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Interactions between Stress and Vestibular Compensation – A Review  [PDF]
Yougan Saman,Mayank B. Dutia
Frontiers in Neurology , 2012, DOI: 10.3389/fneur.2012.00116
Abstract: Elevated levels of stress and anxiety often accompany vestibular dysfunction, while conversely complaints of dizziness and loss of balance are common in patients with panic and other anxiety disorders. The interactions between stress and vestibular function have been investigated both in animal models and in clinical studies. Evidence from animal studies indicates that vestibular symptoms are effective in activating the stress axis, and that the acute stress response is important in promoting compensatory synaptic and neuronal plasticity in the vestibular system and cerebellum. The role of stress in human vestibular disorders is complex, and definitive evidence is lacking. This article reviews the evidence from animal and clinical studies with a focus on the effects of stress on the central vestibular pathways and their role in the pathogenesis and management of human vestibular disorders.
Basic Concepts in Understanding Recovery of Function in Vestibular Reflex Networks during Vestibular Compensation  [PDF]
Kenna D. Peusner
Frontiers in Neurology , 2012, DOI: 10.3389/fneur.2012.00017
Abstract: Unilateral peripheral vestibular lesions produce a syndrome of oculomotor and postural deficits with the symptoms at rest, the static symptoms, partially or completely normalizing shortly after the lesion due to a process known as vestibular compensation. The symptoms are thought to result from changes in the activity of vestibular sensorimotor reflexes. Since the vestibular nuclei must be intact for recovery to occur, many investigations have focused on studying these neurons after lesions. At present, the neuronal plasticity underlying early recovery from the static symptoms is not fully understood. Here we propose that knowledge of the reflex identity and input–output connections of the recorded neurons is essential to link the responses to animal behavior. We further propose that the cellular mechanisms underlying vestibular compensation can be sorted out by characterizing the synaptic responses and time course for change in morphologically defined subsets of vestibular reflex projection neurons. Accordingly, this review focuses on the perspective gained by performing electrophysiological and immunolabeling studies on a specific subset of morphologically defined, glutamatergic vestibular reflex projection neurons, the principal cells of the chick tangential nucleus. Reference is made to pertinent findings from other studies on vestibular nuclei neurons, but no comprehensive review of the literature is intended since broad reviews already exist. From recording excitatory and inhibitory spontaneous synaptic activity in principal cells, we find that the rebalancing of excitatory synaptic drive bilaterally is essential for vestibular compensation to proceed. This work is important for it defines for the first time the excitatory and inhibitory nature of the changing synaptic inputs and the time course for changes in a morphologically defined subset of vestibular reflex projection neurons during early stages of vestibular compensation.
Reconsidering the Role of Neuronal Intrinsic Properties and Neuromodulation in Vestibular Homeostasis  [PDF]
Mathieu Beraneck,Erwin Idoux
Frontiers in Neurology , 2012, DOI: 10.3389/fneur.2012.00025
Abstract: The sensorimotor transformations performed by central vestibular neurons constantly adapt as the animal faces conflicting sensory information or sustains injuries. To ensure the homeostasis of vestibular-related functions, neural changes could in part rely on the regulation of 2° VN intrinsic properties. Here we review evidence that demonstrates modulation and plasticity of central vestibular neurons’ intrinsic properties. We first present the partition of Rodents’ vestibular neurons into distinct subtypes, namely type A and type B. Then, we focus on the respective properties of each type, their putative roles in vestibular functions, fast control by neuromodulators and persistent modifications following a lesion. The intrinsic properties of central vestibular neurons can be swiftly modulated by a wealth of neuromodulators to adapt rapidly to temporary changes of ecophysiological surroundings. To illustrate how intrinsic excitability can be rapidly modified in physiological conditions and therefore be therapeutic targets, we present the modulation of vestibular reflexes in relation to the variations of the neuromodulatory inputs during the sleep/wake cycle. On the other hand, intrinsic properties can also be slowly, yet permanently, modified in response to major perturbations, e.g., after unilateral labyrinthectomy (UL). We revisit the experimental evidence, which demonstrates that drastic alterations of the central vestibular neurons’ intrinsic properties occur following UL, with a slow time course, more on par with the compensation of dynamic deficits than static ones. Data are interpreted in the framework of distributed processes that progress from global, large-scale coping mechanisms (e.g., changes in behavioral strategies) to local, small-scale ones (e.g., changes in intrinsic properties). Within this framework, the compensation of dynamic deficits improves over time as deeper modifications are engraved within the finer parts of the vestibular-related networks. Finally, we offer perspectives and working hypotheses to pave the way for future research aimed at understanding the modulation and plasticity of central vestibular neurons’ intrinsic properties.
