Journal of Vestibular Research, Vol. 1, pp. 279-289, 1990/91 Printed in the USA. All rights reserved.

0957-4271/91 $3.00 + .00 Copyright © 1991 Pergamon Press pic

ASYMMETRIC OPTOKINETIC AFTERRESPONSE IN PATIENTS WITH VESTIBULAR NEURITIS

Krister Brantberg, MD, Mans Magnusson, MD, PhD

Department of Otorhinolaryngology, University Hospital, Lund, Sweden Reprint address: Krister Brantberg, M.D., Department of Otorhinolaryngology,

University Hospital, S-221 85 Lund, Sweden

o Abstract - The symmetry of primary and sec­ondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 14 patients with vestibular neuritis, as well as in 50 normals. The patients were examined at onset of symptoms and at follow-up 3 and 12 months later. At onset, OKAN was found mainly to reflect the spontane­ous nystagmus. Although the spontaneous nystag­mus disappeared in all patients within 3 months, both OKAN I and OKAN II was asymmetric at the 3- and 12-month check-ups. OKAN beating toward the lesioned ear was weaker than the OKAN beat­ing toward the healthy ear. Thus, the asymmetric vestibular function was reflected not only in the OKAN I, but also by an asymmetry in OKAN II. Between the 3- and 12-month check-ups, asymme­try in OKAN declined, even among those patients who showed no improvement in caloric response during that time. The decreasing asymmetry in OKAN with time after lesion was, however, related to the disappearance of a positional nystagmus. Hence, the results may be interpreted as suggesting OKAN not only to be affected by vestibular side­difference, but also to be modified by the process responsible for vestibular compensation following a peripheral vestibular lesion.

o Keywords - optokinetic afternystagmus; primary; secondary; vestibular neuritis.

Introduction

In cases of unilateral sensorineural hearing loss, or in patients suffering from unsteadi-

The preliminary data have been presented at the Baniny Society meeting, Tokyo, 28th May 1990.

ness or vertigo, it is essential to evaluate the functional symmetry of the vestibular end-or­gans and nerves. Stimulus to the vestibular end-organ in the natural state consists of lin­ear or angular acceleration, detected by both labyrinths simultaneously. However, rotatory tests have so far proved to be of limited success in indicating the extent of vestibular side-difference in man (1). In attempting to quantify vestibular side-difference, investiga­tors mainly depend on the caloric test, though the magnitude of caloric response may only be loosely relafed to the severity of peripheral lesion. As caloric irrigation tests only the low frequency response, chiefly of the lateral ca­nal and its afferents (2,3), complementary quantitative tests of vestibular side-difference would be useful.

Optokinetic nystagmus (OKN) is triggered by image slip on the retina. In man, two mechanisms evoke OKN: a cortical (or fast) mechanism, which may be identical with the pursuit system (4), and a subcortical (or slow) mechanism (5). The vestibular nuclei are im­portant premotor structures in the subcortical component of OKN and receive input during retinal image slip (6-8). A summation of ve­locity information from the retina and frOITi

the vestibular nerves has been suggested to take place in the vestibular nuclei (9,10). Thus, the subcortical component of OKN is dependent on the status of received peripheral vestibular input and could, theoretically, be used to demonstrate vestibular side-difference.

Although, the subcortical component of OKN is only accessible to study if the cortical

RECEIVED 14 November 1990; ACCEPTED 18 December 1990.

279

280

component is absent, as it is in certain species (11), it is reflected in the primary optokinetic afternystagmus (OKAN I) (12). During opto­kinetic stimulation, activity related to slow phase eye-velocity in the subcortical pathways of OKN is stored by the "central velocity stor­age integrator" (12-14). When the optokinetic stimulus is abolished by darkness, the integra­tor discharges, generating OKAN I that moves in the same direction as the previous OKN.

OKA.N I is sometimes r'oHowea a nys-tagmus beating in the opposite direction (OKAN II). The mechanism responsible for o KAN II has been suggested to be a "central adaptation operator" (15-17). Although, the anatomical site of this operator is not known, in animal experiments it was found that OKAN II is mediated by the same vestibular nuclei neurons as OKAN I (18,19). Thus, the symmetry of OKAN II might also be affected by asymmetric peripheral vestibular activity.

