Unilateral Vestibular Lesions Research Articles

Nonspecific vertigo with normal otoneurological examination. The role of vestibular laboratory tests.

Vestibular laboratory tests are not generally necessary in the diagnosis of patients with a clear description of vertigo accompanied by positive otoneurological examination findings. The purpose of the study was to investigate the role of conventional vestibular laboratory tests in the diagnosis of patients complaining of nonspecific vertigo, despite their having a documented normal otoneurological examination. The results of the standard electronystagmography (ENG) and sinusoidal harmonic acceleration (SHA) tests of 52 patients referred for ambulatory vestibular laboratory tests due to a nonspecific illusion of movement, but with a normal otoneurological examination, were reviewed. Abnormalities were found in the vestibular tests of 35 patients (67 per cent), 22 of whom (63 per cent) were finally diagnosed as having a unilateral peripheral vestibular lesion, and 13 (37 per cent) benign positional vertigo. These results suggest that a high percentage of patients with nonspecific vertigo and a normal otoneurological examination probably suffer from peripheral vestibular dysfunction, which can be objectively documented by the ENG and SHA tests.

Postural responses to vibration of neck muscles in patients with unilateral vestibular lesions

Postural responses to vibration applied unilaterally to dorsal neck muscles were recorded with a sway platform in nine patients with unilateral vestibular lesions and 19 normal subjects. In normals, the vibration induced a forward postural deviation. In patients, vibration of the neck contralateral to the lesion induced normal forward sway, whereas ipsilateral vibration resulted in sway of lower amplitude than normal and predominantly in the direction of the lesion or backwards. It is suggested that the proprioceptive error signal introduced by the neck vibration combined with an asymmetrical vestibular input due to a unilateral vestibular lesion provoked an erroneous representation of head position in patients resulting in a redirection of their body sway.

Tilt Suppression, OKAN, and Head-Shaking Nystagmus at Long-Term Follow-Up After Unilateral Vestibular Neurectomy1

The functional status of the velocity storage mechanism was studied in patients at long-term follow-up (2 to 4 years) after unilateral vestibular neurectomy. The time constant of the vestibulo-ocular reflex (VORtc), the effect of head tilt on postrotatory nystagmus, optokinetic after-nystagmus (OKAN), and nystagmus after rapid head shaking were studied in 10 patients. In agreement with previous findings, VORtc was found to be short and most patients manifested OKAN, suggesting that unilateral peripheral vestibular loss is associated with a complete loss of storage within the the VOR but only a partial loss of velocity storage for visual input. However, at postrotatory head tilt the VOR time constant was further shortened, supposedly due to discharge of functioning velocity storage. Moreover, most patients manifested nystagmus after head shaking. These findings on tilt suppression and head-shaking nystagmus suggest that velocity storage within the VOR may function even in patients with complete unilateral vestibular lesions.

The Contribution of the Vertical Semicircular Canals to High-Velocity Horizontal Vestibulo-Ocular Reflex (VOR) in Normal Subjects and Patients with Unilateral Vestibular Nerve Section

We have examined to what extent the vertical semicircular canals contribute to the nonlinearity of the horizontal VOR imposed by the driving of primary vestibular afferents into inhibitory cutoff at high velocities of head rotation (Ewald's second law). The gain (eye velocity/head velocity) of the horizontal component of the VOR with the head pitched down 30 degrees and pitched up 30 degrees was examined during constant-velocity rotations in normal subjects and patients following unilateral vestibular nerve section. In normal subjects, VOR gain decreases as chair velocity increases from 60-300 degrees/s when the head is pitched up, but VOR gain remains constant when the head is pitched down. This finding implies that the mechanism by which the gain of the horizontal VOR gain remains constant at all velocities of rotation depends upon the pattern of labyrinthine stimulation. Following unilateral nerve section, we found that the directional preponderance (DP) in horizontal VOR depends upon whether the head is pitched up 30 (mean asymmetry = 5%) or pitched down 30 degrees (mean asymmetry = 20%). This is what is expected based on the degree to which the lateral and vertical semicircular canals sense horizontal head acceleration with the head in different degrees of pitch. Hence, following unilateral vestibular lesions, the DP of horizontal VOR gain is most easily elicited at high velocities of head rotation and with the head pitched down 30 degrees. Evidence for DP at the bedside using the "head-shaking nystagmus" technique may be optimally elicited with the head pitched down 30 degrees.

