Tinnitus db level meter,tinnitus y vertigo tratamiento,piercing keloid tea tree oil usos - Step 1

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INTRODUCTION: Musical training positively influences the cortical plasticity of the brain and has proven to be effective in treating chronic tinnitus. OBJECTIVES: A neuro-music therapy concept, the "Heidelberg Neuro-Music Therapy" treatment was developed and evaluated. MATERIALS AND METHODS: N = 135 patients (mean age 47 years) with chronic, tonal tinnitus attended a standardized protocol for Neuro-Music Therapy (either "standard therapy" ST or "compact therapy" CT). CONCLUSIONS: The "Heidelberg Neuro-Music Therapy" is a method with fast onset and long lasting effect for patients with "tonal" tinnitus.
Apart from emotional disturbances such as anxiety, depression, sleep impairments or irritation1, the main complaints of the persons concerned with ringing in the ear are difficulties in concentrating their attention2 and in auditory perception3.
Data from human neuroimaging support the hypothesis of a final common pathway for tinnitus6 and propose a compromised "noise cancellation mechanism"7 to be liable for the enduring tinnitus percept.
It is known that pleasant music verifiably reduces activities in the amygdala and enhances activity in nucleus accumbens and thalamus8,9. Disadvantages are the rather lengthy application and the passive "sounding" of the tinnitus instead of an active exposition to the tinnitus sound. Therefore a short-term Neuro-Music Therapy based on active treatment modules seems to be fruitful in treating chronic tinnitus.
The novel treatment according to the "Heidelberg Model of Neuro-Music Therapy" is based on the notion that tinnitus is experienced as an auditory percept - just as musical stimuli are experienced as auditory percepts. Two standardized protocols for tinnitus music therapy were defined: a "standard therapy" (ST) and a "compact therapy" (CT) (see patient flow-chart).
All patients receive a comprehensive psycho-educative counseling in order to establish a cognitive model of tinnitus20. As the specific modules used in therapy are based on the individual tinnitus sound, a tinnitus-equivalent has to be set up by means of a commercially available sinus generator. In the Resonance Training the patient learns a vocal exercise stimulating the cranio-cervical resonating cavities. The Neuroauditive Cortex Training uses tone sequences performed live by the therapist on a piano which have to be vocally imitated by the patient.
The Tinnitus Reconditioning offers coping mechanisms related to stress control along with a sound based habituation procedure.
During the relaxation exercise, the tinnitus sound will be integrated intermittently into the background music. Patients were eligible if they suffered from chronic tinnitus (duration > six months) which could be musically compiled (distinct frequency) and had no psychiatric co-morbidity. Since patients were recruited nationwide it was not possible to randomize the patients to the groups in the true sense of the word. Based on data from a pilot study23 we calculated the a priori power and thus estimated the minimum control group size with the power analysis program "GPOWER"24 to n = 15.
As part of the medical history, psychosomatic and audiologic co-morbidities as well as socio-demographic data and tinnitus characteristics were assessed.
On the whole 69% of the patients presented with high frequency hearing loss (> 20 dB hearing impairment present in at least three test frequencies > 3000 Hz) and about 42% presented with low frequency hearing loss (> 30 dB hearing impairment present in at least one test frequency 0-2000 Hz).
Due to the stratified group allocation, no group differences in socio-demographic data were obtained. Patients in the music therapy groups ST and CT received a treatment according to the "Heidelberg Model of Neuro-Music Therapy" as described above. Patients in the control group PT received a psychosocial intervention based on psychological tinnitus treatment strategies25 combined with placebo music therapy elements. Assessment of tinnitus symptoms was performed three times, at admission ("pre"), at discharge ("post") and six months after therapy ("follow-up FU").
Apart from statistical significance, individual changes were assessed according to the concept of clinical significance27. At discharge all patients of the music therapy groups had the opportunity to rate their subjective therapy satisfaction. Statistical analysis of the data was performed using parametrical and non-parametrical tests in SPSS 16 (SPSS Inc. In order to predict parameters possibly influencing therapy outcome, a logistic regression model (CATREG, SPSS 16.0) was calculated using TQ-score immediately after therapy as an indicator for therapy success as a dependent variable.
Analysis of TQ scores revealed a highly statistically significant reduction pre-post (p p =.913). The overall reduction in the music therapy groups can be explained by significant changes in distinct sub-scales of the TQ, especially of "E = emotional problems" (p p p p p >.05).
According to the concept of "clinical significance", more than 80% of the patients the music therapy groups (ST and CT) achieved a reliable reduction in their tinnitus scores from admission to discharge and could thus be categorized as "responder".
On a subjective level, 67% of the patients treated with music therapy regarded their symptoms as "better", 22% observed no change and 11% stated to be worse off. Apart from immediate therapy-related effects, there could be other factors influencing therapy outcome ("moderator variables"). In order to set the results in the context of existing therapies, a psychologically based treatment group was used as control group. Animal models 29 as well as results from research on tinnitus treatments30 suggest the use of very specific stimuli, i.e. The "Heidelberg Model of Neuro-Music Therapy" on the other hand integrates some well known psychological techniques and strategies in order to reduce the tinnitus sensitivity by means of an immediate exploration of the tinnitus sounds by the patient.
The rather low positive feedback rate of the Neuroauditive Cortex Training (only about a quarter of the patients rated this module as helpful) might have been due to the wording during the therapy.
The Resonance Training is a purely vocal exercise that stimulates the auditory pathway by means of somatosensory innervations and enables the patients to control their tinnitus perception. It is known that there are manifold cross-modalities in processing somatosensory and auditory stimuli 35. The Neuroauditive Cortex Training contains a detailed "intonation-training" with purpose-built musical stimuli, based on the individual tinnitus frequency in order to increase the patients" discriminative abilities and enhance their attentive skills. In chronic tinnitus characteristic auditory cortical reorganizations are traceable, which seem to be frequency specific 40,41. Tinnitus Reconditioninghas distinct features in that it combines musical distractors with psychophysiological relaxation and imagination of mental well-being. Since the application of the "well-being image" is linked to acoustic stimuli (relaxation music, tinnitus equivalent sound), the connection "well-being image - relaxation - tinnitus reduction" can be explained in terms of classical conditioning 46. The neurological basis seems to be in an endogenous system located in the medial temporal lobe system (MTLS) 6 and the reticular formation (RF) 47. On the whole, music therapy is a method with short duration, fast onset and long lasting effect for patients with "tonal" tinnitus and light to moderate tinnitus severity (Figure 1 and 2).
