Overview
Clinical Meaning
GI motility is coordinated by the enteric nervous system (ENS, containing approximately 100 million neurons — often called the second brain) working in concert with interstitial...
GI motility is coordinated by the enteric nervous system (ENS, containing approximately 100 million neurons — often called the second brain) working in concert with interstitial cells of Cajal (ICCs), smooth muscle cells, and extrinsic autonomic innervation. ICCs function as the GI pacemaker cells, generating slow wave electrical rhythms that set the baseline frequency of smooth muscle contraction: 3 cycles per minute in the stomach, 12 per minute in the duodenum, and 8 per minute in the ileum. Slow waves alone do not cause contraction — superimposed spike potentials (triggered by ACh from excitatory myenteric motor neurons) must reach threshold to generate contractile force. The migrating motor complex (MMC) is the fasting motility pattern that sweeps undigested residue and bacteria distally every 90-120 minutes in four phases; motilin (released from duodenal M cells) triggers the powerful Phase III contractions, which is why erythromycin (a motilin receptor agonist) is used as a prokinetic agent. Gastroparesis results from damage to any component of this system: diabetic autonomic neuropathy destroys vagal afferents and efferents and causes ICC loss through oxidative stress; post-viral gastroparesis...