CENTRAL CONTROL OF DIGESTIVE FUNCTION 



.67 



testinal motility might indicate that sensory fibers 

 from the stomach also project to this area. 



Another group of cortical structures which seems 

 to be connected with gastrointestinal motor coordina- 

 tion consists of the subgenual portion of the cingulate, 

 the olfactory fibers and the amygdaloid nuclei. 

 Changes in gastric motility on stimulation of one or 

 more of these areas have been observed by se\eral 

 authors (4, 8, 10, 29, 50, 51, 83, 85, 88). These areas 

 may all be part of the same system, and the variation 

 in stimulation effects may be due to variations in the 

 tone of the gastrointestinal tract or to interaction at 

 the brain-stem lev-el. It is also possible to affect gas- 

 tric movements from the sensorimotor corte.x, an 

 influence which may be exerted via the reticular 

 formation. It must be remembered that all of the 

 areas implicated, with the exception of a parietal 

 region described by Eliasson (29), are parts of the 

 cortical areas shown by French et al. (33) to project 

 to the brain stem. The stimulatory effect would then 

 not indicate that these cortical regions are specifically 

 concerned with gastrointestinal regulation. The lack 

 of known projections to the cortical regions dis- 

 cussed (with the exception of the orbital surface) 

 would speak against their specificity. The cingulate 

 cortex is the only part the removal of which seems to 

 lead to increased gastric motility (9). 



The hypothalamus was early implicated in the 

 control of gastrointestinal activity. The earlier litera- 

 ture and the evidence for and against the existence of 

 sympathetic and parasympathetic centers in the 

 anterior and posterior parts of the hypothalamus were 

 reviewed by Sheehan in 1939. Strom & Uvnas (88) 

 and Eliasson (30) found it possible to change the 

 gastrointestinal response to hypothalamic stimula- 

 tion by moving the electrode as little as i mm and 

 could not confirm the division into sympathetic and 

 parasympathetic regions. Probably both afferent and 

 efferent pathways from and to the gastrointestinal 

 tract pass via the hypothalamus, and the richness of 

 responses to electrical stimulation may be due to the 

 large numbers of fibers and cells in one small region. 

 Some of the fibers must synapse since removal of the 

 cortex does not influence the response to electrical 

 stimulation of the hvpothalamus. The changes in 

 intestinal motility that occur on electrical stimulation 

 indicate that adjacent segments of the aliiTientary 

 canal change their motility in the same direction (88). 

 This is not compatible with a normal regulatory func- 

 tion, and it is likely that the intestinal canal under 

 physiological circumstances is relatively independent 

 of central nervous system impulses. 



VOMITING 



\'omiting can be considered as an extremely com- 

 plicated reflex act in which, in response to afferent 

 stimulation, a coordinated reflex involving striated 

 muscles, gastric musculature, respiratory movements 

 and vasomotor reflexes takes place. If a center is to be 

 accepted, this must be localized in the place where 

 immediate connection with all of these different 

 motor neurons are available. This system is not as 

 complicated in lower animals as in man. In the lower 

 animal the expulsion of the food contents of the stom- 

 ach is mainly effected through rapid contraction of the 

 gastric musculature with concomitant opening of the 

 cardia or related structures (42). Most of the experi- 

 mental work in this field has been done on cats and 

 dogs. The earlier investigators thought that there 

 might possibly be two centers, one being responsive to 

 morphine, the other to copper salts. This was dis- 

 proved by Thumas (90) who localized a vomiting 

 center in the dog with definite anatomical limits. 

 He found a small area in the posterior part of the 

 rhomboid fossa vvhicli was more sensitive to the emetic 

 action of apomorpliine than any other and which on 

 destruction made the dog insensitive to the action of 

 apomorpliine. Hatcher & Weisz (43) in repeating 

 Thumas" experiments were led to believe that the 

 true vomiting center was localized in the dorsal 

 nucleus of the vagus nerve. The area localized by 

 Thumas would then be only on tiie pathway for the 

 impulses which induce vomiting. 



From the large number of reflex impulses reaching 

 the dorsal vagus nucleus one would expect vomiting 

 and retching to occur frequently. This apparent con- 

 flict was avoided by the postulate that impulses must 

 arrive to the center at the same time from more than 

 one source. 



Koppanyi (53) working with Hatcher demonstrated 

 that destruction of the vagal nuclei did not interfere 

 with the occurrence of vomiting. Only during the 

 first days after the operation, when edema was prob- 

 ably still present, was there an increased threshold 

 to apomorpliine. Attempts to elicit vomiting by elec- 

 trical stimulation of medullary structures failed con- 

 sistently for several years. The reason for this seems 

 to have been the difficulty to elicit vomiting in anes- 

 thetized animals. More recently, Borison & Wang 

 (16) were able to elicit vomiting in the decerebrated 

 animal in about 50 per cent of cases. They localized a 

 region in the dorsal lateral part of the reticular 

 formation of the medulla the stimulation of which 

 resulted in projectile vomiting. Maximal inspiration 

 occurred simultaneously. No prodromal signs, such 



