Thesis defence : Merrick DIDA

The aetiology of motion sickness (kinetosis) has been the subject of two major theoretical approaches. According to Reason (1978), kinetosis is caused by sensory conflicts arising during movement of the individual in relation to the environment. In contrast, Riccio and Stoffregen (1991) consider that kinetosis is caused by instabilities in postural control. Numerous experimental and modelling studies have been carried out to establish a relationship between postural stability and susceptibility to kinetosis. Although a cause-and-effect relationship has yet to be demonstrated, recent studies suggest that people suffering from motion sickness have a deficit in the selection and reweighting of sensory information to cope with changes in the environment. In this thesis, we studied how postural adaptation develops and how multisensory integration dynamics are modulated according to the degree of susceptibility to kinetosis.

We used a postural task in which participants stood on a posturographic platform with eyes open (YO) or eyes closed (YF) for three minutes. The platform was static during the first minute (baseline phase), oscillated harmonically or was controlled by the ankle angle during the second minute (disturbance phase), and returned to its stable state during the third minute (disruption phase). back). We calculated the power spectral density (PSD) of the anterior-posterior component of the center of pressure over a sliding time window of 10 seconds duration. In the first experiment (oscillation disturbance), principal component (PC) analysis was applied to the PSDs. The results showed that participants less susceptible to motion sickness (measured by the Motion Sickness Susceptibility Questionnaire) had a similar spectral balance in the YO and YF conditions. In contrast, susceptible participants showed a decrease in spectral balance in the YF condition compared to the YO condition. Furthermore, with their eyes closed, people less susceptible to motion sickness returned much later to their reference spectrum. These results suggest that low-susceptibility participants finely adjust their spectrum in the disturbance phase (i.e. reweighting) and therefore take longer to return to their initial postural control, particularly with eyes closed. There is therefore a relationship between the alteration of the capacity for sensory reweighting and susceptibility to motion sickness. In the second experiment (eyes closed, servo-controlled disturbance), energy ratios between the high (0.7 to 1.3 Hz) and low (0.1 to 0.7 Hz) frequency bands were calculated over key time windows. The results revealed a negative correlation between susceptibility to motion sickness (i.e. motion sickness in a car) and the difference in ratio between the end of the disturbance phase and the return to a stationary situation. These results are discussed in terms of differences in vestibular and proprioceptive reweighting dynamics. However, when visual information is available (experiment 3), this correlation becomes non-significant. Although it is widely accepted that the origin of motion sickness is closely linked to the functioning of the vestibular system, Experiments 1 and 2 highlighted the role of visual information for susceptible participants. While most studies in the literature on the relationship between motion sickness and postural control have subjected participants to nauseating situations, our results highlight a relationship between impaired sensory reweighting capacity and susceptibility to motion sickness. in situations that do not induce symptoms. Sensory weighting as well as sensory reorganization capacity could be predictive factors of susceptibility to motion sickness.

Under the supervision of Michel GUERRAZ, University Professor, University of Savoie Mont-Blanc - and Rafael LABOISSIÈRE - Researcher, CNRS Délégation Alpes - Thesis co-director

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