Subjective assessment of visual verticality in follow-up of patients with acute vestibular disease. (Original Article).
We conducted a study of 10 patients with acute unilateral peripheral vestibular failure in order to assess their ability to perceive visual verticality during the acute stage of their disease and during recovery. We also evaluated 31 healthy volunteers to test the reproducibility of our assessment methods. The 10 patients were first evaluated within 4 days of the onset of their vestibular failure, and follow-up tests were conducted 2 and 4 weeks later. The healthy subjects were similarly tested at 2 and 4 weeks following their baseline evaluation. All patients and subjects were tested JO times during each evaluation session, and results from each as well as from the groups as a whole were calculated as a mean of all responses. The mean visual vertical tilt (the amount of deviation from true verticality) among the 10 patients declined from 8.4[degrees] ([+ or -] 2.4[degrees]) at the first examination to 3.2[degrees] ([+ or -] 1.6[degrees]) at week 2 and to 1.4[degrees] ([+ or -]0.7[degrees]) at week 4. These d ecreases coincided with the pace of the resolution of their vestibular symptoms. The rates of reproducibility among the 31 healthy volunteers at 2 and 4 weeks following their initial assessment were 95 and 97%, respectively. We conclude that repeated measurements of the static visual vertical can be useful as a follow-up tool for patients with vestibular neuritis.
In normal persons, the ability to correctly perceive gravitational verticality--"the visual vertical"--is extremely good. (1,2) This ability is dependent on input from visual, vestibular, and proprioceptive systems. It is well known that the perception of the visual vertical is impaired by several types of central nervous system disorders (3,4) and peripheral vestibular lesions. (2,5) However, there is a lack of follow-up studies on the perception of the visual vertical during clinical recovery from acute vestibular disease. To help fill this void, we conducted a study to assess the static visual vertical in patients with acute unilateral peripheral vestibular failure during the course of their disease. Also, because a functional test must be reproducible in a given subject in order to be useful in clinical follow-up, we assessed the reproducibility of the static visual vertical in healthy subjects.
Patients and methods
Our study population was made up of 41 subjects. The test group included 10 patients--five men and five women, aged 26 to 53 years (mean: 41.3)--who had unilateral peripheral vestibular failure. All had been entered into the study within 4 days of the onset of their symptoms. All 10 patients had second- or third-degree spontaneous nystagmus in light, and all reported vertigo and nausea. The nature of their vestibular failure was assessed by caloric stimuli. (6) None had previously experienced otologic disease, and none had evidence of neurologic disease.
The other group was made up of 31 healthy volunteers-25 women and six men, aged 26 to 55 years (mean: 34.4). None had a history of otologic or neurologic disorders.
Following a clinical evaluation, all patients underwent assessments of the static visual vertical. Follow-up assessments were repeated 2 and 4 weeks later. At each session, subjects were seated without back support and with their eyes closed. A circular 3.5-m diameter screen was positioned 30cm from each subject's eyes. A 20-cm straight line, in the form of a motorized bar, was anchored in front of the screen; the center of the bar was able to rotate at the center of the screen. No other visual clues were present. The examiner was able to rotate the position of the line with a joystick. Once the line was rotated, subjects were instructed to open their eyes and to use the joystick to bring the line to vertical. Each subject performed this exercise 10 times. Results were based on the mean value of each series of tests. Based on our experience with receiver operating characteristic curves obtained during a previous study, (7) we determined that a mean deviation of 2[degrees] from true vertical is the best criter ion to identify subjects who have right/left vestibular asymmetry.
The reproducibility of this test was determined in accordance with the Bland-Altman method of assessing agreement between two methods of clinical measurement. (8) Group means and standard deviations of the difference between each consecutive pair of evaluations were used to estimate the 95% coefficients of reproducibility. Comparisons were performed by analysis of variance (ANOVA), with a statistical significance level of 0.05. Our study protocol had been approved by our hospital's research committee.
Study patients. During the 4 weeks of follow-up, the patients with unilateral peripheral vestibular failure experienced a gradual clinical improvement in the degree of their vertigo, autonomic symptoms, and spontaneous nystagmus. This improvement was accompanied by a consistent decrease in the mean visual vertical tilt (the amount of deviation from true vertical) ipsiversive to the lesion (ANOVA, p<0.05) (figure).
During the first evaluation, all 10 patients reported vertigo and nausea, and clinical evaluation detected a 2[degrees] to 3[degrees] spontaneous nystagmus in light. At the 2-week follow-up, no patient reported vertigo or nausea, and the spontaneous nystagmus in light had decreased to 1[degrees] to 2[degrees]. At week 4, no spontaneous nystagmus was evident in either light or dark.