Paper submitted to the RBCMS-SGP (Publishing Management System) on April 1, 2012; and accepted on August,16, 2012. This paper is a preliminary report from the Tinnitus Center, HSCB-SUNY, of hyperacusis in a patient population who request consultation for tinnitus of the severe disabling type. There is a positive correlation between tinnitus and hyperacusis as well as a positive correlation between hyperacusis and the loudness discomfort level test (LDL). The present method of assessment for hyperacusis includes pure tone audiometry, LDL's, Feldmann Masking Curves and the Metz test for recruitment. A classification system exists for hearing loss and a similar system is suggested for hyperacusis.
A review of the literature reflects the difficulty encountered clinically in attempting to diagnose and treat the subjective complaint of hyperacusis.
Jastreboff and Hazell define hyperacusis as a manifestation of increased central gain evaluated by direct frequency measurements of loudness discomfort levels (LDLs). Loudness discomfort levels are most frequently used in the assessment of hyperacusis.12 What frequencies to use for the assessment and how many repetitions per judgement are not universally agreed upon.
Kotsanis and Harjes consider uncomfortable loudness level thresholds (UCLs) under 90 dB HL at 500 - 8000 Hz and 70 dB at 250 Hz as abnormal. Forty-two consecutive cases, 29 males and 13 females, ranging in age between 20-75 years with a mean of 51.9 years with the primary complaint of subjective idiopathic tinnitus (SIT) of the severe disabling type were included in this study. Pure tone audiograms were obtained at the discrete frequencies of 250, 500, 1000, 2000, 3000, 4000, 6000, and 8000 Hz for the right and left ears for each individual. The pitch of the tinnitus was matched to frequency using a two alternative forced choice procedure.18 The ear with the tinnitus is used as the reference for the match. Loudness discomfort levels (LDLs) were obtained for each ear individually at the discrete frequencies tested on the audiogram; 250, 500, 1000, 2000, 3000, 4000, 6000, and 8000 Hz and at the frequency of the tinnitus pitch match. The difference between the pure tone threshold and the loudness discomfort level is considered the dynamic range (DR).
For this study LDLs of 95 dB or greater at all frequencies are considered negative for hyperacusis.
Dynamic range was considered satisfactory or negative for hyperacusis if it was 60 dB or greater at all frequencies. Based on the results of this preliminary study, a methodology for hyperacusis assessment is proposed. A classification system exists for hearing loss 20 and a similar one for hyperacusis is suggested in Table 1.
Thirty (71%) of the 42 patients gave a self-report of hyperacusis while 12 (29%) denied any such complaint. The incidence of hyperacusis in individuals with tinnitus has been reported as high as 40-45%.1,2 The type and severity of the tinnitus from which this figure was derived have not been specified. The LDL test indicates a higher incidence of hyperacusis than the self-report by the patient. In addition, chi square tests indicated significant associations between self report of hyperacusis and an LDL of 90dB for at least one frequency in both ears.
For the criterion of 90dB at two or more frequencies, only the right ear showed a significant association with hyperacusis self report. Jastreboff considers hyperacusis as a pre-tinnitus state.7 However, there are many tinnitus patients who do not report hyperacusis and who exhibit a satisfactory dynamic range on test. If hyperacusis is a central phenomena, then the Feldmann masking curves may reflect this by classification as Type IV or Type V. If hyperacusis is a pre-tinnitus state, then all hyperacusic patients should develop tinnitus and all tinnitus patients should have hyperacusis.
The question which still remains unanswered is what is the significance of positive LDL and positive DR and the subjective difference.
As a loss of hearing does not reflect the severity of tinnitus, so the severity of hyperacusis does not reflect itself in loss of hearing, recruitment, or Feldmann Masking Curve type. Appreciation is extended to the Martha Entenmann Tinnitus Research Foundation and the Lionel Hampton Ear Research Foundation for its support of this effort.
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. Sudden sensorineural hearing loss (SSNHL) remains a controversial problem with respect to etiology and the factors that might predict prognosis. Although previous investigations have assessed the relation of individual factors to outcome, to our knowledge, few studies have used multivariate analysis to evaluate the contributions of multiple factors. The patients had consecutively received a diagnosis of SSNHL and had presented to Fukuoka University Hospital between January 1983 and December 2004.
We evaluated the prognosis for hearing recovery, which was the fixed hearing level, using the criteria established by the Sudden Deafness Research Committee (as described later). We performed logistical regression analyses with outcome as the dependent variable, assigning scores of 0 for no change, 1 for recovered, and 2 for cured. The outcome of SSNHL was cured in 64 ears (22%), recovered in 175 (59%), and no change in 57 (19%).
Logistical regression analysis provides a model for multivariate analyses that can examine at regular intervals the relation between several factors and disease (or all events) after adjusting for the influence of other factors. Time from onset of hearing loss to presentation also appears to be significant in prognosis. The severity of the initial hearing loss is used as an indication of more severe damage to the cochlea. We also saw no significant relation between outcome and therapy (steroids and satellite ganglion block). We presented a case series of 296 patients with SSNHL and used multiple logistical regression analysis to determine which factors are most strongly related to outcome. First, immediately after onset of disease, the patient should consult a physician as soon as possible for diagnosis and treatment.
You must have JavaScript enabled in your browser to utilize the functionality of this website. Hearing loss is a function of exposure time, the average sound level, and the peak level of very loud sounds. Tinnitus (ringing in the ears) and temporary hearing loss can occur from a single concert, sporting event or sudden loud noise like a firecracker.
It is important that hearing protection is carefully selected for each individual, based on the intensity level, duration, and type of noise exposure. Intense airborne ultrasound has been associated with hearing loss, tinnitus, and various nonauditory subjective effects, such as headaches, dizziness, and fullness in the ear. It has long been recognized that intense sound can distort vision and reduce visual acuity, presumably by overpressure of the lens [1-3].
The eye is a mechanical structure capable of sound excitation under certain conditions and constraints. The appreciation value of very-high-frequency music energy has triggered a provocative debate over the use of high digital sampling rates to capture such energy in recordings.
Five normal-hearing adults (ages 20-59 years) with no history of ocular, otic, or neural disease served as our subjects.
We determined the frequency response of the eye by driving sound through the head via transducers on the skin of the head and recording from the eye. In the next experiment, we applied airborne noise within the passband of the eye (25-60 kHz, as depicted in Fig. Broadband noise (5-70 kHz) delivered to the skull at the mastoid, occiput, or forehead excites vibration in the eye.
