Intestinal motility during ontogeny and intestinal pseudo-obstruction in children

From the fragmentary studies performed to date of both functional obstruction and the ontogeny of intestinal motility, several conclusions can be drawn. The development of motor activity that is primarily dependent on neuronal activity, such as sucking, swallow-induced peristalsis of the esophagus, and cyclic fasting small intestinal motor activity, occurs according to a timetable that is similar in all species studies is gestationally dependent, but its timing during gestation is species specific. Postprandial events, including gastric emptying and continuous postprandial motor activity in the small intestine, in contrast seem to be dependent on the nature of the humoral response to food, provided that the musculature of the gut and enteric nerves are able to respond to it. Although these activities are primarily determined by neuronal development, there is a limited amount of information to suggest that their appearance may be pharmacologically manipulated to advance the timing and rate of development. It is commonplace now for cortisol to be used to induce the production of surfactant in mothers of babies who are at risk of hyaline membrane disease. A limited amount of information suggests that cortisol may have similar effects in inducing duodenal motor activity, and, thus, it may be possible to advance the timing and rate of development of intestinal motility in the very preterm infant by its use. There are, however, no studies to date to prove this. It is now clear that intestinal pseudo-obstruction is a heterogeneous disorder associated with various pathologies, some of which are intrinsic to the gut, whereas others are multisystem diseases affecting the intestine. In addition, although intestinal pseudo-obstruction was originally thought to involve the small intestine, it is now realized that it may not affect only one region, as in achalasia or Hirschsprung's disease, but also it may present diffusely throughout the gut. The motility changes caused by the disease processes are nonspecific, although neuropathic and myopathic changes are distinct and due to the destruction of the particular motor control system involved. The mechanisms of the ontogenic and disease changes described in this article are, however, almost totally unexplored. The recent upsurge of interest in the area with the development of advances in cellular and molecular biology, at least the early events, is now beginning to unravel. At the present time, the stage is being set for probably the most exciting phase of understanding of the nature of the ontogeny of intestinal motor activity, which the author expects will enable us to manipulate motor activity in normal preterm infants and, it is hoped, congenital dysmotile states.