Loss Of Peripheral Vestibular Function Research Articles

Restoring vestibular function during natural self-motion: Progress and challenges.

The vestibular system is integral to behavior; the loss of peripheral vestibular function leads to disabling consequences, such as blurred vision, dizziness, and unstable posture, severely limiting activities of daily living. Fortunately, the vestibular system's well-defined peripheral structure and well-understood encoding strategies offer unique opportunities for developing sensory prostheses to restore vestibular function. While these devices show promising results in both animal models and implanted patients, substantial room for improvement remains. Research from an engineering perspective has largely focused on optimizing stimulation protocol to improve outcomes. However, this approach has often been pursued in isolation from research in neuroscience that has enriched our understanding of neural responses at the synaptic, cellular, and circuit levels. Accordingly, this review bridges the domains of neuroscience and engineering to consider recent progress and challenges in vestibular prosthesis development. We advocate for interdisciplinary approaches that leverage studies of neural circuits at the population level, especially in light of recent advancement in large-scale recording technology, to identify impediments still to overcome and to develop more naturalistic stimulation strategies. Fully integrating neuroscience and engineering in the context of prosthesis development will help advance the field forward and ultimately improve patient outcomes.

Acute unilateral vestibulopathy/vestibular neuritis: Diagnostic criteria.

This paper describes the diagnostic criteria for Acute Unilateral Vestibulopathy (AUVP), a synonym for vestibular neuritis, as defined by the Committee for the Classification of Vestibular Disorders of the Bárány Society. AUVP manifests as an acute vestibular syndrome due to an acute unilateral loss of peripheral vestibular function without evidence for acute central or acute audiological symptoms or signs. This implies that the diagnosis of AUVP is based on the patient history, bedside examination, and, if necessary, laboratory evaluation. The leading symptom is an acute or rarely subacute onset of spinning or non-spinning vertigo with unsteadiness, nausea/vomiting and/or oscillopsia. A leading clinical sign is a spontaneous peripheral vestibular nystagmus, which is direction-fixed and enhanced by removal of visual fixation with a trajectory appropriate to the semicircular canal afferents involved (generally horizontal-torsional). The diagnostic criteria were classified by the committee for four categories: 1. "Acute Unilateral Vestibulopathy", 2. "Acute Unilateral Vestibulopathy in Evolution", 3. "Probable Acute Unilateral Vestibulopathy" and 4. "History of Acute Unilateral Vestibulopathy". The specific diagnostic criteria for these are as follows:"Acute Unilateral Vestibulopathy": A) Acute or subacute onset of sustained spinning or non-spinning vertigo (i.e., an acute vestibular syndrome) of moderate to severe intensity with symptoms lasting for at least 24 hours. B) Spontaneous peripheral vestibular nystagmus with a trajectory appropriate to the semicircular canal afferents involved, generally horizontal-torsional, direction-fixed, and enhanced by removal of visual fixation. C) Unambiguous evidence of reduced VOR function on the side opposite the direction of the fast phase of the spontaneous nystagmus. D) No evidence for acute central neurological, otological or audiological symptoms. E) No acute central neurological signs, namely no central ocular motor or central vestibular signs, in particular no pronounced skew deviation, no gaze-evoked nystagmus, and no acute audiologic or otological signs. F) Not better accounted for by another disease or disorder."Acute Unilateral Vestibulopathy in Evolution": A) Acute or subacute onset of sustained spinning or non-spinning vertigo with continuous symptoms for more than 3 hours, but not yet lasting for at least 24 h hours, when patient is seen; B) - F) as above. This category is useful for diagnostic reasons to differentiate from acute central vestibular syndromes, to initiate specific treatments, and for research to include patients in clinical studies."Probable Acute Unilateral Vestibulopathy": Identical to AUVP except that the unilateral VOR deficit is not clearly observed or documented."History of acute unilateral vestibulopathy": A) History of acute or subacute onset of vertigo lasting at least 24 hours and slowly decreasing in intensity. B) No history of simultaneous acute audiological or central neurological symptoms. C) Unambiguous evidence of unilaterally reduced VOR function. D) No history of simultaneous acute central neurological signs, namely no central ocular motor or central vestibular signs and no acute audiological or otological signs. E) Not better accounted for by another disease or disorder. This category allows a diagnosis in patients presenting with a unilateral peripheral vestibular deficit and a history of an acute vestibular syndrome who are examined well after the acute phase.It is important to note that there is no definite test for AUVP. Therefore, its diagnosis requires the exclusion of central lesions as well as a variety of other peripheral vestibular disorders. Finally, this consensus paper will discuss other aspects of AUVP such as etiology, pathophysiology and laboratory examinations if they are directly relevant to the classification criteria.

