Visual Vestibular Mismatch

A poorly understood presentation of balance system disease

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Chapter 3

Dizziness, imbalance and whiplash

Mallinson AI, Longridge NS. Peacock C.

Journal of Musculoskeletal Pain 1996;4(4):105-112.

ABSTRACT

Eighteen patients were evaluated for dizziness and imbalance resulting from whiplash associated disorder. Assessment consisted of standard caloric testing and Computerized Dynamic Posturography (CDP). Although the standard vestibular tests showed no abnormalities in any of these patients, thirteen of them had abnormalities on CDP. The concept of dizziness is variously attributed to problems from the neck, brainstem or bloodflow to the brain and is ill defined in the literature. In our patients, efforts were made to delineate specifically the patient’s complaints by careful history, which included anecdotal problems the patient reported that were recognized as possibly coming from the balance system of the inner ear. Dizziness may be attributable to a vestibular site of lesion, with the CDP results supporting a provisional diagnosis that somehow implicates the balance system of the inner ear.

KEYWORDS: whiplash, dizziness, imbalance, posturography

INTRODUCTION

In a rear end collision, the body accelerates forward while the head’s inertia causes it to lag behind. The resulting extension ends when the soft tissues reach their limit of tension or compression, or when the head is stopped by the headrest of the vehicle. The head then rebounds forward, resulting in a flexion process. This is the motion of so-called whiplash, and is probably associated with extension, flexion, shear, tension, compression, and possibly other features yet to be elucidated (1).

MacNab (2) showed that there was significant injury to the peri-vertebral musculature in serious whiplash injuries. Prognostic indicators appeared to be the severity of early symptoms including radicular symptomatology of the neck.

Dizziness is often mentioned as a symptom in whiplash associated disorder (WAD) (1,3,4,5). The etiology of vertigo, dizziness and imbalance may be due to stretching of the ligaments in the cervical spine, irritation or damage to the vertebral arterial blood supply and damage to the autonomic nervous system in the cervical spine (5,6). Damage to the inner ear is also a possibility (1,7).

The incidence of dizziness in WAD has been quoted as 21% (4) to 85% (1). The aim of the present paper was to elicit from patients the specific dizzy-related complaints of which they suffer. Patients’ complaints were compared to results
of standardly recognized balance assessment techniques of electronystagmography (ENG) and Computerized Dynamic Posturography (CDP).

It has been observed that some patients have subjective vague complaints of lightheadedness, unsteadiness, and dislike of things moving rapidly past them, particularly in malls, supermarkets or at the edge of a busy road. Fluorescent lighting may be distressing and checkered floors may be bothersome. Visual vestibular mismatch is a recognized syndrome where it is assumed that vestibular input and ocular input do not mesh precisely, resulting in symptomatic awareness of particular difficulties. Excessive nausea and motion sickness are frequent complaints. Although dizziness often resolves, prolonged symptomatology sometimes persists. The current treatment for dizziness is vestibular rehabilitation exercises of the Cawthorne-Cooksey (8,9) variety, but the rehabilitation process for dizziness is sometimes limited by concomitant neck pain. In more severe WAD, some patients may be incapacitated for a prolonged period and may not complain of vertiginous symptoms until several weeks after the accident, at a time when they move around enough to become aware of their difficulty. This might account for some of the short delays in apparent dizziness onset following whiplash trauma.

PATIENTS AND METHODS

This retrospective review was obtained by reviewing motor vehicle accident charts of patients seen by one investigator (NSL), including ENG and CDP data from the preceding three years. Only rear end accidents were included. Pedestrians and patients involved with side swipe or head on collisions were excluded. Patients who had a head injury were excluded. There was no random selection and no control group. Patient assessment consisted of history, otolaryngological and balance physical examination, ENG, audiometry and CDP assessment using EquiTest™ protocol. The ENG (10) protocol included assessment for spontaneous nystagmus with eyes open and eyes closed, gaze nystagmus, optokinetic nystagmus and smooth pursuit. Caloric-induced nystagmus was also assessed, including fixation suppression ratio. Postural testing as described by Barber (11) was not undertaken as it had not been found to be helpful in a study of non-traumatic vertiginous patients (12). The CDP protocol followed exactly the EquiTest™ interpretation manual (13). The Sensory Organization Test (SOT) sequence used in this protocol has been described elsewhere (14).

