Motion Sickness Susceptibility Research Articles

Contribution of intravestibular sensory conflict to motion sickness and dizziness in migraine disorders.

Migraine is associated with enhanced motion sickness susceptibility and can cause episodic vertigo [vestibular migraine (VM)], but the mechanisms relating migraine to these vestibular symptoms remain uncertain. We tested the hypothesis that the central integration of rotational cues (from the semicircular canals) and gravitational cues (from the otolith organs) is abnormal in migraine patients. A postrotational tilt paradigm generated a conflict between canal cues (which indicate the head is rotating) and otolith cues (which indicate the head is tilted and stationary), and eye movements were measured to quantify two behaviors that are thought to minimize this conflict: suppression and reorientation of the central angular velocity signal, evidenced by attenuation ("dumping") of the vestibuloocular reflex and shifting of the rotational axis of the vestibuloocular reflex toward the earth vertical. We found that normal and migraine subjects, but not VM patients, displayed an inverse correlation between the extent of dumping and the size of the axis shift such that the net "conflict resolution" mediated through these two mechanisms approached an optimal value and that the residual sensory conflict in VM patients (but not migraine or normal subjects) correlated with motion sickness susceptibility. Our findings suggest that the brain normally controls the dynamic and spatial characteristics of central vestibular signals to minimize intravestibular sensory conflict and that this process is disrupted in VM, which may be responsible for the enhance motion intolerance and episodic vertigo that characterize this disorder.

Chapter 27 - Motion sickness

Over 2000 years ago the Greek physician Hippocrates wrote, "sailing on the sea proves that motion disorders the body." Indeed, the word "nausea" derives from the Greek root word naus, hence "nautical," meaning a ship. The primary signs and symptoms of motion sickness are nausea and vomiting. Motion sickness can be provoked by a wide variety of transport environments, including land, sea, air, and space. The recent introduction of new visual technologies may expose more of the population to visually induced motion sickness. This chapter describes the signs and symptoms of motion sickness and different types of provocative stimuli. The "how" of motion sickness (i.e., the mechanism) is generally accepted to involve sensory conflict, for which the evidence is reviewed. New observations concern the identification of putative "sensory conflict" neurons and the underlying brain mechanisms. But what reason or purpose does motion sickness serve, if any? This is the "why" of motion sickness, which is analyzed from both evolutionary and nonfunctional maladaptive theoretic perspectives. Individual differences in susceptibility are great in the normal population and predictors are reviewed. Motion sickness susceptibility also varies dramatically between special groups of patients, including those with different types of vestibular disease and in migraineurs. Finally, the efficacy and relative advantages and disadvantages of various behavioral and pharmacologic countermeasures are evaluated.

Relationship between Spectral Characteristics of Spontaneous Postural Sway and Motion Sickness Susceptibility.

Motion sickness (MS) usually occurs for a narrow band of frequencies of the imposed oscillation. It happens that this frequency band is close to that which are spontaneously produced by postural sway during natural stance. This study examined the relationship between reported susceptibility to motion sickness and postural control. The hypothesis is that the level of MS can be inferred from the shape of the Power Spectral Density (PSD) profile of spontaneous sway, as measured by the displacement of the center of mass during stationary, upright stance. In Experiment 1, postural fluctuations while standing quietly were related to MS history for inertial motion. In Experiment 2, postural stability measures registered before the onset of a visual roll movement were related to MS symptoms following the visual stimulation. Study of spectral characteristics in postural control showed differences in the distribution of energy along the power spectrum of the antero-posterior sway signal. Participants with MS history provoked by exposure to inertial motion showed a stronger contribution of the high frequency components of the sway signal. When MS was visually triggered, sick participants showed more postural sway in the low frequency range. The results suggest that subject-specific PSD details may be a predictor of the MS level. Furthermore, the analysis of the sway frequency spectrum provided insight into the intersubject differences in the use of postural control subsystems. The relationship observed between MS susceptibility and spontaneous posture is discussed in terms of postural sensory weighting and in relation to the nature of the provocative stimulus.

Relationship between spectral characteristics of spontaneous postural sway and motion sickness susceptibility

Relationship between spectral characteristics of spontaneous postural sway and motion sickness susceptibility

Motion Sickness: Current Knowledge and Recent Advance.

