Vestibular Sensory Information Research Articles

Cortical auditory potentials and cognitive potentials in individuals with and without vestibular dysfunction

Background: Among individuals with vestibular dysfunction, the loss of vestibular sensory information is found to alter cognitive abilities that coordinate spatial and non-spatial information. P300 is an event-related potential commonly used to assess cognitive processing. The aim of the present study was to compare the latency and amplitude of cortical auditory evoked potential and P300 between individuals with vestibular dysfunction and individuals with no vestibular dysfunction. Methods: Forty adults with a mean age of 40.5 ± 13.07 participated in the study. Group I included 20 adults diagnosed with vestibular dysfunction and group II included 20 age-matched adults with no vestibular dysfunction. The P300 was recorded from the electrode site Cz and Pz. It was elicited using pure-tones in odd-ball paradigm. The latency and amplitude of peaks P1, N1, P2, and N2 of the cortical auditory evoked potential and the P300 were measured. Results: Significant amplitude difference was observed in cortical potentials at Cz and Pz. The P300 was present only in 70% of individuals with vestibular dysfunction compared to 100% among individuals with no vestibular dysfunction. The mean amplitude of the P300 was slightly larger in group 1 compared to group 2 and the mean latency of the P300 was similar in both groups. However, the difference in amplitude of the P300 between groups was not statistically significant. Conclusions: Knowing the cognitive function of individuals with vestibular dysfunction enables planning vestibular rehabilitation therapy, which enhances the quality of life in these individuals by improving their vestibular and cognitive functions.

Analysis of abnormal posture in patients with Parkinson's disease using a computational model considering muscle tones.

Patients with Parkinson's disease (PD) exhibit distinct abnormal postures, including neck-down, stooped postures, and Pisa syndrome, collectively termed "abnormal posture" henceforth. In the previous study, when assuming an upright stance, patients with PD exhibit heightened instability in contrast to healthy individuals with disturbance, implying that abnormal postures serve as compensatory mechanisms to mitigate sway during static standing. However, limited studies have explored the relationship between abnormal posture and sway in the context of static standing. Increased muscle tone (i.e., constant muscle activity against the gravity) has been proposed as an underlying reason for abnormal postures. Therefore, this study aimed to investigate the following hypothesis: abnormal posture with increased muscle tone leads to a smaller sway compared with that in other postures, including normal upright standing, under the sway minimization criterion. To investigate the hypothesis, we assessed the sway in multiple postures, which is determined by joint angles, including cases with bended hip joints. Our approach involved conducting forward dynamics simulations using a computational model comprising a musculoskeletal model and a neural controller model. The neural controller model proposed integrates two types of control mechanisms: feedforward control (representing muscle tone as a vector) and feedback control using proprioceptive and vestibular sensory information. An optimization was performed to determine the posture of the musculoskeletal model and the accompanied parameters of the neural controller model for each of the given muscle tone vector to minimize sway. The optimized postures to minimize sway for the optimal muscle tone vector of patients with PD were compared to the actual postures observed in these patients. The results revealed that on average, the joint-angle differences between these postures was <4°, which was less than one-tenth of the typical joint range of motion. These results suggest that patients with PD exhibit less sway in the abnormal posture than in other postures. Thus, adopting an abnormal posture with increased muscle tone can potentially serve as a valid strategy for minimizing sway in patients with PD.

Exploring neurophysiological correlates of visually induced motion sickness using electroencephalography (EEG).

