Sound and postural control during stance tasks in abnormal subjective haptic vertical.

BACKGROUND: Patients with vestibular impairment often suffer from postural instability. This could be compensated by other sensory systems such as the auditory system. OBJECTIVE: The aim of this study was to investigate whether auditory input improves postural stability in patients with abnormal subjective haptic vertical (SHV). METHODS: Participants (n = 13) with normal hearing and vision, but abnormal SHV participated. Participants performed standing on firm ground and foam support (eyes open/closed) and Tandem Romberg test (eyes closed) in quiet (reference), noise and with plugged ears. All tasks were conducted in a soundproofed and reverberant room. Postural stability was recorded close to the body's center of gravity. Reference conditions were compared with a control group. RESULTS: In only two tasks sway increased significantly when noise was presented during challenging tasks in the soundproofed room. Sway of the reference conditions did not differ significantly between control and study group. CONCLUSIONS: This study shows no influence of applied auditory stimulation on posture in participants with abnormal SHV in a reverberant room, but an adverse effect on balance during difficult tasks in the soundproofed room. Noise possibly masked auditory information that was helpful in improving posture in the quiet condition. Futhermore, noise might have distracted participants from maintaining balance.

Neurodegeneration after repeated noise trauma in the mouse lower auditory pathway.

High intensity noise exposure leads to a permanent shift in auditory thresholds (PTS), affecting both peripheral (cochlear) tissue and the central auditory system. Studies have shown that a noise-induced hearing loss results in significant cell loss in several auditory structures. Degeneration can be demonstrated within hours after noise exposure, particularly in the lower auditory pathway, and continues to progress over days and weeks following the trauma. However, there is limited knowledge about the effects of recurring acoustic trauma. Repeated noise exposure has been demonstrated to increase neuroplasticity and neural activity. Thus, the present study aimed to investigate the influence of a second noise exposure on the cytoarchitecture of key structures of the auditory pathway, including spiral ganglion neurons (SGN), the ventral and dorsal cochlear nucleus (VCN and DCN, respectively), and the inferior colliculus (IC). In the experiments, young adult normal hearing mice were exposed to noise once or twice (with the second trauma applied one week after the initial exposure) for 3 h, using broadband white noise (5 - 20 kHz) at 115 dB SPL. The cell densities in the investigated auditory structures significantly decreased in response to the initial noise exposure compared to unexposed control animals. These findings are consistent with earlier research, which demonstrated degeneration in the auditory pathway within the first week after acoustic trauma. Additionally, cell densities were significantly decreased after the second trauma, but this effect was only observed in the VCN, with no similar effects seen in the SGN, DCN, or IC. These results illustrate how repeated noise exposure influences the cytoarchitecture of the auditory system. It appears that an initial noise exposure primarily damages the lower auditory pathway, but surviving cellular structures may develop resistance to additional noise-induced injury.

Individualized Vibrotactile Neurofeedback Training in Patients with Chronic Bilateral Vestibulopathy.

Patients with bilateral vestibulopathy (BVP) suffer from postural imbalance during daily life conditions, which in turn leads to a high frequency of falls. Unfortunately, vestibular rehabilitation has only modest and somewhat inconsistent effects in this patient group. Approximately 50% of BVP patients show an improved postural control after conventional vestibular rehabilitation training. New and more promising approaches are required. The individualized vibrotactile neurofeedback training (IVNT) in stance and gait conditions has already been described as highly effective in patients with various vestibular disorders. The purpose of the present multicenter study was to determine the efficacy of the IVNT in improving balance, reducing self-perceived disability, and improving gait in patients with confirmed BVP. In total, 22 patients performed the IVNT with the Vertiguard® system for 10 daily sessions. The dizziness handicap inventory (DHI), the stance stability score of the sensory organization test (SOT) and the score for everyday life mobility in stance and gait tasks (SBDT) were obtained immediately before and after the rehabilitation training period, as well as 3 and 12 months later. All measures improved significantly after the IVNT. Between 77.3% and 94.4% of patients showed an individual benefit (depending on outcome measure). The effect was not significantly reduced within the follow-up period of 12 months. The results demonstrate a high efficacy of the IVNT for vestibular rehabilitation in BVP patients.

