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Author: admin, 23.12.2014. Category: Medicine For Tinnitus Over The Counter

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. A new strategy for idiopathic subjective tinnitus treatment - sound stimulation during sleep - has been applied. Mechanisms that underlie tinnitus perception are still not well understood; nevertheless, nowadays it is accepted that interactions between altered cochlear inputs and distorted central auditory processing provoke tinnitus. This study was approached on a multidisciplinary basis: otolaryngology, psychology and sleep medicine. Eleven patients with idiopathic subjective tinnitus (10 males and one female, from 31 to 71 years old) were studied during 24 weeks. Sound stimulation during sleep improved the tinnitus intensity in all patients; most of them (8 out of 11) exhibited the greatest decrement in the first week of treatment, while in the remaining 3 patients the tinnitus intensity took 2 or 3 weeks to decrease. In this pilot study we show the positive result -significant decrement in the tinnitus intensity - of the sound stimulation applied during sleep. On the other hand, it is well accepted that mechanisms of learning and memory occur during sleep, organizing sensory inputs and consolidating memories, in a different way than during wakefulness, and even better since less sensory inputs disturb processing, consequently, our protocol is based on stimulation during sleep. Centro de Medicina del Sueňo, Facultad de Medicina, Instituto Universitario CLAEH, Punta del Este, Uruguay. Brief summaries were presented in the following meetings: 2nd Tinnitus Research Initiative Meeting, Principality of Monaco, 2007. III XXX Congress of Association for Research in Otolaryngology, Phoenix, Arizona, USA, 2008 World Association of Sleep Medicine Congress, Sao Paulo, Brazil, 2009. A3™ is Audibel’s newest full family of wireless products featuring next generation 900sync™ Technology that leads the way in performance, comfort, personalization and connectivity. When you proceed to the checkout page, the Seller Discount will be automatically calculated. 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. It was based on the knowledgement that the auditory system also works during sleep, processing the incoming information. The physiological abnormalities that cause subjective tinnitus perception arise in the central nervous system (CNS). Twenty two patients were evaluated; thirteen of them complied with inclusion criteria and were studied, two abandoned the treatment, remaining eleven within the protocol. Patients were evaluated by a psychologist at the beginning of the treatment and also in the middle and at the end of it.
Patients' sleep conditions were clinically evaluated, exploring possible insomnia related to tinnitus or other sleep disturbances (i.e.
Sound generation and stimulation were programmed to reproduce a sound with the same characteristics as that of each patient's tinnitus. Uma, a amplitude da resposta em frequencias diferentes das iPod (cinza traco) eo notebook (preto traco) resposta mostrando apartamento ao longo da largura de banda de trabalho. After concluding the otolaryngology evaluation, eleven patients began the treatment and they were followed up and evaluated during 24 weeks. Each patient was seen by a psychologist three times, at the beginning, the middle and the end of the treatment. Five out of eleven patients had sleep disorders at the beginning of the treatment, four of them suffered insomnia characterized by difficulty to fall asleep with the corresponding daytime consequences such as tiredness, lack of energy, concentration difficulty, irritability.
The present protocol was based on the tenet that most forms of tinnitus are caused by functional changes; thus, it should be possible to reverse them by proper sound treatment taking advantages of the neural plasticity properties of the CNS.


Please use newer version of your browser or visit Internet Explorer 6 countdown page for more information. 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. It is now evident that most forms of subjective tinnitus are caused by changes in the function of the central auditory nervous system while these changes are not associated with any detectable anatomical lesion. Since the sensory information in general is continuously reaching the CNS, its processing will be differentiated according to the current physiological state of the brain: wakefulness, with different levels of motor activity and attention, and sleep5. Tinnitus Retraining Therapy (TRT) is a behavioral treatment that has roots in the hypothesis that tinnitus is caused by expression of the neural plasticity41,42. Every patient was evaluated by an otolaryngologist with a clinical interview and specific tests: impedanciometry, tonal liminal audiometry, high frequency audiometry, logoaudiometry, otoacustic emissions (spontaneous, transients and distortion product) and magnetic resonance imaging (MRI).
Personal interview to evaluate anxiety and depression, and a specific test for tinnitus repercussion (Tinnitus Handicap Inventory, THI) were done. Audio stimulation was performed using commercial iPod Shuffles (Apple, USA) with their own ear buds. Sound stimulation was applied through an ipod, to the same side that patients perceived the tinnitus (unilateral or binaural). Everyone improved their insomnia with the tinnitus treatment, two of them - treated chronically with benzodiazepines- abandoned successfully their chronic treatment. Since we found changes in the auditory tests (TLA, HFA, logo and OAE) in tinnitus patients, we proposed the sound stimulation with the same characteristics in frequencies and intensity as the tinnitus as a way of reinstalling the normal balance in the central level processing of information, hypothesizing that tinnitus emerges to replace an input deficit.