Postural Compensation for Unilateral Vestibular Loss  [PDF]
Robert J. Peterka,Fay B. Horak
Frontiers in Neurology , 2011, DOI: 10.3389/fneur.2011.00057
Abstract: Postural control of upright stance was investigated in well-compensated, unilateral vestibular loss (UVL) subjects compared to age-matched control subjects. The goal was to determine how sensory weighting for postural control in UVL subjects differed from control subjects, and how sensory weighting related to UVL subjects’ functional compensation, as assessed by standardized balance and dizziness questionnaires. Postural control mechanisms were identified using a model-based interpretation of medial–lateral center-of-mass body-sway evoked by support-surface rotational stimuli during eyes-closed stance. The surface-tilt stimuli consisted of continuous pseudorandom rotations presented at four different amplitudes. Parameters of a feedback control model were obtained that accounted for each subject’s sway response to the surface-tilt stimuli. Sensory weighting factors quantified the relative contributions to stance control of vestibular sensory information, signaling body-sway relative to earth-vertical, and proprioceptive information, signaling body-sway relative to the surface. Results showed that UVL subjects made significantly greater use of proprioceptive, and therefore less use of vestibular, orientation information on all tests. There was relatively little overlap in the distributions of sensory weights measured in UVL and control subjects, although UVL subjects varied widely in the amount they could use their remaining vestibular function. Increased reliance on proprioceptive information by UVL subjects was associated with their balance being more disturbed by the surface-tilt perturbations than control subjects, thus indicating a deficiency of balance control even in well-compensated UVL subjects. Furthermore, there was some tendency for UVL subjects who were less able to utilize remaining vestibular information to also indicate worse functional compensation on questionnaires.
Compensation Following Bilateral Vestibular Damage  [PDF]
Bill J. Yates
Frontiers in Neurology , 2011, DOI: 10.3389/fneur.2011.00088
Abstract: Bilateral loss of vestibular inputs affects far fewer patients than unilateral inner ear damage, and thus has been understudied. In both animal subjects and human patients, bilateral vestibular hypofunction (BVH) produces a variety of clinical problems, including impaired balance control, inability to maintain stable blood pressure during postural changes, difficulty in visual targeting of images, and disturbances in spatial memory and navigational performance. Experiments in animals have shown that non-labyrinthine inputs to the vestibular nuclei are rapidly amplified following the onset of BVH, which may explain the recovery of postural stability and orthostatic tolerance that occurs within 10 days. However, the loss of the vestibulo-ocular reflex and degraded spatial cognition appear to be permanent in animals with BVH. Current concepts of the compensatory mechanisms in humans with BVH are largely inferential, as there is a lack of data from patients early in the disease process. Translation of animal studies of compensation for BVH into therapeutic strategies and subsequent application in the clinic is the most likely route to improve treatment. In addition to physical therapy, two types of prosthetic devices have been proposed to treat individuals with bilateral loss of vestibular inputs: those that provide tactile stimulation to indicate body position in space, and those that deliver electrical stimuli to branches of the vestibular nerve in accordance with head movements. The relative efficacy of these two treatment paradigms, and whether they can be combined to facilitate recovery, is yet to be ascertained.
Research progresses of vestibular compensation mechanism and its clinical significance

- , 2016, DOI: 10.3969/j.issn.1674-8115.2016.09.017
Abstract: 前庭系统是一套感知及控制平衡的精密操作系统,司职运动感知、凝视、肢体平衡等功能,并参与情感、记忆等认知功能。前庭功能障碍患者表现为失平衡、视物模糊、眩晕等,并由此导致严重的社会行为障碍。在前庭功能障碍早期,前庭中枢结构具有自发的、功能强大的再平衡功能,亦即前庭代偿。前庭康复是一种外源性干预策略,已经明确在单侧前庭损害中具有积极的促代偿效果。该文阐述了前庭代偿机制的研究新进展,以及基于此的前庭康复理念,亦即最佳前庭代偿效果并非依赖于最佳康复技术,而是有赖于把握神经网络发生内在可塑性改变的时间窗。
: The vestibular system is a complicated operating system contributing to monitor and control balance and has functions such as motion perception, gaze, and truck stability. More recently, the vestibular system has been recognized for its contribution to emotion, memory and social cognition. Patients with vestibular dysfunction present with loss of balance, blurred vision, vertigo and so on, resulting in serious social-behavioral impairments. At the early stage of vestibular dysfunction, the vestibular system often experiences a spontaneous recovery from the static and dynamic deficit, i.e. vestibular compensation. As an extrinsic intervention, vestibular rehabilitation can actively promote the compensation in unilateral vestibular impairment. This article reviews the latest research progresses of vestibular compensation mechanism and vestibular rehabilitation ideas, i.e. the best vestibular compensation relies on cross-talk windows between retraining processes and post-lesion brain-plasticity mechanisms, rather than rehabilitation techniques
Changes in Histamine Receptors (H1, H2, and H3) Expression in Rat Medial Vestibular Nucleus and Flocculus after Unilateral Labyrinthectomy: Histamine Receptors in Vestibular Compensation  [PDF]
Liuqing Zhou, Wen Zhou, Sulin Zhang, Bo Liu, Yangming Leng, Renhong Zhou, Weijia Kong
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0066684
Abstract: Vestibular compensation is the process of behavioral recovery following peripheral vestibular lesion. In clinics, the histaminergic medicine is the most widely prescribed for the treatment of vertigo and motion sickness, however, the molecular mechanisms by which histamine modulates vestibular function remain unclear. During recovery from the lesion, the modulation of histamine receptors in the medial vestibular nucleus (MVN) and the flocculus may play an important role. Here with the means of quantitative real-time PCR, western blotting and immunohistochemistry, we studied the expression of histamine receptors (H1, H2, and H3) in the bilateral MVN and the flocculus of rats on the 1st, 3rd, and 7th day following unilateral labyrinthectomy (UL). Our results have shown that on the ipsi-lesional flocculus the H1, H2 and H3 receptors mRNA and the protein increased significantly on the 1st and 3rd day, with compare of sham controls and as well the contralateral side of UL. However, on the 7th day after UL, this expression returned to basal levels. Furthermore, elevated mRNA and protein levels of H1, H2 and H3 receptors were observed in the ipsi-lesional MVN on the 1st day after UL compared with sham controls and as well the contralateral side of UL. However, this asymmetric expression was absent by the 3rd post-UL. Our findings suggest that the upregulation of histamine receptors in the MVN and the flocculus may contribute to rebalancing the spontaneous discharge in bilateral MVN neurons during vestibular compensation.
