Emmanuel and Kamm reported on the response of behavioural treatment, biofeedback, in constipated patients (Gut 2001;49:214–19). Biofeedback is an established therapy for outlet obstruction due to paradoxical anal sphincter contraction.1 Beyond that, Emmanuel and Kamm demonstrated that slow transit constipation (STC) can also be improved by biofeedback with normalisation of the slow transit in most symptomatic responders. These results contrast with the common belief of STC as a manifestation of a panenteric disease, presumably of the enteric nervous system.
Disturbances of oesophageal motility, gastric emptying, small bowel transit, and gall bladder motility have been described.2 Dysmotility of the small intestine has been thoroughly investigated by manometry in STC patients3,4 Disturbed motility—for example, abnormal configuration or disturbed aboral migration of phase III of the migrating motor complex, bursts, and sustained uncoordinated activity—occur in up to 60% of these patients. In our recent study5 using long term small bowel manometry in 30 clinical STC patients, disturbed aboral migration of phase III was present in 47%, and bursts/sustained uncoordinated activity occurred in 33% of patients, respectively.
It is well established that these manometric findings are markers of a neuropathy of the myenteric plexus and occur in an identical way in patients with chronic intestinal pseudo-obstruction of neuropathic origin. Furthermore, treatment by colectomy has been reported to result in excellent long term outcome in 90% of patients with dysmotility limited to the colon whereas patients with generalised intestinal dysmotility experience a sustained relief in only 13%.6 It is hard to understand how these manifestations of neuropathy, especially in the myenteric plexus of the small intestine, can be successfully treated by biofeedback therapy.
An alternative explanation is that STC is an inhomogeneous group of different aetiologies. In transit studies, slow transit can be the result of a right sided or global delay (the “classical” finding in idiopathic STC), a left sided delay, or a rectal marker accumulation.7 In physiological evaluation, an overlap of slow transit and outlet obstruction can be seen in some patients.8 At least in healthy volunteers, voluntary suppression of defecation resulted in a marked prolongation of colonic transit.9
Of the 22 slow transit patients studied by Emmanuel and Kamm, seven had marker retention predominantly in the rectosigmoid, 13 had a paradoxical sphincter contraction as a marker of outlet obstruction, and seven could not expel a balloon during simulated defecation. In contrast, in our study of small bowel manometry in slow transit patients,5 all patients demonstrated a right sided or global delay and had no signs of outlet obstruction.
Thus the response of behavioural treatment, biofeedback, in constipated patients with slow transit might be influenced by the existence of more than one disease as a possible aetiology of STC. We are looking forward to seeing data on the response of biofeedback therapy in patients with STC with and without pathological small bowel manometry.
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