The symptom set of “visual vertigo” (VV) (Bronstein, 1995) or “visual vestibular mismatch” (VVM) (Longridge and Mallinson, 2002) has been recognized for some time, and it is one that can be debilitating to some patients. To the North American clinician, use of the term “vertigo” implies a spinning sensation and it is unfortunate that this condition has been defined using the term “visual vertigo”, as this has resulted in the failure of its establishment in the literature as a physical entity, except in specialist clinics, where it is recognized as a valid symptom set. Patients with visual vertigo almost always deny a sense of spinning. To the European clinician, vertigo implies any hallucination of movement, hence the use of the term “non-vertiginous vertigo”. As a result of this difference in definitions in papers written on opposite sides of the Atlantic Ocean, there is an inherent risk for misinterpretation of a patient’s complaint during history taking.
The autonomic subset of symptoms relating to vestibular stimulation (e.g. seasickness) was studied by Maitland (1936). He stated that the “eminently seafaring British nation is conspicuous for its neglect of the study of seasickness”. The understanding of seasickness up to that time reflected the idea that it was not generated by the vestibular system, because vestibular pathology as it was understood at the time (semicircular canal pathology) generated nystagmus, and no nystagmus had been observed in seasick individuals. However Maitland advanced the theory that the symptoms associated with seasickness were in fact generated within the vestibular system, because rotation of a subject could produce the same seasickness syndrome. He observed that there were some cases where the labyrinths were “unduly sensitive”, so that there was a range of responses between subjects to a given stimulation. Interestingly, he noted that the group of people who were most susceptible was also affected by other vestibular stimuli, such as train sickness or car sickness, and that they “also disliked waltzing”. Maitland wondered if the susceptibility in this subset of patients might be due to a conflict of stimuli, perhaps between vestibular impulses and visual signal. Supporting his theory was his observation that people with functionless labyrinths were not susceptible to seasickness, train sickness or any other motion stimulation. On the other hand he questioned his own theory, and wondered how visual stimulation could be playing a role, as he was aware that vertiginous symptoms “may still occur on shutting out the visual field by closure of the eyes”.
Preber (1958) embarked on a large study of vegetative or autonomic correlates of vestibular stimulation, elicited either by physiological stimulation or by caloric tests. He attempted to quantify the autonomic responses by correlating the level of the vegetative response with nystagmus elicited during caloric testing. His work suggested an association between motion sickness susceptibility and speed of caloric induced nystagmus. In his detailed account, Preber discussed his findings but also alluded to the fact that labyrinthine stimulation using caloric irrigation may not play a major role in the generation of vegetative responses. He referenced earlier work by Hulk and Henkes (1950) who had studied vegetative reactions of labyrinthine origin by measuring retinal blood pressure. They had found that rotatory vestibular stimulation did not induce reactive changes in retinal blood pressure, but the phenomenon appeared consistently in 50% of patients after a slight otolithic stimulation using a “parallel balance test”, (which was essentially a linear swing, producing a translational, rather than a rotational stimulus). The response was not seen in patients with loss of labyrinthine function, and did not appear after administration of tetra-ammonium bromide (which produces a transitory paralysis of the peripheral vegetative receptors in the labyrinth). Hulk and Henkes concluded that stimuli acting on the semicircular canals do not elicit any vegetative responses, but otolithic stimulation induced a specific and sensitive reaction from the “vegetative nervous system” as they called it, as measured by changes in retinal blood pressure.
Based largely on this work, Preber suggested that “overstimulation of the labyrinths” was the primary factor in the pathogenesis of motion sickness. It was also suggested by Guedry (1970) that while the concept of “overstimulation” of the labyrinths might be important in the generation of motion sickness, “conflicting data from the visual, vestibular and somatosensory systems may be the important aspect of the stimulus”.
HISTORICAL PERSPECTIVES – DIZZINESS THROUGH THE AGES
The awareness of an interface between vertigo and affective symptoms has been recognized since antiquity. Soranus of Ephesus (AD 98 – AD 138) was one of the most learned physicians of classical times, and his obstetrics and gynecology tests were still plagiarized 1500 years later, as they contained many valuable contributions that could have been written in modern times, including the forerunner of the Apgar score still used today. His extensive text about acute and chronic disease has been lost, but a fifth century translation, Tardarum Passionum (Caelius Aurelianus) describes “scotomia” (dizzy complaints), and includes both moving stimuli and gazing down from heights as provocative situations:
“The disease is aggravated if the patient watches the flow of a river from a high point, or gazes at a potter’s wheel or does anything when bending forward”.