Short-term overstimulation affects peripheral but not central excitability in an animal model of cochlear implantation.

Objective: Upper current limits (C-levels) are sometimes extremely increased over time since this procedure can enhance speech perception. It should be clarified if a larger amount of electrical stimulation is tolerated by the remaining peripheral and central auditory pathway.Materials and Methods: An animal electrode array was inserted in mechanically deafened guinea pigs. C-levels were adjusted to a mean of approximately 10 CL ('LOS' group), 40 CL ('MOS' group) or 60 CL ('HOS' group) above the electrode specific electrically evoked compound action potential (eCAP) threshold. The stimulation was performed via a sound processor in standardized auditory environment. Implanted and not stimulated animals served as controls.Results: A significant eCAP threshold shift was observed in the 'HOS'-group aftereight hours of stimulation at basal electrodes. Electrically evoked auditory brainstem thresholds were stable over time in all stimulation groups. The ratio between eCAP- and eABR threshold shifts was significantly enhanced in the 'HOS'- group.Conclusion: Even short-time overstimulation reduces the excitability of peripheral but not central auditory structures. The changed relationship between the excitability of spiral ganglion neurons and inferior colliculus neurons seems to indicate an overstimulation. The results are of utmost importance for a safe CI-processor fitting especially in children or non-compliant patients.

Influence of Auditory Information on Postural Control During Different Gait Tasks in the Elderly.

BACKGROUND: Hearing loss is frequently associated with reduced postural control. This is possibly not only related to simultaneous pathophysiological changes within the hearing and vestibular system. The auditory input itself could provide helpful information for maintaining postural control. Previous studies of our group already showed that continuous or interrupted white noise can significantly improve postural control during gait conditions in young healthy individuals. The present study aimed at investigating if those effects are also active in the elderly. METHODS: Elderly volunteers (mean age 67 years) without any history of disorders to influence gait performance successfully completed 5 walking tasks under 4 different acoustic conditions. Angular sway velocity was measured close to the center of gravity with the Vertiguard® system. RESULTS: Significant changes in body sway velocity were found in 4 of 5 investigated tasks. Only "walking with turning head in rhythm" was not associated with any change in the acoustic input. The sway increased by 8.9% during "walking with open eyes" in the pitch direction and by 11.5% during "tandem walking" in the roll direction if ear protection was applied. The sway was reduced by 9.1% during "walking over barriers" in the pitch direction and by 16.7% in the roll direction during "walking with closed eyes" if a stationary source of continuous white noise was presented. CONCLUSION: The data of the present study indicate that auditory information could significantly alter postural control during walking in the elderly. Continuous white noise seems to be helpful for maintaining balance in different walking tasks.

Cytomegalovirus Seropositivity as a Potential Risk Factor for Increased Noise Trauma Susceptibility.

Context: Cytomegalovirus (CMV) represents the leading congenital viral infection in humans. Although congenital CMV due to vertically transmitted infections is the main cause of CMV-related diseases, adult CMV infections might still be of clinical significance. It is still discussed how far CMV seropositivity, due to horizontal infection in immunocompetent adults, is able to induce significant dysfunction. The present study investigates in how far CMV seropositivity is an additional risk factor for an increasing susceptibility to sensorineural hearing loss induced by acoustic injury during adulthood in a guinea pig CMV (GPCMV) model of noise-induced hearing loss (NIHL). Methods: Two groups (GPCMV seropositive vs. seronegative) of normal hearing adult guinea pigs were exposed to a broadband noise (5-20 kHz) for 2 hours at 115 dB sound pressure level. Frequency-specific auditory brainstem response recordings for determination of auditory threshold shift were carried out and the number of missing outer hair cells was counted 2 weeks after the noise exposure. Results: The data show a slightly increased shift in auditory thresholds in seropositive animals compared to the seronegative control group in response to noise trauma. However, the observed difference was significant at least at high frequencies. The differences in threshold shift are not correlated with outer hair cell loss between the experimental groups. Conclusion: The results point to potential additional pathologies in a guinea pig NIHL model in correlation to GPCMV seropositivity, which should be taken into account when assessing risks of latent/reactivated CMV infection. Due to the relatively slight effect in the present data, the aim of future studies should be a more detailed consideration (e.g., larger sample size) and to localize possible target structures as well as the significance of the infection route.