Motion sickness (MS) is a common physiological response to real or virtual motion. Numerous studies have investigated the neurobiological mechanism and the control measures of MS. This review summarizes the current knowledge about pathogenesis and pathophysiology, prediction, evaluation, and countermeasures of MS. The sensory conflict hypothesis is the most widely accepted theory for MS. Both the hippocampus and vestibular cortex might play a role in forming internal model. The pathophysiology focuses on the visceral afference, thermoregulation and MS-related neuroendocrine. Single-nucleotide polymorphisms (SNPs) in some genes and epigenetic modulation might contribute to MS susceptibility and habituation. Questionnaires, heart rate variability (HRV) and electrogastrogram (EGG) are useful for diagnosing and evaluating MS. We also list MS medications to guide clinical practice. Repeated real motion exposure and combined visual-vestibular interaction training accelerate the progress of habituation. Behavioral and dietary countermeasures, as well as physiotherapy, are also effective in alleviating MS symptoms.

Evaluation of motion sickness susceptibility by motion sickness susceptibility questionnaire in adolescents with idiopathic scoliosis: a case–control study

Adolescent idiopathic scoliosis (AIS) is a three-dimensional deformity of the spine, with unknown origin. Some studies have noted impaired postural balance in AIS, in particular, difficulty to manage situations with sensory conflict. The motion sickness susceptibility can be secondary to a sensory conflict, for example, between visual and vestibular information. Our hypothesis is: patients with AIS have difficulty in managing situations with sensory conflict and therefore have increased motion sickness susceptibility. The purpose of this study was to evaluate in AIS subjects by evaluating their susceptibility to motion sickness, as compared to a control group. We conducted an analysis of data on motion sickness susceptibility collected prospectively from 2012, with the B score of motion sickness susceptibility questionnaire. This evaluation was completed for 65 adolescents (age 14.5 ± 1.6 year) with major right thoracic AIS (Cobb = 40.7° ± 13.1°) and 71 matched controls (14.6 ± 1.6 year). Adolescents with major right thoracic AIS were more susceptible to motion sickness (B score = 5.3 ± 5.8) than controls (B score = 3.4 ± 3.7) with significant difference (p = 0.025). We interpret our results suggesting there is difficulty for patients with AIS to manage situations with sensory conflict. Previous studies focusing on situations with sensory conflict in AIS have required sophisticated technology. They are not accessible for routine patient management. Our research shows the same result with simple, non invasive, low-cost and quick method: B score of motion sickness susceptibility questionnaire.

Simulator sickness incidence and susceptibility during neck motion-controlled virtual reality tasks

To determine the incidence, severity, and predisposing factors to simulator sickness (SS) when using the neck virtual reality (VR) device in asymptomatic individuals to understand the risk of provoking SS in the development of neck VR as a rehabilitation tool. Thirty-two participants used the VR system. Postural stability was measured before and after each VR module [range of motion (ROM), velocity, and accuracy]. The duration of each module was recorded, and participants reported their SS using a visual analogue scale (SS---VAS)/100 mm. Following the VR assessment, participants completed the Motion Sickness Susceptibility Questionnaire (MSSQ) (child and adult subsections) and Simulator Sickness Questionnaire (SSQ). The incidence of motion sickness during the VR immersion was 28 %, and the mean severity was 17.2 mm on VAS. There was a significant difference in ROM time, total time, MSSQ score, and SSQ score (p < 0.05) between those who reported any level of SS---VAS and those with no SS---VAS. The SS---VAS score displayed significant positive correlations with SSQ score, change in postural stability time pre to post, ROM time, and total time. Results indicate a relatively high incidence but low severity of SS which was associated with the MSSQ child subsection score and exposure time.

Differential Gene Expression Profile in the Rat Caudal Vestibular Nucleus is Associated with Individual Differences in Motion Sickness Susceptibility.

