Intestinal motility and transit disorders

The major non-obstructive intestinal motility disorders perturb one peristalsis module. Reducing propulsive drive slows transit monotonically (slow-transit constipation), collapsing below a threshold into refractory colonic inertia. Falling ICC density gives functional pseudo-obstruction with a patent lumen, and a transient drive loss gives reversible paralytic ileus. The same ICC lesion collapses both gastric emptying and gut transit [V].

The non-obstructive intestinal motility disorders perturb the §4 peristalsis module. Reducing propulsive drive slows aboral transit monotonically (slow-transit constipation) and collapses below a threshold (colonic inertia, refractory); falling ICC density gives functional pseudo-obstruction with a patent lumen (CIPO); a transient drive loss gives reversible paralytic ileus. One ICC-depletion lesion collapses both gastric emptying (§11) and gut transit (§14). Mechanisms [V], transit anchors [L]-pending, absolute transit time [O].

The major non-obstructive intestinal motility disorders are perturbations of the single peristalsis module of §4: a slow-wave phase gradient drives a travelling occlusion wave that transports luminal content aborally. Three knobs of that one module — the propulsive drive (the aboral frequency-gradient spread), the ICC pacemaker density, and a transient drive switch — reproduce the whole group.

Reducing the propulsive drive slows aboral transit monotonically: this is slow-transit constipation, and in the model it stays responsive (a restored drive restores transit). Below a threshold the travelling wave can no longer carry content and transport collapses to near zero — colonic inertia, the refractory, treatment-resistant end of the very same axis.

Chronic intestinal pseudo-obstruction is the ICC-density lesion: as pacemaker density falls the wave weakens and propulsion fails — yet the lumen stays patent, so this is a functional, not mechanical, obstruction (there is no fixed stenosis to find). Paralytic ileus is the transient case: a global loss of slow-wave drive halts propulsion, and the model recovers transport when the drive returns — the deficit scales with how long the drive is lost (100.0% after a short loss, 7.3% after a long one), while a permanent loss gives 0.0%.

The unifying result (cross-disease hypothesis #1): one ICC-depletion lesion, many sites. The same density parameter collapses gastric emptying (§11) and intestinal transit (§14) along nearly the same curve — a single cause behind gastroparesis, slow-transit constipation, and pseudo-obstruction.

Treatment (model reading). Each disorder names its own target. Slow-transit constipation: prokinetics raise the propulsive drive and restore transit — effective in the graded regime. Colonic inertia: below the threshold a modest boost stays sub-threshold, so it is refractory to prokinetics and subtotal colectomy is the model-consistent escalation — the threshold is the falsifiable prediction. CIPO: efficacy tracks residual ICC density (no mechanical target exists). Paralytic ileus: remove the transient suppressant (opioids, post-operative inflammation, electrolyte derangement) and propulsion recovers spontaneously — the reversibility is exactly why ileus is waited out, unlike inertia.

The transit mechanisms — the graded drive axis with its inertia threshold, the functional CIPO obstruction, the reversible ileus, and the shared ICC lesion — are all forced by the substrate [V]; clinical transit-time anchors are calibration targets [L] pending; the absolute colonic transit time is open [O], needing radio-opaque-marker / scintigraphy calibration.