The perception of body verticality (subjective postural vertical) in peripheral and central vestibular disorders.

The perception of body verticality (subjective postural vertical, SPV) was assessed in normal subjects and in patients with peripheral and central vestibular lesions and the data were compared with conventional neuro-otological assessments. Subjects were seated with eyes closed in a motorized gimbal which executed cycles of tilt at low constant speed (1.5 degrees s-1), both in the frontal (roll) and sagittal (pitch) planes. Subjects indicated with a joystick when they entered and left verticality, thus defining a sector of subjective uprightness in each plane. The mean angle of tilt (identifying a bias of the SPV) and the width of the sector (defining sensitivity of the SPV) were then determined. In normal subjects, the angle of the "verticality' sector was 5.9 degrees for pitch and roll. Patients with bilateral absence of vestibular function, patients with vertigo, i.e. acute unilateral lesions, benign paroxysmal positional vertigo (BPPV) and Ménière's disease, and patients with positionally modulated up-/downbeat nystagmus all had enlarged sectors (i.e. loss in sensitivity). Mean sector angle in these groups ranged from 7.8 to 11 degrees and the abnormality was present both in pitch and roll, regardless of the direction of nystagmus or body sway. Patients with chronic unilateral peripheral vestibular lesions and those with position-independent vertical nystagmus had normal sensitivities. No significant bias of the SPV was found in any patient group, not even those with acute unilateral vestibular lesions who had marked tilts of the subjective visual vertical (SVV). Complementary experiments in normal subjects tested under galvanic vestibular or roll-plane optokinetic stimulation also failed to show biases of the SPV. In contrast, a significant bias in the SPV could be induced in normal subjects by asymmetric cycles of gimbals tilt, presumably by proprioceptive adaptation. The following conclusions can be drawn. (i) The perception of body verticality whilst seated is mainly dependent on proprioceptive/contact cues but these are susceptible to tilt-mediated adaptation. (ii) Vestibular input improves the sensitivity of the SPV, even in vestibular disorders, as long as the abnormality is stable. (iii) There can be marked dissociation between vestibulo-motor (ocular and postural) phenomena and the perception of body verticality, and between the SPV and SVV. (iv) The postural sway asymmetries in patients with peripheral and central vestibular lesions, like those induced by galvanic or optokinetic stimulation in normal subjects, are not consequences of changes of the SPV.

The role of cervical input in vestibular compensation

The role of proprioceptive input from cervical receptors in vestibular compensation was investigated. Vibratory stimulation to the dorsal neck muscle was given to patients with unilateral vestibular lesions. The length of the displacement of the center of gravity, maximum sway length, and sway area increased markedly during vibratory stimulation to the dorsal neck. In patients in whom compensation had been achieved, a position vector to the side of the lesion increased and the center of gravity moved to the side of the lesion. From these results, it can be speculated that cervical input plays an important role in the process of vestibular compensation.

Unilateral Vestibular Lesions Secondary to Acoustic Neuroma

Unilateral Vestibular Lesions Secondary to Acoustic Neuroma

Vestibular neuritis spares the inferior division of the vestibular nerve.

Acute unilateral vestibulopathy, or vestibular neuritis, is the second most common cause of vertigo. To quantify the involvement of the different semicircular canal (SCC) afferents in this disease, we studied the three-dimensional (3D) properties of the vestibuloocular reflex (VOR) in 16 patients 3-10 days after onset of symptoms. Using 3D magnetic search coil eye movement recordings, we measured the speed and axis of eye rotation during spontaneous nystagmus and during rotation in the planes of the different SCCs. In all patients, spontaneous nystagmus axes clustered between the direction expected with involvement of just one horizontal SCC and the direction expected with combined involvement of the horizontal and anterior SCC on one side. Likewise, dynamic asymmetries were found only during rotations about axes which stimulated the ipsilesional horizontal or ipsilesional anterior SCCs. No asymmetry was found when the ipsilesional posterior SCC was stimulated. Thus, both measurements suggest that vestibular neuritis is a partial and not a complete unilateral vestibular lesion and that this partial lesion affects the superior division of the vestibular nerve which includes the afferents from the horizontal and anterior SCCs.

