Visually induced motion sickness (VIMS) is a relevant limiting factor in the use of virtual reality (VR) devices. Understanding the origin of this problem might help to develop strategies to circumvent this limitation. Previous studies have attributed VIMS to a mismatch between visual, and vestibular information, causing ambiguity of the position of the body in relation to its surrounding. Studies using EEG have shown a shift of the power spectrum to lower frequencies while VIMS is experienced. However, little is known about the relationship between the intensity of the VIMS and the changes in these power spectra. Moreover, the effect of different varieties of VIMS on the causal relationship between brain areas is largely unknown. Here, we used EEG to study 14 healthy subjects in a VR environment who were exposed to increasing levels of mismatch between vestibular and visual information. The frequency power and the bivariate transfer entropy as a measure for the information transfer were calculated. We found a direct association between increasing mismatch levels and subjective VIMS. With increasing VIMS, the proportion of slow EEG waves (especially 1–10 Hz) increases, especially in temporo-occipital regions. Furthermore, we found a general decrease in the information flow in most brain areas but especially in brain areas involved in the processing of vestibular signals and the detection of self-motion. We hypothesize that the general shift of frequency power and the decrease in information flow while experiencing high intensity VIMS represent a brain state of a reduced ability to receive, transmit and process information. We further hypothesize that the mechanism of reduced information flow is a general reaction of the brain to an unresolvable mismatch of information. This reaction aims on transforming a currently unstable model with a high prediction error into a stable model in an environment of minimal contradictory information.
ZUSAMMENFASSUNGEine 55-jährige Patientin stellte sich zur Abklärung eines generalisierten epileptischen Anfalls in der zentralen Notaufnahme unseres Universitätsklinikums vor. Im Rahmen der weiteren Untersuchungen fielen kognitive Einschränkungen und eine axonal-demyelisierende Polyneuropathie auf. Laborchemisch war initial lediglich eine leichte Pleozytose in der Liquoruntersuchung auffällig. Im Rahmen der weiteren Abklärung der klinischen Beschwerden und der Liquorpleozytose konnte bei der Patientin infektionsserologisch eine chronisch-persistierende Treponema-pallidum-Infektion gesichert werden. Die gleiche Diagnose konnte anschließend auch bei dem Lebenspartner der Patientin gestellt werden. Bei generalisierten epileptischen Anfällen, zunehmenden kognitiven Einschränkungen und axonal-demyelinisierender Polyneuropathie unklarer Genese sollte eine Neurolues differenzialdiagnostisch erwogen und eine Liquoruntersuchung durchgeführt werden.
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