The predicted transmission loss was determined by the acoustic mismatch between the impedance of sound in air with that of sound in ocular tissues. We did not measure the TL from the transducer to the eye; however, the air between the transducer and the eye acts as a coupling medium, and the TL may be less than air to body by an estimated 7-17 dB (Table 1).
Finally, to demonstrate that the response recorded from the skin of the head represented the vibrations in the brain, we asked the subjects to perform a Valsalva maneuver, which increases cerebrospinal fluid [20]. Direct vibration of the brain can be communicated to the cochlea via intracranial fluid conduction [13,14], a pathway proposed by Ranke [11] more than 60 years ago and termed the third window by Tonndorf and Tabor [12]. It was von Gierke [23] who first proposed that audible subharmonics of ultrasound and the middle ear (air volume or ossicular displacement or both) were somehow involved in the response of workers to ultrasonic exposure.
Tinnitus has commonly been associated with intense airborne ultrasound exposure [4-6], but quantification details are lacking. Musical airborne energy beyond 22 kHz has been shown to alter the electroencephalogram and evoke physiological activity in the brainstem and thalamus but only when ultrasonic musical frequencies are combined with the musical spectrum below 22 kHz. The eye is an airborne ultrasonic window to the ear and, as such, extends the range of human hearing.
An intriguing concept in cortical audio processing is that some neurons with best frequencies and frequency responses in the mid-audio range may be activated by much higher frequencies [36].
An auditory cortical neuron's sharply tuned frequency response (inverted V shape) is depicted in Figure 5A. Nonlinear distortion produced anywhere in the bone conduction (BC) transmission path could demodulate the AM ultrasound to audible frequencies [37,38]. Propagating ultrasonic components of music toward the body induces brain and behavioral changes [7,8] but, when the body is sound-shielded, these changes are not observed [8].
Is there any evolutionary advantage in having an eye that responds to light and intense ultrasound? Personal headphones could be supplemented or replaced with bone conduction transducers, with frequency responses extending to at least 50 kHz. Musical harmonic information is coded by place on the basilar membrane and temporally in neural firing.
Eye conduction may contribute to industrial highfrequency loss and tinnitus because ultrasound and high audio frequencies overlap in terms of basilar membrane displacement patterns, especially if high audio subharmonics are generated by intense industrial devices. Partial support for this study was kindly provided by Northrop Grumman Newport News Inc., Newport News, Virginia.
Heidelberg Neuro-Music Therapy for chronic-tonal tinnitus - treatment outline and psychometric evaluation. But more than 80% of the music therapy patients (both ST and CT) revealed a reliable improvement ("responder") compared to 44% in the PT group. A number of potential working factors accounting for the treatment success are highlighted. The main reason seems to be the permanent awareness of the tinnitus and the diminished ability to habituate to the sounds4. According to these assumptions, the tinnitus sounds originate from lesions in the auditory pathways. Therefore the patients shall be enabled to actively control the sounds in order to reorganize the underlying neuronal mechanisms maintaining the tinnitus17. The overall therapeutic dose rate (500 minutes of therapy) was equal just as were the intervention modules (including the counseling). The aim is not to reproduce a psychometrical pitch-matched tone but rather a sound that is subjectively equivalent to the patients" "ear sounds". A systematic and targeted training of inaccurately intonated musical sounds enables the patients to exert influence on their auditory processes since they learn to actively filter out irrelevant information and to concentrate on relevant acoustic stimuli. By means of music as calming background stimulus, the balance between the activity of the sympathetic and the parasympathetic branches of the autonomic nervous system shall be restored. The volume is adapted to the individual hearing level compensating for a potential hearing deficit.
The therapy concept was announced by press releases (newspapers and magazines, radio and TV) and offered to patients at the outpatient department of the local ENT-clinic of the university hospital. The therapy was designed as group intervention with five weekly sessions a 90 minutes and an additional individual counselling (50 minutes) leading to therapy duration of 500 minutes equal to the music therapy intervention. The main outcome criteria were the absolute scores of the German version of the tinnitus questionnaire ("Tinnitus-Fragebogen", abbreviated "TQ") by Goebel and Hiller26 as well as the relative decrease in TQ scores. They had to answer three specific questions a) "Was your tinnitus percept changed by the music therapy?" (Answers: worsened - unaffected - improved) and b) "Which elements from therapy did you consider helpful?" (open question). In the logistic regression demographic, therapy and tinnitus related factors were entered in the model to define those factors that are associated with tinnitus and may therefore contribute to therapy success. Therefore there is an urge for a short term therapy with preferably minimal effort but long lasting effect.
In terms of treatment outcome this group was target underperforming since just less than half of the patients achieved the desired symptom reduction. At the core of the "Heidelberg Model of Neuro-Music Therapy", the patients are actively "confronted" with their individual tinnitus sounds and are told to deal with their tinnitus explicitly instead of trying to take no notice of the tinnitus.
These modules enhance the self-determination and the control beliefs of the patients since they learn techniques in order to actively influence their tinnitus. The patients possibly did not know the scientific label of the intervention thus the answers in the feedback-sheet were blurred because the patients could not label this intervention.
One specific of the "Heidelberg Model of Neuro-Music Therapy" is the establishment of a tinnitus-equivalent sound.
Many patients can voluntarily change the percept of their tinnitus by for example teeth clenching, pressure on the occiput, forehead, vertex and temples, head turning and shoulder abductions 36. Frequency discrimination training may interrupt the cortical representations that are generating tinnitus 42,43. This module increases the auditory filtering and supports a modified emotional processing of the tinnitus sound. The MTLS is suspected to be responsible for the establishment of a "tinnitus memory" similar to the pain memory.
Further studies are needed in order to evaluate which elements of the music therapy contribute most to the overall effect and to scrutinize the proposed working factors of the modules.
The treatment of tinnitus related psychological distress is part of the music therapy concept, though the duration is very short and music therapy presents a focal therapy and no in-depth psychotherapy will be possible. University Hospital for Ear, Nose, and Throat - University of Heidelberg - Heidelberg - Germany. Tinnitus outpatient department - German Center for Music Therapy Research - Heidelberg - Germany. Forty-two consecutive patients seen from January to August 1995 were reviewed for this preliminary report.
