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Frontiers in Systems Neuroscience 2022The relationship between the amplitude of motion and the accumulation of motion sickness in time is unclear. Here, we investigated this relationship at the individual...
The relationship between the amplitude of motion and the accumulation of motion sickness in time is unclear. Here, we investigated this relationship at the individual and group level. Seventeen participants were exposed to four oscillatory motion stimuli, in four separate sessions, separated by at least 1 week to prevent habituation. Motion amplitude was varied between sessions at either 1, 1.5, 2, or 2.5 ms. Time evolution was evaluated within sessions applying: an initial motion phase for up to 60 min, a 10-min rest, a second motion phase up to 30 min to quantify hypersensitivity and lastly, a 5-min rest. At both the individual and the group level, motion sickness severity (MISC) increased linearly with respect to acceleration amplitude. To analyze the evolution of sickness over time, we evaluated three variations of the Oman model of nausea. We found that the slow (502 s) and fast (66.2 s) time constants of motion sickness were independent of motion amplitude, but varied considerably between individuals (slow STD = 838 s; fast STD = 79.4 s). We also found that the Oman model with output scaling following a power law with an exponent of 0.4 described our data much better as compared to the exponent of 2 proposed by Oman. Lastly, we showed that the sickness forecasting accuracy of the Oman model depended significantly on whether the participants had divergent or convergent sickness dynamics. These findings have methodological implications for pre-experiment participant screening, as well as online tuning of automated vehicle algorithms based on sickness susceptibility.
PubMed: 35615427
DOI: 10.3389/fnsys.2022.866503 -
Physiology & Behavior Jan 2023The use of virtual reality (VR) with head-mounted displays (HMD) may cause side effects called cybersickness with symptoms comparable to those of motion sickness. In...
The use of virtual reality (VR) with head-mounted displays (HMD) may cause side effects called cybersickness with symptoms comparable to those of motion sickness. In this study, we explored whether individual balance characteristics and self-reported tendency to motion sickness could be related to cybersickness vulnerability. Healthy young people (N = 45) were exposed to a VR application with HMD for four minutes, standing with no support. Balance characteristics were measured before (Sensory orientation test) and during (balance platform) the VR exposure. Symptoms of cybersickness were recorded by the Simulator sickness questionnaire (SSQ). Data were analyzed for subgroups with and without a tendency to motion sickness. The participants were negatively affected by the VR exposure: SSQ-before: 21.3 (19.5); SSQ-after: 31.8 (25.2); p<0.01, and 73% experienced increased discomfort. The SSQ sub-scores Nausea and Disorientation were affected, but not the sub-score for Oculomotor disturbance. Surprisingly, the participants described discomfort already after the initial balance assessment (Sensory orientation test). Participants with a self-reported tendency to motion sickness were relatively more affected by this challenge to their sensory integration. Increased postural instability was evident during the VR exposure, but there was a sizeable individual variance in the postural response. The study identified no individual balance characteristics which could be associated with the cybersickness vulnerability. The adverse effect of the Sensory orientation test is a novel finding and it became a bias that diminished subgroup differences in cybersickness vulnerability.
Topics: Humans; Adolescent; Motion Sickness; Virtual Reality; Surveys and Questionnaires; Sensation
PubMed: 36323375
DOI: 10.1016/j.physbeh.2022.114015 -
Scientific Reports Jun 2023Nausea often occurs in stressful situations, such as chemotherapy or surgery. Clinically relevant placebo effects in nausea have been demonstrated, but it remains... (Randomized Controlled Trial)
Randomized Controlled Trial
Nausea often occurs in stressful situations, such as chemotherapy or surgery. Clinically relevant placebo effects in nausea have been demonstrated, but it remains unclear whether stress has an impact on these effects. The aim of this experimental study was to investigate the interplay between acute stress and placebo effects in nausea. 80 healthy female volunteers susceptible to motion sickness were randomly assigned to either the Maastricht Acute Stress Test or a non-stress control condition, and to either placebo treatment or no treatment. Nausea was induced by a virtual vection drum and behavioral, psychophysiological as well as humoral parameters were repeatedly assessed. Manipulation checks confirmed increased cortisol levels and negative emotions in the stressed groups. In the non-stressed groups, the placebo intervention improved nausea, symptoms of motion sickness, and gastric myoelectrical activity (normo-to-tachy (NTT) ratio). In the stressed groups, the beneficial effects of the placebo intervention on nausea and motion sickness remained unchanged, whereas no improvement of the gastric NTT ratio was observed. Results suggest that placebo effects on symptoms of nausea and motion sickness are resistant to experimentally-induced stress. Stress most likely interfered with the validity of the gastric NTT ratio to measure nausea and thus the gastric placebo effect.
