Visual vestibular mismatch in work-related vestibular injury
Mallinson AI, Longridge NS.
Otol Neurotol 2005 July;26(4):691-4.
Objective: To define and investigate the symptom set known as visual- vestibular mismatch and analyze its nature and occurrence in two groups of patients referred for dizziness.
Study Design: Prospective study of two groups of sequentially referred patients complaining of dizziness, imbalance, or both.
Setting: A tertiary and quaternary care ambulatory referral center.
Patients: Two groups of patients were studied. One was a group of patients who had suffered work-related head trauma and had subsequent complaints of dizziness and/or imbalance. The other was a group of patients referred for dizziness and/or imbalance who had no history of head trauma, work-related injury, or litigation procedures.
Interventions: Standard vestibular assessment including Computerized Dynamic Posturography was carried out on all patients. A series of questions was designed to quantify patients' complaints of symptoms of visual-vestibular mismatch, and patients were scored according to their yes/no answers to the five questions.
Main Outcome Measures: Results of traditional vestibular tests were correlated with the answers to the questions. Computerized Dynamic Posturography and electronystagmography results were compared between both symptomatic and nonsymptomatic patients and also between patients who had traumatic and nontraumatic causes of their symptoms.
Results: We found no correlation between test results and the presence of visual-vestibular mismatch symptomatology. There does seem to be a connection between the presence of motion sickness symptomatology and the development of visual-vestibular mismatch symptoms.
Conclusion: Although visual-vestibular mismatch is of vestibular origin, it is discernible only after obtaining a careful history. It is a genuine symptom set of vestibular origin, and there is a certain group of patients who are more sensitive to this symptom set and who are often debilitated by its presence.
Visual stimulation alone can provoke vertiginous symptoms, and this was clearly outlined in some of the earliest medical writings. Soranus of Ephesus in the first century included moving visual stimuli (e.g., watching water flow or a potter's wheel rotating) as being provocative situations for vertigo. Galen observed that some people “could be affected even if they are not rotated.'' For a delightful account of the history of this phenomenon, the reader is referred to Balaban and Jacob (1).
The term “visual vertigo'' (VV) was originally used by Erasmus Darwin in 1797 (cited in Balaban and Jacob ). The first connection between vertigo and seasickness was made by Hughlings Jackson in 1872 (1). More recently, Dichgans and Brandt (2) described the normal phenomenon of “motion perception,'' in which visual stimuli induce transient sensations of movement and also symptoms of motion sickness.
Bronstein (3) suggested that the clinical symptoms of VV arise when the process of compensation from vestibular injury is disrupted by unusually high reliance on visual cues, leading to abnormal visually induced sway. Guerraz et al. (4) suggested that the development of VV was probably related to some idiosyncratic perceptual style.
The term “visual vestibular mismatch'' (VVM) was originally used in the literature by Benson and King (5). Paige (6) redefined the term in reference to imbalance in the elderly, which he suggested could be the result of a difference in the rates of senescence in visual and vestibular function. However, the term has been redefined (7-9) as a symptom set generated by a discongruency between visual and vestibular signals. One-third of patients develop VVM complaints after intratympanic gentamicin therapy (8). We suspect that the development of VVM may indicate the presence of damage to the balance system. Our findings in treated Ménière's patients supports the statement by Furman and Jacob that these “…situational symptoms appear to be associated specifically with vestibular dysfunction'' (10). Although patients are often markedly symptomatic, this dysfunction is often undetectable using standardized methods of vestibular measurement, such as electronystagmography (ENG) and computerized dynamic posturography (CDP). McCabe in 1975 (11) described a similar set of symptoms and coined the term “supermarket syndrome,'' defined as “an intolerance for looking back and forth… up and down aisles.'' Furman et al. (12) referred to the symptom set as “space motion discomfort'' in 1997 and advanced solid clinical and anatomic evidence that the vestibular system participates in autonomic control, perhaps via vestibular nuclear and cerebellar regions that appear to integrate vestibular and autonomic information (13). Whiplash-related damage to some site in the balance system, either peripheral or central, also results in the generation of VVM (7), and 30% of patients undergoing intratympanic gentamicin therapy for intractable dizziness (i.e., iatrogenic vestibular damage) have been reported to develop VVM (9). VVM has come to be regarded by us as a symptom set that develops in some patients after suffering vestibular injury.