The incidence of hyperacusis in individuals with tinnitus has been reported as high as 40-45%.1,2 Clinical experience based on 4000 patients seen for the primary complaint of subjective idiopathic tinnitus (SIT) of the severe disabling type indicates that not every patient with tinnitus has hyperacusis and not every patient with hyperacusis has tinnitus. This paper is a preliminary report from the Tinnitus Center, HSCB-SUNY, ofhyperacusis in a patient population who request consultation for tinnitus of the severe disabling type.
The American Tinnitus Association defines hyperacusis as an unusual condition in which an individual's ears are unable to tolerate ordinary environmental sounds.
There is significant variability in the interpretation of test data recommended for its identification. The difference between the pure tone threshold and the LDL at the frequency being tested is the dynamic range (DR).
When thresholds are equal to or above 90 dB HL at 500 - 8000 Hz and 70 dB at 250 Hz they are considered as normal.
To the limits of neurotologic physical examination no positive findings were reported for any of the subjects.
In the questionnaire, the patient was asked whether they find loud sounds to be unpleasant both prior to or following the onset of tinnitus. Tympanometry and acoustic reflex thresholds were obtained for those individuals who could tolerate the procedures.
The patient was instructed to indicate when the sound delivered through the earphone from the audiometer became uncomfortable to the ear - not just loud, but uncomfortable.
Hyperacusis should be considered positive if the LDL is 90 dB or less at two or more frequencies or if the dynamic range is 55 dB or less at any frequency.


Hyperacusis should be considered negative when LDLs are 95 dB or greater at all frequencies and if the dynamic range is 60 dB or greater at all frequencies. If we use the criteria of 90 dB or less at any frequency the incidence is 86% for the right ear and 83% for the left ear. Additional numbers of patients are being evaluated to explore this finding and to examine its significance. Will these patients eventually develop an increasing sensitivity to sound i.e., hyperacusis?
This is important with respect to diagnostics and may explain why treatment results are positive with some hyperacusic patients and not with others.
There is a positive correlation between tinnitus and hyperacusis as well as a positive correlation between hyperacusis and the loudness discomfort level test.
Hyperacusis occurs with normal hearing as well as with hearing loss in individuals with tinnitus of the severe disabling type. A standardized new methodology for assessment of hyperacusis is recommended to include a battery of tests: Pure tone audiometry, LDLs, Feldmann Masking Curves, and the Metz test for recruitment. A classification system exists for hearing loss and a similar system for hyperacusis is suggested. Kotsanis C, Harjes C: Pilot study - effects of auditory enhancement training on speech, language, hyperacusis and behavior.
Iastreboff PI: Presentation Fifth International Tinnitus Seminar, Portland, Oregon, July 1995.
Feldmann H: Homolateral and contralateral masking of tinnitus by noise bands and by pure tones. 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. Prognosis for Sudden Sensorineural Hearing Loss: A Retrospective Study Using Logistical Regression Analysis. We used logistical regression analysis to determine which factors are most strongly related to outcome for patients with SSNHL. When more than one factor may affect outcome, multivariate analyses, which can adjust for the effects of other factors, are necessary. SSNHL was diagnosed strictly according to criteria established by Japan's Sudden Deafness Research Committee (Table 1). We also performed analyses for those in the no-change and recovered groups alone and for those in the no-change and cured groups alone.
In patients in the no-change and cured groups, hearing levels at 2 and 4 kHz were significantly related to the outcome.
When more than one factor might affect outcome, multivariate analyses, which can adjust for the effects of other factors, are necessary [4].
A long interval before the presentation and advanced age were associated with lower rates of recovery and cure (full recovery). Most studies have demonstrated that presentation after 7-10 days results in a poor outcome [2,3]. This does not indicate that the outcome would have been the same without treatment, because virtually all patients in this series received some drug therapy. The only treatment that has proven more effective than placebo is the early application of steroids. We found the prognosis for SSNHL to be better in patients who present early and young and who have mild hearing loss and to be worse in those with vertigo.
Then, predicting good prognosis in younger patients with mild hearing loss and no vestibular symptom is possible. Exposure to excessive noise from industrial machinery, heavy construction equipment and vehicles, power tools, aircraft, gunfire, motorcycle and auto race tracks, dental drills, sporting events, fireworks, rock concerts, marching bands, and music from a player's own instrument or nearby instruments can cause hearing loss depending on the intensity and duration of the noise. Shipbuilders, flight crew who stand behind jet aircraft on the flight deck, and army tank operators usually fall in this category. According to the OSHA standard, a person can be exposed to a 95 dB environment for 4 hours before risking hearing damage.
Eyes as Fenestrations to the Ears: A Novel Mechanism for High-Frequency and Ultrasonic Hearing. Yet, when people detect ultrasonic components in music, ultrasound adds to the pleasantness of the perception and evokes changes in the brain as measured in electroencephalograms, behavior, and imaging.
Eye conduction of airborne sound could explain hearing loss and tinnitus in young workers exposed to intense ultrasound (typically cleaners) [4-6] and could explain the perplexing phenomenon that ultrasonic energy influences judgments of music quality and induces changes in electroencephalographic and positron emission tomographic examinations [7,8]. Conventional wisdom [9] since the 1930s has been that high-frequency energy to only 14 kHz was needed to recreate music faithfully. Many instruments produce energy well beyond 20,000 Hz at high levels [10]; even the human voice is capable of ultrasonic output if sufficient vocal effort is mustered (personal observation, 1990). The endolymphatic and cochlear aqueducts (or, frankly, any vascular connection to the cochlea) could act as acoustic fluid pathways, much as the oval or round windows act as aerial pathways.
The eye is a fluid globe that will offer an impedance mismatch to sound in air, much like that of an ear with a fluid-filled middle-ear space. Specifically filtered white noise (10-100,000 Hz) was applied through a custom-designed aluminum ceramic transducer placed on the skin of the head (mastoid, occiput, and forehead).
1B) as sound anterior to the center of the globe and recorded the response from the skull in one subject. The ultrasonic beam was directed at the forehead or into the ear canal as an additional control.
Specifically, acoustic impedance (Z) is the product of density, expressed in kilograms per cubic meter, and ultrasonic velocity, expressed in expressed in meters per second.