Balance Training With Vibrotactile Neurofeedback and Ginkgo Biloba Extract in Age-Related Vertigo.

Background: Balance training with vibrotactile neurofeedback (VNF) can improve balance and subjective impairment in age-related vertigo and dizziness. Ginkgo biloba dry extract EGb 761 has been shown to improve subjective impairment in chronic vertigo and the efficacy of conventional balance training. The combination was expected to work synergistically in this difficult-to-treat population. Objectives: To demonstrate the efficacy of VNF added to EGb 761 for age-related vertigo and dizziness. Design: Multicenter, prospective, controlled, randomized, single-blind, two-arm trial (German Clinical Trials Register https://www.drks.de No. DRKS00007633). Setting: Specialist offices and tertiary care outpatient department. Participants: One hundred and twenty subjects aged 60+ years with chronic dizziness for over 3 months, a Dizziness Handicap Inventory (DHI) Sum Score >25 and fall risk in balance-related situations as measured by the geriatric Standard Balance Deficit Test Composite Score (gSBDT-CS)>40. Patients with other distinct vestibular pathology (e.g., Meniére's disease, stroke, BPPV) were excluded. Intervention: EGb 761 (80 mg twice daily for 12 weeks) plus 10 days of individually adapted balance training with VNF, randomized 1:1 to sensitive (active) or non-sensitive (sham) neurofeedback. Measurements: The change in gSBDT-CS after 6 weeks (primary), other gSBDT outcomes, DHI, cognition, hearing, and safety. Results: One hundred nine of 120 enrolled subjects received both treatments at least once. Over 12 weeks, the gSBDT-CS improved by 6.7 (active) vs. 4.5 (sham). There was a difference in favor of the active treatment of -2.4 (95% CI -5.4; 0.6) after 6 weeks. Under active treatment, more pronounced effects occurred in all secondary analyses and in nearly all secondary endpoints. The DHI sum score decreased from 44.1 to 31.1 in the total sample with a treatment group difference after 6 weeks of -3.1, 95% CI (-7.1; 0.9). No safety issues were reported. Conclusion: Over 12 weeks, the combination of balance training with VNF and Ginkgo biloba dry extract EGb 761 reached a clinically relevant improvement of age-related vertigo and dizziness with a good pharmacological safety profile.

A static sound source can improve postural stability during walking.

BACKGROUND: During walking, postural stability is controlled by visual, vestibular and proprioceptive input. The auditory system uses acoustic input to localize sound sources. For some static balance conditions, the auditory influence on posture was already proven. Little is known about the impact of auditory inputs on balance in dynamic conditions. OBJECTIVE: This study is aimed at investigating postural stability of walking tasks in silence and sound on condition to better understand the impact of auditory input on balance in movement. METHODS: Thirty participants performed: walking (eyes open), tandem steps, walking with turning head and walking over barriers. During each task, acoustic condition changed between silence and presented noise through an earth-fixed loudspeaker located at the end of the walking distance. Body sway velocity was recorded close to the body's center of gravity. RESULTS: A decreased body sway velocity was significant for walking (eyes open), tandem steps and walking over barriers when noise was presented. Those auditory stimuli did not affect sway velocity while walking with turning head. The posture has probably improved due to the localization ability when walking with the head facing forward, while the localization ability was impaired when turning the head. CONCLUSIONS: The localization ability of a fixed sound source through the auditory system has a significant but limited impact on posture while walking.

Can hearing amplification improve presbyvestibulopathy and/or the risk-to-fall ?