Soranus also described vertigo “accompanied by sweating of the upper parts of the body”. For those who do not have the Latin skills to digest the Tardarum Passionum, this understanding is outlined in delightful detail by Balaban and Jacob (2001).
In the 6th century, the famous physician Galen recognized that vertigo could be brought on by being “whirled around in a circle” but could also be brought on in the absence of movement (“if they watch a turning wheel or look at the so-called whirls in a river”). He also recognized individual differences and inferred that there was a wide range of interindividual susceptibility or sensitivity, noting that “some people are affected even if they are not rotated, although others must be rotated several times in a circle”.
This “understanding by observation” 1500 years ago of the vestibular system suggested two aspects of it which are still accepted today:
- There is a large interindividual variation in susceptibility to the symptoms.
- There are certain situations that will generate symptoms
The second point (the idea of a “situation specific” disorder) implies that there is a link between the organic symptoms and psychiatric disorders. This link was initially detailed in the 17th century, when the symptoms of vertigo were regarded as a principal sign of “hypochondriacal melancholy”. By the 19th century vertigo was defined as a neurological disorder. The related affective symptoms were recognized as well, but they had an ambiguous status as being either of neurologic or psychiatric origin.
As dizziness became more accepted as a brain disease, the accompanying signs were still regarded as a physical disorder that accompanied insanity. Westphal in 1871 developed an understanding of the situation specific interface and resulting symptoms of anxiety that were generated by vertigo. He developed the term “agoraphobia” (literally “fear of the marketplace”) to describe his patients’ fear of walking in an open square. As a treatment modality, he also suggested that a patient could overcome their fear by “fixating on a specific line or on an object that is moving away from them”. Westphal was perplexed by the fact that his patients’ symptom set never involved “vertigo” as he understood it (sensation of spinning) (Balaban and Jacob, 2001). Relevance of this observation to Bronstein’s (1995) patients with visual vertigo (i.e. nonvertiginous vertigo) will be discussed later.
Cordes in 1870 wrote of his personal experiences with height phobia and that it generated “sensations of nonrotatory movement, like being on a boat”. As these reports did not conform to the classic complaints of vertigo, they were dismissed as being caused by nervous exhaustion or muscle weakness.
At about the same time, there was also an accumulating body of evidence that symptoms of vertigo might be generated by the ear and the VIIIth cranial nerve. The physiologist Flourens in 1825 published his work in German outlining his experiments (Barany, 1916). Flourens thought it would be possible to get an insight into the workings of the semicircular canal structure in the pigeon by destroying the structure. His work with pigeons, rabbits and other animals demonstrated consistent results, showing for instance that destruction of a horizontal semicircular canal in a pigeon resulted in it turning in circles. Destruction of a vertical canal resulted in it turning somersaults (Barany and Ibershoff, 1910). Although his descriptions were excellent, Flourens did not recognize that the animal was probably suffering from vertigo.
Unknown to Flourens, Purkinje was working in Prague and treating violent prisoners in a cage by inducing nausea, which helped to calm them down. He discovered nystagmus, described the effect of head position on vertigo, and showed that the symptom set arose in the head itself. He was aware of Flourens’ work but failed to “put two and two together”, because he thought that the vertigo in his prisoners arose not from the ear, but from the brain.
Understanding of the inner ear stood still for almost 40 more years. The work of Prosper Ménière, publicized in 1861 (the year he died) was driven by clinical observations in patients (Barany, 1916). Ménière had observed the frequent correlation of vertigo with tinnitus in patients who had normal middle ear function. The cochlea was known at the time to be the site of hearing but the semicircular canal attached to it was thought to have no function at all. Although vertigo was still accepted as a disease of the cerebellum, Ménière’s vertiginous patients developed no signs of brain disease over the years and he had the idea that semicircular canal pathology was responsible for the production of vertigo in his patients.
Barany’s work resulted in the source of vertigo being accepted as arising from the inner ear. It was still accepted that these symptoms had multiple manifestations, many affecting the mental senses. Hughlings Jackson stated that a patient with vertigo also has “horrible depression, he may say that he feels as if he were going to die”. By the early 20th century, the notion of a primal link between loss of a sense of balance and affective disorders became entrenched in psychology. Zwerling (1949) suggested a possibility between “neurotic tendency” and tendency to motion sickness.
