Gastric dysrhythmias: a potential objective measure of nausea

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Abstract
Nausea is a noxious, uncomfortable feeling usually located in the epigastrium. The pathophysiology of nausea encompasses brain–gut and gut–brain interaction. Nausea is associated with myoelectrical dysrhythmias of the stomach, an objective marker in the periphery. The aims of this review were to describe (1) the physiology of normal 3 cycle per minute (cpm) gastric myoelectrical activity and (2) conditions where shifts from normal 3 cpm gastric rhythms to gastric dysrhythmias are associated with the onset of nausea. Illusory self-motion, infusion of drugs such as morphine and glucagon, and ingestion of water or nutrient loads are several of the multitude of stimuli that induce acute nausea and a variety of gastric dysrhythmias such as tachygastrias (3.75–10 cpm) and bradygastrias (1.0–2.5 cpm). In nausea of motion sickness, increased nausea severity correlates with increased plasma vasopressin and epinephrine levels. Gastric dysrhythmias are also present in chronic gastrointestinal neuromuscular disorders such as gastroparesis. When gastric dysrhythmias resolve after drug or device therapies, nausea resolves. The shift in state from comfort in the epigastrium area and normal 3 cpm gastric rhythm to symptoms of nausea and gastric dysrhythmias represents dynamic gut–brain and brain–gut interactions that can be tracked by changes in gastric rhythm. Conclusions: (1) gastric dysrhythmias represent at least one peripheral mechanism underlying the symptom of nausea, and (2) gastric dysrhythmias are an objective biomarker for nausea and potential therapeutic targets for anti-nauseant therapies.

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