Sensory conflict in motion sickness: An observer theory approach

Motion sickness is the general term describing a group of common nausea syndromes originally attributed to motion-induced cerebral ischemia, stimulation of abdominal organ afferent, or overstimulation of the vestibular organs of the inner ear. Sea-, car-, and airsicknesses are the most commonly experienced examples. However, the discovery of other variants such as Cinerama-, flight simulator-, spectacle-, and space sickness in which the physical motion of the head and body is normal or absent has led to a succession of sensory conflict theories which offer a more comprehensive etiologic perspective. Implicit in the conflict theory is the hypothesis that neutral and/or humoral signals originate in regions of the brain subversing spatial orientation, and that these signals somehow traverse to other centers mediating sickness symptoms. Unfortunately, the present understanding of the neurophysiological basis of motion sickness is far from complete. No sensory conflict neuron or process has yet been physiologically identified. To what extent can the existing theory be reconciled with current knowledge of the physiology and pharmacology of nausea and vomiting. The stimuli which causes sickness, synthesizes a contemporary Observer Theory view of the Sensory Conflict hypothesis are reviewed, and a revised model for the dynamic coupling between the putative conflict signals and nausea magnitude estimates is presented. The use of quantitative models for sensory conflict offers a possible new approach to improving the design of visual and motion systems for flight simulators and other virtual environment display systems

Spatial orientation and navigation in microgravity

Manuscript for Spatial Processing in Navigation, Imagery and Perception, F. Mast and L. Janeke, eds.This chapter summarizes the spatial disorientation problems and navigation difficulties described by astronauts and cosmonauts, and relates them to research findings on orientation and navigation in humans and animals. Spacecraft crew are uniquely free to float in any relative orientation with respect to the cabin, and experience no vestibular and haptic cues that directly indicate the direction of “down”. They frequently traverse areas with inconsistently aligned visual vertical cues. As a result, most experience “Visual Reorientation Illusions” (VRIs) where the spacecraft floors, walls and ceiling surfaces exchange subjective identities. The illusion apparently results from a sudden reorientation of the observer’s allocentric reference frame. Normally this frame realigns to local interior surfaces, but in some cases it can jump to the Earth beyond, as with “Inversion Illusions” and EVA height vertigo. These perceptual illusions make it difficult for crew to maintain a veridical perception of orientation and place within the spacecraft, make them more reliant upon landmark and route strategies for 3D navigation, and can trigger space motion sickness. This chapter distinguishes VRIs and Inversion Illusions, based on firsthand descriptions from Vostok, Apollo, Skylab, Mir, Shuttle and International Space Station crew. Theories on human “gravireceptor” and “idiotropic” biases, visual “frame” and “polarity” cues, top-down processing effects on object orientation perception, mental rotation and “direction vertigo” are discussed and related to animal experiments on limbic head direction and place cell responses. It is argued that the exchange in perceived surface identity characteristic of human VRIs is caused by a reorientation of the unseen allocentric navigation plane used by CNS mechanisms coding place and direction, as evidenced in the animal models. Human VRI susceptibility continues even on long flights, perhaps because our orientation and navigation mechanisms evolved to principally support 2D navigation.NASA Cooperative Research Agreement NCC9-58 with the National Space Biomedical Research Institut

Brainstem processing of vestibular sensory exafference: implications for motion sickness etiology

Penultimate version of manuscript accepted 4/20/14, and after minor edits, published online May 18, 2014 at Springer Online First as DOI 10.1007/s00221-014-3973-2The 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 is cancelled 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-cancelled 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, motion sickness has been long debated. Here we review the development of “sensory conflict” theories in relation to recent evidence for brainstem and cerebellar reafference cancellation, and identify some open research questions. We propose that conditions producing persistent activity of these neurons, or their targets, stimulates 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.Dr. Oman was supported in part by the National Space Biomedical Research Institute through NASA NCC 9-58. Dr. Cullen’s research was supported by the Canadian Institutes of Health Research (CIHR), the National Institutes of Health (DC002390), and the Fonds Que´be´cois de la Recherche sur la Nature et les Technologies (FQNRT), and US National Institute of Health Grant R01 DC239

Neurovestibular Effects of Long-Duration Spaceflight: A Summary of Mir-Phase 1 Experiences

Space motion sickness and associated neurovestibular dysfunction though not completely understood - have been relatively well clinically and operationally characterized on short-duration (1-2 week) Space Shuttle missions (Oman, et al, 1984, 1986; Thornton, et al, 1987; Reschke, et al, 1994). Between March 1995 and June 1998, seven NASA astronauts flew on the Russian Mir space station, as "Phase 1" of the joint effort to build the International Space Station, and provided NASA with invaluable experience on the operational and biomedical problems associated with flights of up to six months in duration. The goal of this paper is to provide a summary of the available information on neurovestibular dysfunction, space motion sickness, and readaptation to Earth's gravity on the NASA Mir flights, based on a set of medical questionnaire data, transcripts, and interviews which are available from the NASA-Mir Phase I program. Records were incomplete and anecdotal. All references to specific crewmembers have been removed, to respect their individual privacy. Material was excerpted from multiple sources of information relating to neurologic function, sensory illusions and motion sickness of NASA-Mir Phase I Program crewmembers. Data were compiled by epoch (in-flight vs landing/postflight) and grouped by neurovestibular topic. The information was recorded either contemporaneously during or within days after landing, or retrospectively weeks to months later. Space motion sickness symptoms are more intense and longer in duration. Sense of spatial orientation takes at least a month to become "natural and instinctive" in space station structures, but mental survey knowledge is apparently not completely developed even after 3 months in some cases. Visual reorientation illusions (VRI) are more easily induced after long exposure to weightlessness. Head movements can cause illusory spinning sensations for up to 7 days postflight. Postural and balance control does not fully recover for at least a month postflight

A history of the peninsular war. Vol. VI

Ref. Palau 20141

A history of the peninsular war. Vol. V

Ref. Palau 20141

A history of the peninsular war. Vol. II

Ref. Palau 20141

A history of the peninsular war. Vol. IV

Ref. Palau 20141

Gas and Star Formation in Satellites of Milky Way Analogs

We have imaged the entirety of eight (plus one partial) Milky Way (MW)–like satellite systems, a total of 42 (45) satellites, from the Satellites Around Galactic Analogs II catalog in both Hα and H i with the Canada–France–Hawaii Telescope and the Jansky Very Large Array. In these eight systems we have identified four cases where a satellite appears to be currently undergoing ram pressure stripping (RPS) as its H i gas collides with the circumgalactic medium (CGM) of its host. We also see a clear suppression of gas fraction (M HI/M *) with decreasing (projected) satellite–host separation—to our knowledge, the first time this has been observed in a sample of MW-like systems. Comparisons to the Auriga, A Project Of Simulating The Local Environment, and TNG50 cosmological zoom-in simulations show consistent global behavior, but they systematically underpredict gas fractions across all satellites by roughly 0.5 dex. Using a simplistic RPS model, we estimate the average peak CGM density that satellites in these systems have encountered to be logρcgm/gcm−3≈−27.3 . Furthermore, we see tentative evidence that these satellites are following a specific star formation rate to gas fraction relation that is distinct from field galaxies. Finally, we detect one new gas-rich satellite in the UGC 903 system with an optical size and surface brightness meeting the standard criteria to be considered an ultra-diffuse galaxy