Electrical stimulation of the gastrointestinal (GI) tract is an attractive concept. Since these organs have their own natural pacemakers, the electrical signals they generate can be altered by externally delivering electric currents by intramuscular, serosal, or intraluminal electrodes to specific sites in the GI tract.

Different methods of electrical stimulation have been derived from the variation of stimulation parameters, including long-pulse stimulation, short-pulse stimulation, and stimulation with a train of pulses. Electroacupuncture may also be considered as a methodologic variation of electrical stimulation because electrical stimuli are delivered by needles inserted into acupuncture points associated with the gastrointestinal tract [1].

Patients with slow transit constipation accounted from 5 to 15 % of the constipated population [2], and severe constipation (e.g., bowel movements only twice a month) is seen mainly in young women.

Several studies showed the positive effects of direct colonic stimulation in animal models [3–6].

A recent paper of Martellucci and Valeri [7] reported the first description of a permanent colonic pacing in two young female patients affected by severe slow transit constipation.

The number of bowel movements per week increased from 0.3 to 3.5 in the first patient and from 0.5 to 2.5 in the second patient. Both patients no longer needed laxatives, enemas, or any other treatments.

The two electrodes were placed laparoscopically and under endoscopic control in the muscular layer of the rectosigmoid junction, and then connected to a left inguinal subcutaneous stimulator.

According to the results of Shafik, the presence of a rectosigmoid junction pacemaker and a colosigmoid functional sphincter, regulated by rectosigmoid and recto-colic reflexes, suggested a possible target site for electrical stimulation [8].

The role of the sigmoid colon in the pathophysiology of slow transit constipation is well known, even if not completely clear, considering that megacolon (mainly left) is the main clinical finding in Hirschsprung’s disease, that a dolicho-megacolon (mainly left) is a common feature of patients affected by chronic slow transit constipation, that diverticular disease manifests in left and sigmoid colon, and that an incomplete sigmoid resection for diverticulitis exposes to a higher recurrence rate.

Even if the extent of colonic innervation is still under debate, it is generally believed that vagal innervation to the large bowel terminates at the level of the splenic flexure, while the remainder of the colon, including the rectum, receives parasympathetic input from the pelvic nerves (PN).

A pattern of dual, coordinated, parasympathetic innervation in the left colon may regulate motor activity between the proximal colon and rectum.

The distal colon and rectum also receives sympathetic input from the hypogastric nerves (HGN), mainly derived from the lumbar preganglionic outflow that runs to the inferior mesenteric ganglia (hypogastric ganglion). The innervation and functional role of the HGN on the internal anal sphincter has been well studied. However, it still remains unclear how the HGN regulates colorectal motility.

All these observations suggested that slow transit constipation (or certainly some cases) could be related to conflicting neurogenic input received by the left/sigmoid colon and maybe associated with (or the cause of) hypogangliosis and interstitial cell alteration.

Even if the results are promising, deeper neurophysiopathological studies are needed for a better understanding of the colonic motor function, and further studies with a larger number of patients and a longer follow-up are required.

Dorsal genital nerve (DGN) stimulation has also been investigated as a method against bowel dysfunction. The pudendal nerve dorsal genital branch carries afferent fibers, and it is easily accessible peripherally.

Some studies have analyzed the effect of DGN stimulation for the treatment of fecal incontinence in patients with pudendal neuropathy and idiopathic FI.

In the results of Binnie and colleagues [9], this stimulation results in an immediate rise in the pressure in the anal canal and a significant increase in the electromyographic activity of the external anal sphincter. Maintenance of the stimulus over a 2-month period raised the mean resting pressure significantly in the anal canal and increased the reflex and voluntary responses of the external anal sphincter to coughing and squeezing actions, respectively. The length of the sphincter was not affected. There was widening of the mean motor unit potential duration, though this was not significant. The resting electromyogram was enhanced after the course of treatment, indicating greater spontaneous activity in the external sphincter. In their series, seven of the eight patients studied became continent at the end of the treatment.

Only after about 15 years, Frizelle et al. [10] confirmed these results. In their study biofeedback using a pudendal nerve stimulator comprising a bipolar electrode was applied to the base of the clitoris or penis. Electrical pulse voltage was self-titrated and defined periods of treatment were prescribed. Anorectal manometry and Cleveland incontinence scores were assessed.

There was a significant reduction in incontinence symptom score after pudendal nerve stimulator treatment in the 42 patients treated. This was accompanied by significant improvements in anal sphincter tone, maximal tolerated rectal volume, and the sustained rectoanal inhibitory reflex.

However, Worsøe and colleagues [11] confirmed the efficacy of the treatment but found conflicting functional results. Stimulation was applied twice daily for 3 weeks at the maximal tolerable stimulation amplitude (pulse width, 200 μs; pulse rate, 20 Hz). FI severity scores, FI Severity Visual Analogue Score (VAS), FI Quality of Life Score (FIQL), sphincter function, and rectal volume tolerance were assessed at baseline, immediately after stimulation and 3 weeks after stimulation.

The Wexner score and the St. Mark’s score improved after stimulation in seven and six of the patients and improvement was maintained 3 weeks after stimulation. The number of incontinent episodes was reduced in seven out of nine patients. Improvement was maintained for 3 weeks after stimulation. Interestingly, subjective assessments of FI severity using the VAS score and the FIQL score did not improve during stimulation. Sphincter function and rectal volume tolerability were unaffected.

Moreover the same authors, comparing stimulated with unstimulated phasic distension, found no significant difference in the median rectal cross-sectional area (CSA) measured with impedance planimetry. Comparing stimulated with unstimulated stepwise distension, there was no significant difference in the median rectal CSA. Neither the rectal pressure-CSA relationship (CSA/P(R)) nor the rectal wall tension changed during stimulation. No acute effect on rectal CSA during pressure-controlled distension was demonstrated during DGN stimulation [12].