An Implanted Vestibular Prosthesis Improves Spatial Orientation in Animals with Severe Vestibular Damage.

Gravity is a pervasive environmental stimulus, and accurate graviception is required for optimal spatial orientation and postural stability. The primary graviceptors are the vestibular organs, which include angular velocity (semicircular canals) and linear acceleration (otolith organs) sensors. Graviception is degraded in patients with vestibular damage, resulting in spatial misperception and imbalance. Since minimal therapy is available for these patients, substantial effort has focused on developing a vestibular prosthesis or vestibular implant (VI) that reproduces information normally provided by the canals (since reproducing otolith function is very challenging technically). Prior studies demonstrated that angular eye velocity responses could be driven by canal VI-mediated angular head velocity information, but it remains unknown whether a canal VI could improve spatial perception and posture since these behaviors require accurate estimates of angular head position in space relative to gravity. Here, we tested the hypothesis that a canal VI that transduces angular head velocity and provides this information to the brain via motion-modulated electrical stimulation of canal afferent nerves could improve the perception of angular head position relative to gravity in monkeys with severe vestibular damage. Using a subjective visual vertical task, we found that normal female monkeys accurately sensed the orientation of the head relative to gravity during dynamic tilts, that this ability was degraded following bilateral vestibular damage, and improved when the canal VI was used. These results demonstrate that a canal VI can improve graviception in vestibulopathic animals, suggesting that it could reduce the disabling perceptual and postural deficits experienced by patients with severe vestibular damage.SIGNIFICANCE STATEMENT Patients with vestibular damage experience impaired vision, spatial perception, and balance, symptoms that could potentially respond to a vestibular implant (VI). Anatomic features facilitate semicircular canal (angular velocity) prosthetics but inhibit approaches with the otolith (linear acceleration) organs, and canal VIs that sense angular head velocity can generate compensatory eye velocity responses in vestibulopathic subjects. Can the brain use canal VI head velocity information to improve estimates of head orientation (e.g., head position relative to gravity), which is a prerequisite for accurate spatial perception and posture? Here we show that a canal VI can improve the perception of head orientation in vestibulopathic monkeys, results that are highly significant because they suggest that VIs mimicking canal function can improve spatial orientation and balance in vestibulopathic patients.

Dynamic whole-brain metabolic connectivity during vestibular compensation in the rat.

Unilateral damage to the inner ear results in an acute vestibular syndrome, which is compensated within days to weeks due to adaptive cerebral plasticity. This process, called central vestibular compensation (VC), involves a wide range of functional and structural mechanisms at the cellular and network level. The short-term dynamics of whole-brain functional network recruitment and recalibration during VC has not been depicted in vivo. The purpose of this study was to investigate the interplay of separate and distinct brain regions and in vivo networks in the course of VC by sequential [18F]-FDG-PET-based statistical and graph theoretical analysis with the aim of revealing the metabolic connectome before and 1, 3, 7, and 15 days post unilateral labyrinthectomy (UL) in the rat. Temporal changes in metabolic brain connectivity were determined by Pearson's correlation (|r| > 0.5, p < 0.001) of regional cerebral glucose metabolism (rCGM) in 57 segmented brain regions. Metabolic connectivity analysis was compared to univariate voxel-wise statistical analysis of rCGM over time and to behavioral scores of static and dynamic sensorimotor recovery. Univariate statistical analysis revealed an ipsilesional relative rCGM decrease (compared to baseline) and a contralesional rCGM increase in vestibular and limbic networks and an increase in bilateral cerebellar and sensorimotor networks. Quantitative analysis of the metabolic connections showed a maximal increase from baseline to day 3 post UL (interhemispheric: 2-fold, ipsilesional: 3-fold, contralesional: 12-fold) and a gradual decline until day 15 post UL, which paralleled the dynamics of vestibular symptoms. In graph theoretical analysis, an increase in connectivity occurred especially within brain regions associated with brainstem-cerebellar and thalamocortical vestibular networks and cortical sensorimotor networks. At the symptom peak (day 3 post UL), brain networks were found to be organized in large ensembles of distinct and highly connected hubs of brain regions, which separated again with progressing VC. Thus, we found rapid changes in network organization at the subcortical and cortical level and in both hemispheres, which may indicate an initial functional substitution of vestibular loss and subsequent recalibration and reorganization of sensorimotor networks during VC.

