Motion sickness is induced by unusual patterns of spatial information input, but not by a simple strong acceleration. Thus, in the process of the development of motion sickness, the disturbance of spatial orientation is noticed somewhere in the brain, leading to the expression of autonomic signs and symptoms. What part of the brain plays this key role?
Peripheral vestibular input has repeatedly been proven to be necessary for motion sickness, even for visually-evoked motion sickness. The vestibular nucleus in the brain stem where spatial information including visual and somatosensory as well as vestibular inputs converge, is the primary candidate for this key structure. In the higher brain, the limbic system, particularly the amygdala, is another candidate. In our rat animal model, bilateral amygdala lesions significantly suppressed motion sickness signs, whereas hippocampus lesions did not. Using cFos protein expression as a marker for neuronal activation, we also showed that the central nucleus of the amygdala was activated by vestibular information during the hypergravity stimulation that induced motion sickness in rats.
Involvement of the amygdala may explain some characteristic features of motion sickness, such as its diversity of signs ranging from sympathetic to parasympathetic, and its conditioned occurrence where by some susceptible persons become sick even in motionless vehicles.