The mean visual vertical tilt was 8.4[degrees] ([+ or -]2.4[degrees) at the first evaluation, and no patient had a deviation of less than 2[degrees]. At the 2-week follow-up, the mean visual vertical tilt was 3.2[degrees] ([+ or -] 1.6[degrees]), although eight patients maintained deviations of more than 2[degrees]. At week 4, one patient did not perform the test, but he was able to return to work. The mean visual vertical tilt in the remaining nine patients was 1.4[degrees] ([+ or -]0.7[degrees]), and only one patient maintained a deviation of more than 2[degrees].
Healthy subjects. In the healthy subjects, the mean visual vertical tilt was only 0.4[degrees] ([+ or -]0.50) at both the initial evaluation and the 2-week follow-up, and 0.3[degrees] ([+ or -]0.5[degrees]) at the 4-week evaluation. During all three evaluations, no subject exhibited a single deviation greater than 2[degrees]. The mean difference between the first and second evaluations was -0.1[degrees] ([+ or -0.2[degrees]), and the coefficient of reproducibility was 0.4[degrees]. Between the second and third evaluations, the mean difference was -0.1[degrees] ([+ or -0.3[degrees]), and the coefficient of reproducibility was 0.5[degrees]. The rates of reproducibility were 95% at week 2 and 97% at week 4. No statistically significant differences among the three measurements of the visual vertical were noted in this group.
Human perception of visual verticality is known to be extremely accurate. In this study, repeated measures of the static visual vertical in healthy subjects revealed that it is also highly reproducible. By contrast, our assessments of the static visual vertical in patients who had a unilateral peripheral vestibular lesion revealed a gradual decrease in ipsiversive tilt. The greatest degree of visual vertical tilt was observed during the acute stage of vestibular disease, and the degree of tilt decreased as clinical recovery progressed. These findings were consistent in all 10 of our study patients, and they suggest that otolithic function might be involved in the functional deficit related to vestibular neuritis.
The gradual decrease in visual vertical tilt during recovery might be explained by two factors. First, following the development of a unilateral peripheral vestibular lesion, the level of spontaneous neural activity in the vestibular nucleus is reduced; after a period of compensation, this level can retum to normal.(9) Therefore, it is possible to attribute the deviation in the visual vertical to the temporary vestibular imbalance experienced prior to compensation. Second, during vestibular neuritis, only vestibular input is compromised; other modes of somatosensory input might play roles in the quick recovery of the static visual vertical. It is well recognized that some of the orientation information provided by the somatosensory, visual, and vestibular systems is redundant. Under altered conditions, the central nervous system "reweights" each sensory input and enhances the influence of those senses that provide accurate information and suppresses the influence of conflicting or inaccurate input. (10)
In conclusion, measurements of the static visual vertical in healthy subjects are highly reproducible, and repeated measurements can serve as a useful tool in the follow-up of patients with acute vestibular neuritis.
(1.) Gibson JJ. The relation between visual and postural determinants of the phenomenal vertical. Psychol Rev 1952;59:370-5.
(2.) Friedmann G. The judgement of the visual vertical and horizontal with peripheral and central vestibular lesions. Brain 1970;93:313-28.
(3.) Brandt T, Dieterich M, Danek A. Vestibular cortex lesions affect the perception of verticality. Ann Neurol 1994;35:403-12.
(4.) Dieterich M, Brandt T. Ocular torsion and tilt of subjective visual vertical are sensitive brainstem signs. Ann Neurol 1993;33:292-9.
(5.) Curthoys IS, Dai MJ, Halmagyi GM. Human ocular torsional position before and after unilateral vestibular neurectomy. Exp Brain Res 1991;85:218-25.
(6.) Jongkees LB, Philipszoon AJ. Electronystagmography. Acta Otolaryngol Suppl 1964;189:l-55.
(7.) Aranda MC, Jauregui-Renaud K, Coba PC. Precision de la estimacion visual de la vertical en sujetos con lesion vestibular. Rev Fac Med UNAM 1997;40(Suppl 16):570.
(8.) Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986;1(8476):307-10.
(9.) Fluur E. Vestibular compensation after labyrinthine destruction. Acta Otolaryngol 1960;52:367-75.
(10.) Diener HC, Horak FB, Nashner LM. Influence of stimulus parameters on human postural responses. J Neurophysiol 1988;59:1888-905.
From the Department of Audiology and Otoneurology (Dr. Gomez Garcia) and the Medical Research Unit (Dr. Jauregui-Renaud). H.G. Centro Medico "La Raza," Instituto Mexicano del Seguro Social, Mexico, D.F.
Reprint requests: K. Jauregui-Renaud, MD, Unidad de Investigacion Medica, Hospital General, Centro Medico Nacional "La Raza" IMSS, Avenida Vallejo yJacarandas Colonia La Raza, CP02990, Mexico, D.F. Phone/tax: 52-55-5782-1976; e-mail: email@example.com
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|Publication:||Ear, Nose and Throat Journal|
|Date:||Jun 1, 2003|
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