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Chapter 14

Disturbances of Gastrointestinal Motility and the Nervous System

Michael Camilleri and Adil E. Bharucha

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Figure 14-1 Control of gut motility: interactions between extrinsic neural pathways and the intrinsic nervous system (“enteric brain” or enteric nervous system plexuses) modulate contractions of gastrointestinal smooth muscle. Interactions between transmitters (e.g., peptides and amines) and receptors alter muscle membrane potentials by stimulating bidirectional ion fluxes. In turn, membrane characteristics dictate whether the muscle cell contracts.(Adapted from Camilleri M, Phillips SF: Disorders of small intestinal motility. Gastroenterol Clin North Am 18:405, 1989, by permission of Mayo Foundation.)

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Figure 14-2 The enteric plexuses in the intestinal layers. The chief neural plexuses are in the submucosal and intermuscular layers.

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Figure 14-3 A, Tracing showing normal upper gastrointestinal motility in the fasting and fed states. The fasting tracing shows phase III of the interdigestive migrating motor complex. B, Manometric tracings showing the myopathic pattern of intestinal pseudo-obstruction due to systemic sclerosis (left panel). Note the low amplitude of phasic pressure activity compared with control (middle panel). A manometric example of neuropathic intestinal pseudo-obstruction in diabetes mellitus shows the absence of antral contractions and persistence of cyclical fasting-type motility in the postprandial period (right panel).(A from Malagelada J-R, Camilleri M, Stanghellini V: Manometric Diagnosis of Gastrointestinal Motility Disorders. Thieme, New York, 1986, by permission of Mayo Foundation. B from Camilleri M: Medical treatment of chronic intestinal pseudo-obstruction. Pract Gastroenterol 15:10, 1991, with permission.)

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Figure 14-4 Schema showing normal alternations of pelvic floor, rectoanal angle, and sphincters during defecation.(From Lembo T, Camilleri M: Chronic constipation. N Engl J Med 349:1360, 2003, with permission.)

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Figure 14-5 Algorithm for the investigation of suspected gastrointestinal (GI) dysmotility. ANA, antinuclear antibodies; ANNA, antineuronal enteric antibodies; CK, creatine kinase; CXR, chest radiograph; Ig, immunoglobulin; TSH, thyroid-stimulating hormone.(From Camilleri M: Study of human gastroduodenojejunal motility: applied physiology in clinical practice. Dig Dis Sci 38:785, 1993, with permission.)

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Figure 14-6 Assessment of thoracic vagal function by documentation of sinus arrhythmia and abdominal vagal function by the plasma pancreatic polypeptide (PP) response to modified sham feeding by chewing and spitting a bacon-and-cheese toasted sandwich.