Tinnitus noise trauma quirurgico,my ears constantly ringing bell,ringing in ear only when talking 80,right ear ringing non stop madrid - PDF Review

Author: admin, 01.09.2014. Category: Ring In The Ears

There is no strong conclusive evidence to suggest that there is a link between tinnitus symptoms and any type of food. Monitoring the impact of different foods can be difficult and your tinnitus levels can be better or worse because of a number of different variables. One of the main causes of tinnitus amplification can be stress arousal and because a poor diet has a direct link to stress it is a very important part of managing your tinnitus. Put simply the less well nourished we are the more likely we are to get stressed and the more stressed we are the more we rely on the nutrients that are in our bodies. There are a number of vitamins that can become depleted as a result of increased metabolic rate.
Diets that are over rich and have too much sugar content are also detrimental to managing stress levels. Diets that are high in fats and sugar will result in the diminishment of minerals such as: Thiamine, Niacin, B12, Magnesium and Calcium.
My recent post entitled How to Habituate to Tinnitus looked at Tinnitus Habituation from a mainstream perspective to make sure that you have covered all of your bases with regard to tinnitus treatments. Every journey begins with the first step however preparing the ground before making the first step can be crucial to maintaining longevity for making changes in our lives.
This post will explain the mainstream steps of treatment you might experience in your quest to find a tinnitus solution. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. In this study, we describe differences between neural plasticity in auditory cortex (AC) of animals that developed subjective tinnitus (group T) after noise-induced hearing loss (NIHL) compared to those that did not [group non-tinnitus (NT)]. Despite these severe impairments and the large number of patients affected, there is still no established treatment available to safely and effectively alleviate tinnitus.
Although short or acute tinnitus percepts are experienced occasionally by virtually everyone, chronic tinnitus develops only in a sub-population of humans as well as in the different animal model systems. We have recently published the first report comparing neuronal plasticity following NIHL in animals that develop a tinnitus percept (group T) with plastic changes in animals that do not [group non-tinnitus (NT)], even though both animal groups did not differ in NIHL (17). Based on these results we have proposed a model for tinnitus prevention that points to a global inhibitory mechanism in auditory cortex (AC) that may prevent tinnitus genesis in animals with high overall activity in the auditory system, whereas this mechanism does not seem to be available for tinnitus prevention in animals with low overall activity. In the present follow-up study we present a further, more detailed analysis compared to the Ahlf et al. A total of 35 eight to ten weeks old male gerbils purchased from Charles River Laboratories, Inc. All animals were handled before the beginning of the experiments and accustomed to the setup environment to minimize stress. The setups for behavioral and electrophysiological recordings have been described in detail earlier (17, 18). Three different types of PPI modulated ASR paradigms (17) were performed to assess, first, hearing capacities [behavioral and reflex based audiogram (19)] and, second, the potential existence of a tinnitus percept (20) after the noise trauma. For tinnitus testing we used two modified ASR paradigms in all animals before and after trauma. Of the 35 animals investigated behaviorally, 20 were used for electrophysiological recording in brainstem and AC.
We statistically analyzed behavioral and neuronal response amplitude data as well as FFT frequency spectra by parametric tests; response latencies and durations were assessed by non-parametric tests as one cannot assume normal distribution for these parameters. In tinnitus associated with inner ear damage, and especially that due to noise, it seems reasonable to expect that deficits in inner ear function should be present at the same frequency as the tinnitus.
For the left ear (top), OAEs (the difference between the top and bottom trace) are excellent up to roughly 11,000 Hz. Hearing loss is among the top three chronic health conditions of senior citizens, affecting approximately 50% of the population > 65 years. Hearing depends on highly structured hair bundles in the cochlea properly oriented towards the lateral border of the cochlear duct. Many individuals experience listening difficulty in background noise despite clinically normal hearing and no obvious auditory pathology.
Long-term goal: The overall goal is to understand the role efferent mechanisms in auditory processing, learning and disability.
Our ability to hear and communicate depends primarily on the sensory hair cells (HCs) and their associated spiral ganglion neurons (SGNs). Long term goal of the research – To develop therapeutic interventions to prevent hearing loss and restore lost hearing. Long Term Research Goal: The long-term goal for the current project is to understand tinnitus at the level of neural circuits.
A recent study investigating selective attention abilities in cochlear implant users may point to a novel new method for improving the understanding of speech in a noisy environment.
Long term goal of research: To close the gap in speech understanding performance between cochlear implant users and normal hearing listeners.
Long term goal of research: To understand how different neuromodulators control the neural activity in the central auditory system and their role in pathological auditory processing.
Long term goal of research: To develop mechanism-based treatments for Usher syndrome by understanding the formation of USH protein interactomes and their functions in the development and maintenance of hair bundles in hair cells. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractNoise-induced hearing loss (NIHL) and resulting comorbidities like subjective tinnitus are common diseases in modern societies.
IntroductionA universal characteristic of modern societies, both in developing and developed countries, is the steadily increasing level of noise exposure within our working environments and during leisure time activities (for review see [1]).
