The various. pathological symptoms are, as a rule, less pronounced than in hyperstenosis and change whimsically. Vomiting, which occurs three to four hours after feeding and may even be bulky anti explosive, is no reliable sign of distinction. Several authors (Koplik, for instance) attribute great diagnostic significance to the fact that the stools of true pylorospastie patients are somewhat more frequent and more bulky than in hypertrophie stenosis and as poor in fecal matter as in the latter affection. Similarly, the signs of dyspepsia and diarrhom alternate with pseudo-obstipation. The general condition of nutrition suffers less.
Bulging of the gastric wall is often present, but according to unani mous statements there is no distinctly visible movement of the stomach, at least no true peristalsis with undulating progression; "stiffening of the stomach" is more likely to happen. It will certainly not be possible to exelude true pylorospasim if there is any intimation of peristaltic unrest, relaxation of very lean abdominal walls, or near death. Obser vations of this kind can also be made in eachectic infants with a healthy stomach. On the other hand, a palpable pyloric tumor may for practical purposes be well taken as a very- reliable indication of hypertrophic stenosis, £1R up to the present time eases with negative autopsy findings have only been quite isolated.
Aside from isehoehyrnia, the mixed gastric contents show upon examination a high degree of hyperacidity and frequently hyperehlor hydria; they- are also said to have a diminished fermentative effect and to contain but little mucus.
The etiological factor in pylorospasm is generally taken to consist in the cooperation of a constitutional neuropathic tendency. It is pos sible that in regard to the latter certain factors play a ride similar to those described in the pathogenesis of hypertrophic stenosis (p. 20-1 and following); it is equally possible, however, that in the present instance the causes are of a different nature, for the reason that the assumed pylorospasm has already existed for a comparatively long time without leading to hypertrophy, while Himehsprung's hypertrophy' can evidently develop very rapidly. Furthermore it is possible that there are general disturbances of the entire gastric motion with chiefly hypertonie mani festations rather than true pyloro- or antrospasms. The retention of chyme is not uneonditionally dependent upon a stenosis at the pyloric end of the stomach, but may be attributable to a disturbance of co ordination with spastic character, a spasmogettie asynergy which inter feres with the evacuation of the stomach. There are also concomitant cardio- and enterospasm.
In the course of the illness there are pronounced periods of remis sion and intermission, and the affection does not directly encl fatally.
The therapeutic measures are practically identical with those insti tuted in hypertrophic stenosis. It is advisable, however, to make at least an attempt with gastric irrigation, instantaneous cures having been observed under its application even when the condition had existed for a long time.