Fig. 8.1
In the passenger looking out of the bus and fixating upon the road sign, vestibular (VOR) and visual (pursuit) mechanisms cooperate to stabilise the eyes on the road sign as the bus turns round. In the passenger reading the newspaper, the VOR takes the eyes off the visual target (the newspaper), but pursuit eye movements are used to suppress the VOR. In the latter situation, visual and vestibular inputs are said to be in conflict (From Bronstein and Lempert [23]; with permission)
The intimate relationship between vision and vestibular function implies that visual input may influence vestibular symptoms and modify vestibular function and perception. The interaction between vestibular and visual inputs becomes a significant feature in vestibular disorders in which visual suppression and pursuit mechanisms are evoked to suppress pathological nystagmus and partially restore visual stability. Similarly, absent [1] or altered visual input, as in congenital nystagmus [2] or external ophthalmoplegia [3], modifies vestibular function and perception. The purpose of this section is to review a clinical syndrome in which visuo-vestibular interaction is a prominent mechanism: the syndrome of ‘visual vertigo’ in which vestibular patients and other individuals with certain pathophysiological and ‘psychological susceptibility’ experience significant symptoms of malaise and imbalance provoked by visual motion stimuli in the everyday environment. Of immediate, specific relevance, certain individuals with migraine may find themselves highly susceptible to visual motion stimuli.
8.2.2 Clinical Picture of Visual Vertigo
Some, but not all, ‘vestibular’ patients report worsening or triggering of dizziness and imbalance in certain visual environments. These patients report a dislike of moving visual surroundings, as encountered in traffic, crowds, disco lights and car-chase scenes in films. A frequent presentation is the development of dizziness and imbalance in specific visual environments such as supermarket aisles. The development of these symptoms in some patients with vestibular disorders has long been recognised [4, 5], see Bronstein (2002) for review [6], and was given various names such as visuo-vestibular mismatch and space and motion discomfort [7–10]. The Classification Committee of the Barany Society now recommends the name visually induced dizziness for this symptom [11]. This syndrome should not be confused with oscillopsia, a perception of oscillation of the visual world wherein the symptom is visual. In visual vertigo, the trigger is visual but the symptom is vestibular in kind, such as dizziness, vertigo, disorientation and unsteadiness.
The symptoms of visual vertigo frequently develop after a vestibular insult. A typical patient is a previously asymptomatic person who suffers an acute peripheral disorder (e.g. vestibular neuritis) and, after an initial period of recovery of a few weeks, discovers that the dizzy symptoms do not fully disappear. Furthermore, their symptoms are aggravated by looking at moving or repetitive images, as described above. Patients may also develop anxiety or frustration because symptoms do not go away or because medical practitioners tend to disregard this syndrome.
The origin and significance of the symptoms of visual vertigo in vestibular patients has been the subject of research. We know that tilted or moving visual surroundings have a pronounced influence on these patients’ perception of verticality and balance, over and above what can be expected from an underlying vestibular deficit [9, 10]. This increased responsiveness to visual stimuli is called ‘visual dependency’, a term used to describe people who use visual input, as opposed to inertial inputs, to organise spatial orientation and postural control [12]. Patients with central vestibular disorders and patients combining vestibular disorders and congenital squints or squint surgery can also report visual vertigo and show enhanced visuo-postural reactivity [9].
Overall, these findings suggest that the combination of a vestibular disorder and increased visual dependence in a given patient is precursive to the visual vertigo syndrome. Ultimately, what makes some vestibular patients develop visual vertigo is not yet known; it may be a natural susceptibility to overreliance on visual signals in response to the challenge of a sensory disorder. The role of the associated anxiety-depression, often observed in these patients, and whether this is a primary or secondary phenomenon are not known. The limited evidence so far does not indicate that anxiety or depression levels are higher in visual vertigo patients than in other patients seen in dizzy clinics [9, 10, 13].