Visually induced motion sickness (VIMS) is a common phenomenon when using visual devices such as smartphones and virtual reality applications, with symptoms including nausea, fatigue, and headache. To date, the neuro-cognitive processes underlying VIMS are not fully understood. Previous studies using electroencephalography (EEG) delivered mixed findings, with some reporting an increase in delta and theta power, and others reporting increases in alpha and beta frequencies. The goal of the study was to gain further insight into EEG correlates for VIMS. Participants viewed a VIMS-inducing visual stimulus, composed of moving black-and-white vertical bars presented on an array of three adjacent monitors. The EEG was recorded during visual stimulation and VIMS ratings were recorded after each trial using the Fast Motion Sickness Scale. Time-frequency analyses were conducted comparing neural activity of participants reporting minimal VIMS (n = 21) and mild-moderate VIMS (n = 12). Results suggested a potential increase in delta power in the centro-parietal regions (CP2) and a decrease in alpha power in the central regions (Cz) for participants experiencing mild-moderate VIMS compared to those with minimal VIMS. Event-related spectral perturbations (ERSPs) suggested that group differences in EEG activity developed with increasing duration of a trial. These results support the hypothesis that the EEG might be sensitive to differences in information processing in VIMS and minimal VIMS contexts, and indicate that it may be possible to identify neurophysiological correlate of VIMS. Differences in EEG activity related to VIMS may reflect differential processing of conflicting visual and vestibular sensory information.

Cortical auditory potentials and cognitive potentials in individuals with and without vestibular dysfunction

Background: Among individuals with vestibular dysfunction, the loss of vestibular sensory information is found to alter cognitive abilities that coordinate spatial and non-spatial information. P300 is an event-related potential commonly used to assess cognitive processing. The aim of the present study was to compare the latency and amplitude of cortical auditory evoked potential and P300 between individuals with vestibular dysfunction and individuals with no vestibular dysfunction. Methods: Forty adults with a mean age of 40.5 ± 13.07 participated in the study. Group I included 20 adults diagnosed with vestibular dysfunction and group II included 20 age-matched adults with no vestibular dysfunction. The P300 was recorded from the electrode site Cz and Pz. It was elicited using pure-tones in odd-ball paradigm. The latency and amplitude of peaks P1, N1, P2, and N2 of the cortical auditory evoked potential and the P300 were measured. Results: Significant amplitude difference was observed in cortical potentials at Cz and Pz. The P300 was present only in 70% of individuals with vestibular dysfunction compared to 100% among individuals with no vestibular dysfunction. The mean amplitude of the P300 was slightly larger in group 1 compared to group 2 and the mean latency of the P300 was similar in both groups. However, the difference in amplitude of the P300 between groups was not statistically significant. Conclusions: Knowing the cognitive function of individuals with vestibular dysfunction enables planning vestibular rehabilitation therapy, which enhances the quality of life in these individuals by improving their vestibular and cognitive functions.

Velocity influences the relative contributions of visual and vestibular cues to self-acceleration.

Self-motion perception is based on the integration of visual (optic flow) and vestibular (inertial) sensory information. Previous research has shown that the relative contribution of visual and vestibular cues can change in real time based on the reliability of that information. The present study assessed whether initial velocity and acceleration magnitude influence the relative contribution of these cues to the detection of self-acceleration. Participants performed a simple response time task with visual and vestibular self-acceleration cues as targets. Visual optic flow was presented at three possible initial velocities of 3, 9, or 15m/s, and accelerated to result in three possible final velocities of 21, 27, or 33m/s. Corresponding vestibular cues were presented at magnitudes between 0.01 and 0.04g. The self-acceleration cues were presented at three possible stimulus onset asynchronies (SOAs): visual-first (by 100ms), in-sync, and vestibular-first (by 100ms). We found that presenting the cues in-sync resulted in the fastest responses across all velocities and acceleration magnitudes. Interestingly, presenting the visual cue first resulted in a relative advantage over vestibular-first at the slowest initial velocity of 3m/s, and vice versa for the fastest initial velocity of 15m/s. The fastest overall responses for visual-first and in-sync were observed at 9m/s. The present results support the hypothesis that velocity of optic flow can alter the relative contribution of visual and vestibular cues to the detection of self-acceleration.

Gentle rocking movements during sleep in the elderly.