The head is driven with filtered white noise with a 2- to 50-kHz passband; eyelid recordings are obtained from piezoelectric film sensors as before. Frequency response of two subjects with increased cerebrospinal fluid pressure after performance of a Valsalva maneuver. Thus, transmission of airborne ultrasonic frequencies through the eye to the ear via intracranial fluid conduction helps to explain two mysteries in the human extended range of hearing. Displacement of the round and oval windows as release mechanisms for eye-induced brain vibration could certainly interact with the ossicular chain, producing a detectable audio component. Prevention of hearing loss and tinnitus involves remaining uncoupled from ultrasonic vibrations. The effect is based on the combination of two coherent acoustic routes, one conventional and one solely ultrasonic [7,8]. Personal headphones could be supplemented or replaced with bone conduction transducers with frequency responses > 50 kHz.
The mechanics of ocularly transmitted ultrasound should be similar in all other respects to ultrasound delivered to the skin of the head or neck as vibration [15], with the eventual activation of the auditory cortex in normalhearing and deaf individuals [31,32]. Specifically, amplitude modulation (AM) outside of a neuron's response can be sufficient for activation.
Consistent with the current finding is that the eye is the input window into the ear for high-frequency airborne sound and music. A considerable body of literature reports on sound-vision interactions in humans with forward-facing eyes [40, 41].
The frequency response is in the low ultrasonic range, and this type of hearing is termed eye conduction. Such transducers are already in use for medical treatment of tinnitus and can be readily modified for personal musical use (see Fig. Ultrasound might contribute to the musical harmonic structure and provide more high-frequency treble emphasis in instruments, such as the cymbals, triangles, trumpets, violins, and oboes. Tinnitus distress was assessed using the German version of the Tinnitus-Questionnaire (TQ) at admission, at discharge and six months after therapy. Therapy impact seems to be lasting since TQ scores remained stable until follow-up at six months.
For that reason the predominant wish of the patients is to get rid of the "annoying" and "intrusive" sounds5 and to regain confidence in their sense of hearing. Usually these sounds should be blocked off by feedback connections from limbic regions before reaching the auditory cortex. Musically based interventions11,12,13 also have proven to be highly effective in treating chronic tinnitus - possibly by correcting tinnitus evoking neuronal mechanisms14. If they could actively influence their tinnitus, their control beliefs will rise and thus let down the strains15. Purpose-built music therapeutic interventions were merged to modules and integrated into a standardized manual. During the interval between the sessions, the patients have to exercise themselves in Resonance Training for three minutes every hour. For this purpose, before the training session starts, the patients have to set the background music to a convenient level such that they can easily listen to the music while still being able to follow verbal instructions from the therapist. Only patients coming from the proximity of Heidelberg were allocated in a randomized way (computer generated) either to the ST group or the PT group. The regression analysis reveals a highly significant relationship between the tinnitus score and the independent variables (p 2= 0.43). The proposed therapy concept "Heidelberg Model of Neuro-Music Therapy" seems to be a potential completion of the therapy spectrum. Given that this group received also placebo music therapeutic elements (active listening to preselected musical pieces) and an individual counseling, it seems reasonable to argue that the positive and long lasting effect of the music therapy according to the "Heidelberg Model of Neuro-Music Therapy" is due to the far more specific and active musical training aiming directly at the individual tinnitus sound. There exists a variety of procedures using a combination of counseling and acoustic stimulation. In doing so, the duration of the therapy does not exceed ten weeks (standard therapy) and can even be compacted to five days (compact therapy).
Many patients stated though that they would enjoy singing or listening to music subsequent to the therapy.
Levine 37 proposed interactions between auditory perception and somatosensory input at the dorsal cochlear nucleus. Experimental data indicate that it is more efficient to train at normal hearing frequencies rather than in the region of hearing loss or tinnitus frequency 44,45. Biocybernetics of attention in the tinnitus decompensation: An integrative multiscale modeling approach.
Development and psychometric adequacy of the screening version of the tinnitus handicap inventory. Final common pathway for tinnitus: theoretical and clinical implications of neuroanatomical substrates. Intensely pleasurable responses to music correlate with activity in brain regions implicated in reward and emotion. The rewards of music listening: response and physiological connectivity of the mesolimbic system. Auditive stimulation therapy as an intervention in subacute and chronic tinnitus: a prospective observational study. A multi-centre study on the long-term benefits of tinnitus management using Neuromonics Tinnitus Treatment. Listening to tailor-made notched music reduces tinnitus loudness and tinnitus-related auditory cortex activity. A cognitive model of tinnitus and hyperacusis; a clinical tool for patient information, appeasement and assessment. Musiktherapie bei Tinnitus: Interdisziplinare Pilotstudie zur Uberprufung des Heidelberger Modells.
Clinical significance: a statistical approach to defining meaningful change in psychotherapy research. Enriched acoustic environment after noise trauma reduces hearing loss and prevents cortical map reorganization. Treatment of tinnitus with a customized, dynamic acoustic neural stimulus: underlying principles and clinical efficacy. Cross-modal interactions of auditory and somatic inputs in the brainstem and midbrain and their imbalance in tinnitus and deafness. The effect of a new treatment based on somatosensory stimulation in a group of patients with somatically related tinnitus. Auditory discrimination training for tinnitus treatment: the effect of different paradigms. Auditory perceptual learning at normal hearing frequencies affects changes in tinnitus intrusiveness and percept.
Tinnitus suppression by low-rate electric stimulation and its electrophysiological mechanisms. Classical conditioning as the basis for the effective treatment of tinnitus-related distress. The dorsal cochlear nucleus as a participant in the auditory, attentional and emotional components of tinnitus. There is an absence of attempting to identify types of hyperacusis and few attempts to establish its clinical significance.
Criteria for normal hearing were strict and for the purposes of this study normal hearing was considered to be thresholds of 25 dB or better at all frequencies. What are the results of long term follow-up of tinnitus of patients who were negative by self-report for hyperacusis but demonstrate positive LDL and positive DR?
In: Tinnitus 91, Proceedings of the Fourth International Tinnitus Seminar, Edited by JM Aran and R.
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. Logistical regression analysis provides a model for multivariate analyses that can examine at regular intervals the relation between several factors and disease (or all events) after adjusting for the influence of other factors [4]. Improvement of 10 dB HL or more (mean hearing level at five frequencies) was evaluated as recovered (partial recovery).
The odds ratio expresses the degree of change in odds associated with a 1-unit change in an explanatory variable. A longer period until presentation, subjective vestibular symptom, advanced age, and profound hearing loss were associated with lower rates of cure. Profound hearing loss at 2 kHz and mild hearing loss at 4 kHz were associated with high rates of cure. Furthermore, subjective vestibular symptoms and profound hearing loss were associated with lower rates of cure.
