Tinnitus and normal hearing a study on the transient otoacoustic emissions suppression,sensorineural hearing loss recovery 0810,tenis nike air antigo,noise in ears when blowing nose vertigo - How to DIY

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The aim of this study was to investigate the possible role of cochlear outer hair cell function with TEOAE and DPOAE tests in patients with normal hearing and tinnitus.
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Introduction: Tinnitus, the perception of the sound in the absence of an external acoustic source, disrupts the daily life 1 out of every 200 adults, yet its physiological basis remains largely a mystery. How to cite this article Gentil F, Meireles S, Roza T, Santos C, Parente M, Almeida E, Natal R, et al. INTRODUCTION: Tinnitus is an auditory sensation whose source comes from external stimulus to the body. OBJECTIVE: This study investigates the cochlear function in patients with tinnitus, using Distortion Products Otoacoustic Emissions (DPOAE). MATERIAL AND METHODS: Ears where the subjects referred to feel the tinnitus were considered for the study group while other ears without this sensation of tinnitus acted as a control group. RESULTS AND CONCLUSIONS: Where comparing the control and study group, the highest percentage of cases of DPOAE detected was in the control group, although these differences were not statistically significant. Against some assumptions that an increase in the firing rate of primary auditory nerve fibers produced by hyperactivity of hair cells inside the cochlea will lead to tinnitus, a decreasehas been noted in the otoacoustic emissions (OAE), rather than the increase expected if the above theory were correct2. Recent developments in the cochlear mechanical process research suggests that one origin of tinnitus could be associated to cochlear mechanical tasks. The assumption that a healthy cochlea may shows low intensity tonal or narrow-band sound when there are not acoustic stimulus was introduced by Gold in 19486 who devised a mathematical model of active processes in which the cochlea not only received sounds but also generated acoustic energy. There are different kind of optoacoustic emissions: spontaneous otoacoustic emissions (SOAE), transiently evoked otoacoustic emissions (TEOAE), which is the response to a given auditory stimuli, and distortion product otoacoustic emissions (DPOAE). There are several risk factors for tinnitus identified in the biomedical literature, such as age, drugs or medication, frequent loud noise exposure, otologic diseases such as otosclerosis, otitis media, presbycusis, sudden deafness, Meniere's disease, and acoustic schwannoma or even associated with hypo or hyperthyroidism, cardiovascular and cerebrovascular disease and lifestyle or behavioral factors such as cigarette smoking and alcohol consumption10. The study shows a statistically significant heritability for tinnitus in a sample of 544 monozygotic and same-sex dizygotic elderly female twins who contributed to the fourth wave of the Longitudinal Study of Aging Danish Twins11. As tinnitus can be associated with hearing loss12, the present study was based on the hypothesis that tinnitus without hearing loss or associated with mild hearing loss, can be caused by abnormalities of the central and subcortical level, along with changes in OHC function.
Fifty patients with normal hearing sensitivity or mild hearing loss referring the sensation in the ear of unilateral or bilateral tinnitus were recruited for this study. Patients were questioned in order to obtain relevant information about their clinical history. Audiological assessment was conducted using the Midimate 622 - Clinical Diagnostic Audiometer (Madsen, Denmark). DPOAE were measured using the DP-gram Procedure, in response to pure tones of levels (L1 = 65 dB SPL, L2 = 55dB SPL) in the frequency range 500-8000 Hz using a Capella Cochlear Emission Analyzer (Madsen, Denmark).
Distribution of the perceived tinnitus frequencies in the 66 ears of the study group, obtained from pitch-matching, was also calculated which can be seen in the Figure 1. The most common observed frequency of tinnitus was clearly 8 kHz, reaching 50% of all tinnitus ears. The analysis of DPOAE assessments (Figure 2) showed that it is in the control group (ears without sensation of tinnitus) that the higher percentage of cases where DPOAE were detected for all test frequencies was obtained. Based on Table 2, we are able to say that the p value is higher than 0.05 for all frequencies, with exception of 3 kHz. Therefore, it is important to check what happens when the analyzed frequency is the same as the tinnitus frequency. The chi-square for independence test to test H0, which states that the undetected DPOAE is independent of tinnitus, was used. The theory of tinnitus centred on neurophysiology propose that all auditory systems, and some no auditory systems particularly the limbic system (involved in emotion), and the autonomic nervous system, which controls all body functions, are an essential part of the most cases of tinnitus.
Jastreboff 1 considered that tinnitus frequently starts in the cochlea and then the abnormal activity is generated in the central pathways that prolong the symptoms. The present study intends to test if the cochlear dysfunction has been implicated in tinnitus generation.
Relating the tinnitus prevalence with age and using 1990 Hearing Supplement data, Ries17 reported that from the 15 million adults with bothersome tinnitus, about 27 % have more than 65 years old.