The aims of the present study were to as­certain whether asymmetric peripheral vestib­ular function is reflected in an asymmetry of OKAN, and if so, whether asymmetry in OKAN changes when a patient compensates for the lateral vestibular difference. An addi­tional aim was to evaluate the clinical signif­icance of asymmetry in OKAN by comparing the findings in patients with those in controls.

Materials and Methods

Subjects

Those studied were 14 patients with vestib­ular neuritis (6 males and 8 females, mean age 40.4 years, range 15-65) recruited con­secutively. Diagnosis was based on a sudden onset of severe vertigo with spontaneous nys­tagmus and unilaterally reduced caloric re­sponse (20,21). Patients with cardiovascular or metabolic disease, or on any form of con­tinuous medication, were excluded from the study, as were patients who, either at onset or at follow-up, had histories or signs of co­chlear or central nervous disorders, or who were more than 65 years old. None of the pa­tients reported previous episodes of vertigo.

K. Brantberg and M. Magnusson

The patients were examined at onset of dis­ease (mean 6.0 days, SD 4.6), and again both 3 months later (mean 100.4 days, SD 18.9) and 12 months later (mean 364.9 days, SD 53.6). In two of the 14 patients, the opto­kinetic test was not included in the electro­nystagmographic examination at onset of disease.

Normative values in optokinetic afterre­sponse were determined in 50 healthy subjects (24 females, 26 males), ranging in age from 24 to 65 years, none of whom had any history of cochlear, vestibular, or central nervous dis­orders. The 50 healthy subjects were divided into two groups by age: group 1 comprising those below the age of 40 (13 females, 13 males) and group 2 those over 40 (11 females, 13 males).

Test Procedure

Horizontal optokinetic stimulation was ad­ministered by means of a whole-field optoki­netic drum (diameter 180 em), with alternating black and white stripes, 10 cm broad. During the fest, the subject was seated in a chair with the head fixed by an occipital support (eye­ear axis horizontal), and instructed to stare at, but not to try to follow the moving stripes. Eye movements were recorded with DC electro­oculography (EOG) and transcribed simulta­neously by ink-jet recorder (Mingograph 81, Siemens-Elema, Stockholm). The optokinetic drum was accelerated up to a constant veloc­ity of 90 0/s in complete darkness, after which light was turned on for 60 seconds, recordings being continued until 60 seconds after the light was extinguished.

The patients, but not the controls, were further investigated. Spontaneous and posi­tional nystagmus in darkness were recorded with the subject in the upright position and after gently placing the patient in the supine position (ie, facing upward). The supine po­sition was maintained for at least 30s. The pa­tients were instructed to look straight ahead during the recordings for spontaneous and positional nystagmus, and conversation in se­quencies with the investigator was used to support maintenance of alertness throughout

OKAN and Vestibular Neuritis

the test. Voluntary eye movements and calo­ric response were also evaluated by EOG. In addition, pure tone audiometry and a full clinical otoneurological work-up were done in all patients.

Analysis oj Recordings

Values for eye movement variables were obtained manually from the recordings. Per­sistent nystagmus with a slow phase eye veloc­ity (SPEV) greater than 2°/s in the upright position was described as spontaneous nys­tagmus, and that in the supine position as po­sitional nystagmus.

OKAN I was evaluated as the SPEV mov­ing in the same direction as the previous OKN two seconds (OKAN2s ) after the end of the optokinetic stimulus (ie, lights off), and as the response decay time (OKANdur) for the SPEV to reach 2°/s (measured at the final fast phase of nystagmus to be preceded by a slow phase with a velocity exceeding 2°/s). Nystagmus (SPEV > 2°/s) opposite in direc­tion to, and following, OKAN I was consid­ered to be significant OKAN II, and was characterized by its maximal SPEV.