Vestibular stimulation in the form of rocking movements could be a promising non‐pharmacological intervention for populations with reduced sleep quality, such as the elderly. We hypothesized that rocking movements influence sleep by promoting comfort. We assessed whether gentle rocking movements can facilitate the transition from wake to sleep, increase sleep spindle density and promote deep sleep in elderly people. We assessed self‐reported comfort using a pilot protocol including translational movements and movements along a pendulum trajectory with peak linear accelerations between 0.10 and 0.20 m/s2. We provided whole‐night stimulation using the settings rated most comfortable during the pilot study (movements along a pendulum trajectory with peak linear acceleration of 0.15 m/s2). Sleep measures (polysomnography) of two baseline and two movement nights were compared. In our sample (n = 19; eight female; mean age: 66.7 years, standard deviation: 3 years), vestibular stimulation using preferred stimulation settings did not improve sleep. A reduction of delta power was observed, suggesting reduced sleep depth during rocking movements. Sleep fragmentation was similar in both conditions. We did not observe a sleep‐promoting effect using settings optimized to be comfortable. This finding could imply that comfort is not the underlying mechanism. At frequencies below 0.3 Hz, the otoliths cannot distinguish tilt from translation. Translational movement trajectories, such as used in previous studies reporting positive effects of rocking, could have caused sensory confusion due to a mismatch between vestibular and other sensory information. We propose that this sensory confusion might be essential to the sleep‐promoting effect of rocking movements described in other studies.

Role of somatosensory and/or vestibular sensory information in subjective postural vertical in healthy adults

The body's subjective postural vertical (SPV) has been thought to be affected by somatosensory information. How the SPV is perceived based on what types of somatosensory information has not been determined experimentally by manipulating somatosensory conditions. We investigated the effects of disturbing the somatosensory information from a seat pad and/or vestibular sensory information on the SPV in 15 healthy adults. Their SPV values were measured under four conditions (control, somatosensory, vestibular, and somatosensory + vestibular) in random order. The average and absolute SPV values were measured. In the somatosensory condition, a foam rubber pad was placed on the seating surface and the subject's SPV was measured. In the vestibular condition, the SPV was measured during galvanic vestibular stimulation (GVS). The somatosensory + vestibular condition was used to measure the SPV during combined somatosensory and vestibular stimulation. The mean SPV value was significantly increased in the somatosensory + vestibular condition compared to the other three conditions. The absolute value of SPV was significantly increased in the somatosensory and somatosensory + vestibular conditions compared to the control and vestibular conditions. There was no significant difference in the average or absolute SPV values in the vestibular condition compared to the other conditions. There was no significant difference between SPV errors when somatosensory information was disturbed or when somatosensory + vestibular information was disturbed. When the somatosensory information from the seat was disturbed, the SPV error increased, and it also shifted under the influence of the vestibular sensory information modulation. These results indicate that somatosensory information from the seat plays an important role in SPV in healthy adults.

Auditory P300 and mismatch negativity (MMN) in patients with peripheral vestibular hypofunction

Introduction: There is increasing evidence that the loss of vestibular sensory information may change, possibly permanently, the way that cognitive processing areas of the brain integrate spatial and non-spatial information.Objective: We designed this research to assess attention by auditory P300 and memory by MMN in patients with peripheral vestibular hypofunction.Materials and method: The field included 40 subjects divided into two groups, a study group (SG) and a control group (CG). SG: consisted of 20 adult patients with unilateral uncompensated peripheral vestibular hypofunction. CG: consists of 20 normal individuals with normal vestibular function. All matters were submitted to basic audiological evaluation, VNG, P300 and MMN.The results: Our results presented that in patients with unilateral caloric hypofunction, auditory P300 and MMN showed prolonged latency and smaller amplitude than normal. These parameters were involved not simply in the ear ipsilateral to the affected side, but also the contralateral one.Conclusions: The results of our research confirm the view of the presence of cognitive affection in patient with peripheral vestibular lesion. This cognitive affection appeared in the form of attention and memory deficit.

Cervical Vertigo: Historical Reviews and Advances.