There was also an increase in the number of reports of patients who displayed simultaneous symptoms of ear disease (true vertigo) and agoraphobia. The concept of differing susceptibilities was again raised, and it was suggested that there was a certain population of susceptible individuals who could develop agoraphobia in the face of vertigo. Through the 20th century, further understanding of agoraphobia was gained. Panic anxiety became accepted as a diagnostic entity and initial studies reported that abnormalities of vestibular tests were seen in a large proportion of patients with panic disorder (Jacob et al, 1985) and specifically in patients with agoraphobia (Yardley et al, 1994). Furman et al (1998) also outlined a specific relationship between vestibular dysfunction and agoraphobic avoidance. They stated that “pseudoagoraphobic” syndromes in patients with vestibular disorders have long been recognized and that the psychiatric condition of height phobia is also related to vestibular dysfunction.
In 1935, Koffka in his “Principles of Gestalt Psychology” (cited in Balaban and Jacob, 2001) outlined the important role of vision in balance, stating that we “lean on our eyes as we do with our feet” and “as we do with our hands”. However this phenomenon of sensory integration was largely ignored for the next 40 years until McCabe (1975) described “supermarket syndrome” in patients with Ménière’s disease. He described that these patients had “an intolerance for looking back and forth along aisles and up and down shelves”. He outlined that nausea could be caused by motion of a patient with dizziness, but also described “vestibulo-gastric illness”, which included illness caused by movement of a visual field. In short, motion sickness could occur as a result of:
- Real motion
- Passive exposure to real motion
- Apparent motion (“cinerama sickness”)
Although there was an acceptance of the interaction between visual and vestibular systems, it was unclear how this was postulated to cause symptoms in patients.
The term “visual vertigo” was initially used by Erasmus Darwin in 1797 (Balaban and Jacob, 2001) to designate a visually provoked form of vertigo that arose along with dizziness “when we lose the means of balancing ourselves, or preserving our perpendicularity, by vision”. By the 1870’s, “visual vertigo” referred specifically to vertigo associated with extraocular muscle pathology. Bronstein (1995) has broadened the term to designate any visually induced vertiginous syndrome (using the European definition of vertigo; any sensation of movement of self or surroundings). He has used the term to describe a set of symptoms similar to McCabe’s “supermarket syndrome” (1975) (i.e. the symptom set generated by a visual vestibular disagreement). As discussed previously, Bronstein’s term is a misnomer in North America, as North Americans understand “vertigo” as a spinning sensation. The term “visual vertigo” confuses the situation, as very rarely is there spinning with it. Bronstein initially suggested that visual vertigo resulted from the “dominant role of vision in the control of posture” (1986). He later outlined the problems with this dominant role, as it could result in a symptom complex that arose from a process of compensating for vestibular injury that is interfered with by unusually high visual reliance, leading to intolerance to situations of visual conflict.
The term “visual vestibular mismatch” was first used by Benson and King in 1979. They used the term to describe a “motion cue mismatch”. They suggested that it was a part of the system complex known as neural mismatch. It was postulated that there was some kind of central memory which was linked to a “comparator” (anatomical location unknown and not suggested) where sensory information was correlated with the neural store. If the input signals from the receptors did not agree with the expected (i.e. stored) information, then a mismatch signal was generated. It was postulated that the newly developed signal served two purposes; to update the stored signal, and to initiate the neurovegetative and sensory responses colloquially referred to as motion sickness. The evolutionary role of the response was not addressed, although Longridge (1993) was the first to suggest a role for the autonomic aspects of vestibular response. He postulated that the anorexic part of the vegetative symptoms specifically occurring in vestibular disease may have been beneficial in preventing an unbalanced and vulnerable animal from foraging for food. In other words, the autonomic symptoms of vestibular disease may have evolved to make an animal unwell enough to stay home when vertiginous, keeping it in relative safety.
