Reciprocal inhibitory visual-vestibular interaction : Visual motion stimulation deactivates the parieto-insular vestibular cortex

• Published in: Brain (London, England : 1878) Vol. 121; no. 9; pp. 1749 - 1758
• Main Authors: BRANDT, T, BARTENSTEIN, P, JANEK, A, DIETERICH, M
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.09.1998; Oxford Publishing Limited (England)
• Subjects: Adult; Biological and medical sciences; Brain Mapping; Cerebral Cortex - physiology; Cerebrovascular Circulation - physiology; Female; Fundamental and applied biological sciences. Psychology; Head Movements - physiology; Humans; Male; Middle Aged; Motion Perception; Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration; Photic Stimulation; Psychomotor Performance - physiology; Reference Values; Regional Blood Flow; Space life sciences; Tomography, Emission-Computed - methods; Vertebrates: nervous system and sense organs; Vestibule, Labyrinth - physiology; Visual Cortex - physiology; Radionuclide study; Human; Visual cortex; Reciprocal inhibition; Vection; Vestibular cortex; Physiology; Brain (vertebrata); Positron; Emission tomography
• ISSN: 0006-8950; 1460-2156; 1460-2156
• DOI: 10.1093/brain/121.9.1749

The vestibular system--a sensor of head accelerations--cannot detect self-motion at constant velocity and thus requires supplementary visual information. The perception of self-motion during constant velocity movement is completely dependent on visually induced vection. This can be linear vection or circular vection (CV). CV is induced by large-field visual motion stimulation during which the stationary subject perceives the moving surroundings as being stable and himself as being moved. To determine the unknown cortical visual-vestibular interaction during CV, we conducted a PET activation study on CV in 10 human volunteers. The PET images of cortical areas activated during visual motion stimulation without CV were compared with those with CV. Hitherto, CV was explained neurophysiologically by visual-vestibular convergence with activation of the vestibular nuclei, thalamic subnuclei and vestibular cortex. If CV were mediated by the vestibular cortex, one would expect that an adequate visual motion stimulus would activate both the visual and vestibular cortex. Contrary to this expectation, it was shown for the first time that visual motion stimulation with CV not only activates a medial parieto-occipital visual area bilaterally, separate from middle temporal/medial superior temporal areas, it also simultaneously deactivates the parieto-insular vestibular cortex. There was a positive correlation between the perceived intensity of CV and relative changes in regional CBF in parietal and occipital areas. These findings support a new functional interpretation: reciprocal inhibitory visual-vestibular interaction as a multisensory mechanism for self-motion perception. Inhibitory visual-vestibular interaction might protect visual perception of self-motion from potential vestibular mismatches caused by involuntary head accelerations during locomotion, and this would allow the dominant sensorial weight during self-motion perception to shift from one sensory modality to the other.