This is not to say that certain foods may or may not affect your tinnitus in a positive or negative way. Listening to your tinnitus under relaxed conditions is imperative to finding your solution. If you are stressed and anxious your levels of Cortisol increase making habituation more difficult. This change signals an increased heart rate, muscle tension, cholesterol, increased blood pressure and a number of other metabolic changes. Your irritability levels can increase, nervousness can get worse and your nervous system reactivates the same stress hormones originally produced. Sugary and fatty foods contribute to the development and maintenance of depression and stress.
In most cases finding your tinnitus solution is a long term strategy so preparing for long term changes is more than just taking the first step.
Before posting on more specialised treatments i think it is important to acknowledging the mainstream types of tinnitus habituation treatment available.
The accident resulted in one of our founding members suffering head injuries and hearing damage which caused persistent tinnitus.
This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. To this end, our analysis focuses on the input activity of cortical neurons based on the temporal and spectral analysis of local field potential (LFP) recordings and an in-depth analysis of auditory brainstem responses (ABR) in the same animals. The development of effective therapies for tinnitus is mainly hampered by the fact that the exact neuronal mechanisms leading to the phantom percept and its chronic manifestation are still largely unknown.
We currently do not know why some patients with hearing impairments develop chronic tinnitus while others with the same shift in hearing threshold do not, and vice versa why some but not all subjects without detectable noise-induced hearing loss (NIHL) still develop tinnitus, although first models that may solve this enigma have been published (14–17). As we could demonstrate, NT animals showed higher overall auditory cortical and brainstem activity before noise trauma compared to T-animals.
We suggest that by activating this global inhibitory mechanism the NT animals may actively counteract the development of maladaptive increased response gains in AC seen in T-animals that possibly reflect the tinnitus development. During the first week, animals were tested first, with three different paradigms of pre-pulse inhibition (PPI) of the acoustic startle reflex (ASR) to evaluate the audiograms for each animal and acquire baseline data for the tinnitus percept evaluation. The measurements were performed before and usually 7 days after the acoustic trauma in a single 4 h block. Mean PPI effect (±95% confidence interval) in six exemplary animals classified as non-tinnitus (NT) and tinnitus (T) perceiving. Root mean square (RMS) values of the LFP recordings in AC with 70 dB SPL stimulation intensity. Signals were recorded using a Plexon Multichannel Acquisition Processor (Plexon Inc., Dallas, TX, USA) after amplification by a JHM NeuroAmp 401 (J. Among these, the complete recording protocol in AC could be accomplished in four T and two NT animals.
This conjecture offers a possible for adding objective evidence to substantiate the existance of what would otherwise be an intrinsicially subjective phenomenon.
Despite this high prevalence of hearing loss, only 20% of senior citizens with hearing loss use a hearing aid. Abnormalities in this hair bundle structure or its orientation results in hearing loss, for example in the hereditary disorder Usher syndrome.
This condition has often received a clinical label called auditory processing disorder (APD).
The translational goal is to develop mechanism-based and physiological tests for assessing auditory processing. Unfortunately, mammalian HCs and SGNs are not naturally replaceable, and their loss results in neurosensory hearing loss and balance impairment. To this date, no pharmaceutical drugs have been effective in restoring auditory function after HCs are lost.
Our approach offers a rather unique opportunity to sample activity within large-scale representations and local populations of neurons and, in turn, will reveal precisely how A1 micro-circuits are affected by traumatic insult to peripheral sensory organs. In that study, cochlear implant users showed significant improvement in speech understanding when instructed to attend to a target talker in one ear and ignore an interfering talker in the other.
Currently, we have a limited understanding of how these synapses are maintained in the healthy cochlea and how they can be regenerated after noise overexposure. A substance shown to be effective against NIHL in an animal model is the Ginkgo biloba extract EGb 761.
Consequently, an increasing number of people suffer from hearing disorders that result from an overexposure to noise, that is, noise-induced hearing loss (NIHL). The Internet is full of contradicting reports warning of certain foods affecting tinnitus negatively.
When our metabolic rate increases we use up our food and nutrient stores much more quickly. Vitamin B complex is crucial to a person with tinnitus because it helps to deal with stress, depression and anxiety. Well structured meal plans are often replaced with binge eating, eating more frequently, junk food, fast food, caffeine, alcohol and caffeine addictions.
In response to NIHL in NT animals we find a significant general reduction in overall cortical activity and spectral power as well as changes in all ABR wave amplitudes as a function of loudness. Hence a significant amount of data from both human (6, 7) and animal studies (8–12) on the plastic changes occurring in the involved neuronal networks during tinnitus development is available, a number of different and in part controversial neurobiological models trying to explain the phenomenon do exist. We concluded that animals with low overall neuronal activity in the auditory system might have a predisposition for the development of tinnitus early after noise trauma while animals with higher neuronal activity did not develop such a percept within the time of observation.
According to this model, the high overall AC activity of NT animals before the trauma is a prerequisite for the activation of this hypothetical global inhibition.