Paige (1992) introduced the term “visual vestibular mismatch” into the clinical literature, using it in a different sense from that used by Benson and King. He used the term to refer to the differing signals between two sensory inputs (rather than a differential between a sensory input and a stored template). Paige reviewed the literature showing that anatomical deterioration of all vestibular structures occurs with aging; this reaches 40% by the 9th decade. He also showed that patients had visual problems which were not directly related to the vestibular senesence. Adaptive plastic mechanisms (which normally maintain VOR performance under conditions of head movement) also deteriorate with aging. If the senescence of these two systems did not occur in parallel, (which would prevent them from being effectively integrated), a resulting mismatch between the two signals would occur. Paige found that the performance in his elderly patients on vestibular assessment tests was the same as in younger patients with documented vestibular abnormalities, and he suggested that it was this mismatch in the older patients that had been created by the nonparallel senescence, that “mimicked” the vestibular loss in the younger patients. Paige made the point that there was definitely a senescence of vestibular function but made no guess as to whether it affected the semicircular canals, otolithic structures, or both. He did bring up the frequency of complaints of “imbalance”, as opposed to “vertigo”, in his elderly patients.
Paige’s suggestions were that visual vestibular mismatch might develop as an inability in elderly people to recalibrate the VOR to an appropriate level (although he stated that evidence for this was scant). Alternatively, he suggested that the senescence-related reduction of vestibular input might directly impair adaptive capabilities. He did state that, regardless of the mechanism, the elderly were compromised in their abilities to “control eye movements that serve to maintain gaze, and therefore retinal image stability”.
In this thesis, the term “visual vestibular mismatch” is similar in some respects to the situation outlined by Paige, but the thesis suggests that this mismatch can occur at any age as a result of vestibular pathology. In other words, the development de novo of visual vestibular mismatch is suggestive of a balance system lesion (Mallinson and Longridge 1998). The physiologic mechanisms involved in compensation for balance system damage have been investigated extensively, and can be used to explain why a vestibular lesion can create visual vestibular mismatch. Vision clearly plays a role in postural control in healthy subjects, but the role is secondary, in that vestibular information acts as the template. For example, a visual illusion of movement (e.g. watching a 3D movie) is disregarded by the vestibular system, as the vestibular signal suggests that the illusion of movement is artificial and does not need to be acted on. In the absence of perfectly reliable vestibular information, a dogmatic dependence on visual information is developed to maintain balance, so that patients with vestibular disorders become even more visually dependent for balance (Redfern et al, 2001). Under the 3D movie situation, the “visual preference strategy” can generate an “appropriate” response to the perceived movement, and generate concomitant autonomic responses.
In addition, an increased visual dependence might limit a patient’s ability to compensate fully for a vestibular disorder, particularly where there is a sensory conflict due to excessive visual motion (Guerraz et al, 2001). As a result of this sensory conflict, many patients with vestibular disorders are not able to integrate visual and vestibular function in an appropriate manner. It seems that some patients have an intolerance for any discrepancy between visual and vestibular signals. Some individuals are exceedingly sensitive to any signal disagreement, in the same way that some individuals are exceedingly motion sick. This results in the development of posttraumatic motion sickness, visual vestibular mismatch, or both. These two attributes may be similar in nature, as individuals with other motion sensitivities, such as motion sickness, are unable to disregard erroneous visual cues (Redfern et al, 2001).
Visual vestibular mismatch is difficult to diagnose because of a severe lack of adequate investigation tools, a limited ability to measure degree of injury in these patients, and because there is a wide inter-individual variability between degree of injury and intensity of symptoms.
The exploration of space has vastly improved our understanding of the vestibular system, as microgravity is the only situation in which vestibular responses can be considered to be “off line”. The symptom set of “space motion sickness” (SMS) was reported by Soviet cosmonauts, and also reported consistently by orbiting American astronauts. The “sensory conflict theory” to explain motion sickness was accepted at the time, and it predicted that motion sickness should occur in space (Oman et al, 1986).
The sensory conflict theory did not attempt to pinpoint the anatomic site of space motion sickness. The theory dictated that there was a “conflict between sensory input and a signal originating in centres responsible for processing body movement control and spatial orientation information”.
As we know in patients, there is a wide interindividual variability with respect to symptoms. Oman et al commented on the wide range of interindividual susceptibility that they noted in their space motion sick patients. However they were confused by the fact that when they measured motion sickness susceptibility on earth, and then compared it to space sickness intensity rankings, the least and most susceptible subjects reversed position. They came to the conclusion that space sickness was fundamentally a motion sickness, and that head movements were a clearly identifiable stimulus. As will be seen, this closely parallels patients with symptoms of visual vestibular mismatch, and interestingly, it has been suggested (Mallinson and Longridge 1998, 1998) that the new development of motion sickness in a patient is suggestive of a balance system deficit. Work presented in this thesis helps to form the hypothesis that this may result from disagreement between semicircular canal and otolith signals, similar to Oman’s theory.