ObjectiveTo identify differentially expressed genes associated with motion sickness (MS) susceptibility in the rat caudal vestibular nucleus.MethodsWe identified MS susceptible (MSS) and insusceptible (inMSS) rats by quantifying rotation-induced MS symptoms: defecation and spontaneous locomotion activity. Microarray analysis was used to screen differentially expressed genes in the caudal vestibular nucleus (CVN) after rotation. Plasma stress hormones were identified by radioimmunoassay. Candidate genes were selected by bioinformatics analysis and the microarray results were verified by real-time quantitative-PCR (RT-qPCR) methods. By using Elvax implantation, receptor antagonists or recombinant adenovirus targeting the candidate genes were applied to the CVN to evaluate their contribution to MS susceptibility variability. Validity of gene expression manipulation was verified by RT-qPCR and western blot analysis.ResultsA total of 304 transcripts were differentially expressed in the MSS group compared with the inMSS group. RT-qPCR analysis verified the expression pattern of candidate genes, including nicotinic cholinergic receptor (nAchR) α3 subunit, 5-hydroxytryptamine receptor 4 (5-HT4R), tachykinin neurokinin-1 (NK1R), γ-aminobutyric acid A receptor (GABAAR) α6 subunit, olfactory receptor 81 (Olr81) and homology 2 domain-containing transforming protein 1 (Shc1). In MSS animals, the nAchR antagonist mecamylamine significantly alleviated rotation-induced MS symptoms and the plasma β-endorphin response. The NK1R antagonist CP99994 and Olr81 knock-down were effective for the defecation response, while the 5-HT4R antagonist RS39604 and Shc1 over-expression showed no therapeutic effect. In inMSS animals, rotation-induced changes in spontaneous locomotion activity and the plasma β-endorphin level occurred in the presence of the GABAAR antagonist gabazine.ConclusionOur findings suggested that the variability of the CVN gene expression profile after motion stimulation might be a putative molecular basis for individual differences in MS susceptibility and provide information for the development of new therapeutic strategies for MSS individuals.

Susceptibility to motion sickness is not increased following spinal cord injury.

There are two leading theories on the origin of motion sickness. One, the sensory conflict theory, states that sensory information provided by one sensory channel does not match the expected input from another channel; commonly, these two inputs originate in the vestibular system and the eyes. The second theory - the postural instability theory - states that motion sickness comes about not through sensory conflict, but through an inability to control one's posture. Given that people with a motor-complete spinal cord injury cannot control their muscles below the level of the spinal lesion, we predicted that susceptibility to motion sickness would be higher in individuals who have suffered a spinal cord injury. Twenty-one people living with chronic spinal cord injury (9 quadriplegics, 12 paraplegics) completed the Motion Sickness Susceptibility Questionnaire (MSSQ), via an online survey, to compare susceptibility to motion sickness before and after injury. Spinal cord injury, regardless of level, did not produce an increase in susceptibility to motion sickness. We have tested the general validity of the postural-instability theory by assessing susceptibility to motion sickness in individuals with spinal cord injury. Despite the loss of postural control, there was no increase in motion sickness susceptibility.

Genetic Factors in Vestibular Function and Motion Sickness

Genetic Factors in Vestibular Function and Motion Sickness Objectives: To determine if motion sickness has a genetic basis, and, if so, to determine if there is a correlation between motion sickness genetic factors and genetic factors governing vestibular function. Data sources: The scope of review in this paper includes studies involving collection of primary data on susceptibility to motion sickness, correlated with any genetic factor; and, review articles concerning vestibular function and genetic factors. Study selection: A literature review was conducted to obtain articles that pertained to genetic factors governing vestibular function. To locate articles, sources including PubMed were utilized to locate review articles with the key words genetic,vestibular and motion sickness. Data extraction: Requirement that articles are written in English and published in the past 25 years. Data synthesis: Direct correlation. Conclusions: The selected articles revealed that: (1) Genetic polymorphism of the alpha-2a adrenergic receptor is correlated with motion sickness susceptibility in that the 6.3 Kb gene is correlated with increased susceptibility to motion sickness as compared to the 6.7 Kb polymorph; and (2) There is a lack of significant genetic correlation between the gene for the alpha-2a adrenergic receptor and genetic factors governing vestibular function. This data is in agreement with the observation that individuals who are highly susceptible to motion sickness tend to have normal vestibular function. In other words, subjects with a lack of peripheral vestibular function are generally resistant to motion sickness.