Trauma-induced vestibular dysfunction: Possible functional repair under α1-antitrypsin-rich conditions.

Transient vestibular organ deafferentation, such that is caused by traumatic tissue injury, is presently addressed by corticosteroid therapy. However, restoration of neurophysiological properties is rarely achieved. Here, it was hypothesized that the tissue-protective attributes of α1-antityrpsin (AAT) may promote restoration of neuronal function. Inner ear injury was inflicted by unilateral labyrinthotomy in wild-type mice and in mice overexpressing human AAT. A 2-week-long assessment of vestibular signs followed. All animals responded with peak vestibular dysfunction scores within 4 h after local trauma. While wild-type animals displayed partial or no recovery across 7 days post-injury, AAT-rich group exhibited early recovery: from behavioral score 9-out-of-9 at peak to 4.8 ±â€¯0.44 (mean ±â€¯SD) within 8 h from injury, a time when wild-type mice scored 8.6 ±â€¯0.54 (p < 0.0001), and from vestibular score 15-out-of-15 to 7.8 ±â€¯2.2 within 24 h, when wild-type mice scored 13.0 ±â€¯2.0 (p < 0.01). Thus, recovery and functional normalisation of an injured vestibular compartment is achievable without corticosteroid therapy; expedited tissue repair processes appear to result from elevated circulating AAT levels. This study lays the foundation for exploring the molecular and cellular mediators of AAT within the repair processes of the delicate microscopic structures of the vestibular end organ.

Angular vestibuloocular reflex responses in Otop1 mice. II. Otolith sensor input improves compensation after unilateral labyrinthectomy.

The role of the otoliths in mammals in the normal angular vestibuloocular reflex (VOR) was characterized in an accompanying study based on the Otopetrin1 (Otop1) mouse, which lacks functioning otoliths because of failure to develop otoconia but seems to have otherwise normal peripheral anatomy and neural circuitry. That study showed that otoliths do not contribute to the normal horizontal (rotation about Earth-vertical axis parallel to dorso-ventral axis) and vertical (rotation about Earth-vertical axis parallel to interaural axis) angular VOR but do affect gravity context-specific VOR adaptation. By using these animals, we sought to determine whether the otoliths play a role in the angular VOR after unilateral labyrinthectomy when the total canal signal is reduced. In five Otop1 mice and five control littermates we measured horizontal and vertical left-ear-down and right-ear-down sinusoidal VOR (0.2-10 Hz, 20-100°/s) during the early (3-5 days) and plateau (28-32 days) phases of compensation after unilateral labyrinthectomy and compared these measurements with baseline preoperative responses from the accompanying study. From similar baselines, acute gain loss was ~25% less in control mice, and chronic gain recovery was ~40% more in control mice. The acute data suggest that the otoliths contribute to the angular VOR when there is a loss of canal function. The chronic data suggest that a unilateral otolith signal can significantly improve angular VOR compensation. These data have implications for vestibular rehabilitation of patients with both canal and otolith loss and the development of vestibular implants, which currently only mimic the canals on one side. NEW & NOTEWORTHY This is the first study examining the role of the otoliths (defined here as the utricle and saccule) on the acute and chronic angular vestibuloocular reflex (VOR) after unilateral labyrinthectomy in an animal model in which the otoliths are reliably inactivated and the semicircular canals preserved. This study shows that the otolith signal is used to augment the acute angular VOR and help boost VOR compensation after peripheral injury.

Clinical Assessments of Balance in Adults with Concussion: An Update.

Postural instability is a cardinal indicator of concussion. Assessments of the postural control system range from clinical to laboratory tests that assess the balance of the individual. In a previous article regarding clinical assessment of balance in adults with concussion, we reviewed the importance of balance as a component in concussion evaluations. The purpose of this review article is to update the information previously published in 2014. Since 2014, research has provided evidence for the incorporation of dynamic methods for evaluating balance postconcussion with particular emphasis on sensory system integration and dual tasking. Therefore, this review will examine the current state of knowledge on how concussion injuries affect postural control, advancements in evaluating balance postconcussion, such as novel eye-tracking techniques, and current recommendations for best practices for balance assessment.

