Abstract
Even though reciprocal inhibitory vestibular interactions following visual stimulation have been understood as sensory-reweighting mechanisms to stabilize motion perception; this hypothesis has not been thoroughly investigated with temporal dynamic measurements. Recently, virtual reality technology has been implemented in different medical domains. However, exposure in virtual reality environments can cause discomfort, including nausea or headache, due to visual-vestibular conflicts. We speculated that self-motion perception could be altered by accelerative visual motion stimulation in the virtual reality situation because of the absence of vestibular signals (visual-vestibular sensory conflict), which could result in the sickness. The current study investigated spatio-temporal profiles for motion perception using immersive virtual reality. We demonstrated alterations in neural dynamics under the sensory mismatch condition (accelerative visual motion stimulation) and in participants with high levels of sickness after driving simulation. Additionally, an event-related potentials study revealed that the high-sickness group presented with higher P3 amplitudes in sensory mismatch conditions, suggesting that it would be a substantial demand of cognitive resources for motion perception on sensory mismatch conditions.
Highlights
Vestibular end organs initiate self-motion by sensing linear and angular accelerations rather than by sensing constant velocity (Lishman and Lee, 1973)
Several studies have shown that visual signals processed in the primary visual cortex (V1) are relayed to higher-level visual processing regions, including the Temporal Dynamics of Visually Induced Motion Perception medial temporal gyrus (MT/V5), medial superior temporal region (MST+), dorsomedial area, cingulate sulcus visual area, precuneus motion area, parietoinsular vestibular cortex (PIVC), and ventral intraparietal region (VIP), which all contribute to motion perception (Duffy and Wurtz, 1991; Bradley et al, 1996; Brandt et al, 1998; Fasold et al, 2002)
Cortical areas stimulated by visual signals are activated by vestibular inputs (Brandt et al, 1998; Fasold et al, 2002), which suggests that dynamic sensory reweighting between these multisensory cortices could occur during motion perception
Summary
Vestibular end organs initiate self-motion by sensing linear and angular accelerations rather than by sensing constant velocity (Lishman and Lee, 1973). Several studies have shown that visual signals processed in the primary visual cortex (V1) are relayed to higher-level visual processing regions, including the Temporal Dynamics of Visually Induced Motion Perception medial temporal gyrus (MT/V5), medial superior temporal region (MST+), dorsomedial area, cingulate sulcus visual area, precuneus motion area, parietoinsular vestibular cortex (PIVC), and ventral intraparietal region (VIP), which all contribute to motion perception (Duffy and Wurtz, 1991; Bradley et al, 1996; Brandt et al, 1998; Fasold et al, 2002). Cortical areas stimulated by visual signals are activated by vestibular inputs (Brandt et al, 1998; Fasold et al, 2002), which suggests that dynamic sensory reweighting between these multisensory cortices could occur during motion perception. Deactivation patterns in the vestibular cortices (PIVC and deep posterior insula) were observed during optic flow stimulation (Brandt et al, 1998)
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