In the patient group, asymmetry of OKAN I was calculated as the quotient (Q) between OKAN I with the fast phase beating toward the healthy ear (HE) and OKAN I beating to­ward the lesioned ear (LE): Q = (OKANHE -OKANLE)/(OKANHE + OKANLE). In nor­mals, Q was calculated as the absolute asym­metry between OKAN I beating towards right (R) and left (L): Q = ABS«OKANR -

OKANd/(OKANR + OKANL »). If OKAN T was absent in both directions, the "ahl~

was said to be zero. The caloric ratio was calculated from the

SPEV produced by irrigation: (44 OR + 30 0 R)­(44°L + 30 0 L)/(44°R + 30 0 R + 44°L + 30 0 L), a caloric ratio> 0.20 being considered to be a significant caloric side-difference.

Statistics

Among the 50 normal subjects, the effect of age and sex, both on the symmetry and on

281

the strength of OKAN I, was tested with the Mann-Whitney test and two-way analysis of variance. In the patient group, the difference between OKAN I beating toward the healthy and the lesioned ear, as well as difference in OKAN I between the 3- and 12-month check­up, were evaluated using Student's t test for paired data, the t test being applied where normal distribution was not rejected by the Wilk-Shapiro test.

The Mann-Whitney test was used both in comparing absolute values for asymmetry in OKAN I between the patient and the normal group, and in comparing OKAN I between patients with versus without an OKAN II beating toward the healthy ear.

Kendall's tau was used to test for correla­tion between the discrete variable, presence­absence of positional nystagmus, and variables of OKAN (Q for OKAN2s , Q for OKANdup

and maximal SPEV of OKAN II beating to­ward the healthy ear). In addition, linear re­gression analysis and correlation analysis was used to test for correlation between OKAN2s

and SPEV of spontaneous nystagmus at on­set of the disease. A difference or regression of P < 0.05 was considered significant.

Results

Normals

In response to optokinetic stimulation, 5 normal subjects showed complete absence of OKAN, whereas in 8 subjects OKAN I sym­metrically outlasted the recordings irrespec­tive of the direction of drum rotation. There wa~ difference in values for OKAN I between subjects who were first ex­posed to drum rotation toward the right (n = 23) and those first exposed to drum rotation toward the left (n = 27). The overall mean (n = 50) for OKAN2s was 8.0 0/s (SD 6.1) and that for OKANdur 27.6 s (SD 21.6). Analysis of variance (ANOVA) using the vari­ables age group and sex showed a significant relationship to exist between these variables and the strength of OKAN I among normals (OKAN2s ; P < 0.05, OKANdur ; P < 0.01). Females under 40 years of age manifested sig-

282

nificantly higher mean OKAN2s and longer mean OKANdur than any other subgroups, male or female. Absolute values for asymme­try in OKAN I among the 50 normal subjects (ie, Q for OKAN2s and OKANdur ) are shown in Figure 1. The 90th percentile values of Q for OKAN2s and OKANdur were 0.39 and 0.70, respectively. Asymmetry of OKAN I did not increase with increasing age. OKAN II was not observed in any of the 50 normal subjects.

Patients at Onset of Symptoms

At onset of vestibular neuritis, all patients manifested a caloric ratio greater than 0.20 (mean 0.89, SD 0.12) and spontaneous nys­tagmus in darkness beating toward the healthy ear (mean SPEV 10.9°/s, SD 5.9). Following OKN with fast phases beating toward the le­sioned ear, OKAN changed direction in all patients within 2 s after "lights off." Hence, Q for OKAN was always 1.0 at onset of the disease, as all tested patients showed OKAN

40

30

~ (,,) QJ

:B ::l en

""'"' 0 20 .... ..8 § Z

10

o

° 0,2 0,4 0,6 0,8

quotient (Q) for OKAN2s

(a)

1,0

K. Brantberg and M. Magnusson

I beating toward the healthy ear but no OKAN I beating toward the lesioned ear. Since the duration of OKAN I (OKANdur )

beating toward the healthy ear outlasted the recordings in all patients, the only "informa­tive" parameter of OKAN I at onset of vestib­ular neuritis was the initial SPEV of OKAN I (OKAN2s ) beating toward the healthy ear (mean 20.6°/s, SD 7.9). This variable corre­lated with the SPEV of spontaneous nystag­mus (r = 0 .. 63, p < 0.05), though OKAN2s

was significantly greater (P < 0.001).

