The relation of motion sickness to the spatial?temporal properties of velocity storage

Abstract

Tilting the head in roll to or from the upright while rotating at a constant velocity (roll while rotating, RWR) alters the position of the semicircular canals relative to the axis of rotation. This produces vertical and horizontal nystagmus, disorientation, vertigo, and nausea. With recurrent exposure, subjects habituate and can make more head movements before experiencing overpowering motion sickness. We questioned whether promethazine lessened the vertigo or delayed the habituation, whether habituation of the vertigo was related to the central vestibular time constant, i.e., to the time constant of velocity storage, and whether the severity of the motion sickness was related to deviation of the axis of eye velocity from gravity. Sixteen subjects received promethazine and placebo in a double-blind, crossover study in two consecutive 4-day test series 1 month apart, termed series I and II. Horizontal and vertical eye movements were recorded with video-oculography while subjects performed roll head movements of approx. 45 degrees over 2 s to and from the upright position while being rotated at 138 degrees /s around a vertical axis. Motion sickness was scaled from 1 (no sickness) to an endpoint of 20, at which time the subject was too sick to continue or was about to vomit. Habituation was determined by the number of head movements that subjects made before reaching the maximum motion sickness score of 20. Head movements increased steadily in each session with repeated testing, and there was no difference between the number of head movements made by the promethazine and placebo groups. Horizontal and vertical angular vestibulo-ocular reflex (aVOR) time constants declined in each test, with the declines being closely correlated to the increase in the number of head movements. The strength of vertiginous sensation was associated with the amount of deviation of the axis of eye velocity from gravity; the larger the deviation of the eye velocity axis from gravity, the more severe the motion sickness. Thus, promethazine neither reduced the nausea associated with RWR, nor retarded or hastened habituation. The inverse relationship between the aVOR time constants and number of head movements to motion sickness, and the association of the severity of motion sickness with the extent, strength, and time of deviation of eye velocity from gravity supports the postulate that the spatiotemporal properties of velocity storage, which are processed between the nodulus and uvula of the vestibulocerebellum and the vestibular nuclei, are likely to represent the source of the conflict responsible for producing motion sickness.

Reducing pain by moving? A commentary on Ferrè et al. 2013

“…To quantify the possible influence of motion sickness on our results, we monitored its level after each stimulation trial using a simplified Pensacola scale from 0 to 20 (Dai, Kunin, Raphan, & Cohen, 2003).…”

Human Yaw Rotation Aftereffects with Brief Duration Rotations Are Inconsistent with Velocity Storage

“…Given that derangements in velocity storage have been implicated as a mechanism of human pathology (Dai et al 2003;Bertolini et al 2012), it is also possible that derangements in vestibular aftereffects could also give risk to clinically significant pathology such as motion sickness or motion intolerance.…”

Labyrinthine lesions and motion sickness susceptibility

“…A critical characteristic of the velocity storage integrator is its orienting properties, which tend to align the spatial response vector of eye velocity during rotation with the velocity storage orientation vector, which is close to the gravitational vertical (Dai et al 1991;Raphan and Sturm 1991;Raphan et al 1992;Raphan and Cohen 2002). Based on data obtained from experiments utilizing roll while rotating, we postulated that motion sickness susceptibility is dependent on the indirect velocity storage pathway, i.e., on the aVOR time constant and is not reliant on the direct pathway, i.e., on the gain of the aVOR Dai et al 2003).…”

“…The stimulus alternately brings the vertical and horizontal canals into and out of the plane of rotation, causing subjects to feel tumbling or pitching, disorientation, and nausea, which can finally result in vomiting. The number of head movements that subjects make before overwhelming nausea has been widely used as an operational definition of motion sickness susceptibility (Lackner and Graybiel 1994;Clément et al 2001;Young et al 2001;Dai et al 2003). A motion sickness score can also be calculated to characterize the level of motion sickness (Miller and Graybiel 1969;Hecht et al 2001;Young et al 2001).…”