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Published on: February 3, 2016
Colonic motor abnormalities in slow transit constipation defined by high resolution, fibre-optic manometry
P G Dinning1, L Wiklendt, L Maslen
1Departments of Gastroenterology and Surgery, Flinders Medical Centre, Flinders University, Bedford Park, SA, Australia; St.George Hospital Clinical School, Faculty of Medicine, University of New South Wales, Kogarah, NSW, Australia.
Patients with slow transit constipation (STC) show abnormal colonic motor patterns. A meal does not stimulate normal colonic activity in STC patients, suggesting impaired neural input to the colon.
Area of Science:
- Gastroenterology
- Colorectal Physiology
- Neurogastroenterology
Background:
- Slow transit constipation (STC) is linked to colonic motor abnormalities of unclear origin.
- Healthy colons exhibit a distal propagating motor pattern (2-6 cpm) responsive to meals, indicating extrinsic neural control.
- Investigating meal responses in STC patients is crucial for understanding disease mechanisms.
Purpose of the Study:
- To characterize the colonic motor response to a meal in patients with STC.
- To compare meal-induced colonic activity in STC patients with healthy controls.
Main Methods:
- High-resolution fiber-optic manometry with 72 sensors was used in 14 STC patients and 12 healthy adults.
- Recordings were taken for 2 hours before and after a 700 kCal meal.
- Catheters were placed in the ascending or transverse colon.
Main Results:
- A cyclic propagating motor pattern was present in most STC patients before and after meals.
- Unlike in healthy individuals, meals did not significantly increase this motor pattern in STC patients (7.4 vs. 8.3 per/2h).
- Healthy subjects showed a dramatic increase in motor patterns post-meal (8.3 vs. 59.1 per/2h; p < 0.001).
Conclusions:
- Meals fail to stimulate the normal increase in distal colonic motor patterns in STC patients.
- These findings suggest attenuated extrinsic parasympathetic input to the colon in STC.
- This points to a potential neural basis for colonic dysfunction in slow transit constipation.
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