MSSQ-Short Norms May Underestimate Highly Susceptible Individuals

The aim of this study was to provide more reliable and robust norms for the Motion Sickness Susceptibility Questionnaire (MSSQ-Short). The previous norms for the MSSQ-Short involved a small sample overrepresenting younger female participants, which may provide misleading estimates of susceptibility in the general population. We measured MSSQ-Short scores in a sample of 1,711 members of the general public in New Zealand and Australia. The sample is 6.6 times larger than the original norm sample, and age and gender closely match the general population. Compared with the current study, the original norms underrepresent those of high susceptibility by a factor of 3.6, or 0.52 standard deviations. The analysis detected higher levels of susceptibility in females and significantly lower susceptibility in those ages 65 years and older. This study provides the largest sample of MSSQ-Short scores with more representative demographic characteristics of age and gender. Despite the potential for a self-selection bias toward high levels of susceptibility, we argue that the current norms provide more reliable and robust norms than the original sample. These updated norms provide the tools for researchers and designers to evaluate the likely effect of various motion environments on the general population. Robust norm data can inform research, including general motion sickness research and environmental design.

Use of controlled diaphragmatic breathing for the management of motion sickness in a virtual reality environment.

Evidence indicates that activation of the parasympathetic nervous system (PNS) suppresses physiological responses associated with motion sickness. Research also shows paced breathing increases PNS activation; the current study examines the use of paced diaphragmatic breathing (DB) training to quell motion sickness symptoms. Healthy participants (N=60) were pre-screened for motion sickness susceptibility. Participants were then randomly assigned to either a control condition, focusing on environmental awareness, or to an experimental condition implementing paced DB. Following this, participants were exposed to a virtual reality (VR) motion sickness experience, while heart rate variability, breathing rate (RPM), and motion sickness ratings were collected. Results demonstrated participants in the DB condition had higher PNS activation and reported fewer motion sickness symptoms during the VR experience than the participants in the control condition. Results suggest that the DB protocol can be used to significantly increase PNS tone and decrease the development of motion sickness symptoms.

Effects of motion sickness severity on the vestibular-evoked myogenic potentials.

Motion sickness is a common debilitating condition associated with both actual and perceived motion. Despite the commonality, little is known about the underlying physiological mechanisms. One theory proposes that motion sickness arises from a mismatch between reality and past experience in vertical motions. Physiological tests of the vestibular system, however, have been inconclusive regarding the underlying pathogenesis. Cervical vestibular-evoked myogenic potentials (cVEMPs) arise from the saccule, which responds to vertical motion. If vertical motion elicits motion sickness, the cVEMP should be affected. The purpose of this investigation was to determine if cVEMP characteristics differ among individuals with a range of motion sickness susceptibility from negligible to severe. The hypothesis was that individuals with high susceptibility would have larger cVEMP amplitudes and shorter cVEMP latencies relative to those who are resistant to motion sickness. The study had two parts. The first was quasi-experimental in which participants comprised three groups based on susceptibility to motion sickness (low, mild-moderate, high) as identified on the short version of the Motion Sickness Susceptibility Questionnaire (MSSQ-S). The second part of the study was correlational and evaluated the specific relationships between the degree of motion sickness susceptibility and characteristics of the VEMPs. A total of 24 healthy young adults (ages 20-24 yr) were recruited from the university and the community without regard to motion sickness severity. Participants took the MSSQ-S, which quantifies susceptibility to motion sickness. The participants had a range of motion sickness susceptibility with MSSQ raw scores from 0.0-36.6, which correspond to percent susceptibility from 0.0-99.3%. VEMPs were elicited by 500 Hz tone-bursts monaurally in both ears at 120 dB pSPL. MSSQ-S percent scores were used to divide the participants into low, mild-moderate, and high susceptibility groups. A fixed general linear model with repeated-measures analysis of variance tested cVEMP characteristics for the susceptibility groups (between participants) and ears (within participants). A univariate analysis of variance tested the cVEMP interaural amplitudes across groups. The second analysis was a regression of the severity of motion sickness in percent on cVEMP characteristics. Significance was defined as p < 0.05. Participants in the high susceptibility group had significantly higher cVEMP amplitudes than those in the low susceptibility group. cVEMP amplitudes did not differ between ears, and latencies did not differ between the two groups or between ears. Regression analysis on MSSQ-S percent susceptibility by VEMP amplitudes revealed a best-fit cubic function in both ears, with r(2) values of more than 42%. The interaural asymmetry ratio was negatively associated with motion sickness susceptibility (r(2) = 0.389). The current study is the first to report that greater susceptibility to motion sickness is associated with larger cVEMP amplitudes and lower interaural cVEMP asymmetries. Larger interaural asymmetries in cVEMPs did not promote motion sickness susceptibility. The cVEMP findings implicate the saccule and its neural pathways in the production of motion sickness and are consistent with the theory that vertical motions elicit motion sickness. Motion sickness susceptibility may contribute to the variability in normative cVEMP amplitudes.

