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Author: admin, 12.12.2013. Category: Tinnitus Causes And Cures

To date, no known curative medical or surgical treatment is available for addressing chronic tinnitus. However, habituation to tinnitus is a central auditory process; accordingly, persistent suffering of tinnitus patients is connected to deficits within this process. The functions of sound transfer in the middle ear and the treatment of diseases in that area are well-known. This type of specialization of cells and the anatomy of the entire afferent sound path is well-known. The efferent path descends from the auditory cortex down to the corpus geniculatum mediale. One main target is to develop diagnostic tools to prove these functions or deficits by audiological examinations.
Objective diagnosis of cochlear function, mainly OHC activity, is based on recordings of otoacoustic emissions. Research work on the functions and major characteristics of the psychoacoustical hearing process is based mainly on research by Zwicker [13] but, as mentioned, these elements are not very commonly known within general practices. Certain objective controlling methods with humans were tested according to the idea of brain-mapping; here, especially the group working with Hoke and Hoke [15] and Pantev [16] have achieved high merits mainly because of functional nuclear magnetographic measurements. DP data from 20 normally hearing ears, obtained in the same manner, were used as reference data [20]. To quantify the DP growth, the slope was calculated between L2 = 40 and L2 = 60 dB SPL, where a flat course occurred in the normal hearing state and a steep course in the pathological state. Between 1 and 3 kHz, where the hearing threshold Lt was within normal limits, the DP levels were unusually low. Similar findings led us to examine these functions with hyperacusis patients with normal subjective hearing on pure-tone audiogram. Between the years 2001 and 2002, we examined 127 patients with tinnitus and an almost normal hearing threshold. All these findings give evidence that in a great number of tinnitus and hyperacusis patients, the efferent regulation of the OHCs fails or is even turned off completely. Our audiological data show specific findings in many tinnitus and hyperacusis patients, although they are not similar in all such patients. Similar to these findings with tinnitus patients [26,27], our data show the same effect with 6 8% of normally hearing hyperacusis patients.
These results suggest that in many hyperacusis patients and in tinnitus patients, some alteration of auditory processing already occurs on the cochlear level. Until today, tinnitus perception could not be influenced by any medicine without completely destroying the sense of hearing or incurring the risk of severe side effects. Some approaches involve implanting special catheters, placing them at the area close to the round window and trying to apply medicine with a special dosage pump as a local therapy for the inner ear. Surgical approaches (except, of course, surgery that treats such middle-ear diseases as otosclerosis and thus preserves or restores hearing as the main goal) are restricted to cutting the acoustic nerve, with its known complications.
Therefore, as curative treatments are far from being applicable, the focus of tinnitus therapy is trained on habituation processes [33]. With our clinical data, we could prove that in a large number of tinnitus patients, these deficits of central auditory processing and efferent inhibition can be recorded. This research was presented at the Thirty-First Congress of the Neurootological and Equilibriometric Society, Bad Kissingen, Germany, March 25-27, 2004. Treatment options should be discussed with your audiologist to determine which method is right for you. The Amplicomms Powertel M7000 is an easy to use highly amplified clamshell mobile phone with additional features for the hearing impaired.
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Specific Findings in Distortion Product Otoacoustic Emissions and Growth Functions with Chronic Tinnitus. Latest studies found chronic tinnitus in 4% of the German population, with almost 2% suffering severely in their daily life.
The latest data from Germany showed that 25% of the population experienced tinnitus for a short period at one time of their life, 13.8% did so for a longer period, and approximately 4% suffer from tinnitus to an extent requiring special intervention. We know from our own clinical data that 90% of tinnitus sounds are generated in the internal ear, mainly caused by damage of the outer hair cells (OHCs) [3].
The theoretical background of this auditory sensory habituation is based on understanding the complete process of hearing. Today, even the mechanisms of the inner ear are better known because of new findings of the function and structure of the OHCs [5] and the effective motor protein prestin [6]. The first binaural interaction takes place in the first neuron that ends in the dorsal and ventral nucleus cochlearis in the brainstem. The inferior colliculus seems to have a major function in the control of the efferent sound path and, thereby, of the function of enhancement and inhibition. Function controls for the different sectors of the sound paths are not commonly used in clinical practice; specific microscopical and electrophysiological research is based mainly on findings with cats and rats [11,12].