Some have proposed that this is owing to a self-selection process, whereby those who recover quickly do not seek medical care. None of the therapeutic options has established itself as fully effective in SSNHL, even if some studies found vasodilators, anticoagulants, plasma expanders, and steroids beneficial [1]. Cochlear damage seemed to be limited by the antiinflammatory properties of the steroids [1]. The efficacy of steroids in the treatment of idiopathic sudden hearing loss: A double blind clinical study. Diagnosis and treatment of sudden-onset sensorineural hearing loss: A study of 51 patients. Such individuals can't get enough attenuation for proper protection even with plugs and earmuffs combined. Even if a temporary hearing loss recovers over a period of hours to days, there is a risk that repeated exposure to loud noise will result in permanent hearing loss.
How does the airborne ultrasound get into the ear to create such polaropposite human effects? Further, it is well documented that acoustic energy, including ultrasound, can pass into the eye [3]. Further electroencephalographic and positron emission tomographic changes were documented when frequencies beyond 22 kHz were presented along with conventional audio frequencies [7,8] to human listeners. These fluid pathways were termed the third window of Ranke by Tonndorf and Tabor [12], who later demonstrated cochlear function after sealing both the round and oval windows; thus, for the basilar membrane to be displaced, some compliant window is necessary.
Hearing with a fluidfilled middle ear is not only possible but the degree of loss is small (on the order of 30 dB). We established stimulating parameters and recording techniques over a 2-year period using six additional subjects. We measured the input to the head with a Buel and Kjaer (B&K) high-frequency accelerometer placed on the transducer while mass-loaded to the head. We modified the same type of transducer that delivered contact sound to the skull to produce a narrow beam of airborne ultrasound by fabricating a foam gasket with a 2-mm aperture. When that band of noise was presented as an airborne sound directed at the eye, we measured vibration of the brain and skull at the mastoid, occiput, and forehead in the same frequency range of 25-60 kHz. There is considerable acoustical similarity among the soft tissues suggesting little impedance mismatches contributing to transmission loss. Data in Figure 2 would predict little attenuation for sound passing from the eye to the brain in regard to changes in substrate density; only distance would determine transmission loss. It is argued that an increase in cerebrospinal fluid will damp the vibration in the brain while not substantially altering the spectrum. Increased cerebrospinal fluid increases the damping in the brain, which would lower the intensity of the spectrum recorded from both skull and brain. A number of authors [4-6] have documented harmful, intense airborne ultrasound effects on people.
Such a middle ear-induced audio component would "sound" like a demodulation and could be misinterpreted as demodulation of the primary tone.
Each signal stimulates a separate area on the basilar membrane that would be integrated into a whole as any conventional complex auditory pattern.
Such transducers are already in use for medical treatment of tinnitus [29,30] and can be readily modified for personal musical use (Fig.
If ultrasound is demodulated in the brain [15], the ear would be stimulated at or near brain resonance (14-15 kHz); thus, the auditory cortex that codes high audio frequencies will be involved.


Because ultrasound is coded as high-frequency sound, there is no reason to believe that this is not a potential mechanism. Stimulation of high frequencies outside the frequency response has been shown to cause some neurons to fire. Ultrasonic skull vibration does vary from individual to individual on the basis of geometries [26], but this does not necessarily imply nonlinearities. There is no need to postulate an additional unknown somatosensory route to the ears [8]; nonetheless, the concept of multisensory coding in music perception is intriguing.
Evaluation of acoustic wave propagation velocities in the ocular lens and vitreous tissues of pigs, dogs, and rabbits.
The role of biological system other than auditory air-conduction in the emergence of the hypersonic effect. Ultra-highfrequency acoustic stimulation and tinnitus control: A positron emission tomography study. Auditory cortical responses to amplitude modulations with spectra above frequency receptive fields: Evidence for wide spectral integration. The western heptatonic musical tonality forms the basis of the active music therapy procedures.
The most common side effects are headache and laryngitis if the exercise is not executed properly, either too often, too long or with too much pressure. Group differences of sociodemographic data and audiometric tinnitus characteristics were analyzed with the c2-test or univariate analysis of variance (ANOVA).
About 80% of the patients accomplished a reliable decrease of tinnitus pathology in the course of music therapy and about two thirds of the patients describe their tinnitus symptoms as "improved" after therapy.
Often the musical stimuli are spectrally modulated in order to account for hearing impairments31,32 and are incorporated as a passive means patients have to listen to for rather lengthy intervals (months up to years).
The main parts of the therapy consist of active music therapy modules; hence there is no need and no purpose for spectrally changing the music used. We therefore propose that it is possible to alter the internal tinnitus spectrum by means of the Neuroauditive Cortex Training, which represents a specific perceptual training within the normal hearing frequencies. RF neurons coordinate sensory and motor functions and influence cortical activity via the thalamus. This led us to explore whether or not there was any correlation or statistical verification between the two phenomena. If the acoustic reflex level is less than 60 dB above threshold of hearing at a given frequency recruitment is considered positive. If we use the criteria of 90 dB or less at two or more frequencies, the incidence is 83% for the right ear and 79% for the left ear. It may be that the non-self-report patients who qualify according to the 90 dB criteria are at risk of hyperacusis, despite the fact that they do not report any symptoms of it. Will medical or audiologic intervention prevent them from becoming hyperacusic and, if so, what modalities are to be considered? 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. Many hypotheses have been advanced to explain its etiology: vascular diseases, viral inflammation, trauma, or other lesions.
We used multiple logistical regression analysis to determine which factors are most strongly related to outcome in patients with SSNHL.
On presentation, all patients underwent otorhinological examinations and were confirmed to be free of ear disease, such as otitis media. Age, number of days until presentation, and mean hearing level were handled as continuous variables.
Our observation that age is a significant prognosticator differs with that of Moskowitz et al. Up-sloping audiograms have been reported to have a better prognosis for recovery [1,3,6,8].
However, physicians must discuss with their patients the etiology and treatment options and jointly determine a treatment plan.
But, many industrial workers can be adequately protected with as little as 10 dB of attenuation: the majority of eight-hour equivalent noise exposures fall between 85 and 95 dB. NIOSH values are more conservative.For maximum protection, foam earplugs, muffs or other hearing protection devices are recommended. Surprisingly, ultrasound passes first through the eyes; thus, the eye becomes but another window into the inner ear.