Patients at Follow-up

Caloric ratio (CR). At follow-up, 6 of the 14 patients were found to have recovered normal caloric side-difference (CR :$ 0.20), all 6 of them having done so before the 3-month check-up. These 6 patients manifested a sig­nificant further decrease in CR between the 3-and 12-month check-ups (at 3 mon, CR = 0.11, SD 0.07; at 12 mon, CR = 0.01, SD 0.06, P < 0.05). However, there was no sig-

<n U QJ

E' ::l <n

""'"' 0 ....

15 s ::l Z

40

30

20

10

o

° 0,2 0,4 0,6 0,8

quotient (Q) for OKANdur

(b)

1,0

Figure 1. Histogram of distribution for a) Q for OKAN2s and b) Q for OKANdur among 50 normal subjects. Q is calculated from the difference in response to the two directions of drum rotation.

OKAN and Vestibular Neuritis

nificant difference in caloric ratios between the 3- and 12-month check-ups among the 8 patients who did not recover normal calo­ric side-difference (CR = 0.70, SD 0.31 and CR = 0.71, SD 0.27, respectively).

Spontaneous and positional nystagmus. None of the patients had spontaneous nystagmus in darkness at the 3- or 12-month follow-up. Nevertheless, a nystagmus beating toward the healthy ear was recorded in the supine posi­tion in 7 patients after 3 months (in 2/6 of the patients who recovered normal caloric side­difference, and in 5/8 among those who did not); and after one year, the positional nys­tagmus beating towards the healthy ear was still present in 5 patients (1/6 and 4/8, respec­tively). However, neither at the 3-month nor at the 12-month check-up were any cases of nystagmus beating toward the lesioned ear encountered with the patient in the supine position.

Primary OKAN. At the 3-month check-up, OKAN I was asymmetric (Tables 1 and 2). The OKANdur was significantly shorter after an 0 KN beating toward the lesioned ear than after an OKN beating toward the healthy ear. Among the patients who had not recovered normal caloric side-difference, values for OKAN2s toward the lesioned ear were lower than those for OKAN2s toward the healthy

283

ear. The absolute values for Q among the pa­tients with vestibular neuritis 3 months after onset of disease were significantly higher than those among normals, the difference being sig­nificant both for OKAN2s and for OKANdur ,

both among the patients who recovered nor­mal caloric side-difference (P < 0.05 and P < 0.05, respectively) and among those who did not (P < 0.05 and P < 0.01, respectively).

At the 12-month check-up (Tables 1 and 2), no significant asymmetry in OKAN was found among the patients whose caloric side­difference had recovered. Among the patients who had not recovered normal caloric re­sponse, OKAN I was still asymmetric. How­ever, in neither of these two subgroups were absolute Q values significantly different from those among normals.

Between the 3- and 12-month check-ups, Q for OKAN2s and Q for OKANdur decreased (Figure 2). Among the patients who did not recover normal caloric response, a significant decrease in Q for OKANdur was noted be­tween the 3- and 12-month follow-ups, al­though there was no sign of improved caloric response in the lesioned ear during the 9-month interval.

Secondary OKAN. OKAN II beating toward the healthy ear was observed in 9/14 patients after 3 months (in 4/6 patients who had re­covered normal caloric response and in 5/8

Table 1. Disparity between OKANdur Beating toward the Healthy versus the Lesioned Ear (HE and LE, Respectively) at the

3- and 12-Month Checkups in Patients with Vestibular Neuritis (Means and SOs Are Given)

Not All recovered Recovered

(n = 14) (n = 8) (n = 6)

After 3 months HE 33.1 ± 18.2 38.5 ± 20.7 26.0 ± 12.5 LE 9.2 ± 12.1 10.5±13.4 7.5±11.2 p < 0.001 < 0.01 < 0.05

After 1 2 months HE 26.9 ± 18.9 32.3 ± 17.5 19.8 ± 19.9 LE 15.9 ± 16.3 15.9 ± 12.3 15.8±21.9 P < 0.05* < 0.05 NS*

* indicates non normally distributed differences and the use of the Wilcoxon signed rank test.