Vestibular paroxysmia: clinical characteristics and long-term course

In 2016, the Bárány Society defined new diagnostic criteria for the neurovascular compression syndrome of the eighth nerve, called “vestibular paroxysmia” (VP), differentiating between definite (dVP) and probable (pVP) forms. The aim of this study was (1) to describe clinical symptoms and laboratory findings in a well-diagnosed large patient cohort according to those criteria, and (2) to evaluate the long-term course over years in dVP. We identified 146 patients (73 dVP, 73 pVP) from our tertiary dizziness center registry. Data of structured history-taking, clinical neurological, neuro-ophthalmological/-otological examinations as well as MRI imaging were extracted for analyses. Overall, attack frequency ranged between 5 and 30 attacks per day; spinning vertigo was the most frequent type. In two-thirds of patients, attacks occurred spontaneously; in one-quarter, they were triggered by head movements. The majority (approximately 70%) reported no accompanying symptoms; in those with symptoms, mild unilateral cochlear symptoms prevailed. One-third of patients initially showed hyperventilation-induced nystagmus without specific direction, and a deviation of the subjective visual vertical between 3° and 6°. Complete loss of peripheral vestibular function was never evident. dVP and pVP significantly differed concerning the vertigo type, e.g., spinning vertigo was more frequent in dVP. Fortunately, three-quarters of dVP patients remained attack-free during follow-up (mean 4.8 years, standardized questionnaire), more than half of them even without any medication. Patients with ongoing attacks showed significantly higher attack frequency at baseline, but reported persistent frequency reduction. Overall, the long-term prognosis of VP appears favorable, not necessarily requiring ongoing treatment.

Linking Vestibular Function and Subcortical Gray Matter Volume Changes in a Longitudinal Study of Aging Adults

Emerging evidence suggests a relationship between impairments of the vestibular (inner ear balance) system and alterations in the function and the structure of the central nervous system (CNS) in older adults. However, it is unclear whether age-related vestibular loss is associated with volume loss in brain regions known to receive vestibular input. To address this gap, we investigated the association between vestibular function and the volumes of four structures that process vestibular information (the hippocampus, entorhinal cortex, thalamus, and basal ganglia) in a longitudinal study of 97 healthy, older participants from the Baltimore Longitudinal Study of Aging. Vestibular testing included cervical vestibular-evoked myogenic potentials (cVEMP) to measure saccular function, ocular VEMP (oVEMP) to measure utricular function, and video head impulse tests to measure the horizontal semicircular canal vestibulo-ocular reflex (VOR). Participants in the sample had vestibular and brain MRI data for a total of one (18.6%), two (49.5%), and three (32.0%) visits. Linear mixed-effects regression was used to model regional volume over time as a function of vestibular physiological function, correcting for age, sex, intracranial volume, and intersubject random variation in the baseline levels and rates of change of volume over time. We found that poorer saccular function, characterized by lower cVEMP amplitude, is associated with reduced bilateral volumes of the basal ganglia and thalamus at each time point, demonstrated by a 0.0714 cm3 ± 0.0344 (unadjusted p = 0.038; 95% CI: 0.00397–0.139) lower bilateral-mean volume of the basal ganglia and a 0.0440 cm3 ± 0.0221 (unadjusted p = 0.046; 95% CI: 0.000727–0.0873) lower bilateral-mean volume of the thalamus for each 1-unit lower cVEMP amplitude. We also found a relationship between a lower mean VOR gain and lower left hippocampal volume (β = 0.121, unadjusted p = 0.018, 95% CI: 0.0212–0.222). There were no significant associations between volume and oVEMP. These findings provide insight into the specific brain structures that undergo atrophy in the context of age-related loss of peripheral vestibular function.