RESULTS

The charts of 77 patients who had sustained motor vehicle accident injuries were examined. Only 18 patients (Table 1) were pure rear end accidents. All but one were wearing a seat belt. All but one of them had sought medical attention from either their family doctor or a hospital Emergency Ward.

Computerized Dynamic Posturography was abnormal in 13 of 18 patients. In 11 of these 13 patients the abnormality was a specific pattern of abnormality which suggests impairment in the vestibular system. In particular there was poor performance on SOT conditions 5 and/or 6. Two patients had a more generalized abnormality pattern which we have come to assume indicates mild inability to integrate sensory information of balance.

Eight patients had characteristic vestibular syndromes (Table 1) (15): benign positional vertigo, acute vestibulopathy (vestibular neuronitis), recurrent vestibulopathy. Seven of these eight had abnormal posturography patterns, with five of the seven being specific vestibular abnormality patterns.

TABLE 1. Subject Profiles and Responses to Testing

PATIENT

SUBJECTIVE COMPLAINTS

ONSET LATENCY

EQUITEST

1. (38F)

spinning, lightheaded, imbalance, blurred vision

immediately after

#2, signif. incr. with

#3

abnormal vestibular

2. (54M)

feel drunk constantly, worse with head movement

<30 days

grossly abnormal nonspecific

3. (33M)

nausea with head movement,lightheaded

30 minutes

abnormal vestibular

4. (18F)

Nausea, vague imbalance

6 days

normal

5. (42F)

unsteady, clumsy, might fall, like being on a merry-go- round

not known

abnormal vestibular

6. (60M)

like a drunk, blurry vision, feel funny in malls

3 days

abnormal vestibular

7. (28F)

spinning for a week,

trouble bike riding down hills

minutes

abnormal vestibular

8. (46M)

feel seasick,

unsteady if I get up fast

3 days

normal

9. (29F)

“sea legs”, nausea, woozy imbalance, pull to left

7-14 days

abnormal vestibular

10. (28F)

must focus when I walk, motion sickness

<1 day

abnormal vestibular

11. (45F)

walks like a drunk, nausea trouble in malls, not secure

90 days

abnormal vestibular

12. (48M)

like being on a merry-go- round, nausea waves, wobbly

2-3 days

abnormal vestibular

13. (39F)

2 one hour spells of spinning, brief spins with movement

<1 day

abnormal vestibular

14. (30F)

“sea legs”

also lightheaded

30 days

abnormal nonspecific

15. (53F)

imbalance, like looking at water,

trouble in malls and on stairs

immediate

normal

16. (49M)

whirling, eyes jiggle imbalance, nausea

1 day

abnormal

vestibular

17. (40M)

lightheaded, nausea spin when I look up

4 days

normal

18. (33F)

veering, unsteady

“like stepping off an elevator”

<1 day

normal

DISCUSSION

The concept of vestibular involvement in whiplash injury is poorly discussed in the literature pertaining to cervical spine injury. Although true vertigo is alluded to, we only heard the complaint in eight of our patients, allowing us to make a definitive diagnosis in all eight. We felt that ten patients who denied true vertigo had problems with the vestibular system as supported by the posturography results. A combination of posturography and a very careful history taking is crucial to delineate the problem as coming from the vestibular system.

Hinoki (5) found 87% of patients involved in a flexion extension injury had dizziness whereas it was a much smaller percentage in a study by Sturzenegger (4). Table 1 lists complaints voiced by patients in describing their symptoms. Previous papers, presumably for reasons of simplicity have grouped patients with these complaints as being dizzy, lightheaded or imbalanced. A main purpose of this paper is to draw attention to the fact that, if questioned, many patients with vestibular disease other than WAD also voice complaints mentioned in Table 1. The complaints therefore arise from an abnormality in the balance system.

Although poorly understood, it may be that the differing functions of the vestibular system are managed by discrete parts of the system. This is suggested by the fact that certain “unusual complaints” are described characteristically in a markedly similar fashion by some patients and denied by others. For instance, persistent imbalance (8/18 patients), inability to tolerate excessive optokinetic stimulation (7/18 patients), “feeling drunk” (6/18 patients), and “sea legs” (4/18 patients) are common complaints. However, attempts to delineate a common thread in these groups, or use the complaints as predictors of examination or test results have been unsuccessful.