Regional cerebral blood flow during tinnitus: a PET case studied with lidocaine and auditory stimulation.
Lateralized tinnitus studied with functional magnetic resonance imaging: abnormal inferior colliculus activation.
In vivo approach to the cellular mechanisms for sensory processing in sleep and wakefulness. Firing of inferior colliculus auditory neurons is phase-locked to the hippocampus theta rhythm during paradoxical sleep and waking. Auditory processing during sleep: correlation of cortical unitary activity with hippocampus theta Rhythm.
Sleep and wakefulness modulation of the neuronal firing in the auditory cortex of the guinea-pig. The effects of sleep on the auditory brainstem response (ABR) and the middle latency response (MLR). Late component variants of single auditory evoked responses during NREM sleep stage 2 in man. Auditory stimulation therapy as an intervention in subacute and chronic tinnitus: a prospective observational study.
Treatment of tinnitus with a customized dynamic acoustic neural stimulus: underlying principles and clinical efficacy. Electrical stimulation of auditory and somatosensory cortices for treatment of tinnitus and pain. Transcranial magnetic stimulation(TSM) for treatment of chronic tinnitus: clinical effects. 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.
The stimulus was a sound that mimetized the tinnitus and was fixed at the same tinnitus intensity, applied through an iPod.
The subjective tinnitus may be the result of the expression of neural plasticity and anomalies may develop because of decreased input from the ear, deprivation of sound stimulation, overstimulation or yet unknown factors1.
Early in the twentieth century, the concept of sleep as the result of a blockage of the auditory inflow was introduced6 while, later on, Bremer7 proposed that it was the extensive deafferentation of ascending sensory impulses to the isolated brain that resulted in sleep. The aim of TRT is to psychologically disconnect the patient from dependence on the tinnitus while subjecting the patient to moderate levels of sounds to reverse the effect of sound deprivation on the function of the CNS43. Also general evaluation was done through routine tests (blood lipids, serum thyroid hormones, glucose test, urea and electrolytes, creatinine, complete blood test, urine test). Conventional Polysomnography was recorded in two patients, during two nights each one (first night without sound stimulation and the second one during the stimulation with their specific sound) in order to analyze potential hypnograms changes due to the sound. All sounds were created with custom software developed in Matlab, creating complex sounds by combining pure tones, white and pink noise and filtered white noise (peak filter, Q) at 44100 samples per second.
Aplicando a linearidade dos sons criados, vamos supor que todos os sons mostram a mesma resposta e poder tanto no caderno e saida iPods (tensao).
Each night, patients fixed the sound stimulation intensity at the tinnitus masking level, selecting among the 25 ipods steps.
Between 1 and 6 years of tinnitus evolution were considered, with no differences in the results presented. Everyone has a particular lifestyle, with demanding jobs and no vacation time by own initiative. 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. All patients decreased their tinnitus intensity in the first month of treatment (statistically significant), most of them in the first week.
Furthermore, patients whose sleep was most disturbed rated significantly greater tinnitus annoyance in the evening underscoring the influence of tinnitus on sleep disorders38.
Other tinnitus therapies based on sound are being applied as an special program of music therapy that strives to integrate the tinnitus sound into a musically controllable acoustic process44, sequential sound therapy45 and customized sounds46,47. The inclusion criteria were adult patients with idiopathic subjective tinnitus, with normal imagenology and without any organic causes. Conventional Polysomnography consisted in six electroencephalographic recordings, eye movements, electromyogram, respiration, oximetry and electrocardiogram.
These sounds could be created selecting their frequency, power (relative to full scale), Q and duration. Patients wrote down each night the stimulation intensity and the hours stimulated, together with other observations that they considered important (illnesses, relevant stress situations, etc.). Tinnitus intensities were normalized as steps in the ipod, being 25 the highest for each patient before beginning the treatment (week 0). Three of them have obsessive personality and one was depressive and rejected psychotherapy. 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.