Betahistine Dihydrochloride Treatment Facilitates Vestibular Compensation in the Cat

Unilateral lesion of the vestibular system induces posturo-locomotor deficits that are compensated for with time. Drug therapy is currently used to improve the recovery process and to facilitate vestibular compensation. Betahistine dihydrochloride is an histamine-like substance that has been employed in vestibular pathology; it was found effective in many forms of vertigo and in vestibular-related syndromes. Investigations performed in animal models have shown betahistine-induced neuronal modulations in the vestibular nuclei complex and interactions with the H1 and H3 histamine receptors. Potentially, this substance is therefore capable to interfere with some recovery mechanisms and to improve the behavioral adaptations. But there is at present a total lack of data concerning the influence of betahistine treatment on vestibular compensation in animal models. The aim of this study was to understand the pharmacological activity of betahistine in the restoration of posture and locomotor balance functions in unilateral vestibular neurectomized cats. Posture recovery was assessed by quantifying the surface reaction of the cat's support as measured while standing erect on its four legs, at rest. Locomotor balance recovery was determined using the rotating beam test, by measuring the maximal performance (max. P.) of the cat and its locomotion speed regulation during the postoperative time period. We have compared the recovery profile and time course of these static (posture) and dynamic (equilibrium) functions in three groups of cats. Two experimental groups were treated at daily doses of 50 mg/kg and 100 mg/kg, respectively. Betahistine dihydrochloride was given orally until complete recovery of posturolocomotor functions. One untreated control group served as the reference. Results showed that postoperative treatment strongly accelerated the recovery process in both treated groups, inducing a time benefit of around 2 weeks as compared to the controls. Maximum performance of the cats on the rotating beam as well as locomotion speed regulation were highly correlated to the postoperative development of the cat's support surface, indicating that compensation of the static vestibulospinal deficits conditioned the subsequent locomotor balance recovery. These behavioral data showed that betahistine dihydrochloride constitutes a useful drug therapy for the symptomatic treatment of central vestibular disorders in our animal model of unilateral vestibular lesion. Improvement of vestibular compensation under betahistine postoperative treatment, as evidenced here for the posture and locomotor balance functions, is discussed both in terms of aspecific effect (histamine-induced increase of the level of vigilance) or more direct action in the vestibular nuclei (histamine-induced rebalance of neuronal activity on both sides).

Effect of sensory deprivation or electrical stimulation on acute vestibular symptoms following unilateral labyrinthectomy in rabbit.

The effect of sensory deprivation or electrical stimulation on vestibular compensation was investigated for 7 days after unilateral labyrinthectomy (ULX) in 50 rabbits. Eye movements induced by sinusoidal rotation of the whole body and spontaneous nystagmus were measured for vestibulo-ocular compensation, and head deviation was measured for vestibulospinal compensation. The rabbits were divided into 4 groups: one with ULX only (LX only), ULX with bilateral tarsorrhaphy (LX+TX), ULX with cervical dorsal root ganglionectomy (LX+GX), and a group stimulated electrically on the lesion-sided vestibular system with square pulse for 8 h/day (LX+ES). In LX only, the frequency of spontaneous nystagmus was 2.93 +/- 0.19 beats/sec just after ULX, declining to zero in 4 days. In eye movements induced by sinusoidal rotation on the 7th day after ULX, directional preponderance was 24-43% and gain decreased to 32-48% by rotation toward the intact side and 17-29% by rotation toward the lesion side, compared with that before ULX. Roll head tilt and yaw head tilt were 82 +/- 9 degrees, 45 +/- 6 degrees, respectively, on the 7th day. Recovery of vestibulo-ocular reflex and head deviation was delayed in LX+TX and LX+GX compared with that in ULX only, but recovery was enhanced in LX+ES. Therefore, in this study, electrical stimulation of the lesion side seemed to have a favorable effect on suppression of acute vestibular symptoms induced by unilateral vestibular lesion.

Subjective vertical and vestibular lesion.

Patients with peripheral vestibular disorders may experience postural instability in the standing position, which means disorientation in their environment. The disturbed vestibular function in light reflects the postural instability in space. The present study investigates the relationship between the subjective vertical and the vestibular lesion. The subjects were patients with unilateral vestibular lesion, and the control subjects had no past history of vestibular lesion or any present vestibular lesion. A straight line consisting of 5 spotlights projected on a dome-shaped screen was concentrically moved like a stylus by pressing buttons. We measured the subjective vertical of the subjects using a 5-spotlight straight-line (spotlight-line) on a dome-shaped screen in front of which the subjects were placed. The result showed that the patients with unilateral peripheral disorder had a statistically significantly larger deviation to the impaired ear side, especially when the spotlight-line was moved from the impaired side, as compared with controls.

