PURPOSE: Both motor and sensory dysfunction have been implicated in the pathogenesis of obstructed defecation. We have found that despite preservation of a defecatory urge, patients with obstructed defecation have lost the normal predefecatory augmentation in frequency and amplitude of colonic propagating pressure waves. This observation might be explainable by either altered rectal sensory thresholds or by dysfunction in the colonic motor apparatus. By measuring rectal sensory thresholds and proximal colonic motor responses to rectal mechanical and chemical stimuli, we tested the hypotheses that central perception of rectal stimuli is enhanced and that the proximal colonic motor response to rectal stimulation is attenuated. METHODS: In seven patients with obstructed defecation and ten healthy volunteers we measured proximal colonic motor responses and sensory thresholds in response to both rectal balloon distention and rectal instillation of chenodeoxycholic acid. RESULTS: In controls, but not in patients, rectal mechanical distention significantly reduced and chemical stimulation significantly increased the frequency of proximal colonic propagating sequences (P = 0.01). There was no significant difference in rectal sensory thresholds between patients and controls. Prior instillation of chenodeoxycholic acid significantly reduced (P < 0.03) maximum tolerated balloon volume and defecatory urge volume to comparable degree in both patients and controls. CONCLUSIONS: In obstructed defecation, 1) the normal rectocolonic pathways mediating stimulation-induced proximal colonic propagating pressure waves are nonfunctioning, and. 2) central perception of these rectal stimuli is normal.
PURPOSE: Both motor and sensory dysfunction have been implicated in the pathogenesis of obstructed defecation. We have found that despite preservation of a defecatory urge, patients with obstructed defecation have lost the normal predefecatory augmentation in frequency and amplitude of colonic propagating pressure waves. This observation might be explainable by either altered rectal sensory thresholds or by dysfunction in the colonic motor apparatus. By measuring rectal sensory thresholds and proximal colonic motor responses to rectal mechanical and chemical stimuli, we tested the hypotheses that central perception of rectal stimuli is enhanced and that the proximal colonic motor response to rectal stimulation is attenuated. METHODS: In seven patients with obstructed defecation and ten healthy volunteers we measured proximal colonic motor responses and sensory thresholds in response to both rectal balloon distention and rectal instillation of chenodeoxycholic acid. RESULTS: In controls, but not in patients, rectal mechanical distention significantly reduced and chemical stimulation significantly increased the frequency of proximal colonic propagating sequences (P = 0.01). There was no significant difference in rectal sensory thresholds between patients and controls. Prior instillation of chenodeoxycholic acid significantly reduced (P < 0.03) maximum tolerated balloon volume and defecatory urge volume to comparable degree in both patients and controls. CONCLUSIONS: In obstructed defecation, 1) the normal rectocolonic pathways mediating stimulation-induced proximal colonic propagating pressure waves are nonfunctioning, and. 2) central perception of these rectal stimuli is normal.