In particular, the frequency-specific measurement of distortion product otoacoustic emissions (DPOAE) can characterize the cochlear amplification process of the OHC, originating as a consequence of nonlinear sound amplification. Recently, the binaural masking level difference test, a psychoacoustic test differentiating sound detection in unilateral and bilateral broadband noise, has been evaluated for clinical use [14].
DPs could be recorded well in the frequency range that corresponded to the appearance of tinnitus.
Pure-tone audiometry showed normal thresholds (hearing loss not exceeding 10-15 dB HL) in all frequencies from 250 to 2,000 Hz. We performed pitch and loudness matching of the tinnitus by means of a clinical audiometer [19]. Normal hearing controls and normal, compressive, nonlinear DP-grams, growth function, slope (s), and pure-tone audiogram. Calculation of the slope between 40 and 60 dB SPL was chosen because, in that range, normal and pathological DP growth did differ most. Patient with sudden hearing loss and tinnitus measured at 6 kHz: DP-gram, growth function, slope (s), and pure-tone audiogram.
The DP-grams at high primary tone levels, however, lay close together, indicating normal compressive growth behavior.


Patient with progressive cochlear hearing loss and tinnitus at 8 kHz: DP-gram, growth function, slope (s), and pure-tone audiogram. In normal-hearing individual,distortion product otoacoustic emission amplitudes decreased after contralateral stimulation with a 60-dB broadband noise.
Distortion product otoacoustic emission amplitude reduction in certain frequencies in tinnitus patients. Distortion product otoacoustic emission amplitude reduction in certam frequencies (controls). However, in tinnitus patients without hyperacusis, this inverse reaction or hypermotility of OHCs is restricted to the tinnitus frequency; in hyperacusis patients, it seems to reflect a wider range of frequencies.
Most probably, hyperacusis as an oversensitivity to all sounds is due to an inefficient input control of sounds or even overamplification of incoming sound [28]. Thus, audiological analysis, especially recording of DPOAEs, provides objective signs of different auditory processing in at least 40-50% of tinnitus patients.
Instruments and specific tests for central auditory function also must be developed to give evidence to these deficits of efferent control: They must be easily applicable so as to be used on a wider clinical scale.
Optimization of cochlear blood flow and oxygen supply may be efficient in acute types of OHC damage, especially after acoustic trauma or sudden sensorineural hearing loss. However, even in these cases, more than 50% retain their tinnitus owing to central excitation of a primarily peripherally generated sound [32]. This process works the innate ability of the auditory system to alter the perception of random noise if its meaning is not connected to such emotions as fear or anger.
Our results further indicate that in many tinnitus and hyperacusis patients, abnormal hypermotility of OHCs may occur even if hearing is completely normal. Identification and Treatment of an Underlying Contributor–if impacted earwax, medications, or underlying inflammation or disease are contributing and can be treated effectively, tinnitus symptoms may be significantly reduced. Drug Therapies–although there are currently no drugs approved specifically to treat tinnitus, research on anti-anxiety, antidepressant, and antihistamine medications have shown positive results in some cases.
Using twin amplifiers the Amplicomms Powertel M7000 mobile phone boosts volume by up to 40db and reduces sound distortion to less than 5% which means that even when used with hearing aids sound remains crystal clear. Built-in pulsating alert lights and adjustable volume and tone controls ensure you rise on time.
It comprises five tools for fast and effective daily cleaning including a wax removal brush, wax removal pick, tube and vent cleaner, battery door opener and battery replacement magnet. OtoVita Drying Pellets change colour from orange to white to show when it's time for new one. Because no curative therapeutic approach is available-neither pharmacological nor surgical-the main focus lies in treatments that enhance the habituation of tinnitus. Of these, 1.5% reported that their daily life was greatly affected by the tinnitus, and some 1 % believed that it interfered with their occupation. Noise or acoustic trauma may induce decoupling of the OHCs from the tectorial or the basilar membrane. As each inner ear is connected with both brain halves, one part of the neurons leads from the nucleus cochlearis to the nucleus olivaris superior of the same side, whereas the other part crosses over to the opposite side. This takes up the descending paths from the cortex itself and from the corpus geniculatum mediale. Calculating DPOAE growth functions can illustrate the activity of hair cells and possible compensation mechanisms after injury. The DP slope, however, increased with increasing hearing loss and, therefore, did correlate with the hearing threshold, revealing pathological alteration. Around the tinnitus frequency, the DP levels were up to 10 dB higher than at the maximum hearing loss.