Modification of parameters in vertical optokinetic nystagmus after repeated vertical optokinetic stimulation in patients with vestibular lesions.

Eye movements were recorded in patients with unilateral and bilateral vestibular lesions after upward and downward optokinetic (OK) stimulation before and following 6 weeks' repeated exposure to OK stimulation. In control subjects there was no asymmetry between upward and downward slow-phase velocity (SPV). Before training, less subjects showed that upward and downward SPV was significantly lower than that of controls. There was no asymmetry between upward and downward SPV. After training, in unilateral cases, the values of both upward and downward SPV recovered to the control range. In bilateral cases, the downward SPV values returned to the control range, whereas the values of upward SPV exceeded the control range. The frequencies of both upward and downward OKN in controls were about 3.0 Hz. In unilateral and bilateral cases, before and after training, the OKN frequencies approximated 3.0 Hz, showing no significant differences. The recovery of the SPV in unilateral and bilateral cases after training suggests that OK stimulation acts to stabilize the body and consequently to provoke pronounced OKN, due to eye-head-body co-ordination. The asymmetry of SPV after training in bilateral cases might be a result of the lack of otolith function.

Subjective postural vertical in peripheral and central vestibular disorders.

The perception of subjective postural vertical was assessed in normals and patients with peripheral and central vestibular disorders and spasmodic torticollis. The subjects were seated in a motorized gimbal with the head and torso restrained and their eyes closed. The gimbal executed 7-10 cycles of tilt around the vertical at 1.5 degrees/s in either pitch or roll. Subjects indicated when they began to feel upright and again when they began to feel tilted by an analogous 3-position joystick. Normal subjects felt upright within a sector of 5-6 degrees around vertical in pitch and roll. Five patients with absent vestibular function, 25 torticollis patients and 3 patients with acute unilateral peripheral vestibular lesions showed a significant increase of the sector in pitch and roll, but only the latter had a mild directional bias. Two patients with long standing complete unilateral vestibular deficit and 8 patients with up or downbeat nystagmus in the vicinity of upright had abnormally large sectors within which they felt to be upright. The results suggest that vestibular function is important for the accurate perception of the postural vertical and that a directional asymmetry in vestibulo-ocular function or a head tilt does not necessarily correlate with a directional bias of subjective verticality.

A quantitative analysis of head-shaking nystagmus of peripheral vestibular origin.

A quantitative analysis of horizontal head-shaking nystagmus (HSN) was made on 48 patients with unilateral peripheral vestibular lesions in conjunction with stimulus intensity. Each patient underwent three head-shaking tests with 10, 30 and 50 horizontal head-excursions at a frequency of approximately 2 Hz, and HSN was recorded on ENG with eyes open in total darkness. i) HSN appeared in a biphasic or monophasic pattern. ii) The maximal slow-phase eye velocity (MSV) of the 1st phase (PI) of biphasic HSN increased significantly in proportion to stimulus intensity, and was significantly greater than that of monophasic HSN. iii) The duration of HSN was greater in the 2nd phase (PII) of biphasic HSN than in PI and increased markedly in proportion to stimulus intensity. iv) As the stimulus intensity rose to a high level, the interval between PI and PII (2nd phase latency) shortened, and the PII tended to appear more quickly after head-shaking. It was especially noteworthy that in response to an increase in stimulus intensity, both the MSV in PI and the duration of PII of biphasic HSN increased, but the duration of PI was reversely suppressed by the PII.

"Dumping" of activity within the VOR is possible after unilateral vestibular neurectomy.

The effect of head tilt on postrotatory nystagmus was studied in patients at long time follow-up of complete unilateral vestibular lesions. Ten patients were tested 2-4 years after unilateral vestibular neurectomy. They were all found to have short VOR time constants. However, at postrotatory head tilt the VOR time constant was further shortened. This suggests that the velocity storage mechanisms may function even in cases with complete unilateral vestibular lesions.