Ten patients did not have classical vestibular syndromes but had complaints which suggested an abnormality in the balance system. Interestingly six of these patients had abnormal posturography suggestive of a vestibular abnormality pattern.

Sixteen of 18 patients showed no abnormality on ENG. There was no evidence of spontaneous nystagmus greater than 7° per second, no gaze nystagmus, smooth pursuit abnormality, or optokinetic abnormality noted. There was no caloric abnormality detected in any of the patients. In two patients there was evidence of nystagmus characteristic for benign positional vertigo on position testing. These findings are in significant contradistinction to those of Oosterveld (1) who found significant ENG abnormalities in many patients who were tested after a whiplash.

Computerized Dynamic Posturography may detect abnormalities in patients with vestibular disease when ENG is normal (14). The most useful test was CDP which was abnormal in 13 of 18 patients, all but two of the 13 abnormalities showing a pattern characteristic for inner ear vestibular disease. As Chester (7) found from the legal investigative standpoint, CDP is more frequently abnormal than ENG. Computerized Dynamic Posturography shows a characteristic configuration for normal and abnormal. Normal CDP results occurred in our series despite symptoms of WAD.

Most dizzy patients show neutral or improved function by Cawthorne-Cooksey rehabilitation exercises. In some patients who have flexion extension injury, not only are they not improved, they may be distinctly worse. In our study two patients were symptomatically worse following these exercises. Some patients will demonstrate this in physical terms by stating that their symptoms are very severe the next day, following a day of activity.

Under normal circumstances, there are two main reflexes mediated by the vestibular system utilizing all the afferent information. The vestibulo-ocular reflex (VOR) serves to foveate an image on the back of the eye. Operation of this reflex can be indicated using a simple doll’s eye maneuver. The efficiency of the reflex can be utilized using bedside testing (16) or by caloric tests. The vestibulospinal reflexes (VSR) or “righting” reflexes serve to orient a patient in space with respect to the surroundings and to earth vertical. Patients can often be separated by history as having an abnormality affecting one or the other reflex. For instance, a patient complaining solely of imbalance could be thought of having a VSR impairment, while a patient complaining of intolerance to a patterned rug or to excessive movement in the visual field could be delineated as having a VOR complaint. By this delineation, 9 of our series (50%) had a VSR type of abnormality, 4 had a VOR problem, and 5 had features suggestive of both groups. No other differences could be found among the three groups.

While two patients had generalized abnormalities of balance on posturography, the observation of a specific abnormality pattern in SOT five and/or six in 11 of our patients with WAD allows us to speculate strongly that the inner ear may be the cause of the vestibular compromise in many of these patients, although the presence of visual vestibular mismatch could indicate the possibility of a more central component or a combination of inner ear and central disease.

If we assume that acute trauma has its clinical effects soon after application, then if the vestibular system was damaged in a whiplash event, then some dizzy type symptoms should have their presentation soon after the traumatic event. Among the 18 subjects in this study, 13 had onset within one week, five were delayed in onset by over seven days. Among the early onset subjects, eight had positive CDP and five negative. Among the delayed onset subjects, all five had positive CDP test results that might suggest some vestibular mechanisms for their symptoms. The delay in onset of dizziness is assumed, without proof, to be due to the fact that a patient who is markedly incapacitated becomes aware of symptoms as pain eases and mobility returns.

CONCLUSIONS

Eighteen post-whiplash patients with complaints of dizziness were retrospectively analyzed using sophisticated CDP which found a high incidence of positive findings suggestive of a vestibular disturbance. In the same patients, there was a low incidence of findings of vestibular disturbance using standard ENG. There was no correlation between positive CDP findings and early symptom onset, with many of the early onset patients having negative CDP, and all of the delayed onset having positive CDP. In most of the patients with CDP abnormalities, the pattern of abnormality suggested that the inner ear was the likely cause of the disorder. In those with a nonspecific pattern of abnormality and those with normal CDP, the site was unknown and could be central, from the inner ear, or from the neck.

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