The use and care of animals was approved by the state of Bavaria (Regierungspräsidium Mittelfranken, Ansbach, Germany). All methods used in this paper (except the LFP recordings) have been described previously (17) but still will be explained in detail here for better intelligibility. Second, ABR measurements of the healthy animals were performed to obtain individual audiograms under anesthesia and the far field responses of the auditory pathway in the brainstem up to the inferior colliculus (IC). For obtaining the behavioral hearing thresholds we used a PPI of ASR paradigm in all animals.
Because tinnitus can be a single tone, at nearly any pitch, one really needs to quantify inner ear function at all frequencies. This suggests that there was outer hair cell damage at the same location using an objective test as had already been localized using a subjective test (audiometry). Why do senior citizens reject hearing aids after trying them, despite available advances in hearing aid technology?
In particular, she is interested in the effects of aging and hearing loss on the brain’s speech processing.
The Royal Arch Masons support Emerging Research Grants in the area of Central Auditory Processing Disorder (CAPD).
However, the molecular mechanisms that build the polarized structure of individual hair cells remain poorly understood. He investigates the role of efferent mechanisms in hearing and auditory disorders in humans. To this date, any attempts to regenerate lost sensory HCs have been challenged by the early embryonic lethality of complete knockout mice or massive cell death after conditional deletion of targeted genes. This fact fuels our continuous search for alternative strategies to prevent and treat hearing loss. Tarang is a Postdoctoral Research Associate in the department of Oral Biology at the Creighton University School of Dentistry.
Thus, I intend on using this approach to build a more comprehensive understanding of how cortical micro-circuits change as a result of noise trauma. The dorsal cochlear nucleus (DCN), one of the first stations of the ascending auditory pathway, receives dense serotonergic input.
Gates Research Award, presented annually in perpetuity to an outstanding Emerging Research Awardee.
The overall goal of this study is to examine the potential of the neurotrophic factor, neurotrophin-3 (NT-3), to assist in preserving or regenerating these synaptic connections in cochlea after noise overexposure. Further effects of the extract on the cellular and systemic levels of the nervous system make it a promising candidate not only for protection against NIHL but also for its secondary comorbidities like tinnitus.


Statistical data show that in 2000 about 9% of the general population in the USA display hearing impairments [2].
Listening to your tinnitus as part of your relaxation therapy or meditation can be very beneficial. Our use of fats, carbohydrates and protein speeds up and our stores of blood sugar, fatty acids and protein can become depleted.
Having a higher intake of magnesium, iron, selenium, zinc, phosphorus, and calcium can also help to reduce the likelihood and impact of stress. In contrast, T-animals show no significant change in overall cortical activity as assessed by root mean square analysis of LFP amplitudes, but a specific increase in LFP spectral power and in the amplitude of ABR wave V reflecting activity in the inferior colliculus (IC). Furthermore, within a week after the acoustic trauma T-animals showed increased activity in auditory cortical neurons representing the tinnitus frequencies, whereas NT animals exhibited decreased activity at moderate sound intensities at that point in time. We suggest that a certain dynamic range for unspecific gain reduction across the whole AC is needed to successfully counteract the response gain increase that is associated with tinnitus development. The authors declare that there is no conflict of interests regarding the publication of this paper.
After these measurements surgery for implantation of the head holder and the recording chamber over the left AC was performed and electrophysiological single electrode recordings in primary AC field AI of the healthy anesthetized animal were carried out on two to three sessions within 1 week after the surgery. We startled the animals with 90 dB SPL pure tones (6 ms length including 2 ms rise and fall ramps) ranging from 0.5 to 16 kHz in a pseudo-randomized order in octave steps. 0) and no changes in PPI effect were found comparing pre (blue) and post trauma (red) data by t-tests. The recordings were identical to those described in the earlier report (17) allowing us to additionally analyze single unit responses within AC.
Unfortanately, it is impractical to test hearing in a continuous fashion because each single frequency takes roughly a minute to test. This technique might be useful for medico-legal situations where there is noise trauma and tinnitus. She uses her clinical experience as an audiologist to conduct translational work to address the speech understanding difficulties experienced by older adults, and to assess the impact of intervention (hearing aids, cochlear implants, and auditory training) on neural processing and speech understanding. Our research focuses on the role of a novel secreted protein, URB, in hair bundle morphogenesis and cochlear development. One mechanism thought to aid in listening-in-noise is the medial olivocochlear (MOC) inhibition— a part of the descending auditory system.
In this light, we sought to design a new system that combines the inducible nature of an antibiotic-controlled system with the lysosomal fusion protease pre-procathepsinB (CB) to generate an inducible, temporal, and reversibly conditional mouse model. One brain area thought to be at least partly responsible for the tinnitus percept is the primary auditory cortex (A1).
Such a level of understanding is essential to advance our efforts to reduce or even reverse the impact noise trauma has on its patients and our society. The aim of this work is to evaluate the feasibility of a novel strategy that takes advantage of these observations.