Topics: Female; Humans; Motion Sickness; Nausea; Placebo Effect; Stomach
PubMed: 37336972
DOI: 10.1038/s41598-023-36296-w -
Journal of Neurophysiology Mar 2019Although motion of the head and body has been suspected or known as the provocative cause for the production of motion sickness for centuries, it is only within the last... (Review)
Review
Although motion of the head and body has been suspected or known as the provocative cause for the production of motion sickness for centuries, it is only within the last 20 yr that the source of the signal generating motion sickness and its neural basis has been firmly established. Here, we briefly review the source of the conflicts that cause the body to generate the autonomic signs and symptoms that constitute motion sickness and provide a summary of the experimental data that have led to an understanding of how motion sickness is generated and can be controlled. Activity and structures that produce motion sickness include vestibular input through the semicircular canals, the otolith organs, and the velocity storage integrator in the vestibular nuclei. Velocity storage is produced through activity of vestibular-only (VO) neurons under control of neural structures in the nodulus of the vestibulo-cerebellum. Separate groups of nodular neurons sense orientation to gravity, roll/tilt, and translation, which provide strong inhibitory control of the VO neurons. Additionally, there are acetylcholinergic projections from the nodulus to the stomach, which along with other serotonergic inputs from the vestibular nuclei, could induce nausea and vomiting. Major inhibition is produced by the GABA receptors, which modulate and suppress activity in the velocity storage integrator. Ingestion of the GABA agonist baclofen causes suppression of motion sickness. Hopefully, a better understanding of the source of sensory conflict will lead to better ways to avoid and treat the autonomic signs and symptoms that constitute the syndrome.
Topics: Animals; Baclofen; GABA-B Receptor Agonists; Humans; Motion Sickness; Vestibular Nuclei; Vestibule, Labyrinth
PubMed: 30699041
DOI: 10.1152/jn.00674.2018 -
Acta Oto-laryngologica May 2017Elevated Motion Sickness Susceptibility (MSS) in Meniere?s disease (MD) is likely to be a consequence of the onset of MD and not migraine per se.
CONCLUSION
Elevated Motion Sickness Susceptibility (MSS) in Meniere?s disease (MD) is likely to be a consequence of the onset of MD and not migraine per se.
OBJECTIVES
Pathologies of the vestibular system influence MSS. Bilateral vestibular deficits lower MSS, vestibular neuritis or benign paroxysmal positional vertigo have little overall effect, whereas vestibular migraine elevates MSS. However, less is known about MSS in MD, a condition in which many patients experience vestibular loss and migraine symptoms.
METHODS
The authors conducted an online survey that posed diagnostic and disease questions before addressing frequency of headaches, migraines, visual display dizziness (VDD), syncope, social life, and work impact of dizziness (SWID4) and motion sickness susceptibility (MSSQ). The two groups were: diagnosed MD individuals with hearing loss (n = 751) and non-MD individuals in the control group (n = 400).
RESULTS
The MD group showed significantly elevated MSS, more headache and migraine, increased VDD, higher SWID4 scores, and increased syncope. MSS was higher in MD than controls only after the development of MD, but not before, nor in childhood. Although elevated in MD compared with controls, MSS was lower than migraine patients from past data. Multivariate analysis revealed VDD, SWID4, and MSS in adulthood as the strongest predictors of MD, but not headache nor migraine.
Topics: Adult; Case-Control Studies; Female; Humans; Male; Meniere Disease; Middle Aged; Migraine Disorders; Motion Sickness; Surveys and Questionnaires; United Kingdom
PubMed: 27918236
DOI: 10.1080/00016489.2016.1255775 -
International Journal of Pediatric... Jul 2022Easily available clinical tests to evaluate postural control are needed. Furthermore, motion sickness (MS) and postural control are correlated. The aims of this study...
OBJECTIVE
Easily available clinical tests to evaluate postural control are needed. Furthermore, motion sickness (MS) and postural control are correlated. The aims of this study were to compare the internal validity of a set of clinical tests of postural control with the internal validity of static posturography and to evaluate possible associations between postural control and MS.
METHODS
We included healthy subjects from a primary school in Denmark who completed questionnaires about MS and underwent two rounds of clinical tests of postural control and static posturography using a Tetrax Interactive Balance System two weeks apart. For clinical tests of postural control, subjects were observed for up to 30 s standing on both legs, on one leg, on a pillow both with their eyes open and again with their eyes closed.
RESULTS
Twenty-one subjects were included: 71% males with an average age of 13.7 years. Agreement rates ranged from 62% to 95% between test and retest in clinical tests.; lowest for subjects standing on their non dominant leg with their eyes open and highest for subjects performing Romberg's test with their eyes closed along with subjects standing on a pillow with their eyes open. For several of these tests, almost all subjects were able to hold their balance for the full 30 s. Test-retesting using static posturography by Bland Altman plot showed datapoints scattered equally above and below the mean line indicating no systematic bias. Results of clinical tests and static posturography were not associated. MS was reported from 43% of subjects and a trend was observed with high sway scores from subjects suffering from MS. This was statistically insignificant.