What has not been examined in any of these studies is the possibility that the acoustic energy that passes through the eye may also serve as a source of auditory perception.
No ultrasonic route to the ear was proposed in these studies, but certainly possible is that the ultrasonic energy in music-and for that matter, industrial noise-could pass through the eye and be detected by the ear. More recently, it has been shown that direct vibration of the brain [13,14] could elicit evoked responses from the auditory nerve, confirming that a brain can be a passive "fluid" conductor of sound, even an amplifier near resonance [15] and, at the same time, a physiological responder to the sound propagated through it. After the impedance mismatch is overcome with sufficient energy, is the eye, like the fluid-filled middle ear, capable of transmitting the absorbed sound to the brain?
High-frequency stimulating transducers were custom-made ceramic aluminum bimorphs attached with tape to the skin of the skull. The assumption is that the eye dimensions are small in regard to the near field, and so scattering within the eye may not be anticipated. Air coupling to the eye might reduce the transmission loss to about 33 dB, whereas skin-brain-skull transmission loss might be as high as 50 dB (depending on frequency).
Thus, the energy leaving the eye should be more intense at the forehead than at the mastoid, correcting for impedance changes from fluid to bone. There are, nonetheless, airborne sources as intrusion alarms, which do not have audible subharmonics that can induce audible and subjective effects.
This personal protection should provide ample safety; nonetheless, the current Occupational Safety and Health Administration regulations [25] regarding hearing safety in airborne ultrasound should be reviewed.
A case is made here for a separate airborne ultrasonic input, but the final pathway is the same because ultrasound activates the auditory cortex in normal-hearing and deaf listeners. If the ultrasound acts directly on the base of the cochlea, just the tip of the basilar membrane would be stimulated [33], also resulting in high-frequency area activation of the auditory cortex [31]. Assuming the music scenario, conventional audio and ultrasound may drive some units, supporting the perception that ultrasonic components of music are important for apprehension. The stimulation in this case is in a form of AM that is a process in which one sound is multiplied by another.
The hair cells could act as a demodulator, but the most likely demodulator is the brain itself [15]. An auditory cue can trigger a visual shift in attention, and a louder cue is more effective than a softer one. Mutual stimulation via both the thalamic and paralimbic pathways ultimately lead to tonotopic changes in the auditory cortex7 while reciprocal innervations of the medial temporal lobe system give rise to memory consolidation leading to a paradoxical "tinnitus memory"6. Therefore the Neuro-Music Therapy is indicated only if the patients indentify their tinnitus as "tonal" (sinus tones). Any psychiatric disorder or ongoing medication with antidepressants or antipsychotic drugs yields to exclusion of the patients. Selection of the musical pieces was based on the individual musical taste and preferences as well as on the emotion evoking impact of the musical pieces.
Therapy outcome as assessed by the TQ and the CPT were evaluated using univariate analysis of variance (ANOVA) for repeated measure procedures. This effect was independent of the patient"s treatment allocation to standard therapy or compact therapy. Additionally, a tinnitus-equivalent sound provides the possibility to deal with the symptoms in an immediate and direct way. Therefore an activation of cranio-cervical and cranio-facial muscles and nerves by means of the Resonance Training might correct the auditory pathway by means of indirect stimulation of the joint "relay-station" cochlear nucleus 36.
Furthermore it is very important to ensure the training regime is intrinsically motivating. Stress is considered to potentiate the severity of tinnitus due to the proposed accompanying reduction and alteration in auditory masking 6. The present method of assessment and a classification system for hyperacusis will be presented. In no case of self-report of hyperacusis (N=30), did both the LDL and DR indicate negative results. There was an incidence of 34%, Type IV curves, considered clinically to represent central problems.
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. The outcome of SSNHL was cured (full recovery) in 64, recovered (partial recovery) in 175, and no change in 57.
The strength of this study was its use of relatively rigorous diagnostic procedures, reasonable case representation, and the large number of consecutive patients (suggesting that the reported associations might not be chance findings). The correlation between high-tone SSNHL and poor prognosis was presented in a study by Linssen and Schultz-Coulon [9]. Further, could airborne ultrasonic energy entering the eye secondarily induce tinnitus and hearing loss?
Is the eye pathway the reason that live music sounds better than recordings or the reason why ultrasonic instruments can cause hearing loss and tinnitus?
To record the sound spectra from the eye, we taped a piezoelectric film sensor, constructed of a piezoelectric polymer polyvinylidene fluoride [16], over the closed eyelid, being careful not to make contact with the orbit, to detect the frequency response of the globe to white noise propagating around the skull and through the brain. The effective band of eye frequency response is from 25 to approximately 60 kHz (double-headed arrow).
Tactile responses to airborne ultrasound have been reported in the oral and nasal cavities if the mouth is open, likely owing to a standing wave phenomenon [4] that directly stimulates epithelial cilia.
Placing the aluminum transducer on the skin results in a TC of 0.3 and a transmission difference of 10 dB. The predicted difference was 10 dB (see Table 1); the measured difference was 6 dB, given the short distance along the skull.
The damped tracing during the Valsalva maneuver (solid line) is some 5 dB lower in intensity in both subjects; the variability between subjects is also evident, yet consistent with the concept of the eye as an acoustic sensor for ultrasound. In a related report, swimming into a 50-kHz beam produced an audible perception, and merely immersing the jaw into water with a 50-kHz beam present produced a lower sensation [24]. Certainly our study sets forth a method of quantifying the transmission of airborne ultrasound into brain vibrations. Simply put, three tones beyond the frequency range of some auditory cortical neuron will cause it to fire. As mentioned earlier, the ossicles can be displaced by the oval-window movement with brain vibration, resulting in an audible tone near middle-ear resonance of 3 kHz, which is not primary demodulation of the ultrasound [23]. Abrupt onset of sound can improve the detection of a subsequent flash, the opposite of masking [42]. According to the results from the regression analysis, there was - apart from tinnitus masking level - no influence of tinnitus characteristics or otological co-symptoms on therapy success.
A deliberate regulation of emotional responses towards the tinnitus sounds might enhance gate control mechanisms and restore misdirected "filter functions" of thalamic and limbic areas.
This correlation may support the concept of different types of hyperacusis and could explain why some individuals respond to treatment and others do not. Of the nine who did not report hyperacusis, only two were substantiated by test results while the other seven had one or both tests positive. 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.