284 K. Brantberg and M. Magnusson

Table 2. Disparity between OKAN2s Beating toward the Healthy versus the Lesioned Ear (HE and LE, Respectively) at Onset

of Vestibular Neuritis and at 3- and 12-Month Checkups (Means and SDs Are Given)

All

At onset (n = 12) HE 20.6 ± 7.9 LE 0.0 ± 0.0

After 3 months (n = 14) HE 11.9±4.1 LE O. ::t 6.9 p < 0.01

After 1 2 months (n = 14) HE 12.9±7.5 LE 10.1 ± 7.7 p < 0.05

patients who had not), and in 4/14 patients after 12 months (1/6 and 3/8, respectively). The max SPEV of the observed OKAN II was in the range of 3° to 8°/s after 3 months and 3° to 5°/s after 12 months. The patients with OKAN II beating toward the healthy ear manifested more pronounced asymmetry in OKAN I, as reflected in greater values for Q

1.0

fJ'l 0.8

g .... .s g d .~ '0

0.6

0.4

5- 0.2

*

all not reeov. reeov.

c=:J 3 months

~ 12 months

(a)

Not recovered Recovered

(n = 6) (n = 6) 19.2±9.1 22.0 ± 7.0

0.0 ± 0.0 0.0 ± 0.0

(n = 8) (n = 6) 11.8 ± 4.5 12.0 ± 4.0

6.5 ± 7.2 7.0 ± 7.2 < 0.01 NS

(n = 8) (n = 6) 14.3±9.1 11.2 ± 4.9 11.0±9.7 9.0 ± 4.3

< 0.01 NS

both at the 3- and 12-month check-ups (Fig­ure 3). The duration of OKAN I preceding an OKAN II was significantly shorter than that of OKAN I among those who manifested no OKAN II, both at the 3- and 12-month check-ups (P < 0.01 and P < 0.05, respec­tively). No case of OKAN II beating toward the lesioned ear was observed.

1.0

.... 0.8

~ g 0.6 .... .s q _ 0.4

5 'g 5- 0.2

**

all

* *

not reeov. reeov.

c=:J 3 months

~ 12 months

(b)

Figure 2. Quotients a) Q for OKAN2s and b) Q for OKANdur at 3- and 12-month follow-up, showing decreasing asymmetry in OKAN I with time after onset of vestibular neuritis for all 14 patients together ("all"), for patients who recovered normal caloric side-difference (" recoy.") and for those who did not (" not recoy. "). Means, SEM, and levels of significance (Student's t test for paired data) are given.

OKAN and Vestibular Neuritis

§ -= .S:2 '0 6-.... 0

~ U

1.0 **

0.8

0.6

0.4

0.2

o.o~~~~~--~~--~~~--

OKAN2s C.R. OKANdur

c=J wi th OKAN II (n-g)

~ wi thout OKAN II (n-5)

(a)

1.0

0.8

§ -= 0.6 .S:2 '0 :::l 0" ....

0.4 0

~ U

0.2

0.0

285

** **

C.R. OKANdur

c=J with OKAN II (n .. 4)

~ without OKAN II (n-i0)

(b)

Figure 3. The difference in caloric ratio (CR), Q for OKAN2s and Q for OKANdur between patients with versus without OKAN II beating toward the healthy ear. Patients with OKAN II demonstrate a preponderance of OKAN I beating toward the healthy ear, which is reflected in their greater values for Q, both at the 3- and 12-month check-ups (Figures 3a and 3b, respectively). Means, SEM, and levels of significance (Mann-Whitney test) are given.

Relationship between OKAN and positional nystagmus. Rank correlation showed a, sig­nificant correlation to exist between positional nystagmus and variables Q for OKANdur and maximal SPEV of OKAN II at the 3-month check-up (correlation coefficient r = 0.44 and r = 0.51, respectively). At the 12-month check-up, the presence of a positional nystag­mus was correlated to Q for OKAN2s , Q for OKANdur , and maximal SPEV of OKAN II (r = 0.51, r = 0.61, and r = 0.80, respec­tively). From. values of Q for OKANdw . it was possible to predict the presence or ab­sence of a positional nystagmus correctly in 13/14 patients at the 12-month check-up. No significant correlation was found between the presence of a positional nystagmus and the magnitude of the caloric ratio.

