatation of the esophagus incident to spasm at its lower extremity is situated above the diaphragm. In passing it may be stated that the pinchcock action, plus the kinking of the esophagus normally prevents regurgitation when a man with a full stomach "stands on his head" or inverts his body. For the upward escape of food from the stomach an involuntary co-ordinated antiperistaltic cycle is necessary. The dilatation resulting from phrenospasm may reach great size (Fig. 96a), and the capacity of the sac may be as much as two liters. While the esophagus is usually dilated, the stomach on the other hand is often contracted, largely from lack of distention by food, but possibly also because of a spastic state due to the same causes as the phrenospasm. Recently Mosher has demonstrated that hepatic abnormality may furnish an organic cause in many cases formerly considered spasmodic.