Introduction

Bowel disturbances in patients with inflammatory bowel disease (IBD) range from abdominal pain, tenesmus, diarrhea, rectal bleeding and passage of mucus. Intestinal pseudo-obstruction and toxic megacolon can occur as frightening complications of either ulcerative colitis (UC) or Crohn's disease (CD). Altered small and large intestinal motility patterns are a possible cause of the spectrum of symptoms of which patients complain [1]. Little is known about motility alterations in IBD and, most of all, how important they are in determining the patient's symptoms. Presumably, interactions between epithelial transport and abnormal motor activity are the key mechanisms. The disparity between severity of symptoms and degree of inflammation and small hard stools often passed with blood and mucus suggest a contribution of gut dysmotility to clinical features. Evidence of altered gut motility have been reported as being not only confined to the lower gut, but also to the small intestine, stomach and gallbladder [2, 3].

Patients with IBD generally experience periods of active disease followed by resolution of the mucosal injury and healing. This may be followed by a period of inactivity or quiescence that is interrupted by an acute relapse, the most frequent symptom of which is diarrhea. Impaired colonic absorption and/or increased secretion of fluids may partially explain liquid diarrhea [4].

Factors that might be involved in dysmotility include changes in the smooth muscle cell function, changes in innervation or variations in the sensory components. Herein, we try to give an overview of what has been discovered so far on motility modifications in patients with inflammatory bowel disease and in animal models.

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