In addition, our proposed experimental paradigm offers a unique opportunity to study auditory attention mechanisms used in understanding speech in noisy environments. Recent evidence indicates that the DCN may be a site of central tinnitus, and it is possible that serotonin might play a role in the generation or modulation of central tinnitus. We have generated genetic mouse models that allow us to remove or overproduce NT-3 from the supporting cells, which are the cells surrounding the sensory hair cells.
It is classified into three clinical types according to the severity of hearing and vestibular symptoms. Following an earlier study we here tested the potential effectiveness of prophylactic EGb 761 treatment against NIHL and tinnitus development in the Mongolian gerbil. Similar data were published for Germany in 2006, where 8% of the 18- to 79-year-old adults appear to be hearing impaired [3]. Keeping a food diary is one approach to monitoring the impact of food on your tinnitus levels. They both directly affect each other meaning you might be craving foods that are making you more stressed and your tinnitus worse. The mineral Zinc can also be seriously depleted by stress and an increase in metabolic rate. If the overall neuronal activity in AC is already low before the trauma, as in the case of T-animals, this activity may not be reduced further and tinnitus develops because of un-resisted response gain increase in those regions of AC representing the tinnitus percept. Acoustic trauma (2 kHz, 115 dB SPL, 75 min) under deep anesthesia was used to induce a mild NIHL (evaluated by ABR analysis directly after the trauma and PPI audiogram after 1 week) and a persistent tinnitus percept in the majority of the animals (26 of 35 animals, 74%; evaluated by PPI measurement one week after trauma). The same pure tones were used as pre-stimulus probes ranging from 0 to 50 dB SPL in 10 dB steps 100 ms before the startle stimulus. In both cases, a silent 15 ms gap within the noise (white or band pass) 100 ms before the startle stimulus served as pre-pulse. The right panel gives the comparison of time of recording averaged over all frequencies as part of the 2-factorial ANOVA. In particular, we are testing whether URB functions as part of a Planar Cell Polarity (PCP) signaling pathway, a highly conserved pathway of widespread biological interest. Xiaowei Lu at the University of Virginia where she studied signaling mechanisms underlying inner ear development and hair cell polarization.
The purpose of this translational project is to evaluate whether the functioning of the MOC system is altered in individuals with APD. To build upon our laboratory’s expertise, we applied this technology to generate a mouse model carrying a transgenic version of the of the retinoblastoma (Rb1) gene. However, the precise changes in neural activity within local neuron populations have not been investigated directly. He conducted postdoctoral research at Stanford University and the University of Maryland and is now an Assistant Research Scientist in the Institute for Systems Research at the University of Maryland.
This will help further develop our understanding of the human auditory system so that we can bridge the gap in hearing-in-noise performance between hearing impaired and normal hearing listeners. Moreover, serotonin reuptake inhibitors (SSRIs) typically used as antidepressants in the treatment of depression and anxiety disorders, have been explored as a treatment for tinnitus. We have found that NT-3 produced from the supporting cells is critical for regulation of hearing sensitivity and synaptic density in the cochlea. Zou's studies focus on type 2, which is the dominant form of Usher syndrome and characterized by congenital moderate degree of hearing loss, normal vestibular function, and retinitis pigmentosa.
We monitored the effects of EGb 761 and noise trauma-induced changes on signal processing within the auditory system by means of behavioral and electrophysiological approaches. What remains an open question in our model is the source of the hypothetical global inhibition, whether it is generated intra-cortically (within AC), sub-cortically or even in higher cortical or limbic structures. Within the first week after the trauma all electrophysiological recordings in AC were performed in two to three recording sessions. The rationale of these paradigms is that an animal that perceives a tinnitus would be impaired in gap detection because it would hear its own tinnitus within the silent gap [cf. Stimulation was pseudo-randomized using a fixed list of all combinations of stimulus frequencies and sound pressure levels (0–90 dB SPL in 5 dB steps).
We are also investigating possible links between URB and the Usher syndrome network of proteins. She is currently a research instructor at Emory University where she investigates cochlear development. The benefits of measuring MOC inhibition in individuals with APD are twofold: 1) it could be useful to better define APD and identify its potential mechanisms, and 2) it may elucidate the functional significance of MOC efferents in listening in complex environments.
The goal of the proposed project is to probe how noise trauma affects both large- and local-scale organization of A1 brain circuits with unprecedented spatial and cellular resolution in an animal model of tinnitus.
The goal of this research is to identify the cellular targets of serotonin and SSRIs in the DCN and understand their functional roles. Based on this finding, we propose that NT-3 may present a novel therapeutic agent for NIHL.
PDZD7 was recently reported to exacerbate the symptoms and contribute the digenic form of Usher syndrome type 2 when patients carry heterozygous PDZD7 mutations.
We found significantly reduced NIHL and tinnitus development upon EGb 761 application, compared to vehicle treated animals. All experiments were carried out in an IAC (Industrial Acoustics Company GmbH, Niederkrüchten, Germany) acoustic chamber on a TMC (Technical Manufacturing Corporation, Peabody, MA, USA) low-vibration table.