Discussion

An asymmetry in horizontal optokinetic afterresponse was demonstrated in patients

with vestibular neuritis. Asymmetric periph­eral vestibular function was reflected, not only in the OKAN I, but also in asymmetry of OKAN II. The asymmetry of OKAN was not, however, merely a representation of the peripheral vestibular function, as reflected in the caloric side-difference, but also during follow-up showed changes corresponding to the process of vestibular compensation.

A sudden onset of severe vertigo with spontaneous nystagmus and unilaterally re­duced caloric response. in the absence of co­chlear symptoms, suggests a diagnosis of vestibular neuritis. Neurological signs indicat­ing lesion to the central nervous system are found in one-third of such cases (22-24). Therefore, we excluded from the study all pa­tients with any sign or history of metabolic, cardiac or vascular disease, or with ocular­motor abnormalities consistent with the pos­sibility of a central nervous lesion (22).

Different instructions to a subject exposed to an optokinetic stimulation may effect the

286

generation of OKN and OKAN. An instruc­tion to "stare" at the optokinetic stimulus may favor the subcortical optokinetic mech­anism (5), as retinal image slip is considered to constitute the stimulus for this mechanism (4,5,12,25), while the cortical optokinetic mechanism has been suggested to be identical with the pursuit eye movement mechanism (4,5). Since OKAN I is associated with the subcortical mechanism (5,11,12,25) one would assume a stimulus favoring this mechanism to be appropriate when investigating OKAN. Nevertheless, if subjects are instructed to "look" at the optokinetic stimulus, most sub­jects will still have an adequate retinal slip to evoke OKAN (26,27,30). However, when a subject is instructed to "look," the retinal slip will depend on the subjects' capacity for pur­suit eye movements. Subjects with a high ca­pacity may reduce the retinal slip more prominently than others. To minimize such variations, the subjects in the present study were instructed to focus on the stimulus but not to try to follow the moving stripes during the test.

Few studies have been made of QKAN in peripheral vestibular disorders in man, per­haps due to the problem of quantifying OKAN. The decay of SPEV in OKAN may be due to the output from three separate sys­tems in each of which eye-velocity informa­tion is stored. In addition to the central velocity storage integrator, discharges from the smooth pursuit system (27) and the mech­anism responsible for OKAN II (16,17) may be involved. Identification of individual vari­ables of these systems leads to practical dif­ficulties, however. In this study were used two readily accessible variables of OKAN (OKAN2s and OKANdur ) that have been demonstrated to reflect asymmetric vestibular activity in man (28). However, evaluation of cumulative slow phase eye displacement or area under the decay curve may add further information.

Normals in this study manifested consider­able asymmetry of OKAN I in their response to drum rotation toward right and left. Such asymmetry may be consistent with the sugges-

K. Brantberg and M. Magnusson

tion of two separate velocity storage integra­tors, one for either side of the brain stem (12,13). However, changes in alertness during the test might also affect the symmetry of OKAN (29). Moreover, large intrasubject variability in OKAN I has been reported in man (30).

Asymmetry in OKAN I did not increase with age among the 50 normals in this study. However, the strength of OKAN I is known to decrease with increasing age (30,31), a re­lationship also noted in this study, where OKAN I was more prominent among females under the age of 40 than in any other sub­group, male or female.

Among the patients with vestibular neuri­tis, OKAN I beating toward the lesioned ear was weaker than OKAN I beating toward the healthy ear, a finding in accord with those of other studies on unilateral peripheral vestib­ular disorders in man (32-36). The asymme­try in OKAN I has been interpreted as being due to the loss of spontaneous activity of sec­ondary vestibular neurons on the lesioned side (25). In animal experiments, recovery of tonic activity in the ipsilateral vestibular nu­cleus has "been demonstrated to occur with time after a unilateral peripheral lesion (37). Such a recovery after a lesion may cause a de­crease in the relative side-difference between the tonic activity in two vestibular nuclei. As velocity information from the subcortical op­tokinetic mechanism and the activity of the vestibular nucleus are considered to have an aggregate net effect (9,10), a decrease in asymmetry of OKAN I with time after a uni­lateral peripheral lesion may be expected. Indeed, in the monkey after unilateral laby­rinthectomy, the initial asymmetric OKAN I was found to have become nearly symmetri­cal at long-term follow-up (38,39). However, additional mechanisms may also be involved in resolving the side-differences in OKAN af­ter a vestibular lesion.