Physical Therapy Management of Adults with Mild Traumatic Brain Injury.

Rehabilitation for individuals after mild traumatic brain injury (mTBI) or concussion requires emphasis on both cognitive and physical rest, with a gradual return to activity including sports. As the client becomes more active, the rehabilitation professional should pay close attention to symptoms associated with mTBI, such as headache, dizziness, nausea, and difficulty concentrating. The systematic approach to return to play provided by the Berlin Consensus Statement on Concussion in Sport can apply to adults with mTBI. This protocol calls for gradually increasing the intensity of physical activity while attending to postconcussion symptoms. During the incident that led to an mTBI, the injured individual may incur injuries to the vestibular and balance system that are best addressed by professionals with specific training in vestibular rehabilitation, most commonly physical therapists. Benign paroxysmal positional vertigo is a condition in which otoconia particles in the inner ear dislodge into the semicircular canals, resulting in severe vertigo and imbalance. This condition frequently resolves in a few sessions with a vestibular physical therapist. In conditions such as gaze instability, motion sensitivity, impaired postural control, and cervicogenic dizziness, improvement is more gradual and requires longer follow-up with a physical therapist and a home exercise program. In all of the above-stated conditions, it is essential to consider that a patient with protracted symptoms of mTBI or postconcussion syndrome will recover more slowly than others and should be monitored for symptoms throughout the intervention.

Reduced choice-related activity and correlated noise accompany perceptual deficits following unilateral vestibular lesion.

Signals from the bilateral vestibular labyrinths work in tandem to generate robust estimates of our motion and orientation in the world. The relative contributions of each labyrinth to behavior, as well as how the brain recovers after unilateral peripheral damage, have been characterized for motor reflexes, but never for perceptual functions. Here we measure perceptual deficits in a heading discrimination task following surgical ablation of the neurosensory epithelium in one labyrinth. We found large increases in heading discrimination thresholds and large perceptual biases at 1 wk postlesion. Repeated testing thereafter improved heading perception, but vestibular discrimination thresholds remained elevated 3 mo postlesion. Electrophysiological recordings from the contralateral vestibular and cerebellar nuclei revealed elevated neuronal discrimination thresholds, elevated neurometric-to-psychometric threshold ratios, and reduced trial-by-trial correlations with perceptual decisions ["choice probabilities" (CPs)]. The relationship between CP and neuronal threshold was shallower, but not significantly altered, suggesting that smaller CPs in lesioned animals could be largely attributable to greater neuronal thresholds. Simultaneous recordings from pairs of neurons revealed that correlated noise among neurons was also reduced following the lesion. Simulations of a simple pooling model, which takes into account the observed changes in tuning slope and correlated noise, qualitatively accounts for the elevated psychophysical thresholds and neurometric-to-psychometric ratios, as well as the decreased CPs. Thus, cross-labyrinthine interactions appear to play important roles in enhancing neuronal and perceptual sensitivity, strengthening interneuronal correlations, and facilitating correlations between neural activity and perceptual decisions.

Brain or strain? Symptoms alone do not distinguish physiologic concussion from cervical/vestibular injury.

OBJECTIVE: To compare symptoms in patients with physiologic postconcussion disorder (PCD) versus cervicogenic/vestibular PCD. We hypothesized that most symptoms would not be equivalent. In particular, we hypothesized that cognitive symptoms would be more often associated with physiologic PCD. DESIGN: Retrospective review of symptom reports from patients who completed a 22-item symptom questionnaire. SETTING: University-based concussion clinic. PATIENTS: Convenience sample of 128 patients who had symptoms after head injury for more than 3 weeks and who had provocative treadmill exercise testing. INDEPENDENT VARIABLES: Subjects were classified as either physiologic PCD (abnormal treadmill performance and a normal cervical/vestibular physical examination) or cervicogenic/vestibular PCD (CGV, normal treadmill performance, and an abnormal cervical/vestibular physical examination). MAIN OUTCOME MEASURES: Self-reported symptoms. Univariate and multivariate methods, including t tests, tests of equivalence, a logistic regression model, k-nearest neighbor analysis, multidimensional scaling, and principle components analysis were used to see whether symptoms could distinguish PCD from CGV. RESULTS: None of the statistical methods used to analyze self-reported symptoms was able to adequately distinguish patients with PCD from patients with CGV. CONCLUSIONS: Symptoms after head injury, including cognitive symptoms, have traditionally been ascribed to brain injury, but they do not reliably discriminate between physiologic PCD and cervicogenic/vestibular PCD. Clinicians should consider specific testing of exercise tolerance and perform a physical examination of the cervical spine and the vestibular/ocular systems to determine the etiology of postconcussion symptoms. CLINICAL RELEVANCE: Symptoms after head injury, including cognitive symptoms, do not discriminate between concussion and cervical/vestibular injury.