For sound generation, the frequency response function of the speaker was calibrated to produce an output spectrum that was flat within ±1 dB measured within the acrylic tube.
Note that we did not find any significant change over time and no interaction of the two predictors in these animals. To obtain ABR-based audiograms the mean ABR wave amplitudes were compared to the mean amplitude 200–100 ms before the stimulus (baseline).
We hope that defining these roles for URB in bundle morphogenesis will help in the design of rational therapies for the treatment of Usher syndrome and other forms of hereditary hearing loss in the future. The potential role of the MOC system in APD pathophysiology, should it be confirmed, would be of significant clinical interest because current APD clinical test batteries lack mechanism-based physiologic tools. In addition to its role in cell proliferation, Rb1 expression in the inner ear also affects differentiation and survival of HCs and their associated supporting cells (SCs). Proposed experiments will use state-of-the-art optical imaging approaches to investigate how entire auditory cortical areas (large-scale) and auditory cortical microcircuits (local-scale) are disrupted by noise trauma. Notably, this work is particularly important and relevant for children fitted with cochlear implants since they need to contend with noisy environments, such as classrooms, every day. The ultimate goals of this research are to understand how serotonin influences the output of the DCN, and whether serotonin may have a role in tinnitus.
In this proposal, we will use these mouse models to address the following questions: does removing NT-3 exacerbate the damage to the loss of synapses and hearing sensitivity after noise overexposure? These protective effects of EGb 761 were correlated with changes in auditory processing, both at peripheral and central levels. As the prevalence of hearing impairments increases with age, it appears to be sensible to assume that when these children grow up the number of patients with hearing impairments will increase dramatically in the future.
The data obtained were checked by eye via a custom-made Matlab program, trials in which the animals moved within 100 ms before the startle stimulus were discarded; in the valid trials only peak-to-peak amplitudes of responses within the first 50 ms after startle stimulus onset were used for further analysis. Animals were again ketamine-xylazine anesthetized, placed on a 37°C warm heating pad and fixated via the aluminum head-post.
A multi-level understanding of circuit dynamics underlying tinnitus (from single neurons to complete representations) will enhance our understanding of precisely how cortical circuits remodel after noise trauma and, in turn, develop and identify strategies by which this debilitating condition can be repaired. The ability to hear better in these environments will lead to improved long-term social and educational development for these children. Does overproducing NT-3 prevent or promote recovery from noise-induced loss of synapses and hearing? Using this animal model, Zou plans to investigate the function of PDZD7 during hair bundle development in the cochlea. We propose a model with two main effects of EGb 761 on auditory processing, first, an increase of auditory brainstem activity leading to an increased thalamic input to the primary auditory cortex (AI) and second, an asymmetric effect on lateral inhibition in AI. Furthermore, as hearing loss may be etiologically responsible for the development of a number of secondary diseases, like hyperacusis (for review see [5]), tinnitus [6, 7], or depression due to social isolation [8], the problem of NIHL should be of immensely growing importance. Finally, the exact relations between cochlear damage, hearing impairment, and tinnitus development are still elusive. The evaluation was performed independently by the principal investigator and a technical assistant, who was blind to the state of the animal. Consequently, when using a gap as pre-pulse, animals with tinnitus should produce smaller PPI of ASR than animals without tinnitus (cf. For additional analysis the root mean square (RMS) value of the ABR signal was calculated from 1 to 5 ms after stimulus onset and single waves of the ABR responses representing the different levels within the brainstem (25) were detected by a custom-made Matlab program at 70 dB SPL for each stimulation frequency.
However, just like a number of other genes considered potential candidates for HC regeneration, complete and permanent elimination of Rb1 results in massive apoptosis, and as such, should be avoided at all costs. These experiments will provide us with a better understanding of the pathophysiology of NIHL and the potential of neurotrophin-based therapeutics for treating hearing loss. This study will be significant for the future diagnosis and treatments for Usher syndrome type 2. This study will allow us to characterize this newly generated model of transient and reversible gene ablation and gather information supporting pre-clinical studies on HC regeneration. In this context, two main types of strategies are conceivable: reducing noise exposure by technical measures or preventing the development of NIHL via pharmacological interventions. We made sure that the animals were always (pre and post trauma = trauma status) responding to the 90 dB SPL startle stimulus (cf. In humans, it is known that the majority of tinnitus percepts (around 70%) exhibit a pure tone-like character while the remaining part consists of ringing tones, noises or even more complex sounds (22). The recorded LFPs were analyzed with custom-made Matlab programs and statistically evaluated with Statistica.
Whereas many technical measures, for example, for noise reduction in working environments or public, have the advantage that they may be effective for a large number of people, they are often very expensive and have no effect if the source of noise is self-inflicted [10].During the last few years a large number of substances have been tested both in animal and human studies in search of a powerful drug that is able to prevent NIHL.
We used the two different paradigms to determine possible tinnitus percepts in the animals because the exact nature of these percepts is unknown.