An exploratory investigation on spatiotemporal parameters, margins of stability, and their interaction in bilateral vestibulopathy

Integration of accurate vestibular, visual, and proprioceptive information is crucial in managing the centre of mass in relation to the base of support during gait. Therefore, bilateral loss of peripheral vestibular function can be highly debilitating when performing activities of daily life. To further investigate the influence of an impaired peripheral vestibular system on gait stability, spatiotemporal parameters, step-to-step variability, and mechanical stability parameters were examined in 20 patients with bilateral vestibulopathy and 20 matched healthy controls during preferred overground walking. Additionally, using a partial least squares analysis the relationship between spatiotemporal parameters of gait and the margins of stability was explored in both groups. Patients with bilateral vestibulopathy showed an increased cadence compared to healthy controls (121 ± 9 vs 115 ± 8 steps/min; p = 0.02; d = 0.77). In addition, although not significant (p = 0.07), a moderate effect size (d = 0.60) was found for step width variability (Coefficient of Variation (%); Bilateral vestibulopathy: 19 ± 11%; Healthy controls: 13 ± 5%). Results of the partial least squares analysis suggest that patients with peripheral vestibular failure implement a different balance control strategy. Instead of altering the step parameters, as is the case in healthy controls, they use the single and double support phases to control the state of the centre of mass to improve the mechanical stability.

Acute consequences of a unilateral VIIIth nerve transection on vestibulo-ocular and optokinetic reflexes in Xenopus laevis tadpoles

Loss of peripheral vestibular function provokes severe impairments of gaze and posture stabilization in humans and animals. However, relatively little is known about the extent of the instantaneous deficits. This is mostly due to the fact that in humans a spontaneous loss often goes unnoticed initially and targeted lesions in animals are performed under deep anesthesia, which prevents immediate evaluation of behavioral deficits. Here, we use isolated preparations of Xenopus laevis tadpoles with functionally intact vestibulo-ocular (VOR) and optokinetic reflexes (OKR) to evaluate the acute consequences of unilateral VIIIth nerve sections. Such in vitro preparations allow lesions to be performed in the absence of anesthetics with the advantage to instantly evaluate behavioral deficits. Eye movements, evoked by horizontal sinusoidal head/table rotation in darkness and in light, became reduced by 30% immediately after the lesion and were diminished by 50% at 1.5 h postlesion. In contrast, the sinusoidal horizontal OKR, evoked by large-field visual scene motion, remained unaltered instantaneously but was reduced by more than 50% from 1.5 h postlesion onwards. The further impairment of the VOR beyond the instantaneous effect, along with the delayed decrease of OKR performance, suggests that the immediate impact of the sensory loss is superseded by secondary consequences. These potentially involve homeostatic neuronal plasticity among shared VOR-OKR neuronal elements that are triggered by the ongoing asymmetric activity. Provided that this assumption is correct, a rehabilitative reduction of the vestibular asymmetry might restrict the extent of the secondary detrimental effect evoked by the principal peripheral impairment.

‘Excess anxiety’ and ‘less anxiety’: both depend on vestibular function

To present evidence of a functional interrelation between the vestibular and the anxiety systems based on a complex reciprocally organized network. The review focuses on the differential effects of various vestibular disorders, on psychiatric comorbidity, and on anxiety related to vertigo. Episodic vertigo syndromes such as vestibular migraine, vestibular paroxysmia, and Menière's disease are associated with a significant increase of psychiatric comorbidity, in particular anxiety/phobic disorders and depression. Chronic unilateral and bilateral vestibulopathy (BVP) do not exhibit a higher than normal psychiatric comorbidity. Anxiety related to the vertigo symptoms is also increased in episodic structural vestibular disorders but not in patients with chronic unilateral or bilateral loss of vestibular function. The lack of vertigo-related anxiety in BVP is a novel finding. Several studies have revealed special features related to anxiety in patients suffering from BVP: despite objectively impaired postural balance with frequent falls, they usually do not complain about fear of falling; they do not report an increased susceptibility to fear of heights; they do not have an increased psychiatric comorbidity; and they do not report increased anxiety related to the perceived vertigo. Subtle or moderate vestibular stimulation (by galvanic currents or use of a swing) may have beneficial effects on stress or mood state in healthy adults, and promote sleep in humans and rodents. The intimate structural and functional linkage of the vestibular and anxiety systems includes numerous nuclei, provincial and connector hubs, the thalamocortical network, and the cerebellum with many neural transmitter systems. The different involvement of emotional processes and anxiety - to the extent of 'excess anxiety' or 'less anxiety' - in structural vestibular disorders may be due to the specific dysfunction and whether the system activity is excited or diminished. Both psychiatric comorbidity and vertigo-related anxiety are maximal with excitation and minimal with loss of peripheral vestibular function.