PURPOSE: The decline of sensory systems during aging has been widely investigated and several papers have correlated the visual, hearing and vestibular systems and the consequences of their functional degeneration. Hearing loss and presbyvestibulopathy have been found to be positively correlated as is with the risk-to-fall. MATERIAL AND METHODS: The present study was therefore designed as systematic review (due to PRISMA criteria) which should correlate hearing amplification by hearing aids and/or cochlear implants with balance outcome. However, the literature review (Cochrane, PubMed) revealed ten paper (prospective, controlled trials and acute trials) with heterogenous patient popiulations and non-uniform outcome measures (i.e., gait analysis, questionnaires, postural stabilometry) so that no quantitative, statistical analysis could be performed. RESULTS: The qualitative analysis oft he identified studies showed that hearing amplification in the elderly improves spatio-temporal orientation (particularly with cochlear implants) and that the process of utilizing auditory information for balance control takes some time (i.e., the neuroplasticity-based, learning processes), usually some months in cochlear implantees. DISCUSSION: Hearing and balance function degenerate independently from each other and large interindividual differences require a separate neurotological examination of each patient. However, hearing amplification is most helpful to improve postural stability, particularly in the elderly. Future research should focus on controlled, prospective clinical trials where a standardized test battery covering the audiological and neurotological profile of each elderly patient pre/post prescription of hearing aids and/or cochlear implantation should be followed up (for at least 1 year) so that also the balance improvements and the risk-to-fall can be reliably assessed (e.g., by mobile posturography and standardized questionnaires, e.g., the DHI).

Neuroprotective Effect of Near-Infrared Light in an Animal Model of CI Surgery.

INTRODUCTION: The preservation of residual hearing has become an important consideration in cochlear implant (CI) recipients in recent years. It was the aim of the present animal experimental study to investigate the influence of a pretreatment with near-infrared (NIR) light on preservation of sensory hair cells and residual hearing after cochlear implantation. METHODS: NIR was applied unilaterally (15 min, 808 nm, 120 mW) to 8 guinea pigs, immediately before a bilateral scala tympani CI electrode insertion was performed. The nonirradiated (contralateral) side served as control. Twenty-eight days postoperatively, auditory brainstem responses (ABRs) were registered from both ears to screen for hearing loss. Thereafter, the animals were sacrificed and inner hair cells (IHCs) and outer hair cells (OHCs) were counted and compared between NIR-pretreated and control (contralateral) cochleae. RESULTS: There was no IHC loss upon cochlear implantation. OHC loss was most prominent on both sides at the apical part of the cochlea. NIR pretreatment led to a statistically significant reduction in OHC loss (by 39.8%). ABR recordings (across the frequencies 4-32 kHz) showed a statistically significant difference between the 2 groups and corresponds well with the apical structural damage. Hearing loss was reduced by about 20 dB on average for the NIR-pretreated group (p ≤ 0.05). DISCUSSION/CONCLUSION: A single NIR pretreatment in this animal model of CI surgery appears to be neuroprotective for residual hearing. This is in line with other studies where several NIR posttreatments have protected cochlear and other neural tissues. NIR pretreatment is an inexpensive, effective, and noninvasive approach that can complement other ways of preserving residual hearing and, hence, should deserve further clinical evaluation in CI patients.

Correction to: Constant severe imbalance following traumatic otoconial loss: a new explanation of residual dizziness.

The original article was updated.

Near-infrared-light pre-treatment attenuates noise-induced hearing loss in mice.

Noise induced hearing loss (NIHL) is accompanied by a reduction of cochlear hair cells and spiral ganglion neurons. Different approaches have been applied to prevent noise induced apoptosis / necrosis. Physical intervention is one technique currently under investigation. Specific wavelengths within the near-infrared light (NIR)-spectrum are known to influence cytochrome-c-oxidase activity, which leads in turn to a decrease in apoptotic mechanisms. It has been shown recently that NIR can significantly decrease the cochlear hair cell loss if applied daily for 12 days after a noise exposure. However, it is still unclear if a single NIR-treatment, just before a noise exposure, could induce similar protective effects. Therefore, the present study was conducted to investigate the effect of a single NIR-pre-treatment aimed at preventing or limiting NIHL. The cochleae of adult NMRI-mice were pre-treated with NIR-light (808 nm, 120 mW) for 5, 10, 20, 30 or 40 minutes via the external ear canal. All animals were noised exposed immediately after the pre-treatment by broad band noise (5-20 kHz) for 30 minutes at 115 dB SPL. Frequency specific ABR-recordings to determine auditory threshold shift were carried out before the pre-treatment and two weeks after the noise exposure. The amplitude increase for wave IV and cochlear hair cell loss were determined. A further group of similar mice was noise exposed only and served as a control for the NIR pre-exposed groups. Two weeks after noise exposure, the ABR threshold shifts of NIR-treated animals were significantly lower (p < 0.05) than those of the control animals. The significance was at three frequencies for the 5-minute pre-treatment group and across the entire frequency range for all other treatment groups. Due to NIR light, the amplitude of wave four deteriorates significantly less after noise exposure than in controls. The NIR pre-treatment had no effect on the loss of outer hair cells, which was just as high with or without NIR-light pre-exposure. Relative to the entire number of outer hair cells across the whole cochlea, outer hair cell loss was rather negligible. No inner hair cell loss whatever was detected. Our results suggest that a single NIR pre-treatment induces a very effective protection of cochlear structures from noise exposure. Pre-exposure of 10 min seems to emerge as the optimal dosage for our experimental setup. A saturated effect occurred with higher dosage-treatments. These results are relevant for protection of residual hearing in otoneurosurgery such as cochlear implantation.