Tinnitus intensity continued decreasing in the following weeks; three patients presented periods of total silence. In a number of patients subjective tinnitus may be initiated by a discontinuity in the spontaneous or low-level stimulus inducing neural activity across auditory nerve fibers with different characteristic frequencies (CFs). Electrophysiological approaches as unitary recordings, immunoreactive staining techniques as well as functional magnetic resonance imaging in humans are some contributions to such concept8-10. On the other hand, daytime sleepiness is more common in subjects with tinnitus and it is even more frequent in patients with both tinnitus and poor sleep39. Many of these therapies are still under investigation and only some of them have been objectively evaluated in clinical trials48.
This research has been approved by the Ethical Committee of the Faculty of Medicine CLAEH University, according to the International Ethic Guidelines for human research.
Table 2 shows audiological evaluation; while all patients showed alteration in at least one of the parameters explored, no one needed to be equipped with audiphones. Personal interviews with the psychologist showed the patients' evolution much better than the THI scale, which did not appear as a precise technique to evaluate evolution, at least when the degree of tinnitus repercussions were not severe. Patients were continuously clinically evaluated and two of them were also studied by polysomnography.
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. This discontinuity may be caused by functional loss of outer hair cells in those regions where inner hair cells are preserved. Velluti and co-workers postulated the sensory systems as a main factor in active participation in sleep processes11-14. After the sound mimicked the perceived tinnitus, it was saved as a .wav file (16 bit, PCM) and consequently loaded to the iPod Shuffle.
Changes neither in the sleep stages percentages nor in the sleep architecture (hypnogram) were exhibited when comparing two completed nights (with and without sound stimulation) in each patient.
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.
The reduced spontaneous activity for nerve fibers with CFs in the hearing loss range may result in a reduction of inhibition, mediated by the auditory efferent system, at more central levels4. The processing of sensory information is definitely present during sleep, since profound modifications occur. These facts underscore the importance of identification and successful treatment of sleep disorders in patients with tinnitus.
Drugs have not demonstrated to provide replicable long-term reduction of tinnitus49; many of them are still at a research level, such as transcranial magnetic or cortical electric stimulation of the auditory cortex50,51. 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]. This reduced inhibition of neurons with CFs induces hypersensitivity and hyperactivity in these neurons, generating a "phantom sensation", that is a sensation referred in a different location on the body (in this case usually the ear) than the anatomical location of the abnormality that causes the symptoms1. All sensory systems reviewed, visual, auditory, somesthetic and olfactory, as well as temperature receptors, etc., demonstrate some influence on sleep and, at the same time, the sensory systems undergo changes that depend on the CNS sleep or waking condition.
The custom software was programmed to adjust the power of the sound signal in order to have equal full scale voltage output.
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. Since most forms of severe tinnitus are caused by functional changes, it should be possible to reverse it with proper sound treatment, taking advantages of the neural plasticity properties of the CNS.
From several viewpoints, the auditory is a special system related to sleep neurophysiology, exhibiting a series of unique associated changes12,15,16.
The same ear buds were used to mimic and deliver the stimulus, thus ensuring that equal voltage would be transduced into equal sound pressure. Otoacoustic Emissions (OAE) -spontaneous, transient and distortion product- were recorded in each patient.
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 auditory incoming signals to the CNS may change the sleep characteristics, while, conversely, the CNS can control by feedback mechanisms the auditory input in close correlation with the sleep-wakefulness cycle11. The slope was calculated if at least three data points fell in the range between L2 = 40 and L2 = 60 dB SPL. Receptor and auditory nerve action potentials exhibited amplitude changes when analyzed during quiet wakefulness, Slow Wave Sleep (SWS) and Paradoxical Sleep (PS) in guinea-pigs16,17. 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. Auditory evoked potentials recorded from the primary cortical area in rats also exhibited amplitude shifts when the animal passed from wakefulness (W) to sleep. 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. All evoked potentials components of the averaged waveform were larger during SWS than in W or PS18. 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.
Most relevant, reciprocally, auditory deprivation (experimental deaf guinea pigs and hamsters) produces changes in the sleep stages percentages26,27. Reports in humans showed marked changes on the evoked potentials later components during sleep28-31. A high amplitude complex waveform dominates in SWS stages 2, 3 and 4, which is the result of summed K-complexes evoked by sensory stimuli32.
Semantic information is possible in SWS stage 2 and PS33, whereas the presence of P3 seems to be essential for stimulus encoding, despite the question if W and sleep P3 could be considered equivalent remains to be answered32. Moreover, this negativity has been reported also in newborns "quiet sleep" and linked to learning35. Intracochlear implanted humans changed their sleep characteristics when implant remained "on" during the night36.



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