Vertigo is one of the most common presentations in adult patients. Among the various causes of vertigo, so-called cervical vertigo is still a controversial entity. Cervical vertigo was first thought to be due to abnormal input from cervical sympathetic nerves based on the work of Barré and Liéou in 1928. Later studies found that cerebral blood flow is not influenced by sympathetic stimulation. Ryan and Cope in 1955 proposed that abnormal sensory information from the damaged joint receptors of upper cervical regions may be related to pathologies of vertigo of cervical origin. Further studies found that cervical vertigo seems to originate from diseased cervical intervertebral discs. Recent research found that the ingrowth of a large number of Ruffini corpuscles into diseased cervical discs may be related to vertigo of cervical origin. Abnormal neck proprioceptive input integrated from the signals of Ruffini corpuscles in diseased cervical discs and muscle spindles in tense neck muscles secondary to neck pain is transmitted to the central nervous system and leads to a sensory mismatch with vestibular and other sensory information, resulting in a subjective feeling of vertigo and unsteadiness. Further studies are needed to illustrate the complex pathophysiologic mechanisms of cervical vertigo and to better understand and manage this perplexing entity.

PID Controller Design for FES Applied to Ankle Muscles in Neuroprosthesis for Standing Balance.

Closed-loop controlled functional electrical stimulation (FES) applied to the lower limb muscles can be used as a neuroprosthesis for standing balance in neurologically impaired individuals. The objective of this study was to propose a methodology for designing a proportional-integral-derivative (PID) controller for FES applied to the ankle muscles toward maintaining standing balance for several minutes and in the presence of perturbations. First, a model of the physiological control strategy for standing balance was developed. Second, the parameters of a PID controller that mimicked the physiological balance control strategy were determined to stabilize the human body when modeled as an inverted pendulum. Third, this PID controller was implemented using a custom-made Inverted Pendulum Standing Apparatus that eliminated the effect of visual and vestibular sensory information on voluntary balance control. Using this setup, the individual-specific FES controllers were tested in able-bodied individuals and compared with disrupted voluntary control conditions in four experimental paradigms: (i) quiet-standing; (ii) sudden change of targeted pendulum angle (step response); (iii) balance perturbations that simulate arm movements; and (iv) sudden change of targeted angle of a pendulum with individual-specific body-weight (step response). In paradigms (i) to (iii), a standard 39.5-kg pendulum was used, and 12 subjects were involved. In paradigm (iv) 9 subjects were involved. Across the different experimental paradigms and subjects, the FES-controlled and disrupted voluntarily-controlled pendulum angle showed root mean square errors of <1.2 and 2.3 deg, respectively. The root mean square error (all paradigms), rise time, settle time, and overshoot [paradigms (ii) and (iv)] in FES-controlled balance were significantly smaller or tended to be smaller than those observed with voluntarily-controlled balance, implying improved steady-state and transient responses of FES-controlled balance. At the same time, the FES-controlled balance required similar torque levels (no significant difference) as voluntarily-controlled balance. The implemented PID parameters were to some extent consistent among subjects for standard weight conditions and did not require prolonged individual-specific tuning. The proposed methodology can be used to design FES controllers for closed-loop controlled neuroprostheses for standing balance. Further investigation of the clinical implementation of this approach for neurologically impaired individuals is needed.