Postural compensation for vestibular loss and implications for rehabilitation

This chapter summarizes the role of the vestibular system in postural control so that specific and effective rehabilitation can be designed that facilitates compensation for loss of vestibular function. Patients with bilateral or unilateral loss of peripheral vestibular function are exposed to surface perturbations to quantify automatic postural responses. Studies also evaluated the effects of audio- and vibrotactile-biofeedback to improve stability in stance and gait. The most important role of vestibular information for postural control is to control orientation of the head and trunk in space with respect to gravitoinertial forces, particularly when balancing on unstable surfaces. Vestibular sensory references are particularly important for postural control at high frequencies and velocities of self-motion, to reduce trunk drift and variability, to provide an external reference frame for the trunk and head in space; and to uncouple coordination of the trunk from the legs and the head-in-space from the body CoM. The goal of balance rehabilitation for patients with vestibular loss is to help patients 1) use remaining vestibular function, 2) depend upon surface somatosensory information as their primary postural sensory system, 3) learn to use stable visual references, and 4) identify efficient and effective postural movement strategies.

Abnormal Eye Movements Associated with Unilateral Loss of Vestibular Function

Acute unilateral loss of peripheral vestibular function causes spontaneous nystagmus. Initially, nystagmus is present during visual fixation.

Vestibular-Evoked Myogenic Potentials as a Test of Otolith Function

Objectives: To evaluate the use of 75 auditory clicks rather than the usual 100–256 for production of the vestibular-evoked myogenic potential (VEMP) response and to assess if the VEMP correlates with measures of cochlear function such as hearing loss (decibels on pure-tone testing) or auditory brainstem response (ABR). Subjects and Methods: Testing of the VEMP was carried out on 24 subjects: 7 normal individuals and 13 hard-of-hearing patients, 2 patients with known vestibular lesions, 1 with profound sensorineural hearing loss and 1 patient with unilateral acoustic neuroma prior to resection. The recording was performed using a conventional ABR machine. Using 75 refraction clicks as auditory stimuli, VEMP responses were measured from a surface electrode applied to the sternocleidomastoid muscle. The 75 responses were averaged. Results: A consistent unilateral biphasic response, the first negative and the second positive (nI, pII), was elicited from 39 of 40 ears (7 normal and 13 hard-of-hearing subjects with no known vestibular dysfunction). No statistical difference was found between the right and left ear responses for nI or pII wave latencies. Two patients with loss of peripheral vestibular function showed no VEMP responses on the affected side. The responses, however, were elicited bilaterally in a patient with congenital profound sensorineural hearing loss. In addition, ABR latencies did not correlate with VEMP latencies. Conclusion: Clear VEMP responses were elicited by using only 75 auditory clicks. This shortens the testing time and facilitates the procedure for the tested subject. Our data also indicate that the VEMP is generated secondary to auditory stimulation of the vestibular end organs (specifically the saccule) and does not correlate with cochlear function.

Head-shaking Nystagmus (HSN): the Theoretical Explanation and the Experimental Proof

Head-shaking nystagmus (HSN) is induced by oscillating the head at high frequency in the horizontal plane. This test is used in the clinic to detect the presence of a unilateral loss of vestibular function. HSN has been described as monophasic with fast-phase direction towards either side, or biphasic with the direction of fast phases reversing after a few seconds. Loss of vestibular function amplifies existing non-linearities in the vestibular system, so that imposed sinusoids can induce biases which are the source of HSN. Fifty-one patients suffering from loss of peripheral vestibular function (43 partial, 11 total unilateral tests) were exposed to whole-body sinusoidal stimulation, with increasing head velocities (90-220°/s) at 1/6Hz, to explore the consistency of per-rotatory induced biases. A bias was induced in all cases, but it wandered on either side, healthy or pathologic, unless test head velocities were larger than ~180°/s. Given this condition, the slow-phase bias was located towards the pathologic side for all patients with significant bias (>5°/s). These observations demonstrate that the sign and amplitude of the bias is variable and is not correlated with the lesioned side, unless high head velocities are imposed. This explains why the direction of the initial phase of HSN in the clinic seems so labile. Subsequent monophasic or biphasic characteristics of HSN are simply the reflection of interactions between two main time constants associated with ?velocity storage? and ?gaze holding? in the vestibular central processes.

