Neuroendocrine and gastric myoelectrical responses to illusory self-motion in humans

Abstract

We compared gastric myoelectrical activity and endogenous neuroendocrine responses in subjects with and without motion sickness elicited by illusory self-motion or vection. Rotating a drum with black and white vertical stripes around seated stationary subjects (n = 22) produced vection. Gastric myoelectrical activity was recorded with cutaneous electrodes. Thirteen subjects developed gastric dysrhythmias [4- to 9-cycles/min (cpm) signals] and motion sickness during vection, whereas nine subjects maintained normal 3-cpm gastric rhythms and remained symptom free. Base-line plasma cortisol and beta-endorphin levels were significantly greater (P less than 0.01) in the subjects who would develop gastric dysrhythmias and nausea compared with the subjects who would not develop motion sickness. Norepinephrine levels increased in the nauseated group immediately after vection ceased (354.6 +/- 41.1 pg/ml) compared with the symptom-free subjects (223.1 +/- 22.8 pg/ml, P less than 0.05). Epinephrine increased significantly (P less than 0.05) after vection only in the nauseated subjects, whereas dopamine levels were not altered by vection in either group. We conclude that 1) anticipatory increases in plasma cortisol and beta-endorphin occurred in subjects who would develop nausea and gastric tachyarrhythmias during vection; 2) endogenous epinephrine and norepinephrine were increased in subjects who had vection-induced nausea and gastric dysrhythmias; and 3) vection stimulates brain-gut interactions, resulting in gastric tachyarrhythmias and complex neuroendocrine responses in subjects with motion sickness.

Gastric myoelectrical and autonomic cardiac reactivity to laboratory stressors

“…As expected, these patterns of autonomic response were observed in conjunction with a decrease in 3-cpm gastric myoelectrical activity and an increase in gastric tachyarrhythmia. These findings are consistent with prior motion sickness research showing that similar patterns of gastric myoelectrical reactivity are observed in conjunction with a reciprocal pattern of autonomic response (Hasler et al, 1995;Hu et al, 1991;Koch, Stern, Vasey, Seaton et al, 1990;Money et al, 1996;Uijtdehaage et al, 1992). We do not recommend, however, that inferences regarding gastric autonomic activity be made from PEP or RSA.…”

“…Furthermore, several studies have shown that the expression of gastric tachyarrhythmia during the experience of nausea is associated with an increase in sympathetic and decrease in parasympathetic activation . Prior research, for example, has shown that motion sickness-induced gastric tachyarrhythmia is associated with decreased parasympathetic cardiac activity (Hu, Grant, Stern, & Koch, 1991;Uijtdehaage, Stern, & Koch, 1992, increased skin conductance Miller, Sharkey, Graham, & McCauley, 1993), and increased plasma catecholamine levels (Koch, Stern, Vasey, Seaton et al, 1990). Prior experiments investigating the effects of laboratory stressors on gastric myoelectrical activity have shown that 3-cpm activity decreases in response to the cold pressor test (Riezzo, Porcelli, Guerra, & Giorgio, 1996;Stern, Vasey, Hu, & Koch, 1991) and viewing aversive films (e.g., limb mutilation; Stewart, 1987), and that 3-cpm activity decreases and gastric tachyarrhythmia increases during shock avoidance (Muth, Koch, Stern, & Thayer, 1999).…”

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

“…Motion or intravenous infusion of vasopressin elicited gastric dysrhythmia in humans, and the dysrhythmia was recording prior to reported nausea (Stern et al, 1987;Koch et al, 1990a;Caras et al, 1997). Gastric dysrhythmia is closely correlated with reported nausea in a variety of conditions that produce nausea, including surgery, pregnancy and chemotherapy (Pezzolla et al, 1991;Riezzo et al, 1992;DiBaise et al, 2001).…”

Gastric Arrhythmia and Nausea of Motion Sickness Induced in Healthy Japanese Subjects Viewing an Optokinetic Rotating Drum

“…Koch et al [29] have shown that subjects who subsequently develop symptoms of motion sickness when exposed to a rotating optokinetic drum have a significantly higher level of peripheral beta-endorphins than subjects who experienced no symptoms. It was suggested that central endorphins might play a role in inhibiting the development of optokinetic motion sickness.…”

“…During drum rotation, neurosensory afferent information from the vestibular and proprioceptive systems indicates no movement of the individual. Thus in susceptible subjects, the rotating drum induces a neurosensory mismatch that results in the symptoms of nausea and tachygastria and increased beta-endorphin [29], vasopressin [30,32], and epinephrine [33]. However, neurohumoral mechanisms that mediate vection-induced tachygastria are still not well understood.…”