The important differential diagnosis in these patients is, however, one of a purely psychological disorder or panic attacks [12]. An accepted set of criteria to distinguish between psychological and vestibular symptoms are not agreed presently [14–17]; however, in the absence of a clear history of vestibular disease, or findings on vestibular examination and with visual triggers restricted to a single particular environment (e.g. only supermarkets), a patient with visual vertigo would be more likely to suffer from a primary psychological disorder or a psychosomatic disorder such as chronic subjective dizziness [17]. Reciprocally, a patient with no premorbid psychological dysfunction who after a vestibular insult may develop car tilting illusions when driving [18] or dizziness when looking at moving visual scenes (traffic, crowds, movies) is more likely to have the visual vertigo syndrome. A third diagnostic category comprises certain individuals with migraine who have an exceptionally high susceptibility to whole field visual motion, particularly of the kind which readily imparts vection [19]. These appear not to have been thoroughly studied as a group, but such susceptibility in certain individuals is a familiar encounter in both vestibular and motion sickness studies [20]. By way of illustration; a large rotating disk, viewed by a subject in primary gaze, is a commonplace and powerful device used to reveal visual dependency and challenge postural control. The visual motion readily induces laterally tilting vection and postural leaning in the majority of normal subjects. However, this subgroup of migraineurs is highly susceptible, becoming unstable within a few seconds of exposure to motion, developing nausea and, if exposure continues by merely tens of seconds, developing migraine-like headache. In our experience, these subjects appear also to be highly susceptible to motion sickness, but a full quantitative evaluation of the relationship has not been established.
8.2.3 Treatment of Visual Vertigo
There are three aspects in the treatment of patients with the visual vertigo syndrome. The first is specific measures for the underlying vestibular disorder, e.g. Meniere’s disease, BPPV and migraine, and these will be found elsewhere in this book. However, a specific etiological diagnosis cannot be confirmed in many patients with chronic dizziness.
Secondly, patients benefit from general vestibular rehabilitation with a suitably trained audiologist or physiotherapist. These exercise-based programmes can either be generic, like the original Cawthorne-Cooksey approach or, preferably, customised to the patient’s needs. All regimes involve progressive eye, head and whole body movements (bending, turning) as well as walking exercises ([21–23]; see video in [23]).
Thirdly, specific measures should be introduced in the rehabilitation programme in order to reduce the patient’s hyperreactivity to visual motion. The aim is to promote desensitisation and increase tolerance to visual stimuli and to visuo-vestibular conflict. Patients are therefore exposed, under the instruction of the vestibular physiotherapist, to optokinetic stimuli which can be delivered via projection screens, head-mounted virtual reality systems, video monitors, ballroom planetariums or optokinetic rotating systems [24, 25]. Initially patients watch these stimuli whilst seated, then standing and walking, initially without and then with head movements, in a progressive fashion (Fig. 8.2). Recent research has shown that these patients benefit from repeated and gradual exposure to such visual motion training programmes; both the dizziness and associated psychological symptoms improve over and above conventional vestibular rehabilitation [25].
Fig. 8.2
Optokinetic or visual motion desensitisation treatment for patients with vestibular disorders reporting visual vertigo symptoms. Left: roll (coronal) plane rotating optokinetic disk; middle: planetarium-generated moving dots whilst the subject walks; right: ‘Eye-Trek’ or head-mounted TV systems projecting visual motion stimuli. In this case, in advanced stages of the therapy, the patient moves the head and trunk whilst standing on rubber foam (Based on Pavlou et al. [25], with permission). Patients should look at the central part of the disk (arrow) for maximal visual field cover
Finally, although there is not much published regarding the presence of visual vertigo in patients with migraine [19], the fact that migraine symptoms increase on self- and visual motion [26] dictates that patients with visual vertigo and migraine should be treated with prophylactic medication before entering a visuo-vestibular rehabilitation programme. However, on the basis of limited evidence, it seems that migraine patients do benefit from this rehabilitation approach and, in a recent study that would require confirmation, they seemed to respond better to rehabilitation than non-migraineous dizzy patients [27].