Assessment of otolith function using cervical and ocular vestibular evoked myogenic potentials in individuals with motion sickness

The involvement of otolith organs in motion sickness has long been debated; however, equivocal findings exist in literature. The present study thus aimed at evaluating the otolith functioning in individuals with motion sickness. Cervical and ocular vestibular evoked myogenic potentials were recorded from 30 individuals with motion sickness, 30 professional drivers and 30 healthy individuals. The results revealed no significant difference in latencies and amplitudes between the groups (p>0.05). Nonetheless, thresholds were significantly elevated and inter-aural asymmetry ratio significantly higher in motion sickness susceptible group (p < 0.001) for both the potentials. All the individuals in the motion sickness group had high asymmetry ratio at least on one of the two potentials. Thus, reduced response and/or asymmetric otolithic function seem the likely reasons behind motion sickness susceptibility.

Epidemiological Differences in Visual Height Intolerance between Primary School Children and Adolescents/Adults

In 2012, the first cross-sectional epidemiological study was conducted on 3,517 individuals from throughout Germany, aged 14 years and above, to determine the prevalence, typical symptoms, situations of occurrence, restrictions, and types of compensational behavior occurring in visual height intolerance (vHI). The lifetime prevalence of vHI was found to be 28%. It was higher in women (32%) than in men (25%), and increased with age. Individuals with a family history of vHI or the accompanying diseases, for example, motion sickness susceptibility, Menière disease, migraine, or anxiety disorders, also had a higher prevalence. Initial attacks occurred most often (30%) in the second decade; however, attacks could manifest throughout life.

Motion sickness prevalence in school children.

This study aimed to determine the prevalence of motion sickness in schoolchildren and related the finding to the postural balance and quality of life. A population-based cross-sectional study was carried out with 831 children aged 7 to 12years. The frequency of motion sickness was evaluated based on the Motion Sickness Susceptibility Questionnaire-Short (MSSQ-short). Postural balance was assessed using the Romberg test under different sensory conditions. The Dizziness Handicap Inventory was used in order to assess the quality of life. The statistical analyses were performed using the chi-square, Kruskal-Wallis, Mann-Whitney, and Spearman correlation tests. The prevalence of motion sickness was 43.4% in car, 43.2% on bus, 11.7% on park swing, and 11.6% on Ferris wheel. Mean unadjusted scores on the MSSQ-short ranged from 5.0 (SE = 0.5) for 10-year-olds to 6.8 (SE = 0.5) for 9-year-olds. The most prevalent symptoms following the balance tests were dizziness (89.2%), vertigo (54.9%), headache (10.6%), and nausea (8.2%). Significant correlations were found between the MSSQ-short score and all postural balance tests. Significant correlations were found between the MSSQ and modified DHI (Dizziness Handicap Inventory) at all ages. The prevalence of motion sickness in schoolchildren is greater when in a car or on a bus. An association was found between motion sickness and postural balance tests and motion sickness and quality of life.

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

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.

Effect of an emetic gastrointestinal input on the processing of labyrinthine inputs by cerebellar rostral fastigial nucleus neurons (1130.7)