We performed separate analyses on those in the no-change and partial-recovery groups and on those in the no-change and fullrecovery groups. The lack of understanding of the etiological mechanism of SSNHL has rendered the development of a specific treatment very difficult and, currently, empirical therapies are used.
A longer period until presentation and advanced age were associated with lower rates of recovery.
The correlation between high-tone hearing loss and vertigo was explained by the anatomical proximity of the basal turn of the cochlea and vestibule.
To prove a treatment is effective, a statistical analysis in a randomized double-blind study must be used. These persons risk hearing damage, but have compromised so they have auditory awareness of sounds around them. We also mounted calibration accelerometers either to the transducer sensors or to the skin of the skull for mass-loaded measurements.
The piezoelectric film transducer acted as a sensor for calibration trials but was removed during measurements of ocular transmission. The propagation speeds and densities of the relative tissues for this study are depicted in Figure 2. Skull-to-skull measurements are wider in frequency response, with a peak at approximately 15 kHz, presumably reflecting brain resonance as well as less attenuation. The brain, skull, and eye are coupled acoustically; with the skull essentially rigid, the compression of the brain against the skull is the source of change in Figure 3. A parsimonious explanation (not suggested by the authors) is that the eyes were responsive for the lowered threshold of ultrasound detection when the head is submerged by providing an efficient route to the ear via the brain, as the acoustic impedance of the eye and seawater are very similar (see Table 1).
Though no acoustic standards have been promulgated for measuring ultrasonic sound in human bone or fluid, guidance is available [26,27]. Very-high-frequency recordings (6-21 kHz) have activated the thalamus and other regions in the brain [28] in patients who have high-frequency tinnitus; thus, the thalamus plays a role in high-frequency and ultrasonic hearing. The cilia of hair cells in the base of the basilar membrane are very short (5-10 ยต), are immersed in fluid, and resonate in the ultrasonic frequencies. The product of the multiplication is the carrier, the carrier plus the modulator (C + M), and the carrier minus the modulator (C-M). Finally, a tactile response to airborne ultrasound has been reported in the oral and nasal cavities if the mouth is open, likely owing to standing wave phenomena [4]. So it appears that intense high frequencies that pass through the eye window as opposed to just surpassing the impedance barrier to the body [43] might indeed lead to multisensory coordination and, hence, survivability for humans, but there is a limit [24] that, if exceeded, may result in hearing loss and tinnitus. If one accepts the thought for discussion that tinnitus is a pre-condition for hyperacusis, does this not suggest that there are different types of hyperacusis reflecting a difference in clinical types of tinnitus with the same or different site(s) of lesion?
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.
Two hundred and nine patients were admitted to the hospital for treatment, and 87 received treatment on an outpatient basis. We tested statistical significance with the Wald chi-square test (two-sided), and we estimated odds ratio and 95% confidence interval by logistical regression. According to several reports, advanced age, hypertension, diabetes, and hyperlipidemia are poor prognostic factors, suggesting that microvascular dysfunction in the cochlea gives rise to poor outcome [1,7].
Cochlear lesions may cause vestibular damage by endolymphatic alterations via ductus reunions. In effect, the conservative estimate of 20 kHz as the upper range of hearing has resulted in a too-slow digital sampling to support high fidelity without distortions. We found the frequency transfer from the brain to the eye to be in the passband from 25 to 60 kHz. The film has the acoustic impedance of water and a flat frequency response in the range of interest, allowing relative monitoring of the peak SPL. The Valsalva maneuver supports the interpretation that the eye data reflect the acoustic properties of the brain-skull. An aftereffect of listening to the intense water-coupled tone was persistent tinnitus [24]. The lack of a mechanism for airborne sound to act on the ear directly has, no doubt, influenced the lack of research.
Musical instruments that have high-frequency and ultrasonic components are, for the most part, percussive; thus, the high audio and ultrasonic spectra would complement conventional audio frequencies consistent with the findings that the full spectrum is a better activator of the auditory system than is the ultrasound alone [7,8]. Cilia directly driven by ultrasound have been proposed as another possible mechanism in humans [34], and the concept was demonstrated in isolated turtle hair cells [35]. 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 the first analysis, for patients in the no-change and recovered groups, the factors most strongly related to outcome were the number of days until presentation and age. The lack of a universally accepted definition for SSNHL and for its recovery limits the ability to compare and evaluate the treatment protocols. If frequencies higher than 20 kHz are audible or useful, clearly sampling at 96 kHz is a necessity for true high fidelity. The threshold for hearing at 25 kHz is approximately 125 dB SPL [17], and the present stimulus was inaudible, but the induced head vibration was recordable. Animal studies are limited in that the ratio of surface area to mass is small and that fur readily absorbs ultrasound.
Ultrasound may contribute to pitch perception by extending the spectrum upward in frequency and by enhancing temporal cues. All methods would result in ultrasound's having a high pitch, as documented by studies over the last 60 years [15]. AM stimulation may not be necessary to obtain this effect; it was merely the mode of stimulation in our study. Nevertheless, the relative reduction and the individual improvement (reliable change index) were independent from the basic TQ-value - therefore also patients with comparatively lower strains still benefit from the therapy in equal measure. Is hyperacusis a unitary symptom or are there different types of hyperacusis as there are different types of tinnitus? Of the 12 individuals not complaining of hyperacusis, four had LDLs and DRs substantiating the absence of hyperacusis.
This suggests that hyperacusis may be present in individuals with tinnitus before they become symptomatic.
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]. The second analysis, for the nochange and cured groups, revealed that the number of days until presentation, vestibular symptom, age, and initial mean hearing level were most strongly related to outcome.
In previous reports, the prognosis of SSNHL was affected by various factors, such as age, the number of days from onset until presentation, initial hearing level, the method used for treatment, and the presence of vestibular symptoms and the like [1-3].
The transmission loss (TL) from bone to brain or eye is predictable on the basis of the acoustic properties related to tissue density and propagation speed [18]. A simple test of the eye window's role in concert music would be to assess music quality with and without goggles.
Musical harmonic information is coded by place both on the basilar membrane and temporally in neural firing. The value of this test would be to identify such individuals and provide treatment before they become symptomatic for hyperacusis. 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.
Goggles, as used as a control in this study, eliminated the eye window for airborne ultrasound. Ultrasound might contribute to the musical harmonic structure but may just provide more high-frequency energy to emphasize the treble in such instruments as the cymbals, triangles, trumpets, violins, and oboes (see Fig. 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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