Constant severe imbalance following traumatic otoconial loss: a new explanation of residual dizziness.

Benign paroxysmal positional vertigo (BPPV) is the most common type of vertigo, caused by otoconia falling from the utricle into a semicircular canal (SCC). After successful repositioning maneuvers residual dizziness (RD) has been described and several reasons are used to explain RD. It can last for only a few days or weeks, but also much longer. We present a patient with a severe traumatic loss of otoconia from both maculae utriculi and a persistent imbalance more than 9 years. We think that the loss of otoconia from the utricular and probably also saccular macula induced a sudden reduction of her ability to sense gravity thus logically explaining her symptoms. We show the vestibular test results also supporting our hypothesis and we extrapolate this support to other forms of so far unexplained dizziness especially increasing imbalance with aging. We also discuss the normal c- and oVEMP indicating intact haircell function and supporting our hypothesis of isolated otoconial loss as the major cause for imbalance.

Auditory influence on postural control during stance tasks in different acoustic conditions.

BACKGROUND: Postural stability might be influenced by auditory input as humans utilize spatiotemporal information to localise sound sources. Earlier studies investigated the acoustic influence on posture but unfortunately experimental setup, room acoustics and conditions of participants varied widely. OBJECTIVE: This study aimed at recording body sway velocity under clearly defined acoustic conditions in a homogenous group of young healthy participants. METHODS: Thirty participants performed five stance tasks (standing eyes open/closed, standing on a foam support eyes open/closed, Tandem Romberg test eyes closed) under four acoustic conditions (in quiet, with a loudspeaker presenting continuous/interrupted noise, with ear protectors) in two different rooms (long/short reverberation time). Body sway velocity was determined close to body's centre of gravity. RESULTS: Postural stability decreased significantly when continuous noise was applied and increased significantly when interrupted noise was presented in the reverberant room. The usage of ear protectors increased body sway velocity compared to quietness in both rooms. CONCLUSIONS: An impaired auditory input by plugging/acoustic masking reduced postural control. Interrupted noise seems to provide a continuously repeated feedback about the postural position in a reverberant room. Hence, the effect of hearing on posture highly depends on the structure of the auditory signal, the sensorimotor condition and the acoustic environment.

Acute Noise Exposure Is Associated With Intrinsic Apoptosis in Murine Central Auditory Pathway.

