Developments in autonomic research: a review of the latest literature

Motion sickness is characterized by several autonomic signs: pallor, sweating, loss of appetite, nausea and vomiting. Gastric myoelectrical activity is reduced and gastric emptying delayed, and the high-frequency to low-frequency ratio of heart rate variability increases with motion sickness. Children showing a high incidence of vasovagal syncope during head-up tilt are also more susceptible to motion sickness, arguing strongly for a vestibular contribution to both conditions. Typically, motion sickness is caused by slow oscillatory movements (~0.2 Hz), and is considered by many to be dependent on inputs from the vestibular system. However, given that signs of motion sickness can be induced by moving visual stimuli, changes in inputs from the vestibular system are evidently not required. Indeed, visually induced motion sickness—cybersickness—is common in games relying on virtual reality. Our current understanding of motion sickness is based on the sensory conflict hypothesis, which postulates that sickness occurs when there is a mismatch between the current pattern of sensory inputs about movement of the body and the pattern that is expected on the basis of previous experience. The fluid shift hypothesis, in which shift of fluid into the head (and inner ears) has also been proposed to account for space sickness.