Gallbladder hypomotility provides opportunity for crystallization, aggregation of crystals, and
growth to macroscopic stones from supersaturated bile. Gallbladder hypomotility may be determined in patients and controls by ultrasound or nuclear medicine studies of fasting volume, ejection volume, and contracted volume. Although there is great overlap of values, asymptomatic cholesterol gallstone patients, in general, have greater fasting and postprandial gallbladder volume and decreased percent gallbladder emptying compared to gallstone-free individuals.5 Greater fasting volume and decreased percent emptying of the gallbladder persist 1 year after dissolution of stones by oral ursodeoxycholic acid therapy, suggesting that altered gallbladder function is not necessarily caused by the stones, but may be an underlying disorder. On the other hand, studies in animal gallstone models reveal that supersaturated bile induces defects in contractility of gallbladder muscle, implying that motility defects may be a result of an abnormality in bile. Gallbladder muscle from patients with cholesterol stones has increased membrane cholesterol/phospholipid ratio and decreased membrane fluidity resulting in impaired muscle contractility.6 These abnormalities are corrected by removing the excess cholesterol from the plasma membranes. Gallstones and Gallbladder Disorders 25 Impaired gallbladder emptying and increased incidence of gallstones occur in the latter part of pregnancy, in individuals treated with oral contraceptives or somatostatin, following spinal cord injury, with diabetes mellitus, after vagotomy, and in patients receiving long-term parenteral nutrition. These associations suggest that alteration of gallbladder motility contributes to gallstone formation. In none of these situations, however, is gallbladder hypomotility likely to be the only factor leading to stone formation. For instance, patients with severe spinal cord injury have a threefold increase in risk of gallstones, but these patients may have disorders of gastric, duodenal, and colonic motility; dietary changes; muscle atrophy; and weight loss, in addition to decreased gallbladder motility.