Concussion History And Kinematics Of Dynamic Balance In Division I Athletes

A concussion is one of the most complex injuries in sports and can have potentially catastrophic results if not treated correctly. The central nervous system (CNS) integrates visual, proprioceptive, and vestibular sensory information to maintain balance during all movements. Ample clinical evidence exists that a concussion disrupts normal function of the CNS and results in postural instability. However, the long-term effects of concussion on balance control, particularly during dynamic functional movements, are not clear. PURPOSE: To determine the effects of concussion history on the kinematics of athletes performing dynamic balance tasks on dynamic balance on athletes. METHODS: Division I athletes without (n=5; 20.0±1.0 yrs) and with a history of concussion (n=5; 19.4±0.9 yrs 1.5±1.2 yrs post injury) performed dynamic balance tasks including gait, gait while stepping over an obstacle, get up and go (GUG), and GUG with a dual task. Speed was recorded for each task, and straightness of trajectory was calculated for normal gait and stepping over an obstacle as a root mean square (RMS) of the mediolateral deviation of the pelvis trajectory from a straight line. Cohen’s d effect sizes between groups were bootstrapped given the small sample size. Effect sizes greater than 0.8 were considered large, 0.5-0.8 moderate, and less than 0.5 as no effect. RESULTS: Athletes with history of concussion performed the dual task GUG 1.7 m/s slower than the control (large effect size: d=0.90). In addition, those with history of concussion performed normal gait with an RMS deviation of 30.9 cm compared to 25.1 cm in control (mod effect size: d=0.66) when instructed to maintain a straight trajectory. No effect of concussion history occurred for normal gait speed, speed of stepping over an obstacle, speed of GUG without dual task, or mediolateral deviation when stepping over an obstacle. CONCLUSIONS: Deficits in dynamic balance control during functional movements in Division I athletes were evident even as long as 1.5 years following concussion event. These data are part of a large prospective investigation (current enrollment: n=207), and athletes who sustain a concussion over the course of the study will be re-evaluated at regular intervals to observe changes in postural control during recovery.

The Role of the Vestibular Nucleus in the Multimodal Coordination of Balance

Balance is a complex neurological process that makes use of multimodal sensory information. Regulation of balance relies on the integration of sensory information about the body's position and acceleration relative to gravity (vestibular inputs, provided by organs in the inner ears) with information about the body's position relative to itself (proprioceptive inputs, provided by receptors in joints and muscles). In addition, vestibular reflexes can be modified by feedback from the limbs. However, the neural populations and mechanisms underlying multimodal balance control remain to be determined. We hypothesized that neurons in the vestibular nuclei (VN) participate in multimodal balance control by integrating vestibular and proprioceptive sensory information. To test this hypothesis, we recorded activity from single VN neurons in decerebrate and conscious cats, and determined whether they responded to movement of the limb (to activate proprioceptors) and whole body (to activate vestibular receptors). Hindlimb extension‐flexion (movement of the limb in the rostral‐caudal plane) stimuli were generated via a limb‐attached motor, and vestibular stimuli were generated using a hydraulic table. In the decerebrate preparation, 70 neurons histologically demonstrated to be in the VN exhibited a response to hindlimb stimulation. These responses were classified on the basis of cell activity changes during each of four movements (midline‐to‐extension, extension‐to‐midline, midline‐to‐flexion, and flexion‐to‐midline). Most (81.4%, 57/70) of these neurons encoded information about the direction of limb movement, while the others responded similarly to movement in any direction. Of 51 of these neurons tested for a vestibular response, 56.9% (29/51) demonstrated a significant response (signal‐to‐noise ratio&gt; 0.5). In conscious animals, vestibular stimulation was used as a search stimulus to localize VN neurons. Two‐thirds (67.7%, 65/96) of the VN cells whose activity was modulated by vestibular stimulation had a significant response to hindlimb stimulation. Only 41.5% (27/65) of these neurons encoded the direction of the leg stimulation in their responses. These results demonstrate the convergence of vestibular and somatosensory information onto individual VN neurons. However, the responses of VN neurons to hindlimb movement differed in the conscious and decerebrate preparations: responses in decerebrate preparations were much more likely to encode the direction of limb movement (p&lt;0.001, Fisher's exact test). This indicates the presence of cortical modulation of these responses. Our future work will delve further into the role of higher brain centers in modulating the responses of VN neurons to vestibular and proprioceptive inputs.

Activation of the thalamic parafascicular nucleus by electrical stimulation of the peripheral vestibular nerve in rats.