Stapediovestibular dislocation depicted on temporal bone computed tomography with 3D rendering.

Stapediovestibular dislocation is an unusual form of ossicular trauma. In this article, a case of medial stapediovestibular dislocation and pneumolabyrinth due to penetrating injury with a stick diagnosed on temporal bone CT is described. In particular, 3D CT renderings can aid in the evaluation of the displaced ossicles.

Restricted neural plasticity in vestibulospinal pathways after unilateral labyrinthectomy as the origin for scoliotic deformations.

Adolescent idiopathic scoliosis in humans is often associated with vestibulomotor deficits. Compatible with a vestibular origin, scoliotic deformations were provoked in adult Xenopus frogs by unilateral labyrinthectomy (UL) at larval stages. The aquatic ecophysiology and absence of body-weight-supporting limb proprioceptive signals in amphibian tadpoles as a potential sensory substitute after UL might be the cause for a persistent asymmetric descending vestibulospinal activity. Therefore, peripheral vestibular lesions in larval Xenopus were used to reveal the morphophysiological alterations at the cellular and network levels. As a result, spinal motor nerves that were modulated by the previously intact side before UL remained permanently silent during natural vestibular stimulation after the lesion. In addition, retrograde tracing of descending pathways revealed a loss of vestibular neurons on the ipsilesional side with crossed vestibulospinal projections. This loss facilitated a general mass imbalance in descending premotor activity and a permanent asymmetric motor drive to the axial musculature. Therefore, we propose that the persistent asymmetric contraction of trunk muscles exerts a constant, uncompensated differential mechanical pull on bilateral skeletal elements that enforces a distortion of the soft cartilaginous skeletal elements and bone shapes. This ultimately provokes severe scoliotic deformations during ontogenetic development similar to the human syndrome.

Vestibular loss promotes procedural response during a spatial task in rats.

Declarative memory refers to a spatial strategy using numerous sources of sensory input information in which visual and vestibular inputs are assimilated in the hippocampus. In contrast, procedural memory refers to a response strategy based on motor skills and familiar gestures and involves the striatum. Even if vestibular loss impairs hippocampal activity and spatial memory, vestibular-lesioned rats remain able to find food rewards during complex spatial memory task. Since hippocampal lesions induce a switch from declarative memory to procedural memory, we hypothesize that vestibular-lesioned rats use a strategy other than that of hippocampal spatial response to complete the task and to counterbalance the loss of vestibular information. We test, in a reverse T-maze paradigm, the types of strategy vestibular-lesioned rats preferentially uses in a spatial task. We clearly demonstrate that all vestibular-lesioned rats shift to a response strategy to solve the spatial task, while control rats use spatial and response strategies equally. We conclude that the loss of vestibular informations leading to spatial learning impairments is not offset at the hippocampus level by integration process of other sense mainly visual informations; but favors a response strategy through procedural memory most likely involving the striatum, cerebellum, and motor learning.

Trauma-Induced Vestibular Dysfunction: Improved Repair Under Local Treatment With α1-Antitrypsin.