8.3 Motion Sickness
8.3.1 Signs and Symptoms
The primary signs and symptoms of motion sickness are nausea and vomiting although migraine-like headache can be a marked feature in a significant number of individuals. Other commonly related symptoms include stomach awareness, sweating and facial pallor (so-called cold sweating), increased salivation, sensations of bodily warmth, dizziness, drowsiness, loss of appetite and increased sensitivity to odours. Motion sickness can be provoked by a wide range of situations – in cars, tilting trains, funfair rides, aircraft, weightlessness in outer space, virtual reality and simulators. The term ‘motion sickness’ embraces car sickness, air sickness, space sickness, sea sickness, etc. Physiological responses associated with motion sickness may vary between individuals. For the stomach gastric stasis occurs with an increased frequency and reduced amplitude of the normal electrogastric rhythm [28]. Other autonomic changes include sweating and vasoconstriction of the skin causing pallor (less commonly skin vasodilation and flushing in some individuals) with the simultaneous opposite effect of vasodilation and increased blood flow of deeper blood vessels, changes in heart rate which are often an initial increase followed by a rebound decrease and inconsistent changes in blood pressure [29]. A whole host of hormones are released, mimicking a generalised stress response, amongst which vasopressin is thought to be most closely associated with the time course of motion sickness [30], and the observation of cold sweating suggests that motion sickness disrupts aspects of temperature regulation [31].
Motion sickness is unpleasant, but also under some circumstances, it may have adverse consequences for performance and even survival. Motion sickness preferentially causes decrements on performance of tasks which are complex, require sustained performance and offer the opportunity of the person to control the pace of their effort [32]. For pilots and aircrew, it can slow training in the air and in simulators and even cause a minority to fail training [33]. For survival-at-sea, such as in liferafts, seasickness can reduce survival chances by a variety of mechanisms, including reduced morale and the ‘will to live’, failure to consistently perform routine survival tasks, dehydration due to loss of fluids and electrolytes through vomiting and possibly due to the increased risk of hypothermia [29].
8.3.2 Causes and Reasons for Motion Sickness
The physical intensity of the stimulus is not necessarily related to the degree of nauseogenicity. Indeed with optokinetic stimuli, there is no real motion. A person sitting at the front in a widescreen cinema experiences self-vection and ‘cinerama sickness’, but there is no physical motion of the body. In this example, the vestibular and somatosensory systems are signalling that the person is sitting still, but the visual system is signalling illusory movement or self-vection. Consequently, the generally accepted explanation is based on some form of sensory conflict or sensory mismatch. The sensory conflict or sensory mismatch is between actual versus expected invariant patterns of vestibular, visual and kinaesthetic inputs [33]. Benson [29] categorised neural mismatch into two main types: (i) conflict between visual and vestibular inputs or (ii) mismatch between the canals and the otoliths. A simplified model was proposed by Bos and Bles [34] that there is only one conflict: between the subjective expected vertical and the sensed vertical. However, despite this apparent simplification, the underlying model is necessarily complex and finds difficulty in accounting for the observation that motion sickness can be induced by types of optokinetic stimuli which pose no conflict concerning the Earth vertical [35]. A useful set of rules was proposed by Stott [36], which, if broken, will lead to motion sickness: Rule 1. Visual-vestibular: motion of the head in one direction must result in motion of the external visual scene in the opposite direction; Rule 2. Canal-otolith: rotation of the head, other than in the horizontal plane, must be accompanied by appropriate angular change in the direction of the gravity vector; and Rule 3. Utricle-saccule: any sustained linear acceleration is due to gravity, has an intensity of 1 g and defines ‘downwards’. In other words, the visual world should remain space stable, and gravity should always point down and average over a few seconds to 1 g.