The parafascicular nucleus (PFN) of the thalamus is a primary structure in the feedback circuit of the basal ganglia-thalamo-cortical system, as well as in the neural circuit of the vestibulo-thalamo-striatal pathway. We investigated the characteristics of the functional connectivity between the peripheral vestibular system and the PFN in rats. A single electrical stimulation was applied to the horizontal semicircular canal nerve in the peripheral vestibular end-organs. This resulted in polysynaptic local field potentials (LFPs) in the PFN, which were composed of long-lasting multiple waves. The LFPs were prominently seen contralateral to the stimulation site. The PFN LFPs were suppressed by transient chemical de-afferentation of peripheral vestibular activity using a 5% lidocaine injection into the middle ear. The spontaneous firing rate of the single units increased after electrical stimulation to the horizontal canal nerve in a frequency-dependent manner. The induction of cFos protein was more prominent in the contralateral PFN than in the ipsilateral PFN following horizontal semicircular canal nerve stimulation. The functional vestibulo-parafascicular connection is a neural substrate for the transmission of vestibular sensory information to the basal ganglia.

Neuroanatomy of the Parietal Association Areas

The parietal association cortex comprises the superior and inferior parietal lobules, the precuneus and the cortices in the intraparietal, parietooccipital and lunate sulci. By processing somatic, visual, acoustic and vestibular sensory information, the parietal association cortex plays a pivotal role in spatial cognition and motor control of the eyes and the extremities. Sensory information from the primary and secondary somatosensory areas enters the superior parietal lobule and is transferred to the inferior parietal lobule. Visual information is processed through the dorsal visual pathway and it reaches the inferior parietal lobule, the intraparietal sulcus and the precuneus. Acoustic information is transferred posteriorly from the primary acoustic area, and it reaches the posterior region of the inferior parietal lobule. The areas in the intraparietal sulcus project to the premotor area, the frontal eye fields, and the prefrontal area. These areas are involved in the control of ocular movements, reaching and grasping of the upper extremities, and spatial working memory. The posterior region of the inferior parietal lobule and the precuneus both project either directly, or indirectly via the posterior cingulate gyrus, to the parahippocampal and entorhinal cortices. Both these areas are strongly associated with hippocampal functions for long-term memory formation.

Bioinspired Autonomous Visual Vertical Control of a Quadrotor Unmanned Aerial Vehicle

Near-ground maneuvers, such as hover, approach, and landing, are key elements of autonomy in unmanned aerial vehicles. Such maneuvers have been tackled conventionally by measuring or estimating the velocity and the height above the ground, often using ultrasonic or laser range finders. Near-ground maneuvers are naturally mastered by flying birds and insects because objects below may be of interest for food or shelter. These animals perform such maneuvers efficiently using only the available vision and vestibular sensory information. In this paper, the time-to-contact (tau) theory, which conceptualizes the visual strategy with which many species are believed to approach objects, is presented as a solution for relative ground distance control for unmanned aerial vehicles. The paper shows how such an approach can be visually guided without knowledge of height and velocity relative to the ground. A control scheme that implements the tau strategy is developed employing only visual information from a monocular camera and an inertial measurement unit. To achieve reliable visual information at a high rate, a novel filtering system is proposed to complement the control system. The proposed system is implemented onboard an experimental quadrotor unmanned aerial vehicle and is shown to not only successfully land and approach ground, but also to enable the user to choose the dynamic characteristics of the approach. The methods presented in this paper are applicable to both aerial and space autonomous vehicles.

Deficient recovery response and adaptive feedback potential in dynamic gait stability in unilateral peripheral vestibular disorder patients.