CONCLUSIONS
Due to a ceiling effect, subjects achieved the same scores in both rounds of testing in several of the clinical tests, reducing the clinical importance of these tests. Compared to clinical tests, static posturography seemingly remains the superior method when it comes to evaluation of postural control, although not as easily applicable in a daily clinical setting. When comparing MS and postural control a trend was observed, indicating higher sway scores in subjects suffering from MS.
Topics: Adolescent; Denmark; Female; Humans; Male; Motion Sickness; Postural Balance
PubMed: 35580384
DOI: 10.1016/j.ijporl.2022.111139 -
Proceedings of the National Academy of... Oct 2023Travel can induce motion sickness (MS) in susceptible individuals. MS is an evolutionary conserved mechanism caused by mismatches between motion-related sensory...
Travel can induce motion sickness (MS) in susceptible individuals. MS is an evolutionary conserved mechanism caused by mismatches between motion-related sensory information and past visual and motion memory, triggering a malaise accompanied by hypolocomotion, hypothermia, hypophagia, and nausea. Vestibular nuclei (VN) are critical for the processing of movement input from the inner ear. Motion-induced activation of VN neurons recapitulates MS-related signs. However, the genetic identity of VN neurons mediating MS-related autonomic and aversive responses remains unknown. Here, we identify a central role of cholecystokinin (CCK)-expressing VN neurons in motion-induced malaise. Moreover, we show that CCK VN inputs onto the parabrachial nucleus activate -expressing neurons and are sufficient to establish avoidance to novel food, which is prevented by CCK-A receptor antagonism. These observations provide greater insight into the neurobiological regulation of MS by identifying the neural substrates of MS and providing potential targets for treatment.
Topics: Animals; Mice; Motion Sickness; Movement; Neurons; Vestibular Nuclei; Vestibule, Labyrinth
PubMed: 37847729
DOI: 10.1073/pnas.2304933120 -
Temperature (Austin, Tex.) 2014Principal symptoms of motion sickness in humans include facial pallor, nausea and vomiting, and sweating. It is less known that motion sickness also affects... (Review)
Review
Principal symptoms of motion sickness in humans include facial pallor, nausea and vomiting, and sweating. It is less known that motion sickness also affects thermoregulation, and the purpose of this review is to present and discuss existing data related to this subject. Hypothermia during seasickness was firstly noted nearly 150 years ago, but detailed studies of this phenomenon were conducted only during the last 2 decades. Motion sickness-induced hypothermia is philogenetically quite broadly expressed as besides humans, it has been reported in rats, musk shrews and mice. Evidence from human and animal experiments indicates that the physiological mechanisms responsible for the motion sickness-induced hypothermia include cutaneous vasodilation and sweating (leading to an increase of heat loss) and reduced thermogenesis. Together, these results suggest that motion sickness triggers highly coordinated physiological response aiming to reduce body temperature. Finally, we describe potential adaptive role of this response, and describe the benefits of using it as an objective measure of motion sickness-induced nausea.
PubMed: 27626043
DOI: 10.4161/23328940.2014.982047 -
Journal of Neurology Apr 2016The two most common vestibular disorders are motion sickness and vestibular migraine, affecting 30 and 1-2% of the population respectively. Both are related to migraine... (Review)
Review
The two most common vestibular disorders are motion sickness and vestibular migraine, affecting 30 and 1-2% of the population respectively. Both are related to migraine and show a familial trend. Bilateral vestibular hypofunction is a rare condition, and some of patients also present cerebellar ataxia and neuropathy. We present recent advances in the genetics of vestibular disorders with familial aggregation. The clinical heterogeneity observed in different relatives of the same families suggests a variable penetrance and the interaction of several genes in each family. Some Mendelian sensorineural hearing loss also exhibits vestibular dysfunction, including DFNA9, DFNA11, DFNA15 and DFNA28. However, the most relevant finding during the past years is the familial clustering observed in Meniere's disease. By using whole exome sequencing and combining bioinformatics tools, novel variants in DTNA and FAM136A genes have been identified in familial Meniere's disease, and this genomic strategy will facilitate the discovery of the genetic basis of familial vestibular disorders.
Topics: Computational Biology; DNA-Binding Proteins; Extracellular Matrix Proteins; Genetic Association Studies; Genetic Predisposition to Disease; Homeodomain Proteins; Humans; Mitochondrial Proteins; Myosin VIIa; Myosins; Transcription Factor Brn-3C; Transcription Factors; Vestibular Diseases
PubMed: 27083884
DOI: 10.1007/s00415-015-7988-9