Three response measures were evaluated, first, the amplitude and timing of the first negative peak (N1) and the second positive peak (P2) waves of the recorded data (reflecting mainly the slower extralemniscal and intracortical input [for review see Ref. Based on their physiological mechanisms of effectiveness against NIHL, a number of substance classes may be distinguished. For validation of the PPI effect of the pre-stimuli we performed 1-factorial ANOVAs for the valid response amplitudes dependent on the pre-stimulus intensity for each frequency and trauma status separately for each individual animal. With the pure tone stimulus over a white noise and the click stimulus over band pass filtered noise we aimed to cover as many different percepts as possible. Among these, antioxidants that reduce oxidative stress by elimination of reactive oxygen species (ROS) [11], glucocorticoids, and substances that improve cochlear blood flow (for review see [12]), activate inhibitory transmitter systems [13], or block apoptosis pathways in hair cells were most successfully employed (for review see [14]).A substance that has been shown to protect against NIHL in guinea pigs is the Ginkgo biloba extract EGb 761 [15, 16]. The mean responses before and after trauma of the six animals used for electrophysiological recordings in AC are given in Figure S1 in Supplementary Material.
If a tinnitus is detected, the different tone frequencies and noise spectra used should give a rough estimate of the spectral content of the tinnitus percept.


Stange and coworkers demonstrated that animals which were treated with EGb 761 before exposing them to different types of noise trauma exhibited a smaller reduction in auditory nerve compound action potentials (CAP) than untreated controls. Responses in this threshold paradigm were fitted with a sigmoidal Boltzmann function for each frequency, trauma status, and animal separately. Each frequency and gap-condition was repeated 15 times and each test was performed before and after the acoustic trauma. EGb 761 is a plant extract that is composed of about 80 different compounds which deploy not only one but also a number of different mechanisms presumed to counteract the development of NIHL.
Hearing thresholds were defined as the sound level at the inflection point of the Boltzmann function for each frequency before and after trauma (18). Again the data obtained were checked by eye by the same two experimenters as above via a custom-made Matlab program. Well-documented are the protection of neuronal mitochondrial ATP synthesis in the presence of oxidative stress [17, 18], the protection of erythrocyte membranes against oxidative damage, which results in reduced blood viscosity and improved blood flow [19, 20], and neuroprotection through antiapoptotic properties [21–25]. Trials in which the animals moved within 100 ms before the startle stimulus were discarded; in the valid trials only peak-to-peak amplitudes of responses within the first 50 ms after startle stimulus onset were used for further analysis (17). In addition, the extract displays a number of effects that may counteract the development of secondary consequences of NIHL like tinnitus.
This approach allowed the determination of a possible frequency-specific tinnitus-related behavior at one octave precision. These include increased extracellular dopamine levels in the prefrontal cortex [26], which may reduce depressive behavior that may foster the development of tinnitus [27], by partial inhibition of the norepinephrine transporter [28] or adult neurogenesis of hippocampal neurons [29], which additionally could both lead to cognition increasing effects.
After the trauma only some animals showed an undisturbed gap-effect at all frequencies tested while other animals showed no gap-effect at some but not all frequencies (cf. Therefore, EGb 761 is a promising candidate substance for protective measures against NIHL and its consequences.As detailed above, one of the consequences of NIHL may be the development of a tinnitus percept. Figure 1), which gave a first hint of a possible tinnitus percept but was not yet used as the final classification of the animals in the tinnitus or NT group (cf. In a previous study we have described the development of noise trauma-induced tinnitus in the Mongolian gerbil both on a behavioral and neurophysiological level [31]. We were able to detect a number of neuroplastic changes in auditory brainstem and cortex that were correlated with the development of a tinnitus percept as tested with a well-characterized behavioral paradigm [32]. To avoid possible effects of the acoustic trauma on different stimulation frequencies all startle response data were normalized to minimize variance of the response amplitudes. In particular we could demonstrate a neuronal predisposition for the development of tinnitus. Normalization was performed as described earlier (17, 23); briefly, we divided each amplitude by the corresponding median amplitude of the 90 dB SPL only condition (which reflects the full startle response of the animal for the loudest condition at each specific frequency, 0 dB SPL pre-stimulus intensity Figure S1 in Supplementary Material). We were able to show that animals developing such a mispercept after an acoustic trauma show significantly less cortical activity already in the healthy state compared to tinnitus-resistant animals. Thus we attempted to control for differences in the startle amplitudes resulting from the hearing loss at the trauma frequency. The latter animals are able to counteract tinnitus development after noise trauma while animals without this ability develop a chronic tinnitus percept.While studies in humans with different Ginkgo biloba extracts so far failed to show any reliable effect on tinnitus perception when given after its development [34, 35], we here tested the effectiveness of a prophylactic treatment with EGb 761 in the context of NIHL and tinnitus development in this animal model.
This normalization also guarantees that the reduced ASR response after acoustic trauma is not due to hearing loss but likely due to a tinnitus percept (23).