The above describes what might be termed the ‘how’ of motion sickness in terms of mechanisms. By contrast it is necessary to look elsewhere for an understanding of the ‘why’ of motion sickness. Motion sickness itself could have evolved from a system designed to protect from potential ingestion of neurotoxins by inducing vomiting when unexpected central nervous system inputs are detected, the ‘toxin detector’ theory [37]. This system would then be activated by modern methods of transport that cause mismatch. This theory is consistent with the observation that people who are more susceptible to motion sickness are also more susceptible to emetic toxins, chemotherapy sickness, and postoperative nausea and vomiting (PONV) [38]. In addition, this theory has been experimentally tested with evidence of reduced emetic response to challenge from toxins after bilateral vestibular ablation [39]. Less popular alternatives to the toxin detector hypothesis propose that motion sickness could be the result of aberrant activation of vestibular-cardiovascular reflexes [40] or that it might originate from a warning system that evolved to discourage development of perceptual motor programmes that are inefficient or cause spatial disorientation [41].
8.3.3 Individual Differences in Motion Sickness Susceptibility
Individuals vary widely in their susceptibility, and there is evidence from twin studies that a large proportion of this variation can be accounted for by genetic factors with heritability estimates around 55–70 % [42]. Some groups of people have particular risk factors. Infants and very young children are immune to motion sickness with motion sickness susceptibility beginning from perhaps around 6–7 years of age and peaking around 9–10 years. Following the peak susceptibility, there is a subsequent decline of susceptibility during the teenage years towards adulthood around 20 years which may reflect habituation. Women appear somewhat more susceptible to motion sickness than men; women show higher incidences of vomiting and report a higher incidence of symptoms such as nausea and vomit more than men (surveys of passengers at sea indicate a five to three female to male risk ratio for vomiting) with susceptibility varying over the menstrual cycle, peaking around menstruation [43]. The elevated susceptibility of females to motion sickness, postoperative nausea/vomiting or chemotherapy-induced nausea/vomiting may serve an evolutionary function. Thus, more sensitive sickness thresholds in females may serve to prevent exposure of the foetus to harmful toxins during pregnancy.
8.3.4 Special Groups: Vestibular Disorders and Migraine
Individuals who have complete bilateral loss of labyrinthine (vestibular apparatus) function are largely immune to motion sickness. However, this may not be true under all circumstances since some bilateral labyrinthine defective individuals are still susceptible to motion sickness provoked by visual stimuli designed to induce self-vection during pseudo-coriolis stimulation, i.e. pitching head movements in a rotating visual field [44]. Certain groups with medical conditions may be at elevated risk. Many patients with vestibular pathology and disease and vertigo can be especially sensitive to any type of motion. The well-known association amongst migraine, motion sickness sensitivity and Meniere’s disease dates back to the initial description of the syndrome by Prosper Meniere in 1861. Patients with vestibular migraine are especially susceptible to motion sickness [45]. The reason for the elevated motion sickness susceptibility in migraineurs (without overt vestibular disease) is not known, but may be due to altered serotonergic system functioning [46]. Support for this possibility was provided by the observation that the serotonin 1B/1D agonist rizatriptan provided significant anti-motion sickness effects in migraineurs [47]. However, rizatriptan did not provide significant protection against exposure to more provocative vestibular stimulation, suggesting that the role of rizatriptan in this context is more likely to be as a modulator of susceptibility rather than a direct ‘blocker’ of motion sickness. It is possible that there are several underlying and overlapping mechanisms for this link, including pain pathways and autonomic reactivity [48]. The complexity of any association between migraine and motion sickness is illustrated by Bosser et al. [49] who surveyed the general population (i.e. unselected for severe migraine as in migraineurs requiring medical help or attending migraine clinics). This survey demonstrated the expected significant bivariate association between elevated motion sickness susceptibility and migraine. However, when these data were reanalysed using multivariate techniques, the existence of any independent association of motion sickness with migraine disappeared and was replaced by other more important predictors such as syncope and autonomic reactivity [49].
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