Abstract
Full-field visual rotation around the vertical axis induces a sense of self-motion (vection), optokinetic nystagmus (OKN), and, eventually, also motion sickness (MS). If the lights are then suddenly switched off, optokinetic afternystagmus (OKAN) occurs. This is due to the discharge of the velocity storage mechanism (VSM), a central integrative network that has been suggested to be involved in motion sickness. We previously showed that visually induced motion sickness (VIMS) following optokinetic stimulation is dependent on vection intensity. To shed light on this relationship, the current study investigated whether vection intensity is related to VSM activity, and thus, to the OKAN. In repetitive trials (eight per condition), 15 stationary participants were exposed to 120 s of visual yaw rotation (60°/s), followed by 90 s in darkness. The visual stimulus either induced strong vection (i.e., scene rotating normally) or weak vection (central and peripheral part moving in opposite directions). Eye movements and subjective vection intensity were continuously measured. Results showed that OKAN occurred less frequently and with lower initial magnitude in the weak-vection condition compared to the strong-vection condition. OKAN decay time constants were not significantly different. The results suggest that the stimuli that produced strong vection also enhanced the charging of the VSM. As VSM activity presumably is a factor in motion sickness, the enhanced VSM activity in our strong-vection condition hints at an involvement of the VSM in VIMS, and could explain why visual stimuli producing a strong sense of vection also elicit high levels of VIMS.
Highlights
Motion in the whole visual field induces both optokinetic nystagmus (OKN) and a compelling sense of self-motion in stationary observers
We investigated whether the optokinetic afternystagmus (OKAN), occurring after a period of optokinetic stimulation, was related to the occurrence of vection during the optokinetic stimulation
The OKAN response is a manifestation of the velocity storage mechanism (VSM) and both the VSM and vection have been associated to motion sickness
Summary
Motion in the whole visual field induces both optokinetic nystagmus (OKN) and a compelling sense of self-motion (vection) in stationary observers. Involvement of the VSM in vection has been suggested by Brandt and Dichgans (1972) and Brandt et al (1974), who showed that oculomotor and perceptual aftereffects (i.e., OKAN and vection, resp.) following full-field optokinetic stimulation are similar in terms of duration and direction, and that both show peripheral dominance These observations led Cohen et al (1977) to propose that circular vection is the result of monitoring the activity in the integrators associated with OKN and OKAN. As vection is positively related to VIMS, a comparison of OKAN responses following weak- and strong-vection-inducing stimuli sheds light on the question whether the VSM can be seen as a common denominator in vection and VIMS
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