During the one-year follow-up of the pa­tients in the present study, asymmetry of OKAN declined, not only among those who recovered normal caloric response, but also in those with unchanging asymmetry of caloric

OKAN and Vestibular Neuritis

response. The decreasing asymmetry of OKAN was, however, correlated to the presence or absence of a positional nystagmus. Disap­pearance of positional nystagmus during fol­low-up may indicate progress in recovery after a lesion. Therefore, these findings may be in­terpreted as suggesting that symmetry of OKAN is subject to modification by the pro­cess responsible for vestibular compensation. However, the nonappearance of improved ca­loric response does not exclude a partial res­toration of the peripheral vestibular apparatus. Change in functional status of the otolith or­gans or of the superior and posterior canals may not be reflected in caloric response.

Habituation to an optokinetic stimulus is known to effect OKAN in man. Jell and col­leagues in 1985 (26) found a decrease in OKAN during repeated trials in one session, most noticeably between trials 3 and 4. Retesting after 1 week, and up to 8 weeks later revealed no recovery. Blakely and col­leagues in 1989 (36) studied the effect of re­peated testing with a single OKN stimulation at different times after the first stimulation (3 days, 3 weeks, 6 weeks, 3 months, 6 months), but did not find any significant changes in OKAN during that time. Hence, habituation is unlikely to have a major effect on the rel­ative side difference of OKAN in the present study, as single exposures of an optokinetic stimulus were given at intervals of 3 and 9 months.

There have been only a few reports on OKAN II in man. Using stimulus velocities of 120° to 150 0/s and a stimulus duration of 60 s, Simmons-Buttner found OKAN II to be present in more than 10070 of normals (31). Both repetitive and persislent optokinetic stimulation have been demonstrated to in­crease the strength of OKAN II (40), a habit­uation effect that may partly explain the present discrepant finding of OKAN II in none of the 50 normals. In Simmons­Buttner's study, the subjects had already been exposed to optokinetic stimulation prior to that used for evaluation of OKAN II, whereas in our study the subjects were new to the experimental situation.

287

Among patients with vestibular neuritis, asymmetries in OKAN II were common, a finding in accord with the suggestion that both OKAN I and OKAN II are dependent on an intact peripheral vestibular apparatus (41). OKAN II was observed only after drum rotation generating OKAN I beating toward the lesioned ear. The OKAN I toward the le­sioned ear was of shorter duration when it preceded an OKAN II than it was in patients who manifested no OKAN II. This finding is in agreement with the suggestion that the "ve­locity storage integrator" and the storage element responsible for OKAN II are inter­connected in a negative feedback loop (16,17).

Taken together, the asymmetry of OKAN II in patients with vestibular neuritis and the absence of asymmetry in 50 normal subjects indicate that clinically valuable information can be obtained by investigating OKAN II in cases of suspected peripheral vestibular disor­ders. The magnitude of asymmetry in OKAN I among normals in this study suggests testing OKAN I with the variables used here to be of limited clinical value. In any individual, however, asymmetry may be subject to fluc­tuation, and the importance of repeated mea­surements has been emphasized (30).

The finding of asymmetry in optokinetic afterresponse does not indicate whether there is a lesion to the peripheral or central vestib­ular pathways (42), but may be considered to reflect asymmetry in the performance of ves­tibular reflexes. Consequently, testing OKAN should not be the sole test used when investi­gating a suspected vestibular lesion. However, as a complementary quantitative test of ves­tibular asymmetry, it may well prove useful, particularly at follmN-up after a lesion or dur­ing the course of Meniere's disease.

Acknowledgments- The authors wish to thank Bjorn Holmquist, D.Sc., Department of Mathe­matical Statistics, Lund Institute of Technology, for valuable advice regarding the statistical anal­yses. The study was supported by the Swedish Medical Research Council (grant no. 17X-05693) and by the Soderberg Foundations.

288 K. Brantberg and M. Magnusson

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