Synaptic Plasticity in Medial Vestibular Nucleus Neurons: Comparison with Computational Requirements of VOR Adaptation  [PDF]
John R. W. Menzies,John Porrill,Mayank Dutia,Paul Dean
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013182
Abstract: Vestibulo-ocular reflex (VOR) gain adaptation, a longstanding experimental model of cerebellar learning, utilizes sites of plasticity in both cerebellar cortex and brainstem. However, the mechanisms by which the activity of cortical Purkinje cells may guide synaptic plasticity in brainstem vestibular neurons are unclear. Theoretical analyses indicate that vestibular plasticity should depend upon the correlation between Purkinje cell and vestibular afferent inputs, so that, in gain-down learning for example, increased cortical activity should induce long-term depression (LTD) at vestibular synapses.
Recovery of Vestibular Ocular Reflex Function and Balance Control after a Unilateral Peripheral Vestibular Deficit  [PDF]
J. H. J. Allum
Frontiers in Neurology , 2012, DOI: 10.3389/fneur.2012.00083
Abstract: This review describes the effect of unilateral peripheral vestibular deficit (UPVD) on balance control for stance and gait tests. Because a UPVD is normally defined based on vestibular ocular reflex (VOR) tests, we compared recovery observed in balance control with patterns of recovery in VOR function. Two general types of UPVD are considered; acute vestibular neuritis (AVN) and vestibular neurectomy. The latter was subdivided into vestibular loss after cerebellar pontine angle tumor surgery during which a vestibular neurectomy was performed, and vestibular loss following neurectomy to eliminate disabling Ménière’s disease. To measure balance control, body-worn gyroscopes, mounted near the body’s center of mass (CoM), were used. Measurement variables were the pitch (anterior–posterior) and roll (lateral) sway angles and angular velocities of the lower trunk/pelvis. Both patient groups showed balance deficits during stance tasks on foam, especially with eyes closed when stable balance control is normally highly dependent on vestibular inputs. Deficits during gait were also present and were more profound for complex gait tasks such as tandem gait than simple gait tasks. Major differences emerged between the groups concerning the severity of the deficit and its recovery. Generally, the effects of acute neuritis on balance control were more severe but recovered rapidly. Deficits due to vestibular neurectomy were less severe, but longer lasting. These results mostly paralleled recovery of deficits in VOR function. However, questions need to be raised about the effect on balance control of the two modes of neural plasticity occurring in the vestibular system following vestibular loss due to neuritis: one mode being the limited central compensation for the loss, and the second mode being some restoration of peripheral vestibular function. Future work will need to correlate deficits in balance control during stance and gait more exactly with VOR deficits and carefully consider the differences between insufficient central compensation compared to inadequate peripheral restoration of function.
Unilateral Vestibular Loss Impairs External Space Representation  [PDF]
Liliane Borel, Christine Redon-Zouiteni, Pierre Cauvin, Michel Dumitrescu, Arnaud Devèze, Jacques Magnan, Patrick Péruch
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0088576
Abstract: The vestibular system is responsible for a wide range of postural and oculomotor functions and maintains an internal, updated representation of the position and movement of the head in space. In this study, we assessed whether unilateral vestibular loss affects external space representation. Patients with Menière's disease and healthy participants were instructed to point to memorized targets in near (peripersonal) and far (extrapersonal) spaces in the absence or presence of a visual background. These individuals were also required to estimate their body pointing direction. Menière's disease patients were tested before unilateral vestibular neurotomy and during the recovery period (one week and one month after the operation), and healthy participants were tested at similar times. Unilateral vestibular loss impaired the representation of both the external space and the body pointing direction: in the dark, the configuration of perceived targets was shifted toward the lesioned side and compressed toward the contralesioned hemifield, with higher pointing error in the near space. Performance varied according to the time elapsed after neurotomy: deficits were stronger during the early stages, while gradual compensation occurred subsequently. These findings provide the first demonstration of the critical role of vestibular signals in the representation of external space and of body pointing direction in the early stages after unilateral vestibular loss.
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