Management of Fecal Incontinence by Massimo Mongardini & Manuel Giofrè

Author:Massimo Mongardini & Manuel Giofrè
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

9.5 Mechanism of Action

Anorectal and pelvic floor innervation is derived from both the autonomic and the somatic nervous systems. Motor innervation of the levator ani muscle and puborectalis sling originates in the sacral nerve roots (S2-S5) [54–56]. The external anal sphincter muscle is mainly innervated by a branch of the pudendal nerve, the inferior rectal nerve [54]. Autonomic innervation is both sympathetic and parasympathetic. Parasympathetic innervation is through the pelvic plexus, derived from the sacral nerves (S2-S4) [54]. Anal and distal rectal sensory innervation is mainly through the pudendal nerve [57]. Electrical stimulation of this dual innervation seems to excite both systems and cause both direct and reflex-mediated responses in the fecal continence mechanism [58, 59]. The exact mechanism of action of SNS in the treatment of bowel and urinary dysfunctions is not completely understood. Most of the studies were conducted in patients affected by urinary dysfunctions. For infants, who have not yet achieved voluntary control, a critical level of bladder distention is required to stimulate the voiding reflex. This sensory input, on reaching the pontine micturition center, simultaneously allows for a coordinated detrusor contraction and concomitant urethral relaxation. Gaining voluntary control, the voiding reflex becomes a complex process mediated at a higher level in the cerebral cortex. Voluntary voiding is a result of inhibition of the sympathetic system and activation of the sacral parasympathetic system [60]. For patients with urinary retention, SNS is believed to activate the pudendal nerve afferents originating from the pelvic organs into the spinal cord. At the level of the spinal cord, pudendal afferents may turn on voiding reflexes by suppressing exaggerated guarding reflexes, thus relieving the symptoms of patients with urinary retention. Research with positron emission tomography (PET) scans in urge-incontinent individuals suggests that SNS influences brain areas involved in bladder alertness and awareness [61]. In patients with fecal incontinence, limited information is available to explain the mechanism of action. A small study demonstrated that SNS was associated with higher tolerance of rectal distention, but the neurologic mechanism behind this is unclear [62]. Probably, the pudendal afferent somatic fibers work by inhibiting colonic propulsive activity and activating the internal anal sphincter [63]. The action on colonic motility may explain why patients with significant anal sphincter defects may benefit from SNS. Nevertheless, chronic constipation is also an approved indication for SNS in Europe. Dinning et al. have demonstrated increased colonic peristalsis and frequency of bowel movements in slow-transit constipation patients with SNS stimulation [64, 65]. As with the bladder, it is difficult to understand how SNS may be effective in both bowel storage and emptying disorders.

Download

Copyright Disclaimer:
This site does not store any files on its server. We only index and link to content provided by other sites. Please contact the content providers to delete copyright contents if any and email us, we'll remove relevant links or contents immediately.