Visual Vertigo, Motion Sickness and Disorientation in vehicles

The normal vestibular system may be adversely affected by environmental challenges which have characteristics that are unfamiliar or ambiguous in the patterns of sensory stimulation they provide. A disordered vestibular system lends susceptibility even to quotidian environmental experiences as the sufferer becomes dependent on potentially misleading, non-vestibular sensory stimuli. In both cases the sequela may be dizziness, incoordination, imbalance and unpleasant autonomic responses. Many forms of visual environmental motion, particularly busy places such as supermarkets, readily induce inappropriate sensations of sway or motion and imbalance referred to as visual vertigo. All people with intact vestibular function can become motion sick although individual susceptibility varies widely and is partially determined by inheritance. Motorists learn to interpret sensory stimuli in the context of the car stabilised by its suspension and guided by steering. A type of motorist disorientation occurs in some individuals that develop a heightened awareness of false perceptions of car orientation, readily experiencing stereotypical symptoms of threatened rolling over on corners and veering on open highways or in streaming traffic. This article discusses the putative mechanisms, consequences and approach to managing patients with visual vertigo, motion sickness and motorist disorientation syndrome in the context of chronic dizziness and motion sensitivity

Impairment of spatial cognitive function with preservation of verbal performance during spatial disorientation

Spatial disorientation, which is responsible for up to 30% of aircraft accidents causes impairment of cognitive function which may further compromise a pilot's ability to think his way out of the situation and regain control [1,]. The functional-anatomical separation of spatial and verbal processing [10,11] raises the possibility of selective interference between the task of resolving spatial disorientation and the ability to perform concurrent spatial, as opposed to verbal, secondary tasks. We report for the first time a degradation of spatial task performance with preservation of verbal performance when subjects in a simulator are disoriented by conflict between self- motion and visual flow in the view of the external environment

Electrocortical therapy for motion sickness

Given a sufficiently provocative stimulus, almost everyone can be made motion sick, with approximately one-third experiencing significant symptoms on long bus trips, on ships, or in light aircraft.1–4 Current countermeasures are either behavioral or pharmacologic. Behavioral measures include habituation/desensitization treatment protocols5 as well as positioning the head in alignment with the direction of the gravito-inertial force and maintaining a stable horizontal reference frame.5 Pharmacologic measures include antimuscarinics, H1 antihistamines, and sympathomimetics, which all detrimentally impact upon cognitive function, rendering them inappropriate for occupational use.5 All current therapies are only partially effective

Pathophysiology and treatment of motion sickness

Purpose of review Motion sickness remains bothersome in conventional transport and is an emerging hazard in visual information technologies. Treatment remains unsatisfactory but advances in brain imaging, neurophysiology, and neuropharmacology may provide insights into more effective drug and behavioural management. We review these major developments. Recent findings Recent progress has been in identifying brain mechanisms and loci associated with motion sickness and nausea per se. The techniques have included conventional neurophysiology, pathway mapping, and functional MRI, implicating multiple brain regions including cortex, brainstem, and cerebellum. Understanding of the environmental and behavioural conditions provocative of and protective against motion sickness and how vestibular disease may sensitize to motion sickness has increased. The problem of nauseogenic information technology has emerged as a target for research, motivated by its ubiquitous applications. Increased understanding of the neurophysiology and brain regions associated with motion sickness may provide for more effective medication in the future. However, the polysymptomatic nature of motion sickness, high interindividual variability, and the extensive brain regions involved may preclude a single, decisive treatment. Summary Motion sickness is an emerging hazard in information technologies. Adaptation remains the most effective countermeasure together with established medications, notably scopolamine and antihistamines. Neuropharmacological investigations may provide more effective medication in the foreseeable future

Vertigo and dizziness from environmental motion: visual vertigo, motion sickness, and drivers' disorientation

The normal vestibular system may be adversely affected by environmental challenges which have characteristics that are unfamiliar or ambiguous in the patterns of sensory stimulation they provide. A disordered vestibular system lends susceptibility even to quotidian environmental experiences as the sufferer becomes dependent on potentially misleading, nonvestibular sensory stimuli. In both cases, the sequelae may be vertigo, incoordination, imbalance, and unpleasant autonomic responses. Common environmental motion conditions include visual vertigo, motion sickness, and motorists' disorientation. The core therapy for visual vertigo, motion sickness, and drivers' disorientation is progressive desensitization within a cognitive framework of reassurance and explanation, plus anxiolytic tactics and autogenic control of autonomic symptoms

A motion sickness maximum around the 0.2 Hz frequency range of horizontal translational oscillation

Background: Low frequency translational oscillation can provoke motion sickness in land vehicles, ships and aircraft. Although controlled motion experiments indicate a progressive increase in nauseogenicity as frequency decreases toward 0.2 Hz, few data are available on the existence of a definite maximum nauseogenic potential of motion around 0.2 Hz, or decreased nauseogenicity below this frequency. Hypothesis: Nauseogenicity should be maximal around 0.2 Hz. Methods: We selected 12 subjects for high motion sickness susceptibility, and they were exposed to horizontal sinusoidal motion (1.0 m.s-2 peak acceleration) at 3 different frequencies (0.1, 0.2 and 0.4 Hz), at 1-wk intervals at the same time of day, according to a factorial design. Subjects were seated comfortably in the upright position with head erect. Fore-aft motion was through the body and head X-axis. Motion was stopped (motion endpoint) at moderate nausea or after 30 min. Results: The proportion of subjects experiencing moderate nausea was maximal at the intermediate frequency: 8/12 at 0.1 Hz, 12/12 at 0.2 Hz, 7/12 at 0.4 Hz. The mean time to motion endpoint was significantly (p < 0.01) shorter at the intermediate frequency: 18.0 min at 0.1 Hz; 11.2 min at 0.2 Hz; 20.2 min at 0.4 Hz. Similar frequency patterns emerged for other sickness ratings. The equivalent times to achieve moderate nausea using estimated values to correct for subjects who reached the 30 min time cut-off were: 22.7 min at 0.1 Hz; 11.2 min at 0.2 Hz; 28.1 min at 0.4 Hz. Conclusions: A maximum nauseogenic potential around 0.2 Hz was substantiated

Motion sickness susceptibility fluctuates through the menstrual cycle

Background: Motion sickness is a common and potentially debilitating condition that characteristically occurs in situations of conflicting sensory input. While the precise stimuli that give rise to this trait are increasingly well characterized, the underlying determinants of individual susceptibility to motion sickness remain unclear. This study uses a classical twin design to assess the influence of genetic and environmental factors. Methods: A postal survey was conducted in an age-matched sample of 3652 monozygotic (MZ) and dizygotic (DZ) adult female twins selected from the TwinsUK Registry. Study participants were asked to complete items from a validated questionnaire relating to their lifetime susceptibility to motion sickness. The relative contribution of genetic and environmental factors to motion sickness susceptibility was assessed using variance components analysis. Results: The response rate to the questionnaire was 78%. Approximately 40% of respondents reported at least moderate susceptibility to motion sickness. The pattern of responses among twins indicated a significant genetic contribution with heritability for a motion sickness factor score estimated as 57% (95% CI: 51%, 63%). The heritability of recalled motion sickness was at its highest in childhood (70% [59%, 80%]) and declined through puberty and the early adult years. Discussion and Conclusions: The findings highlight the importance of genetic factors in determining an individual's underlying propensity to motion sickness and should stimulate the search for specific susceptibility genes