Unilateral peripheral vestibular disorder (UPVD) causes deficient locomotor responses to novel environments due to a lack of accurate vestibular sensory information, increasing fall risk. This study aimed to examine recovery response (stability recovery actions) and adaptive feedback potential in dynamic stability of UPVD‐patients and healthy control subjects during perturbed walking. 17 UPVD‐patients (>6 months since onset) and 17 matched healthy control participants walked on a treadmill and were subjected to eight unexpected perturbations during the swing phase of the right leg. For each perturbation, the margin of stability (MS; state of body's centre of mass in relation to the base of support), was determined at touchdown of the perturbed leg and during the following six recovery steps. The first perturbation caused a reduced MS at touchdown for the perturbed leg compared to baseline, indicating an unstable position, with controls requiring five recovery steps to return to MS baseline and UPVD‐patients not returning to baseline level within the analyzed six recovery steps. By the eighth perturbation, control subjects needed two steps, and UPVD‐patients required three recovery steps, both thereby improving their recovery response with practice. However, MS at touchdown of the perturbed leg increased only for the controls after repeated perturbations, indicating adaptive feedback‐driven locomotor improvements for the controls, but not for the UPVD‐patients. We concluded that UPVD‐patients have a diminished ability to control dynamic gait stability during unexpected perturbations, increasing their fall risk, and that vestibular dysfunction may inhibit the neuromotor system adapting the reactive motor response to perturbations.

Thalamic cholinergic innervation and postural sensory integration function in Parkinson’s disease

The pathophysiology of postural instability in Parkinson's disease remains poorly understood. Normal postural function depends in part on the ability of the postural control system to integrate visual, proprioceptive, and vestibular sensory information. Degeneration of cholinergic neurons in the brainstem pedunculopontine nucleus complex and their thalamic efferent terminals has been implicated in postural control deficits in Parkinson's disease. Our aim was to investigate the relationship of cholinergic terminal loss in thalamus and cortex, and nigrostriatal dopaminergic denervation, on postural sensory integration function in Parkinson's disease. We studied 124 subjects with Parkinson's disease (32 female/92 male; 65.5 ± 7.4 years old; 6.0 ± 4.2 years motor disease duration; modified Hoehn and Yahr mean stage 2.4 ± 0.5) and 25 control subjects (10 female/15 male, 66.8 ± 10.1 years old). All subjects underwent (11)C-dihydrotetrabenazine vesicular monoaminergic transporter type 2 and (11)C-methylpiperidin-4-yl propionate acetylcholinesterase positron emission tomography and the sensory organization test balance platform protocol. Measures of dopaminergic and cholinergic terminal integrity were obtained, i.e. striatal vesicular monoaminergic transporter type 2 binding (distribution volume ratio) and thalamic and cortical acetylcholinesterase hydrolysis rate per minute (k3), respectively. Total centre of pressure excursion (speed), a measure of total sway, and sway variability were determined for individual sensory organization test conditions. Based on normative data, principal component analysis was performed to reduce postural sensory organization functions to robust factors for regression analysis with the dopaminergic and cholinergic terminal data. Factor analysis demonstrated two factors with eigenvalues >2 that explained 52.2% of the variance, mainly reflecting postural sway during sensory organization test Conditions 1-3 and 5, respectively. Regression analysis of the Conditions 1-3 postural sway-related factor [R(2)adj = 0.123, F(5,109) = 4.2, P = 0.002] showed that decreased thalamic cholinergic innervation was associated with increased centre of pressure sway speed (β = -0.389, t = -3.4, P = 0.001) while controlling for covariate effects of cognitive capacity and parkinsonian motor impairments. There was no significant effect of cortical cholinergic terminal deficits or striatal dopaminergic terminal deficits. This effect could only be found for the subjects with Parkinson's disease. We conclude that postural sensory integration function of subjects with Parkinson's disease is modulated by pedunculopontine nucleus-thalamic but not cortical cholinergic innervation. Impaired integrity of pedunculopontine nucleus cholinergic neurons and their thalamic efferents play a role in postural control in patients with Parkinson's disease, possibly by participating in integration of multimodal sensory input information.

