ReviewExperimental brain research2014
Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology.
Review in Experimental brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 94 citations in OpenAlex.
- Transcutaneous Auricular Vagus Nerve Stimulation for Visually Induced Motion Sickness: An eLORETA Study.Brain topography · 2024Trial
- An old approach to a novel problem: effect of combined balance therapy on virtual reality induced motion sickness: a randomized, placebo controlled, double-blinded study.BMC medical education · 2024Trial
- Virtual reality stimulation modulates saccular activity and vestibular system responses.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026Article
- From Reflexes to Prediction: Kathleen E. Cullen's Contribution to Modern Vestibular Neuroscience and Clinical Otoneurology-A Conceptual Narrative Review.Audiology research · 2026Review
- Functional brain network analysis of VR motion sickness.Experimental brain research · 2025Article
- The gut feeling in motion sickness.Communications biology · 2025Review
- Neural correlates of vestibular adaptation in cosmonauts after long duration spaceflight.NPJ microgravity · 2025Article
- Motion sickness susceptibility modulates the impact of electrical vestibular stimulation on postural control.Scientific reports · 2025Article
- Reducing motion sickness during simulated astronaut post-spaceflight water landings using anticipatory cues or postural control.NPJ microgravity · 2025Article
- Validating sensory conflict theory and mitigating motion sickness in humans with galvanic vestibular stimulation.Communications engineering · 2025Article
- The microgravity environment affects sensorimotor adaptation and its neural correlates.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- A computational model of motion sickness dynamics during passive self-motion in the dark.Experimental brain research · 2024Article
- On labyrinthine function loss, motion sickness immunity, and velocity storage.Frontiers in neurology · 2024Article
- A computational model of motion sickness dynamics during passive self-motion in the dark.Experimental brain research · 2023Article
- Recovery time from VR sickness due to susceptibility: Objective and quantitative evaluation using electroencephalography.Heliyon · 2023Article
- Modeling orientation perception adaptation to altered gravity environments with memory of past sensorimotor states.Frontiers in neural circuits · 2023Article
- Association of Lymphatic Fluid Volume in the Inner Ear of Beagle Dogs with the Susceptibility to Motion Sickness.The journal of international advanced otology · 2022Article
- Expansion to the Motion Sickness Susceptibility Questionnaire-Short Form: A Cross-Sectional Study.Journal of audiology & otology · 2022Article
- Brain and Behavioral Evidence for Reweighting of Vestibular Inputs with Long-Duration Spaceflight.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Bio-mimetic high-speed target localization with fused frame and event vision for edge application.Frontiers in neuroscience · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The origin of the internal "sensory conflict" stimulus causing motion sickness has been debated for more than four decades. Recent studies show a subclass of neurons in the vestibular nuclei and deep cerebellar nuclei that respond preferentially to passive head movements. During active movement, the semicircular canal and otolith input ("reafference") to these neurons are canceled by a mechanism comparing the expected consequences of self-generated movement (estimated with an internal model-presumably located in the cerebellum) with the actual sensory feedback. The un-canceled component ("exafference") resulting from passive movement normally helps compensate for unexpected postural disturbances. Notably, the existence of such vestibular "sensory conflict" neurons had been postulated as early as 1982, but their existence and putative role in posture control and motion sickness have been long debated. Here, we review the development of "sensory conflict" theories in relation to recent evidence for brainstem and cerebellar reafference cancelation, and identify some open research questions. We propose that conditions producing persistent activity of these neurons, or their targets, stimulate nearby brainstem emetic centers-via an as yet unidentified mechanism. We discuss how such a mechanism is consistent with the notable difference in motion sickness susceptibility of drivers as opposed to passengers, human immunity to normal self-generated movement and why head restraint or lying horizontal confers relative immunity. Finally, we propose that fuller characterization of these mechanisms and their potential role in motion sickness could lead to more effective, scientifically based prevention and treatment for motion sickness.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.