AIM: To characterize vestibular recovery in a mouse model of unilateral labyrinthotomy under local AAT and dexamethasone treatment. BACKGROUND: Alpha1-antitrypsin (AAT) is a circulating tissue-protective molecule that rises during inflammatory conditions and promotes inflammatory resolution. Its local concentration in human perilymph inversely correlates with the severity of inner ear dysfunction; concomitantly, mice that overexpress AAT and undergo inner ear trauma rapidly restore vestibular function. Locally applied AAT has yet to be examined in this context, nor has it been directly compared with anti-inflammatory corticosteroid treatment. METHODS: Wild-type mice C57BL/6 underwent a unilateral inner ear injury. Nine microliters of saline, clinical-grade AAT (180 µg/site), dexamethasone (4 mg/site), or both were applied locally on Days 0, 1, and 2 (n = 5/group). Vestibular function was assessed for 7 days. An in vitro human epithelial gap closure assay was performed using A549 cells in the presence of AAT and/or dexamethasone. RESULTS: Upon labyrinthotomy, all groups displayed severe vestibular dysfunction. Saline-treated mice showed the longest impairment. That group and the dexamethasone group displayed partial to no recovery, while AAT-treated mice exhibited complete recovery within 7 days; at this time point, dexamethasone-treated mice exhibited 50% recovery. Objective vestibular testing showed similar outcomes. In vitro, cotreatment with AAT and dexamethasone resulted in a gap closure dynamic that was superior to AAT alone at 6 h and superior to DEX alone at 48 h. CONCLUSION: Locally applied AAT treatment is superior to locally applied dexamethasone in promoting vestibular recovery in vivo. Ongoing studies are exploring the potential advantages of AAT combined with early low-dose dexamethasone therapy.

Effective sensory modality activating an escape triggering neuron switches during early development in zebrafish.

Developing nervous systems grow to integrate sensory signals from different modalities and to respond through various behaviors. Here, we examined the development of escape behavior in zebrafish [45-170 h postfertilization (hpf)] to study how developing sensory inputs are integrated into sensorimotor circuits. Mature fish exhibit fast escape upon both auditory/vestibular (AV) and head-tactile stimuli. Newly hatched larvae, however, do not respond to AV stimuli before 75 hpf. Because AV-induced fast escape in mature fish is triggered by a pair of hindbrain neurons known as Mauthner (M) cells, we studied functional development of the M-cell circuit accounting for late acquisition of AV-induced escape. In fast escape elicited by head-directed water jet, minimum onset latency decreased throughout development (5 ms at 45-59 hpf, 3 ms after 75 hpf). After 75 hpf, lesioning the otic vesicle (OV) to eliminate AV input resulted in loss of short-latency (<5 ms) fast escape, whereas ablation of the sensory trigeminal ganglion (gV) to block head-tactile input did not. Before 75 hpf, however, fast escape persisted after OV lesion but disappeared after gV ablation. Laser ablation of the M-cell and Ca²âº imaging of the M-cell during escape demonstrated that M-cell firing is required to initiate short-latency fast escapes at every developmental stage and further suggest that head-tactile input activates the M-cell before 75 hpf, but that after this point AV input activates the M-cell instead. Thus, a switch in the effective sensory input to the M-cells mediates the acquisition of a novel modality for initiating fast escape.

Posttraumatic vertigo and dizziness.

Dizziness and vertigo are common symptoms following minor head trauma. Although these symptoms resolve within a few weeks in many patients, in some the symptoms may last much longer and impede ability to return to work and full functioning. Causes of persisting or recurrent dizziness may include benign paroxysmal positional vertigo, so-called labyrinthine concussion, unilateral vestibular nerve injury or damage to the utricle or saccule, perilymphatic fistula, or less commonly traumatic endolymphatic hydrops. Some dizziness after head trauma is due to nonlabyrinthine causes that may be related to structural or microstructural central nervous system injury or to more complicated interactions between migraine, generalized anxiety, and issues related to patients self-perception, predisposing psychological states, and environmental and stress-related factors. In this article, the authors review both the inner ear causes of dizziness after concussion and also the current understanding of chronic postconcussive dizziness when no peripheral vestibular cause can be identified.

Processing of vestibular inputs by the medullary lateral tegmental field of conscious cats: implications for generation of motion sickness.

