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. 2000 Winter;23(4):270-5.
doi: 10.1080/10790268.2000.11753536.

Physiologic basis of digital-rectal stimulation for bowel evacuation in patients with spinal cord injury: identification of an anorectal excitatory reflex

Affiliations

Physiologic basis of digital-rectal stimulation for bowel evacuation in patients with spinal cord injury: identification of an anorectal excitatory reflex

A Shafik et al. J Spinal Cord Med. 2000 Winter.

Abstract

Background and purpose: Although advances in rehabilitation practices, pharmacology, and surgery offer new bowel program alternatives, digital-rectal stimulation is still utilized to facilitate defecation in patients with spinal cord injury (SCI). We speculated that defecation induced by such a technique is mediated through a reflex mechanism.

Methods: The study comprised 18 healthy volunteers (10 men, 8 women, mean age 36.6 +/- 9.7 years) and 9 patients with SCI (6 men, 3 women, mean age 35.1 +/- 11.2 years). The anal canal was dilated by a balloon inflated in 2-mL increments to 10 mL, and rectal pressure response was then recorded. The test was repeated after separate block of the external and internal anal sphincters and after individual anesthetization of the anal canal and rectum.

Results: In normal subjects, the rectal pressure rose significantly (p < 0.01) with 2-mL inflation. Increases in anal dilatation effected further rectal pressure elevations (p < 0.001), although there were no significant differences among the 4-, 6-, and 10-mL distensions (p > 0.05). The rectal pressure rise occurred with external, but not with internal, sphincter paralysis. In the subjects with paraplegia, there was no rectal pressure response to the 2- and 4-mL anal dilatations, while the 6-, 8-, and 10-mL distensions effected significant pressure increases (p < 0.001, p < 0.001, p < 0.001, respectively) that did not differ significantly among the 3 distending volumes. Internal sphincter inhibition, in contrast to the external sphincter, produced no rectal pressure response. In both normal subjects and subjects with paraplegia, the rectal pressure response did not occur after individual anesthetization of the rectum and anal canal.

Conclusions: Anal dilatation induces rectal contraction through stimulation of mechanoreceptors, possibly in the internal sphincter. Rectal contraction upon anal dilatation suggests a reflex relationship that was absent on individual anesthetization of the possible 2 arms of the reflex arc: anal canal and rectum. This relationship, which we term the "anorectal excitatory reflex," appears to be evoked on digital anal dilatation. The reflex might be of diagnostic significance in defecation disorders and has the potential to be used as an investigative tool.

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