Corresponding to the threshold run, the slope increased rapidly on the low-frequency side of the notch but gradually decreased on the high-frequency side. Here, the DP level decrease between 2 and 4 kHz corresponded to the increasing hearing loss, resembling most of the nontinnitus ears. Acting as controls were 41 normally hearing nontinnitus individuals (average age, 33.5 years). Decreased DP levels and increased growth functions seem to be proof of diminished sensitivity and tuning of the cochlear amplifier.
This dysfunction is mainly the result of disturbances in the cortical network of auditory processing that leads either to ineffective or diminished efferent control of the auditory pathway [9] or to an efferent overactivity on all levels, including that of the OHCs. Therein, the cortical reflection of incoming sound or electric activity leads, via smaller or ineffective efferent inhibition, to hyperactivity in the OHCs, where it then can be recorded. Antiarrhythmic agents such as lidocaine can stop tinnitus in perhaps 50% of cases but only temporally for the time of infusion [29]. This ability of the auditory perception can be developed and trained even in older people by using the filter capacities of the efferent system, with its effects on all parts of the auditory pathway, including the OHCs.
Thus, training of these central auditory abilities and functions [34] is a promising approach to facilitate tinnitus and hyperacusis habituation [14]. Physiology of cochlear efferent and afferent neurons: Direct comparisons in the same animal. Salicylate and quinine selectively increase spontaneous firing rates in secondary auditory cortex. Wandel in Diagnostik und Therapie: Auditorische reiz- und ereigniskorrelierte Potentiale und Magnetfelder in der audiologischen Diagnostik.
Contingent Magnetic Variation (CMV) Studied with Stimuli Close to the Hearing Threshold in Normal Subjects and Tinnitus Patients. The level and growth behavior of the 2f1-f2 distortion product otoacoustic emission and its relationship to auditory sensitivity in normal hearing and cochlear hearing loss. The ipsilaterally evoked olivocochlear reflex causes rapid adaptation of the 2f1-f2 distortion product otoacoustic emission. Otoakustische Emissionen und Tinnitus: DPOAE, eine Messmethode zum objektiven Nachweis des auf der Ebene der auBeren Haarzellen entstehenden Tinnitus?
Distortion product otoacoustic emissions in patients with innerear highfrequency hearing loss and tinnitus.
Der Round Window Cath zur Lokaltherapie des Innenohres - Ergebnisse einer plazebokontrollierten, prospektiven Studie bei chronischem Tinnitus. Hearing therapy: A way to intensify auditory perception in the treatment of chronic tinnitus.
Habituation occurs in almost 5 0% of affected patients as a normal process, leading to a complete compensation. These data, published by the German Tinnitus League (DTL) [1], probably are the same for all industrialized countries.
Ionic channels of the OHCs may tear off, viral toxins or other toxic agents may influence stimulus transduction in the hair cells, and stimulus transmission may be disturbed at the synaptic level.


Already the differentiation between afferent and efferent supply of the hair cells [7] shows the existence of complicated regulating loops controlling the entire auditory pathway, with Corti's organ situated at the peripheral end.
From there, efferent fibers run to all subordinate brain centers that, in the end, reach again the OHCs of the inner ear [9,10]. Another group of tinnitus patients showed a congruent relation between DP levels and threshold and also a congruent relation between threshold and slope or growth function.
Auditory brainstem responses were recorded, and the wave I -V interpeak interval was measured in an attempt to exclude retrocochlear pathology. Only with a lowering primary tone level does the DP-gram reflect the audiogram notch, which decreases by some 20 dB. Most distinctly, the DP level decreased at lower primary levels, as indicated by the spread of the DP-grams, changing the DP growth functions to a linear process.
DPOAEs were recorded according to the described paradigm in a session with and without a contralateral sound stimulus of 60 dB HL. The recorded audiological data play an important role in our understanding of tinnitus generation in at least some patients.
HH Naumann, C Herberhold, E Kastenbauer (eds), Oto-Rhino-Laryngologogie in Klinik und Praxis, Band 1 Ohr. Presented at the Second Annual Meeting of the German Society for Audiology (DGA), Munich, 1999. In L Deecke, C Baumgartner, G Stroink, SJ Williamson (eds), Biomagnetism: Fundamental Research and Clinical Applications.