The Vestibular System Implements a Linear–Nonlinear Transformation In Order to Encode Self-Motion

Author SummaryUnderstanding how the coding of sensory information changes at different stages of sensory processing remains a fundamental challenge in systems neuroscience. Here we address this question by studying early sensory processing in vestibular pathways of monkeys, a system for which sensory stimuli are relatively easy to describe. Peripheral vestibular afferents detect and encode head motion in space to ensure posture and gaze is accurate and stable during everyday life. In this study, we show that central vestibular neurons nonlinearly integrate their afferent inputs, which helps explain the mechanisms that generate enhanced feature detection in sensory pathways. In addition, our results overturn conventional wisdom that early vestibular processing is linear, revealing a striking boosting nonlinearity that is a hallmark of the first central stage of vestibular processing. Studies from other sensory systems have shown that higher-order neurons can more efficiently detect specific features of sensory input, and that nonlinear transformations can increase this efficiency. We suggest that nonlinear integration of afferent input by central vestibular neurons extends their coding range and facilitates the detection of natural vestibular stimuli.

Human eye-head gaze shifts preserve their accuracy and spatiotemporal trajectory profiles despite long-duration torque perturbations that assist or oppose head motion

Humans routinely use coordinated eye-head gaze saccades to rapidly and accurately redirect the line of sight (Land MF. Vis Neurosci 26: 51-62, 2009). With a fixed body, the gaze control system combines visual, vestibular, and neck proprioceptive sensory information and coordinates two moving platforms, the eyes and head. Classic engineering tools have investigated the structure of motor systems by testing their ability to compensate for perturbations. When a reaching movement of the hand is subjected to an unexpected force field of random direction and strength, the trajectory is deviated and its final position is inaccurate. Here, we found that the gaze control system behaves differently. We perturbed horizontal gaze shifts with long-duration torques applied to the head that unpredictably either assisted or opposed head motion and very significantly altered the intended head trajectory. We found, as others have with brief head perturbations, that gaze accuracy was preserved. Unexpectedly, we found also that the eye compensated well--with saccadic and rollback movements--for long-duration head perturbations such that resulting gaze trajectories remained close to that when the head was not perturbed. However, the ocular compensation was best when torques assisted, compared with opposed, head motion. If the vestibuloocular reflex (VOR) is suppressed during gaze shifts, as currently thought, what caused invariant gaze trajectories and accuracy, early eye-direction reversals, and asymmetric compensations? We propose three mechanisms: a gaze feedback loop that generates a gaze-position error signal; a vestibular-to-oculomotor signal that dissociates self-generated from passively imposed head motion; and a saturation element that limits orbital eye excursion.

Influence of vestibular input on spatial and nonspatial memory and on hippocampal NMDA receptors

It has recently been shown that a lack of vestibular sensory information decreases spatial memory performance and induces biochemical changes in the hippocampus in rodents. After vestibular neurectomy, patients display spatial memory deficit and hippocampal atrophy. Our objectives were to explore: (a) spatial (Y maze, radial-arm maze), and non-spatial (object recognition) memory performance, (b) modulation of NMDA receptors within the hippocampus using radioligand binding, and (c) hippocampal atrophy, using MRI, in a rat model of bilateral labyrinthectomy realized in two operations. Chemical vestibular lesions (VLs) were induced in 24 animals by transtympanic injections of sodium arsanilate (30 mg/0.1 ml/ear), one side being lesioned 3 weeks after the other. The control group received transtympanic saline solution (0.1 ml/ear) (n = 24). Spatial memory performance (Y maze and radial maze) decreased after VL. Conversely, non-spatial memory performance (object recognition) was not affected by VL. No hippocampal atrophy was observed with MRI, but density of NMDA receptors were increased in the hippocampus after VL. These findings show that the lack of vestibular information induced specific deficits in spatial memory. Additionally, quantitative autoradiographic data suggest the involvement of the glutamatergic system in spatial memory processes related to vestibular information. When studying spatial memory performances in the presence of vestibular syndrome, two-step labyrinthectomy is a suitable procedure for distinguishing between the roles of the specific components of vestibular input loss and those of impaired locomotor activity.