We describe the effects of the EGb 761 extract on the behavioral level (acoustic startle response (ASR) audiometry), the auditory brainstem level (electrophysiological recordings of auditory brainstem responses (ABR)), and the central level (electrophysiological recording of local field potentials (LFP) and single and multiunit responses in auditory cortex (AC)).
Our results point to massive neuroplastic effects of EGb 761 on auditory processing both at the peripheral and central level. Significant positive values for PPI change reflect impaired PPI and therefore indicate the development of a tinnitus percept. These changes in processing may underlie the observed protective effects against NIHL and in the consequence tinnitus development.2.
Only such animals were therefore classified as probably perceiving a tinnitus (T group) that showed at least one impaired frequency after the trauma independent of the affected frequency itself. As it turned out, in all cases where a tinnitus was detected according to one of the two gap-ASR paradigms used, the second gap-ASR paradigm was also positive for tinnitus. Ethics Statement and AnimalsMongolian gerbils (Meriones unguiculatus) were housed in standard animal racks (Bio A.S.
Animals without such a significant increase in PPI change were classified as NT perceiving animals (NT group). It became apparent that animals classified as T or NT based on these behavioral measures also differed in neurophysiological response measures (ABR and AC responses; cf. While the tests used here may only detect acute tinnitus, exemplary animals were re-tested in regular intervals for up to 16 weeks and did not show any changes in tinnitus frequencies.
Based on these results we think that the classification of NT and T-animals is not only valid in acute but also in the chronic state of the disease. Two weeks prior to trauma (yellow bar) oral application of vehicle or EGb 761 was performed on a daily basis.
Pretrauma measurements included behavioral startle responses (turquoise; hearing threshold and gap-noise tinnitus paradigms), ABR measurements (dark green), and electrophysiological recordings in auditory cortex (light green) both under anesthesia. After the acoustic trauma the measurements were repeated within the first seven days after the trauma.During the oral administration the measurements were started (cf.
These included the behavioral testing in the first week of application, the pretrauma auditory brainstem response (ABR) measurements, and the pretrauma recording from the AC within the second week of substance administration. This procedure was performed before the acoustic trauma and during the week after that event.
We made sure that the animals were always (pre- and posttrauma = trauma status) responding to the 90 dB SPL startle stimulus (cf. For validation of the PPI effect of the prestimuli we performed 1-factiorial ANOVAs for the valid response amplitudes dependent on the prestimulus intensity for each frequency and trauma status separately for each individual animal. The mean responses of all 36 animals (19 V, 17 E) before and after trauma are given in Figure 2.
Responses in this threshold paradigm were fitted with a sigmoidal Boltzmann functions for each frequency, trauma status, and animal separately. The left panel documents the mean hearing thresholds with their 95% confidence interval for clicks and all tested tone frequencies with the -statistics of the interaction of the 2-factorial ANOVA. The center panel depicts the 1-factorial part of the same ANOVA with the factor group (mean values over all tested frequencies and click). Right panels show the same data separated into animals that do not develop a tinnitus percept (upper panel) and those that did show a tinnitus percept after the trauma (lower panel). The grey area in the left panel indicates significant hearing loss (single sample -test versus 0) in both groups (, ), which is also significant if averaged over all tested frequencies and the click stimulus (center panel, asterisks).
Note that relative changes of thresholds measured with either ABR or ASR have been demonstrated to be identical [33]. The rational of these paradigms is that an animal that perceives tinnitus would be impaired in gap detection because it would hear its own tinnitus within the silent gap (cf.
Consequently, when using a gap as prepulse, animals with tinnitus should produce smaller PPI of ASR than animals without tinnitus (cf.
If tinnitus is detected, the different tone frequencies and noise spectra used should give a rough estimate of the spectral content of the tinnitus percept.
Each frequency and gap-condition were repeated 15 times and each test was performed before and after the acoustic trauma.
After the trauma only a part of the animals showed an undisturbed gap-effect at all frequencies tested while other animals showed no gap-effect at some but not all frequencies (cf. Figure 4) which gave a first hint of a possible tinnitus percept but was not yet used as the final classification of the animals in the tinnitus or nontinnitus group (cf.
Thus we were able to control for differences in the startle amplitudes resulting from the hearing loss at the trauma frequency. This normalization also guarantees that the reduced ASR response after acoustic trauma is not due to hearing loss rather than a tinnitus percept [39].
Finally, the PPI of ASR in the healthy animal (before trauma) and after the trauma was calculated and the change in PPI relative to pretrauma (in %) was tested against 0 (no change) for each frequency separately with a -test ().
Only such animals were therefore classified as probably perceiving tinnitus (T groups) that showed at least one impaired frequency after the trauma independent of the affected frequency itself. As it turned out, in all cases where tinnitus was detected according to one of the two gap-ASR paradigms used, the second gap-ASR paradigm was also positive for tinnitus. Animals without such a significant increase in PPI change were classified as nontinnitus perceiving animals (NT groups) (cf. As it turned out, animals classified as T or NT based on these behavioral measures also differed in neurophysiological response measures (ABR and AC; for example, Figures 7 and 12), thereby strengthening the classification (cf.