Presented at the Seventh International Tinnitus Seminar, Fremantle, Western Australia, 2002. This finding is based on the ability of the auditory perception to habituate random noise and focus on important acoustic information.
Strain may cause spasms of the precapillary blood vessels, resulting in temporary malnutrition of the cochlea.
In the inner ear, sounds are mainly treated according to the discrimination of place (tonotopy) and time, whereas in higher brain centers and auditory neurons, more and more complex sound patterns are involved. Through further stations of the sound paths via corpus geniculatum mediate and the radiatio auditiva, the auditory cortex is reached. Besides providing three-dimensional hearing, a major advantage of such a complex sound path is a sophisticated hearing ability in high-noise areas or in the presence of disturbing sounds. Exactly one-half of patients (110) reported high-frequency, tonal tinnitus; the other 110 did not. Even at lower primary tone levels, the DP level did not decrease with increasing hearing loss.
With contralateral stimulation, the tuning curves of the cochlea and the acoustic nerve flatten.
Presumably, this matches only for so-called motor tinnitus, the type of tinnitus confined to destruction or decoupling of the OHCs [4]. They are also very helpful for the counseling of patients and for preventing further frustrating and expensive therapeutic failures. According to our audiological data, 9 0% of tinnitus patients have deficits in inner-ear function as a generator of tinnitus, mainly in the outer hair cells.
The main outcome of this study shows that many people experience or suffer from tinnitus, but only a small proportion suffer to an extent requiring treatment.
As a rule, the patients estimated the loudness of the tinnitus somewhat above the audiometric threshold around the tinnitus frequency.
In the region of normal hearing below 3 kHz, the DP-grams were widely spaced at lower primary tone levels but lay close together at the higher levels, indicating compressive growth. Taking into account the amount of hearing loss around the tinnitus, these high DP levels are fairly surprising and could result in incorrect conclusions about cochlear integrity. Also, high slopes were found between 2 and 3 kHz, possibly revealing a disturbance that was not reflected in the behavioral audiogram (Fig. Regarding the DPOAE recordings, contralateral sound decreases the emissions; thus, the amplitudes are reduced. This occurrence can be verified by registration of distortion products of otoacoustic emissions. This is certainly owing to the normal habituation process, which allows for people who have tinnitus to no longer experience it as disturbing. In the notch region and around the tinnitus, the DP-grams were widely spaced and actually equidistant, revealing linear growth. Accordingly, if tinnitus is influenced by malfunction or is even due to deregulation of efferent auditory control, it should be interesting to examine the effects of lateral inhibition (via contralateral sound) with tinnitus patients.
Thus, the main origin of tinnitus is peripheral, and most patients suffer from accompanying hearing loss, even though it is sometimes mild or subjectively not even noticed. They react to the increase or decrease of frequency or to the beginning or ending of sound impulses. In almost 50% of our patients, we find hyperfunction of outer hair cells, again recorded via distortion products of otoacoustic emissions and their growth functions. Thereby, sound impulses are prepared for further treatment within the auditory cortex by the extraction of certain characteristics: Thus, only the content of information, not the entire signal, is transported to the cortex (processing of information) [8]. Normal efferent reduction of distortion products through contralateral acoustic stimulation does not take place in most tinnitus patients. This can be seen in a comparison of the individual data and its range of plus or minus the standard deviation of the DP level of the normally hearing control group at the corresponding frequencies. This finding shows that central auditory functions are also disturbed in chronic tinnitus patients, leading to reduced efferent effects on the hair cells and thus impeding habituation. The slope was calculated if at least three data points fell in the range between L2 = 40 and L2 = 60 dB SPL. We have data on diminished ability to distinguish stimuli from random noise by bilateral sound processing: The so-called bilateral masking difference test results are pathological in almost 3 0% of patients suffering from chronic tinnitus. We concluded from our audiological data that chronic tinnitus is primarily a cochlear dysfunction, but habituation is impeded by accompanying or consecutive deficits of the central auditory pathway. Regarding therapeutic approaches, these central functions can be trained by hearing therapy, as we know from patients' rehabilitation.
Before the actual experimental is run, in each case the patient's pure-tone threshold is obtained by means of a conventional clinical audiometer.



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