The importance of a mismatch between vestibular and visual input was alluded to by Brandt et al. (14) in describing “physiological height vertigo,'' in which the distance between observer and visible stationary contrasts is very large. We postulate that this mismatch is analogous to VVM and can also be created by vestibular injury, and we have come to regard the new development of fear of heights as indicative of a vestibular insult. Where is VVM generated? We have had the opportunity to examine the occurrence of VVM in two groups of patients: quaternary care referrals to our clinic from otolaryngologists and neurologists with various complaints of nontraumatic dizziness, and workers' compensation patients suffering dizziness and imbalance after work-related head injury. We felt this provided us with an ideal setting in which to examine the genesis of VVM. Did it result from peripheral end-organ symptoms or from perhaps more central damage suffered in a head blow? We also wished to determine whether VVM symptoms could be diagnosed by the “traditional'' vestibular assessment techniques of CDP and ENG.
PATIENTS AND METHODS
In a prospective study, 61 patients referred to our clinic for assessment of nontraumatic dizziness were analyzed. All patients underwent an extensive otoneurologic history, completed a dizziness questionnaire, and underwent laboratory balance assessment with ENG according to Barber and Stockwell (15) and CDP using the Equitest (Neurocom, Inc., Clackamas, OR, U.S.A.).
Included in the history-taking was the questioning in a non-leading fashion about VVM symptoms, using five VVM-specific questions (Table 1). We have purposely avoided putting the five questions into our questionnaire, which might serve to cue a patient in advance. Our history-taking is structured so that the five VVM questions are asked in a more roundabout manner, rather than being posed directly.
We excluded certain patients from the group of 61, as follows:
- Patients who had been involved in motor vehicle accidents.
- Patients who had developed symptoms after any type of head blow.
- Patients who did not have the language skills to answer our five VVM questions.
- Patients who were physically unable to complete posturography.
One hundred nine patients referred to us by the Workers' Compensation Board (WCB) were assessed in an identical manner. All patients had complaints of dizziness that came on after some type of work-related head trauma. All patents had had a neurologic examination, and it was felt that their complaints were not of neurologic origin.
All medical examinations were carried out by one of us (N.S.L.) and all diagnostic assessments and interpretations were carried out by the other (A.I.M.). Each assessor was blinded for the duration of the assessment with regard to impressions that might have been formed by the other. Three patients of the original WCB referrals were excluded, as follows:
- A patient with a sole complaint of tinnitus.
- A patient with a sole complaint of anosmia.
- A patient who had suffered recent gentamicin toxicity related to infection of orthopedic injuries from his accident.
TABLE 1. VVM questions asked during history-taking
Are you made unwell by any of the following stimuli?
- Going on an escalator
- Watching traffic at an intersection
- Being in a supermarket
- Walking in a mall
- Seeing checkerboard floor patterns
Of the two groups we studied, our trauma patients (the WCB-referred patients) were slightly younger and much more male-dominated, likely because most “dangerous'' occupations (e.g., forestry workers, construction, longshoremen) are traditionally dominated by younger men. One WCB patient was unable to complete posturography because of extreme nausea. Two patients in this group were unable to answer our VVM questions, as they had had no exposure to any of the offending stimuli.
