ON THE STOMACH IN MAN AND THE ANTHROPOID APE. 23 



When sections through the stenosed pyloric canal are examined under the microscope, 

 the general arrangement of the muscular fasciculi — both circular and longitudinal — is 

 seen to have undergone little or no alteration. The great strands of longitudinal fibres 

 which enter the sphincteric ring are particularly conspicuous, whilst the felt work of 

 mixed longitudinal and superficial circular fibres forms a thick layer at the duodeno- 

 pyloric constriction which is carried on to the initial part of the duodenum. It should 

 be noted that it is usual to find the muscular coat of the duodenum close to the pylorus 

 (for a distance of from 6 to 8 mm.) much hypertrophied (PL II. fig. 19). 



Three of the leading views advanced as to the nature of the stenosis and the 

 interference with the free outflow of gastric contents may now be briefly alluded to. 

 Pfaundler (41) holds that there is no muscular hypertrophy in the wall of the pyloric 

 canal, and that the appearances which seem to indicate this, as well as the results which 

 ensue, are all due to a spasmodic contraction of the circular musculature of this portion 

 of the stomach. The stenosis, therefore, according to this author, is not caused by a 

 structural change, but is produced by a functional disturbance of the nervous mechanism 

 which presides over the movements of the stomach. 



Others are of the opinion that the primary and real cause of the stenosis is a true 

 congenital hypertrophy of the muscle in the region involved. Dr Jusstjf Ibrahim (26) 

 is an able exponent of this theory. 



Dr John Thomson (53, 54, 55) has enunciated a more elaborate hypothesis. He 

 points out the difficulty involved in conceiving a hyperplasia of muscle-fibres except 

 under the influence of increased functional activity. He therefore considers that 

 spasm of the muscular coat of the pyloric canal is the initial and primary mischief, and 

 that this takes place in the foetus in utero through some defect in the nervous 

 mechanism which co-ordinates the expelling and retaining forces of the stomach wall. 

 It is well to note that in the stenosed pylorus the retaining forces are represented by 

 the entire length of the sphincteric muscular cylinder of the pyloric canal. The 

 hypertrophy of the musculature, according to Thomson, is secondary, and is due to its 

 excessive activity as indicated by its state of spasmodic contraction. 



This is not the place to take part in a controversy in which so many matters 

 completely outside the main object of this investigation are involved. Still, there are 

 some points mixed up with the question which specially bear on the structure and 

 function of the pyloric canal, and in so far as these are concerned it may be admissible 

 to pursue the subject. 



I must admit that in the first instance I was much biassed in favour of Pfaundler's 

 contention, that the stenosis was merely due to a spasm of the sphincteric cylinder of 

 the pyloric canal, and that the appearance of hypertrophy was entirely due to the strong 

 degree of contraction of the muscle-fibres. Sections which I had made through other 

 contracted portions of the stomach wall had shown me how greatly thickened the 

 circular coat may become when strongly contracted. When I came, however, to 

 study the sections through the stenosed pyloric canal and compare these with normal 