Recovery of vestibulo-ocular reflex-function in subjects with an acute unilateral peripheral vestibular deficit

The centrally controlled compensation for a reduced horizontal vestibulo-ocular reflex (VOR) gain caused by a unilateral afferent deficit is usually studied following a selective surgical procedure which completely lesions the vestibular nerve or blocks the horizontal semicircular canal. The more common, unilateral, vestibular deficit encountered clinically, is a partial loss of peripheral vestibular function, following which peripheral recovery and/or central compensation may occur. We investigated changes of the VOR gain in response to a sudden, idiopathic, unilateral vestibular deficit in 64 subjects by examining the responses to low-frequency, whole-body, rotations about an earth vertical axis with different accelerations (5, 20 and 40 deg/sec2) during in- and out-patient visits separated by 4 months in an attempt to identify changes brought about by peripheral recovery and by central compensation processes. Peripheral function was assumed to be measured by the response to caloric irrigation. It improved some 30% on average between the two visits. VOR responses for rotations towards the deficit side also improved between the two visits. Most improvement occurred for 20 deg/sec2 accelerations. However, the correlation coefficient between rotation and caloric responses was always less than 0.6. Unlike caloric responses which improved over time, responses for rotations to the intact side did not change between the visits. For this reason, the majority of observed VOR rotation responses were nearly symmetrical at the time of the second visit, despite being below normal levels. These findings suggest that both peripheral recovery and central compensation processes help restore symmetrical VOR function for head rotations after a partial unilateral vestibular deficit. However the improvement of VOR response symmetry, particularly to slow (< 40 deg/sec2) accelerations, is largely independent of the recovery of peripheral sensitivity.

Long-term deficits of goal-directed vestibulo-ocular function following total unilateral loss of peripheral vestibular function.

Brief whole-body movements (+/- 5 to 170 degrees/s peak velocity; approximately equal to 0.5 s duration), applied during 1.44-s intervals of total darkness while subjects "looked" at a just-viewed target, were used to examine vestibulo-ocular function in 3 patients who had compensated to total unilateral loss of peripheral vestibular function. We found that the combined effects of slow-phase and saccadic eye movements both tended to keep the eyes stabilized on the unseen target. Compensatory slow-phases elicited during rapid head movements ipsilateral to (i.e., towards) the lesion were only about 60% as effective as those elicited during rapid contralateral movements. Compensatory gaze-correcting saccades tended to supplement deficient slow-phase movements, especially during rapid ipsilateral head movement. However, the gaze-correcting effect of saccades was only about half of the required for perfect stabilization. Thus, two functional vestibular deficits were observed during rapid ipsilateral head movements: (1) reduced slow-phase stabilization, and (2) reduced saccadic ability to adequately supplement the deficient slow phases. However, overall vestibular functional capability, as assessed by observation of the net effect of both slow phases and saccades, was much better than would be indicated by conventional observation of slow-phase movements alone.

Unilateral loss of peripheral vestibular function in patients: degree of compensation and factors causing decompensation.

Unilateral surgical ablation of peripheral vestibular function has been suggested for the treatment of a number of diseases that involve vestibular dysfunction. The postoperative distressing symptoms usually subside with time, whereupon the patient is said to have clinically compensated. However, even in well-compensated patients, the initial symptoms may reappear--under certain conditions that are briefly discussed (decompensation)--and, in addition, vestibular gaze stabilization deficits, (apparently permanent) appear whenever moderately rapid head movements are imposed. Thus, surgical ablation of unilateral peripheral vestibular function should not be considered "a treatment of choice," and should be performed in only carefully selected cases.

Vestibulo-toxicity of tobramycin

The case histories are described of two patients with normal renal function who developed permanent complete bilateral loss of peripheral vestibular function during tobramycin therapy. Despite the low incidence of the cochleotoxic and and vestibulotoxic side-effects of tobramycin, it seems advisable to monitor patients on tobramycin therapy for signs of vestibular dysfunction and hearing loss.