The dorsolateral reticular formation of the caudal medulla, the lateral tegmental field (LTF), participates in generating vomiting. LTF neurons exhibited complex responses to vestibular stimulation in decerebrate cats, indicating that they received converging inputs from a variety of labyrinthine receptors. Such a convergence pattern of vestibular inputs is appropriate for a brain region that participates in generating motion sickness. Since responses of brainstem neurons to vestibular stimulation can differ between decerebrate and conscious animals, the current study examined the effects of whole-body rotations in vertical planes on the activity of LTF neurons in conscious felines. Wobble stimuli, fixed-amplitude tilts, the direction of which moves around the animal at a constant speed, were used to determine the response vector orientation, and also to ascertain whether neurons had spatial-temporal convergence (STC) behavior (which is due to the convergence of vestibular inputs with different spatial and temporal properties). The proportion of LTF neurons with STC behavior in conscious animals (25 %) was similar to that in decerebrate cats. Far fewer neurons in other regions of the feline brainstem had STC behavior, confirming findings that many LTF neurons receive converging inputs from a variety of labyrinthine receptors. However, responses to vertical plane vestibular stimulation were considerably different in decerebrate and conscious felines for LTF neurons lacking STC behavior. In decerebrate cats, most LTF neurons had graviceptive responses to rotations, similar to those of otolith organ afferents. However, in conscious animals, the response properties were similar to those of semicircular canal afferents. These differences show that higher centers of the brain that are removed during decerebration regulate the labyrinthine inputs relayed to the LTF, either by gating connections in the brainstem or by conveying vestibular inputs directly to the region.

[Sensorineural hearing loss after dull head injury or concussion trauma]. / Innenohrschwerhörigkeit nach stumpfem Schädelhirntrauma bzw. Kopfanpralltrauma.

A dull head injury can lead to isolated damage of the inner ear (cochlear labyrinthine concussion) or damage of the otolithe organ (vestibular labyrinthine concussion) due to a bone conduction pressure . A typical sign is a high frequency SNHL in form of a c5-dip. The c5-dip can be bilateral or unilateral or different on each side - dependant on the side of injury. In case of a unilateral skull base fracture a contralateral labyrinthine concussion is also possible. Moreover a lot of cases also show an accompanying tinnitus. This knowledge is based on animal and human experiments, as well as data from clinical and medical report examinations over decades. It is important to differentiate between a SNHL caused by accident or uni- or bilateral endogenic degenerative hearing loss.

Evidence that spatial memory deficits following bilateral vestibular deafferentation in rats are probably permanent.

Previous studies of rats with bilateral vestibular deafferentation (BVD) have demonstrated spatial memory deficits, suggesting adverse effects on the hippocampus. However, the longest post-operative time interval that has been studied was approx. 5-7 months post-surgery. In this study, we investigated whether rats exhibited spatial memory deficits at 14 months following BVD and whether these deficits could be exacerbated by administration of cannabinoid (CB) drugs. Twenty-eight adult rats were divided into four groups: (1) sham surgery+vehicle; (2) sham surgery+the CB1/CB(2) receptor agonist WIN55,212-2 ('WIN'); (3) BVD+vehicle; and (4) BVD+WIN. WIN (1.0 or 2.0 mg/kg/day) or vehicle, was administered (s.c.) on days 1-10 and 11-20 (respectively), 30 min before the rats performed in a foraging task. On day 21, the CB receptor inverse agonist, AM251 (3.0 mg/kg, s.c.), was administered before WIN or vehicle. To our surprise, BVD animals were impaired in using the visual cues during the probe test in light. In the dark trials, when visual cues were unavailable, BVD animals were unable to use self-movement cues in homing. However, WIN at 2 mg/kg, significantly improved BVD animals' homing time and number of errors in the dark through strategies other than the improvement in using self-movement cues. Furthermore, AM251 significantly improved heading angle in vehicle-treated animals and the first home choice in WIN-treated animals. These results suggest that at 14 months post-BVD, the animals are not only impaired in path integration, but also piloting and that the spatial memory deficits may be permanent. The involvement of the cannabinoid system is more complicated than expected.

Vestibular control of intermediate- and long-term cardiovascular responses to experimental orthostasis.