Noise that is capable of inducing the hearing loss (NIHL) has a strong impact on the inner ear structures and causes early and most obvious pathophysiological changes in the auditory periphery. Several studies indicated that intrinsic apoptotic cell death mechanisms are the key factors inducing cellular degeneration immediately after noise exposure and are maintained for days or even weeks. In addition, studies demonstrated several changes in the central auditory system following noise exposure, consistent with early apoptosis-related pathologies. To clarify the underlying mechanisms, the present study focused on the noise-induced gene and protein expression of the pro-apoptotic protease activating factor-1 (APAF1) and the anti-apoptotic B-cell lymphoma 2 related protein a1a (BCL2A1A) in the cochlear nucleus (CN), inferior colliculus (IC) and auditory cortex (AC) of the murine central auditory pathway. The expression of Bcl2a1a mRNA was upregulated immediately after trauma in all tissues investigated, whereas the protein levels were significantly reduced at least in the auditory brainstem. Conversely, acute noise has decreased the expression of Apaf1 gene along the auditory pathway. The changes in APAF1 protein level were not statistically significant. It is tempting to speculate that the acoustic overstimulation leads to mitochondrial dysfunction and induction of apoptosis by regulation of proapoptotic and antiapoptotic proteins. The inverse expression pattern on the mRNA level of both genes might reflect a protective response to decrease cellular damage. Our results indicate the immediate presence of intrinsic apoptosis following noise trauma. This, in turn, may significantly contribute to the development of central structural deficits. Auditory pathway-specific inhibition of intrinsic apoptosis could be a therapeutic approach for the treatment of acute (noise-induced) hearing loss to prevent irreversible neuronal injury in auditory brain structures and to avoid profound deficits in complex auditory processing.

Apoptosis in the cochlear nucleus and inferior colliculus upon repeated noise exposure.

The time course of apoptosis and the corresponding neuronal loss was previously shown in central auditory pathway of mice after a single noise exposure. However, repeated acoustic exposure is a major risk factor for noise-induced hearing loss. The present study investigated apoptosis by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) assay after a second noise trauma in the ventral and dorsal cochlear nucleus and central nucleus of the inferior colliculus. Mice [Naval Medical Research Institute (NMRI) strain] were noise exposed [115 dB sound pressure level, 5-20 kHz, 3 h) at day 0. A double group received the identical noise exposure a second time at day 7 post-exposure and apoptosis was either analyzed immediately (7-day group-double) or 1 week later (14-day group-double). Corresponding single exposure groups were chosen as controls. No differences in TUNEL were seen between 7-day or 14-day single and double-trauma groups. Interestingly, independent of the second noise exposure, apoptosis increased significantly in the 14-day groups compared to the 7-day groups in all investigated areas. It seems that the first noise trauma has a long-lasting effect on apoptotic mechanisms in the central auditory pathway that were not largely influenced by a second trauma. Homeostatic mechanisms induced by the first trauma might protect the central auditory pathway from further damage during a specific time slot. These results might help to understand the underlying mechanisms of different psychoacoustic phenomena in noise-induced hearing loss.

Apoptotic mechanisms after repeated noise trauma in the mouse medial geniculate body and primary auditory cortex.

A correlation between noise-induced apoptosis and cell loss has previously been shown after a single noise exposure in the cochlear nucleus, inferior colliculus, medial geniculate body (MGB) and primary auditory cortex (AI). However, repeated noise exposure is the most common situation in humans and a major risk factor for the induction of noise-induced hearing loss (NIHL). The present investigation measured cell death pathways using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) in the dorsal, medial and ventral MGB (dMGB, mMGB and vMGB) and six layers of the AI (AI-1 to AI-6) in mice (NMRI strain) after a second noise exposure (double-exposure group). Therefore, a single noise exposure group has been investigated 7 (7-day-group-single) or 14 days (14-day-group-single) after noise exposure (3 h, 5-20 kHz, 115 dB SPL peak-to-peak). The double-exposure group received the same noise trauma for a second time 7 days after the initial exposure and was either TUNEL-stained immediately (7-day-group-double) or 1 week later (14-day-group-double) and data were compared to the corresponding single-trauma group as well as to an unexposed control group. It was shown that TUNEL increased immediately after the second noise exposure in AI-3 and stayed upregulated in the 14-day-group-double. A significant increase in TUNEL was also seen in the 14-day-group-double in vMGB, mMGB and AI-1. The present results show for the first time the influence of a repeated noise trauma on cell death mechanisms in thalamic and cortical structures and might contribute to the understanding of pathophysiological findings and psychoacoustic phenomena accompanying NIHL.

Antivertiginous drug therapy does not hinder the efficacy of individualized vibrotactile neurofeedback training for vestibular rehabilitation - a randomized trial.