Multiple inputs can elicit nausea and vomiting, including ingested toxins and vestibular signals. Amongst the nervous system regions believed to participate in generating motion sickness is the cerebellar rostral fastigial nucleus (rFN). In addition, there is evidence that gastrointestinal inputs are transmitted to rFN through a variety of pathways, including projections from the dorsal motor nucleus of the vagus and area postrema. These observations raise the hypothesis that GI inputs could change motion sickness susceptibility by altering the processing of labyrinthine inputs by rFN neurons. To test this hypothesis, we recorded activity from rFN neurons in decerebrate cats, and compared their responses to whole‐body rotations before and after the intragastric infusion of the emetic compound copper sulfate (CuSO4). Some (18%) rFN neurons had complex responses to vestibular stimulation, particularly responses to only one direction of rotation (known as STC behavior). Such complex responses would be expected in a brain area that participates in generating motion sickness. The spatial and temporal characteristics of these responses changed little after injection of CuSO4. Although infusion of CuSO4 affected gains of responses to rotations of ~25% rFN neurons, the effects were inconsistent (CuSO4 augmented responses in some cells and decremented responses in others). CuSO4 resulted in pronounced changes in responses to rotations of a significantly larger fraction (Chi‐squared test, p&lt;0.05) of neurons in other brain regions that mediate nausea and vomiting, including the parabrachial nucleus and the “vomiting center” (caudal medullary lateral tegmental field). These data suggest that integration of vestibular and GI inputs by rFN neurons plays a limited role in affecting motion sickness susceptibility.Grant Funding Source: NIH grant R01‐DC03732

Integration of vestibular and gastrointestinal inputs by cerebellar fastigial nucleus neurons: multisensory influences on motion sickness

Previous studies demonstrated that ingestion of the emetic compound copper sulfate (CuSO4) alters the responses to vestibular stimulation of a large fraction of neurons in brainstem regions that mediate nausea and vomiting, thereby affecting motion sickness susceptibility. Other studies suggested that the processing of vestibular inputs by cerebellar neurons plays a critical role in generating motion sickness and that neurons in the cerebellar fastigial nucleus receive visceral inputs. These findings raised the hypothesis that stimulation of gastrointestinal receptors by a nauseogenic compound affects the processing of labyrinthine signals by fastigial nucleus neurons. We tested this hypothesis in decerebrate cats by determining the effects of intragastric injection of CuSO4 on the responses of rostral fastigial nucleus to whole-body rotations that activate labyrinthine receptors. Responses to vestibular stimulation of fastigial nucleus neurons were more complex in decerebrate cats than reported previously in conscious felines. In particular, spatiotemporal convergence responses, which reflect the convergence of vestibular inputs with different spatial and temporal properties, were more common in decerebrate than in conscious felines. The firing rate of a small percentage of fastigial nucleus neurons (15%) was altered over 50% by the administration of CuSO4; the firing rate of the majority of these cells decreased. The responses to vestibular stimulation of a majority of these cells were attenuated after the compound was provided. Although these data support our hypothesis, the low fraction of fastigial nucleus neurons whose firing rate and responses to vestibular stimulation were affected by the administration of CuSO4 casts doubt on the notion that nauseogenic visceral inputs modulate motion sickness susceptibility principally through neural pathways that include the cerebellar fastigial nucleus. Instead, it appears that convergence of gastrointestinal and vestibular inputs occurs mainly in the brainstem.

Mal de debarquement, motion sickness and the effect of an artificial horizon

Exposure to unfamiliar motion patterns commonly results in motion sickness and a false perception of motion, termed mal de debarquement, on the return to stable conditions. To investigate whether motion sickness severity is correlated with the duration and severity of mal de debarquement; to study the possible preventive effect of projecting earth-referenced scenes (an artificial horizon) during exposure to motion on the development of mal de debarquement. Thirty subjects were exposed to the recorded motion profile of a boat in a 3-degrees-of-freedom ship motion simulator. During the simulated voyage, the study participants were repeatedly put through a performance test battery and completed a motion sickness susceptibility questionnaire, while self-referenced and earth-referenced scenes were projected inside the simulator cabin. Six hours post disembarkation, subjects completed a questionnaire on mal de debarquement duration and severity. Mal de debarquement, mostly of mild severity, was reported following 59% of the exposures to the provocative motion profile, and in 79% of cases lasted less than 6 hours. The incidence of mal de debarquement, its duration, and the severity of symptoms did not differ between the various artificial horizon projection modes. Significant correlations were found between motion sickness severity and the duration and severity of the mal de debarquement that followed. The significant correlations found between motion sickness severity and mal de debarquement duration and severity imply that both syndromes might stem from a failure to adapt to new motion conditions. There is a disparity between the previously reported reduction in motion sickness symptoms by an artificial horizon, and its failure to influence the duration and symptoms of mal de debarquement. This might be explained by the different response in the two syndromes, physical versus cognitive.