Table 1 outlines our VVM-specific questions asked during history-taking in a nonleading fashion. We identified them as being VVM specific (i.e., the most common indicators of complaints of VVM) in a previous study (9). For the purposes of this study, we regarded a VVM-positive patient as one having a positive response to at least three of the five aggravating factors. Patients reporting a positive response to zero, one, or two of the five questions were categorized as VVM-negatives. We felt that positive answers to one or even two of the questions could represent suggestion or perhaps coincidence. We consider that sensitivity to three different aggravating factors suggests the presence of VVM. Table 2 outlines our data in the two groups of patients. All data were analyzed using a _Χ_² analysis to determine significance. The only significant differences seen between the trauma and nontrauma groups were in the VVM-negative patients. Posturography results were significantly different in the VVM-negatives between the trauma and nontrauma groups. It was abnormal in 87% of the trauma group but in only 56% of the non-trauma group.
Table 2. Comparison of nontrauma and trauma patients
||Trauma (n=109) (%)
||Nontrauma (n=61) (%)
||100/9 (92% male)
||23/38 (38% male)
|Negative VVM (0, 1, or 2 VVM score)
|Positive VVM (3, 4, or 5 VVM score)
|ANALYSIS OF POSITIVE VVM POPULATION
| Number of patients
| Abnormal posturography
| Abnormal calorics
|ANALYSIS OF NEGATIVE VVM POPULATION
| Number of patients
| Abnormal posturography
| Abnormal calorics
ap < 0.001
Table 3. Comparison of VVM groups
|No. of patients
ap < 0.001
The concept of VVM has only recently come to be accepted as a physiologic rather than a psychological phenomenon and to perhaps be of balance system origin. Our patients with VVM differ from the patients described by Bronstein (3) in that some of them are not physically destabilized by orientationally inaccurate visual stimuli. This is evidenced by the fact that there was no difference in CDP performance between our VVM-positives and our VVM- negatives. However, our VVM patients characteristically develop autonomic symptoms (e.g., nausea, sweating, pallor, and panic), which are all components of the space motion discomfort symptoms outlined by Furman et al. (12). Certain patients are rendered totally incapacitated by the severity of this symptom set, and it can become a chronic condition.
Where is the VVM-causing abnormality located? It does not seem to be caused by head injury; 30% of our nontrauma group fell into the VVM-positive category, and 29% of our trauma group was VVM-positive. The trauma group's complaints were felt not to be neurologic, and both groups of patients voiced markedly similar complaints that were characteristically vestibular, in addition to their complaints of VVM. From this, it seems to us that VVM has arisen from damage that has occurred somewhere in the balance system. If VVM were brought on by head injury itself, we would expect to see a very high percentage of VVM-positives in our head-injured group.
Table 3 shows that measurement of VVM is difficult from an objective point of view, which can pose a challenge to the assessment of such patients. There was no difference in CDP performance between VVM-positive and VVM-negative patients. Calorics also were of no use in differentiating VVM-positives from VVM- negatives. The only distinguishing feature between the two groups was the significant difference in motion sickness, with only 27% of the VVM-negatives being motion sick, as opposed to 76% of the VVM-positives. Although it is possible that there is a psychological aspect to the complaints of some of our patients, “psychiatric dizziness'' has recently been redefined as “dizziness occurring exclusively in combination with other symptoms as part of a recognized psychiatric symptom cluster'' (10). This was not evident in any of our patients.
The histories of our VVM patients are virtually identical to patients we have seen who have developed symptoms after suffering whiplash-associated injuries but no head injury and patients who developed symptoms after intratympanic gentamicin therapy.
VVM is not physically destabilizing, but we repeatedly encountered patients in whom the unpleasant symptom set can be severe. It can only be elucidated by obtaining a very careful history. VVM does not seem to be brought on by head injury as such, and it cannot be delineated using standard vestibular investigations. We have delineated a category of “susceptible'' patients in whom the vestibular disruption is not necessarily destabilizing but rather invokes an autonomic motion sickness-like cascade of symptoms. These symptoms are physiologic rather than psychogenic, and we recognize them in patients with a variety of vestibular disorders. They encompass a wide variety of symptoms, and standard vestibular assessments are often not helpful in measuring their deficits. Nevertheless, we regard the development of VVM symptoms (which sometimes can be debilitating) as arising from the inner ear.
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