Vestibular rehabilitation using individualized vibrotactile neurofeedback training (IVNT) can lead to significant improvement in the postural stability of patients with vestibular symptoms of different origins. However, some of these patients have complex, severe dizziness, meaning that a pharmacological pretreatment or parallel (to vestibular rehabilitation) treatment can help them perform the rehabilitation exercises. Hence, the present study investigated the influence of a pharmacological treatment on the efficacy of vibrotactile neurofeedback training in patients with chronic, noncompensated vestibulopathies. All participants performed IVNT for ∼10 min each day for 2 weeks. In addition, every second participant was selected randomly to receive oral medication (20 mg cinnarizine and 40 mg dimenhydrinate per tablet), taking three tables per day. Trunk and ankle sway and postural stability were measured. In addition, the dizziness handicap inventory was evaluated immediately before training on the last day of training and 6 months after training. After the 10-day period of IVNT, both groups showed a statistically significant improvement in all parameters tested. A follow-up analysis after 6 months showed a long-term efficacy for the IVNT, that is, the patients remained significantly improved in their postural stability. The antivertiginous therapy did not hinder the efficacy of the IVNT. The present results indicate that IVNT even in combination with an antivertiginous drug therapy is an effective treatment regime for patients with disabling vertigo of different origins.

Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex.

It has previously been shown that acoustic overstimulation induces cell death and extensive cell loss in key structures of the central auditory pathway. A correlation between noise-induced apoptosis and cell loss was hypothesized for the cochlear nucleus and colliculus inferior. To determine the role of cell death in noise-induced cell loss in thalamic and cortical structures, the present mouse study (NMRI strain) describes the time course following noise exposure of cell death mechanisms for the ventral medial geniculate body (vMGB), medial MGB (mMGB), and dorsal MGB (dMGB) and the six histological layers of the primary auditory cortex (AI 1-6). Therefore, a terminal deoxynucleotidyl transferase dioxyuridine triphosphate nick-end labeling assay (TUNEL) was performed in these structures 24 h, 7 days, and 14 days after noise exposure (3 h, 115 dB sound pressure level, 5-20 kHz), as well as in unexposed controls. In the dMGB, TUNEL was statistically significant elevated 24 h postexposure. AI-1 showed a decrease in TUNEL after 14 days. There was no statistically significant difference between groups for the other brain areas investigated. dMGB's widespread connection within the central auditory pathway and its nontonotopical organization might explain its prominent increase in TUNEL compared to the other MGB subdivisions and the AI. It is assumed that the onset and peak of noise-induced cell death is delayed in higher areas of the central auditory pathway and takes place between 24 h and 7 days postexposure in thalamic and cortical structures.

What Could Posturography Tell Us About Balance Problems in Parkinson's Disease?

OBJECTIVE: Impaired balance in patients with Parkinson's disease (PD) leads to loss of balance and frequent falls. Computerized dynamic posturography allows the assessment of stance tasks whereas mobile posturography analyzes the balance in free-field conditions, where falls among PD patients commonly occur (e.g. sitting down or standing up). The aim of the present study is to assess postural stability in PD patients with both techniques. STUDY DESIGN: Prospective study. SETTING: University Hospitals, ambulatory care (outpatient clinic). PATIENTS: Thirty-three patients diagnosed with idiopathic PD. INTERVENTION: Balance assessment. MAIN OUTCOME MEASURES: Dizziness handicap inventory (DHI), activities-specific balance confidence scale (ABC), composite score of sensory organization test (SOT), results of free-field body sway analysis (standard balance deficit test (SBDT)), or geriatric SBDT. RESULTS: PD patients showed a significantly higher sway in the roll direction in almost all of the SBDT conditions. Also, pathological sway compared with normative values was more prominent in complex tasks. There is a significant correlation between the different objective variables of the postural study (SOT and SBDT) and the ABC, but not with the DHI. Finally, the percentage of PD patients with a pathological score in SOT-composite score was 54.5% whereas in SBDT-composite score it was significantly higher (93.9%). CONCLUSION: Mobile posturography is more accurate in depicting the reality of balance impairment in PD patients than platform posturography. Also, ABC relates better than DHI to the significant psychological consequences of balance impairments. An increased lateral trunk sway seems to be a key factor of postural instability in PD patients.