Black et al (1999) recognized that in addition to space motion sickness, disturbances in postural equilibrium and gait upon return from space were among the most consistently observed consequences of space flight. In their study of four astronauts, post flight performance variabilities were compared between astronauts, and it was found that that one of them performed balance tests very poorly post flight. This was totally unexpected, as he had not shown these deficits after his previous flights. However this astronaut had undergone an additional eccentric pitch axis rotation test after landing, and the theory was that this additional stimulation had interfered with the readaptation process post flight. They concluded that the stimuli to the otoliths in this one individual was what disrupted his recovery, and that post flight postural instability in astronauts resulted from disrupted processing of otolithic inputs.
Disturbances of postural equilibrium are also seen in patients, to the point where they have measurable abnormalities on Computerized Dynamic Posturography (Equitest®), but these abnormalities are nonspecific, and patients often show below par performance on all six Sensory Organization Test conditions.
The two aspects of space motion sickness (i.e. symptoms of nausea and also signs of extreme imbalance) are well documented. Do they have a common origin? In microgravity, there is no reason to suspect that canal stimuli or canal function would be radically altered by microgravity (Parker, 1998). This suggests that the sensory conflict in space motion sickness and also on earth relates to a canal-otolith conflict. The conclusion was that this conflict was responsible for postural instability and disorientation in astronauts after landing (Black et al, 1999), and it was suggested that the otoliths also play a major role in the development of space motion sickness (Parker, 1998). It is unclear whether the symptoms of space motion sickness precede or occur after the postural instability, but the understanding has developed to the point where the balance and autonomic/visceral control centres, traditionally viewed as separated, should now be considered as one functional entity (Oman 1998). This was originally proposed by Preber (1958) who stated that “ … the symptoms [of motion sickness] are the same whether they result from the movement of ships, aircraft or cars”.
While the evidence presented suggests that these symptoms arise from (and are suggestive of the presence of) peripheral balance system disease, a clinician cannot rule out other causes, as it is possible that in neurological disease, this symptom complex can occur due to central dysfunction.
Why does the high visual reliance suggested by Bronstein (1995) develop and cause the symptom set known as visual vestibular mismatch? It is now clear that the symptoms of VVM (in some people at least) are not suggestive of “neurologic damage” or “psychiatric disease”. Bronstein suggested that visual reliance was the natural compensation mechanism and that visual information would now automatically dominate a situation where previously reliable vestibular information had been compromised. The probable mechanism as outlined by Mallinson and Longridge (1998) related to the fact that even under normal environmental conditions, physiological flaws in sensory systems exist. Under normal environmental circumstances, visual and vestibular information often do not match, and physiological shortcomings of one system can be looked after by the other. In the normal individual, vestibular information is regarded as the most reliable frame of reference signal (always reliable because it is referenced to gravity) and the vestibular system is most capable of accurately detecting movement within this frame of reference. For example, if a passenger is sitting in a car at a stop sign on a hill and observes movement of a car in front, the visual signal alone is incapable of determining which car is moving (i.e. “them rolling back, or me creeping forward”), because the visual signal will be identical for either situation. The advantage of the vestibular system is that it can detect the presence or absence of acceleration. If an accurate vestibular signal is incorporated into the paradigm, then it can be determined whether it is the individual, or the surroundings that are moving. It has been suggested that detecting the presence or absence of self movement in this way is a role of the otoliths, because as discussed earlier, disrupted processing of otolith inputs upon return from orbital flight is probably the source of postural instability of astronauts post flight (Black et al, 1999).
It is important to reiterate that Paige (1992) suggests that creation of visual vestibular mismatch occurs due to an asymmetric senescence, but the use of the term by Mallinson et al (1995), and Mallinson and Longridge (1998 , 1998 ) refers to a certain clinical situation; one where a distorted, impaired or adulterated vestibular signal is generated. The signal distortion creates a mismatch between visual environmental information and the vestibular reference signal. Our initial work has suggested strongly that the deficit is otolithic, and this thesis postulates that in the presence of an otolithic deficit, there is a decreased ability of the vestibular system to calculate self movement in an accurate manner. Under these circumstances, the visual signal is “over relied” on and, as suggested by Bronstein, the hypothesis is that in many cases visual information becomes the new “template” for maintaining stability with respect to one’s environment (Mallinson and Longridge, 1998).
