Illusory self motion and simulator sickness

Presented here is a discussion of simulator sickness (with applications to motion sickness and space sickness) based on the notion of senses as perceptual systems, and the sensory conflict theory. Most forms of the sensory conflict theory unnecessarily propose the existence of a neural store. The neural store is thought to consist of a record of previous perceptual experiences against which currently experienced patterns of stimulation are compared. The authors seek to establish that in its most parsimonious form the sensory conflict theory does not require a construct such as the neural store. In its simpler form, the sensory conflict theory complements and extends Gibson's view of the senses as perceptual systems

Visuo-vestibular interaction in the reconstruction of travelled trajectories

We recently published a study of the reconstruction of passively travelled trajectories from optic flow. Perception was prone to illusions in a number of conditions, and not always veridical in the others. Part of the illusionary reconstructed trajectories could be explained by assuming that subjects base their reconstruction on the ego-motion percept built during the stimulus' initial moments . In the current paper, we test this hypothesis using a novel paradigm: if the final reconstruction is governed by the initial percept, providing additional, extra-retinal information that modifies the initial percept should predictably alter the final reconstruction. The extra-retinal stimulus was tuned to supplement the information that was under-represented or ambiguous in the optic flow: the subjects were physically displaced or rotated at the onset of the visual stimulus. A highly asymmetric velocity profile (high acceleration, very low deceleration) was used. Subjects were required to guide an input device (in the form of a model vehicle; we measured position and orientation) along the perceived trajectory. We show for the first time that a vestibular stimulus of short duration can influence the perception of a much longer lasting visual stimulus. Perception of the ego-motion translation component in the visual stimulus was improved by a linear physical displacement: perception of the ego-motion rotation component by a physical rotation. This led to a more veridical reconstruction in some conditions, but to a less veridical reconstruction in other conditions

Migraine and motion sickness: what is the link?

The brainstem is a structurally complex region, containing numerous ascending and descending fibres that converge on centres that regulate bodily functions essential to life. Afferent input from the cranial tissues and the special senses is processed, in part, in brainstem nuclei. In addition, brainstem centres modulate the flow of pain messages and other forms of sensory information to higher regions of the brain, and influence the general excitability of these cortical regions. Thus, disruptions in brainstem processing might evoke a complex range of unpleasant symptoms, vegetative changes and neurovascular disturbances and that, together, form attacks of migraine. Migraine is linked with various co-morbid conditions, the most prominent being motion sickness. Symptoms such as nausea, dizziness and headache are common to motion sickness and migraine; moreover, migraine sufferers have a heightened vulnerability to motion sickness. As both maladies involve reflexes that relay in the brainstem, symptoms may share the same neural circuitry. In consequence, subclinical interictal persistence of disturbances in these brainstem pathways could not only increase vulnerability to recurrent attacks of migraine but also increase susceptibility to motion sickness. Mechanisms that mediate symptoms of motion sickness and migraine are explored in this paper. The physiology of motion sickness and migraine is discussed, and neurotransmitters that may be involved in the manifestation of symptoms are reviewed. Recent findings have shed light on the relationship between migraine and motion sickness, and provide insights into the generation of migraine attacks