Functional loss of the horizontal doll's eye reflex following unilateral vestibular lesions

The doll's eye reflex represents the vestibulo-ocular reflex (VOR) elicited by high-acceleration head rotation. After complete unilateral vestibular lesions, the ipsilateral, horizontal doll's eye reflex is replaced by a series of "catch-up" saccades. These cause permanent symptoms of blurred vision and dizziness during ipsilateral turns. We compared normal controls and patients with complete surgical lesions or canal paresis of up to 9 years duration via electronystagmography (ENG) to determine the usefulness of the doll's eye test as a diagnostic test for complete vestibular lesions. This test was found to be more sensitive in diagnosis of such lesions than head-shaking nystagmus, rotatory directional preponderance, and spontaneous nystagmus. It is also useful to document VOR function in patients in whom caloric irrigation is contraindicated.

Monocular and Binocular Testing to Improve the Diagnostic Value of Horizontal Optokinetic Nystagmus.

This report describes the effects of unilateral peripheral vestibular lesions on the binocular and monocular optokinetic nystagmus (OKN). Six subjects who had undergone surgical removal of an acoustic neuroma were compared to 14 normal subjects. Stimuli consisted of 15° vertical stripes projected onto a flat screen 1 m from the subject. Stimulus velocities were 15, 30, 45, and 60°/sec. Before surgery, contralateral gain of the slow phase velocity was low, approximately 0.6, compared to 0.9 for ipsilateral gain at 60°/sec. In the acute postoperative period (<30 days), the gains of horizontal OKN were low and symmetrical for both stimulus directions. In the intermediate period (30-60 days postoperative), the OKN was asymmetrical (contralateral gain lower than ipsilateral gain), with the greatest discrepancy at 60°/sec. During the chronic phase (>2 months) the OKN was still asymmetrical in 3 of the 6 subjects. These data suggest that monocular and binocular optokinetic testing can be used to monitor the vestibular compensation of subjects following vestibular nerve section.

Off-vertical axis rotational responses in patients with unilateral peripheral vestibular lesions.

Off-vertical axis rotation (OVAR) stimulates the otolith organs in a manner that is suitable for assessment of the otolith-ocular reflex. To further assess the potential clinical usefulness of OVAR, the eye movement responses of seven patients with surgically confirmed unilateral peripheral vestibular lesions were compared with the eye movement responses of a group of age-matched, healthy, asymptomatic control subjects. Patients and controls were tested with constant velocity rotations that followed a brief period of angular acceleration (velocity trapezoid) using either earth-vertical axis (EVA) rotation or OVAR. Both EVA and OVAR sinusoidal velocity profiles were also performed. Results indicated that each patient had 1) an asymmetric OVAR response, ie, a bias component whose direction was opposite normal when rotating toward the lesioned ear, and 2) a normal modulation component. Population data suggested that patients had 1) a more rapid decay of response than normal subjects during OVAR velocity trapezoids, 2) an increased phase lead as compared to normal subjects during sinusoidal OVAR, and 3) like normal subjects, a less rapid decay of response during OVAR velocity trapezoids than during EVA rotational velocity trapezoids. Taken together, these findings suggest that patients with unilateral peripheral vestibular deficits have abnormal otolith-ocular and semicircular canal-ocular reflexes but that a single labyrinth appears to provide an otolithic signal sufficient for qualitatively normal semicircular canal-otolith interaction.

Velocity storage in labyrinthine disorders.

We studied 13 patients with unilateral peripheral vestibular lesions following removal of acoustic neurinomas. The time constant of the VOR after surgery was 6.4 +/- 2.6 seconds (normal is 18.5 +/- 7.7 seconds). The time constant of OKAN after surgery was 7.2 +/- 1.8 seconds (normal is 11.3 +/- 3.2 seconds). The mean initial velocity of OKAN after surgery was 9.7 +/- 2.4 deg/second (normal is 11.7 +/- 5.9 deg/second). These data suggest that unilateral peripheral vestibular loss is associated with a complete loss of velocity storage for canal input but only a partial loss of velocity storage for visual input. These results can be accounted for by current mathematical models of the velocity storage mechanism.

The Role of the Cervical Input in Vestibular Compensation

The role of proprioceptive input from cervical receptors in vestibular compensation was investi-gated. Vibratory stimulation to the dorsal neck muscle was given to patients with unilateral vestibular lesions and to normal subjects. In normal subjects, the center of gravity shifted forward after vibratory stimulation without any right-left deviation. In patients whose compensation had been achieved, the center of gravity moved to the side of the lesion. From these results, it can be speculated that cervical input plays an important role in the process of vestibular compensation.