Gastric myoelectrical and neurohormonal changes associated with nausea during tilt-induced syncope.

Abstract

Nausea is a common prodromal symptom of neurally mediated syncope, but the biological factors linking nausea with syncope have not been studied. We aimed to characterize nausea during tilt-induced syncope by exploring related changes in gastric myoelectrical activity and plasma epinephrine, norepinephrine, and vasopressin concentrations across study phases of recumbency, tilt, syncope, and recovery. Electrogastrographic and plasma hormone changes were compared between patients with tilt-induced syncope and nausea (n=18) and control subjects (n=6) without symptoms or hemodynamic changes during tilt-table testing. Over a 4-minute period preceding syncope, sequential electrogastrography epochs demonstrated an increase over time in bradygastria (P=.003) and tachygastria (P=.014) power ratios, while the dominant frequency (P<.001) and the percent normogastria (P=.004) decreased. Syncope led to significant differences between cases and controls in electrogastrographic power ratios in each frequency range: bradygastria (P=.001), tachygastria (P=.005), and normogastria (P=.03). Nausea always followed electrogastrographic changes, and nausea resolution always preceded electrogastrographic normalization. Plasma vasopressin (676.5±122.8 vs 91.2±15.3pg/mL, P=.012) and epinephrine (434±91.3 vs 48.7±2.5pg/mL, P=.03), but not norepinephrine (P>.05), also differed with syncope between cases and controls. The nausea related to tilt-induced syncope is temporally associated with changes in gastric myoelectrical activity and increases in plasma vasopressin and epinephrine. The biological mechanisms that induce syncope are physiologically distinct from other experimental models of nausea such as illusory self-motion, yet nausea with syncope appears to have similarly associated electrogastrographic and hormone changes. Thus, tilt-induced syncope could serve as an informative experimental model for nausea research.