This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of
nausea and
vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias.
Antral distension and increased intestinal delivery of
lipids may cause slow-wave disruption and development of
nausea. This may be mediated by
cholinergic and serotonergic pathways. Similarly,
progesterone and
estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals.
Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central
cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with
motion sickness. This may be mediated by
vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of
nausea and
vomiting, the search has begun for novel
antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of
prostaglandin synthesis inhibitors, central
muscarinic receptor antagonists, and
dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically
implanted neurostimulator has shown promise in reducing
emesis in patients with
gastroparesis and gastric dysrhythmias.