Sustained orthostasis elicits the elevation of arterial blood pressure (BP) via sympathetic activation in conscious Wistar rats for at least 2 hours. We tested the hypothesis whether vestibular apparatus plays a role in BP and heart rate (HR) control in response to prolonged gravitational stress. BP and HR responses to 45 degrees head-up for either 2 or 24 hours were monitored by telemetry. Vestibular lesions (VL) were performed by a modified microsurgical-chemical technique. Horizontal BP and HR were not influenced by VL preceding 2-hour tilt. VL abolished the sustained 2-hour BP response to head-up tilt (8.3+/-0.9 mm Hg relative to horizontal values) while suppressed HR transiently only. VL eliminated diurnal BP fluctuations and decreased HR in horizontal position for 24 hours. Head-up tilt for 24 hours increased BP and HR progressively in intact animals, raising their daily average value by 5.6+/-0.7 mm Hg and 22.2+/-6 BPM, respectively. VL resulted in an initial BP rise followed by progressive BP reduction in response to long-term head-up tilt (4+/-2.2 mm Hg) without eliminating the tachycardia (34.4+/-5.4 BPM). Thus, blockade of labyrinthine inputs attenuates the BP responses elicited by both intermediate and long-term gravitational stress of orthostatic type. However, other sensory inputs derived from non-vestibular cues (e.g. proprioceptive, visual, visceral, cutaneous etc.) seem to be effective enough to maintain BP normal.

The real identity and sensory overlap mechanism of special vestibular afferent neurons that sense both rotation and linear force.

AIMS: Although the vestibular system has been widely investigated over the past 50 years, there is still an unsolved mystery. Some special vestibular afferent (SVA) neurons responding to both rotation and linear force were found through neurophysiological techniques, however, the sensory overlap mechanism of SVA neurons is still unclear, which may be closely related to vestibular-related diseases. MATERIALS AND METHODS: To address the above-mentioned problem, a cupula buoyancy theory was established in the present study, where SVA neurons were considered semicircular canal afferent (SCCA) neurons. Then labyrinth anatomy and neural response dynamics of vestibular afferent neurons in chinchilla were investigated through vestibular labyrinth reconstruction and single unit recording technique, respectively. KEY FINDINGS: We analyzed the deflections of cupulae under multiple conditions with the help of Amira Software and predicted the neural response law of SCCA neurons to linear force based on the cupula buoyancy theory. Data analysis confirmed that the basic response characteristic of SVA neurons had no significant difference to those of SCCA neurons, but were significantly different from those of otolith afferent neurons. Further, the actual responses of SVA neurons to linear force are completely consistent with our predictions. These results strongly suggest that SVA neurons actually are SCCA neurons, and the cupula buoyancy theory is the key to the sensory overlap mechanism of SCCA neurons. SIGNIFICANCE: Our study revealed the real identity of SVA neurons and provided a reasonable mechanism for sensory overlap of rotation and linear force, which improved our understanding about the vestibular system.

Topography of the lesion in idiopathic sudden sensorineural hearing loss.

INTRODUCTION: Etiology of ISSNHL includes cessation of vascular perfusion, viral infection and cochlear membrane injury. Precise location of injury should be defined for a target-oriented treatment. Vestibular complaints in ISSNHL are hypothesized as involvement of vestibule. Vestibular complaints can be either due to involvement of inner ear or neural tract at any level. OBJECTIVES: In the present study we aimed to demonstrate involvement of vestibular organs in the absence of vestibular symptoms. It was aimed to evaluate superior and inferior vestibular neural pathways. METHODS: c-vemp and o-vemp were applied to patients suffering ISSNHL without vertigo. Pure tone averages, audiogram configurations, degree of hearing loss were analyzed. Latencies of P1 and N1 waves, amplitudes of P1-N1 waves were evaluated. Asymmetrical vemp wave patterns were compared between two ears regarding difference of PTA. RESULTS: Latencies of c-vemp waves were longer and amplitudes were smaller. o-vemp parameters were similar on both sides. Positive correlation was observed between c-vemp latencies and degree hearing loss. CONCLUSION: Inferior vestibular nerve pathway is affected in the absence of vertigo in ISSNHL with spared superior vestibular nerve pathway. Damage in IVN pathway correlates with degree of ISSNHL.