In addition to the well known vegetative responses related to visual vestibular mismatch, there are also other factors at play and these have been recognized, albeit not understood for some time. The symptoms of visual vestibular mismatch can involve vegetative and also postural symptoms to varying degrees. I have wondered why some patients have predominantly postural, rather than vegetative signs and symptoms. Some patients are aware of only the postural features (“I feel like I’m on a boat all the time”) while some are aware of only the vegetative features (“I feel sweaty and nauseated all the time”). Again, there is a complete lack of tests to document this malfunction. Any movement in one’s visual environment can potentially be interpreted as self movement, and this can create symptoms of newly developed visual vestibular mismatch in subjects who are sensitive to such signal differences. The resulting over reliance or mismatch between vestibular and visual signals can create an unsafe environment at heights, on ladders, and in other situations where good balance is necessary. In addition, it can put people at risk recreationally. For example jogging through a sunny forest with the sunlight flickering through the trees, jogging along a beach watching the waves roll in, or even enjoying carnival rides are examples of recreational pursuits that could cause symptoms and/or create potentially injurious situations. Sports pursuits requiring exact knowledge of body position (golf, skiing, horseback riding, basketball, badminton, among many) are all pursuits that could potentially be injurious or much less enjoyable.
In summary, these patients sometimes have signs of imbalance, but sometimes only symptoms of imbalance (patients and their family/friends often deny any noticeable imbalance). Sometimes (but not always) autonomic symptoms (motion sickness and space motion sickness) can be present. It can be seen that the symptom set (whether autonomic or just a perception of imbalance) can generate distress which could result in avoidance behaviour (hence the labeling of these patients as agoraphobics), and ironically the best advice might be a reiteration of that offered by Borde in 1547: “Such men having this passion let them beware of climbing or going up upon high hills or round stairs” (cited in Balaban and Porter, 1998).
Identifying visual vestibular mismatch requires careful history taking. While obtaining the history, it is important to ask questions specific to visual vestibular mismatch in a roundabout, indirect, non-leading manner. A nine-question questionnaire was originally developed and then refined into a set of five questions related to visual vestibular mismatch (Longridge and Mallinson, 2005) (Appendix one). This questionnaire has been introduced into the literature for guidance during history taking. Modern day patients often volunteer complaints of nausea or instability in specific visual environments such as crowds or shopping malls, and are often bothered by escalators or traffic. Mallinson and Longridge (1998 ) suspected that visual vestibular mismatch was not an ingrained symptom that is seen in normal people, and regarded its development de novo as being representative of balance system disease. A set of five questions was developed to delineate a patient’s sensitivity, and classify them as “VVM positive” (3, 4 or 5 positive answers) or “VVM negative” (0, 1 or 2 positive answers). This question set is still used in the clinical setting.
Visual vestibular mismatch is often seen in patients with work related head trauma (Longridge and Mallinson, 2005) and after whiplash type injury (Mallinson and Longridge, 1998(2)), and can also be caused by intratympanic gentamicin treatment for Ménière’s disease (Longridge, Mallinson and Denton, 2002). It can rarely occur spontaneously without other vestibular complaints.
It became apparent that visual vestibular mismatch could occur in many circumstances:
- After head trauma (McCabe, 1975)
- Resulting from recognized ear disease (e.g. diagnosed Ménière’s disease) (Longridge et al, 2002)
- After intratympanic gentamicin therapy for Ménière’s disease.
- Related to other vestibular disease (e.g. acute or recurrent vestibulopathy)
- Spontaneously (in very rare instances)
It was also suggested that in patients with vestibular disease arising from a wide variety of causes, a common thread in a subgroup of patients from each category was that they developed the symptom set outlined as visual vestibular mismatch. I wondered if it might be seen in the whiplash population, head injury population, or in the group of patients with more traditional complaints (spinning vertigo sometimes seen in patients who have traditional vestibular disease). If this could be answered, it might be easier to make inferences about the causes of VVM. It was possible that otolithic decline might be partly responsible for the development of imbalance. A hypothesis was developed that there might be a common mechanism of damage, as the symptoms caused were identical regardless of the category of patient (i.e. a given patient could not be categorized according to their history). It was further hypothesized that the common pathogenic process involved a lesion in the balance system, and if the cause of injury could be identified, it might be possible to allege a certain mechanism of injury. This was the initial intention of the experiments discussed in my thesis.