The upper two animals received the vehicle and the lower two animals received the EGb 761 extract before the trauma. In other cases (KS 42 and KS 07) gap detection was impaired and did not show any significant change after the trauma at least at some frequencies; this was a first indication of T categorization (cf.
2-factorial ANOVA (only interaction shown) depict the changes in no-gap and gap conditions before and after trauma. Note that even when gap-effects are small on the group level they were always significant in the single animals before trauma. Significant positive values of PPI change reflect an impaired PPI, indicating the development of a tinnitus percept.
2-factorial ANOVA indicates that EGb 761 treated animals develop tinnitus percepts at lower frequencies than vehicle treated controls. Asterisks below or above the abscissa indicate significant change of PPI (-test versus 0): , . To obtain ABR-based audiograms the mean ABR waves were compared to the mean amplitude 200 to 100 ms before the stimulus (baseline). Thresholds were defined automatically by a custom-made Matlab program at the highest attenuation at which the evoked amplitude raised over 2 standard deviations of the baseline; data were discarded at frequencies where this procedure was not possible, for example, at low signal to noise ratios.
For additional analysis the root mean square (RMS) value of the ABR signal was calculated from 1 to 5 ms after stimulus onset. For further analysis data from both ears of each animal were used.As behavioral audiograms using PPI of ASR (cf. We have demonstrated earlier [33] that these different methods to assess audiograms in our animal model yield different absolute thresholds but identical relative shifts in hearing thresholds after noise trauma. Electrophysiological Unit Recordings in Primary Auditory Cortex (AI)In a subset of the 36 animals (3 vehicle, 4 EGb 761) used in this study we performed electrophysiological recordings in auditory cortex in addition to the behavioral and ABR measurements described above.
Two to three days after obtaining baseline ASR and ABR data, that is, before the acoustic trauma, the skull of the anesthetized animals was trepanned to expose the left auditory cortex. In addition to these iso-intensity measurements, tuning curves were recorded using pure tones in the mentioned frequency range but at different intensities ranging from 0 to 90 dB SPL. The recorded unit activity was analyzed with custom-made Matlab and IDL programs (IDL 7.06, Exelis Visual Information Solutions, McLean, VA, USA).
Where appropriate, either parametric statistics (Student's -test, one- and two-factorial ANOVA with Tukey post-hoc-test) or nonparametric statistics (Kolmogorov-Smirnov-test, Kruskal-Wallis ANOVA with post hoc Median-test, and Mann-Whitney -test) were applied.3. Effects of Prophylactic EGb 761 Treatment on NIHL and Tinnitus EmergenceWe used the PPI of the ASR to obtain behavioral audiograms from all 36 animals before and after the acoustic trauma. The responses to the different prestimulus intensities were checked by 1-factorial ANOVAs for each frequency and trauma status (before or after trauma) and for each individual animal separately.
For an overview of the different response characteristics before and after trauma the mean response amplitudes of the 19 vehicle treated and 17 EGb 761 treated animals are given in Figure 2.
Note that we find different response characteristics dependent on the stimulation frequency and trauma status but always find the significant prestimulus intensity effect of the PPI, that is, a decrease in ASR amplitude with increasing prestimulus intensity, which is not only true for the mean response but also for the individual responses.
To these individual responses we fitted sigmoidal Boltzmann functions obtaining the individual behavioral hearing thresholds for each frequency.Additional to these behavioral thresholds we obtained individual ABR based hearing thresholds under anesthesia before and after the trauma. Nevertheless, the impact of the trauma on the hearing thresholds was significantly stronger in group V compared to group E (Figure 3(b) center). Furthermore, the degree of NIHL that developed differed between the V and E groups during the first week after trauma (Figures 3(c) and 3(d)).
Whereas the frequency specificity of the NIHL vanished in both groups resulting in flat NIHL functions, the overall threshold shift completely recovered in group E, resulting in audiograms not significantly different from pretrauma conditions 7 days after trauma.
The temporal development was entirely different between NT and T animals (Figures 3(c) right, 3(d) right).
While NT animals showed no remaining hearing loss only 1 day after trauma, all vehicle treated animals and the T animals of the E group showed increased NIHL until day 7 after trauma.
Note that we show the relative hearing loss compared to pretrauma level as we want to keep the two different methods of hearing threshold level measurements comparable. As we have demonstrated in an earlier study [33] ABR and ASR thresholds differ in absolute values so that audiograms show a parallel upward or downward shift. Relative changes due to hearing loss on the other hand were identical for both methods.As described above, both EGb 761 and vehicle treated groups contained T and NT animals.
Exemplarily the mean response amplitudes to both gap-ASR paradigms of four animals are depicted in Figure 4.
The two upper animals were treated with the vehicle and the two lower ones with the substance. In animals KS 51 and KS 16 significant gap detection (-tests, ) was found before and after the trauma at all frequencies tested. This impairment was a first hint for the classification of these two animals into the tinnitus group (cf. The mean startle response amplitudes for all these animals before and after the acoustic trauma are depicted in Figure 5(a).




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