In the same way, DPOAE amplitudes have been found to be larger in younger subjects and in women than in men18. Based on previous reports and in accordance with the results found in the present study, we can say that whatever the etiology, at the same levels of hearing thresholds, DPOAE seems to be lower when chronic tinnitus is present22-26. Shiomi et al.25 studied cochlear activity in 9 tinnitus patients who had normal hearing and 55 who had also hearing impairment, and compared both groups to a control one with 26 normal-hearing individuals without any symptoms of tinnitus. Dall'Igna et al.27 investigated about the OAE in patients with symptoms of tinnitus and normal hearing. Granjeiro et al.30 tested the hypothesis that tinnitus begins with OHC dysfunction by recording DPOAE in 32 tinnitus patients with normal hearing and 37 patients without tinnitus but similar thresholds. Figure 1 of the present study shows that a higher incidence of tinnitus was found for a frequency range between 4 and 8 kHz, reaching an incidence of 83% of all ears analyzed. The presence of tinnitus, with or even without hearing loss, has also been shown to alter DPOAE9.
Until now, a few studies have investigated DPOAE by including tinnitus patients with normal audiometric thresholds9,22,29,30-32.
Quite different results were found by Gouveris et al.33 who compared the cochlear OHC function by DPOAE-grams of 32 ears with acute tonal tinnitus and normal hearing or minimal hearing loss with 17 healthy nontinnitus ears.
Based on that, they suggested that a cochlear lesion results in a decreased activity of the OHC. Sztuka et al.34 measured the features of DPOAE in a 44 tinnitus patients group without hearing loss and compared to 33 individuals without tinnitus and normal hearing sensibility (control group).
Differently from what happened in all the surveys listed above, Singh et al.35 who studied 25 normal-hearing patients with tinnitus and 20 patients with normal hearing and no tinnitus. Paglialonga et al.32 studied the probable role played by both OHC and cochlear efferent system functionality in tinnitus ears with normal hearing.
Although others reason than tinnitus could be possibly involved in the reduced DPOAE, different results seems to be found in the present study, since no significant differences were found between tinnitus ears and nontinnitus ears at all test frequencies when DPOAEs were compared between the two groups at each frequency independently of the tinnitus frequency (Table 2).
This study has shown that DPOAE has a potential value in the assessment of tinnitus, providing information on the structural integrity of the cochlea, especially OHC functioning. Paper submitted to the RBCMS-SGP (Publishing Management System) on October 3, 2015; and accepted on November 11, 2015. Mariana Lopes Favero*, Jihane Romanos**, Regina Celia Mingroni-Netto***, Clay Rienzo Balieiro****, Talita Sunaitis Donini*****, Mauro Spinelli******. Introduction: Auditory neuropathy is due to a disorder of inner hair cells or of auditory nerve function and can be associated with a number of etiological factors, including mutations in the OTOF gene encoding otoferlin, that acts in IHC synaptic vesicle fusion.
Objective: To describe our first auditory neuropathy case due to a gene OTOF mutation, discussing the clinical implication of this diagnostic. Case report: Female child with auditory neuropathy diagnosis due to otoacoustic emissions and cochlear microphonics normal records and absence of neural auditory function was submitted to a genetic study which evidenced a 1552-1567del116 mutation in the 15 exon of the OTOF gene. Conclusions: In spite of technical difficulties to detection of the OTOF gene mutation, this diagnosis leads to important discussion about the early diagnostic methods of auditory neuropathy and therapeutic options. INTRODUCTIONHearing neuropathy is due to an alteration on hearing stimulus transport by any lesions of internal ciliated cells of the hearing nerve or synapsis in them (1).These patients clinically present pre or post-lingual hearing loss, from the most different levels up to complete deafness, and they are normally distinguished as incompatible hearing with tonal threshold.
INTRODUCTION: The general consensus on the roles of hearing loss in triggering tinnitus seems not applicable in patients with normal hearing thresholds. OBJECTIVE: To scrutinize auditory functioning in a sample of tinnitus subjects with normal hearing thresholds and non-tinnitus normally hearing control participants using transient evoked and distortion product otoacoustic emission (TEOAE and DPOAE) and Threshold Equalising Noise (TEN) test.
METHODS: Twenty-seven tinnitus adult patients with normal hearing thresholds and 27 normally hearing volunteers were tested with TEOAE, DPOAE and TEN test.
CONCLUSION: These results suggest the possible existence of subtle auditory deficit in normally hearing tinnitus patients, which may be an early sign of diseases that are only diagnosed after the onset of hearing loss. Keywords: coustic neuroma, otoacoustic emissions, tinnitus, threshold equalising noise test. Tinnitus is defined as the perception of sound that results completely from activity within the nervous system without any corresponding mechanical, vibratory activity within the cochlea, and not related to external stimulation of any kind1.
An increasing amount of epidemiology studies provide both self-reported data on tinnitus and hearing status which allows closer examination on the relationship between tinnitus and hearing status. Although some studies have different theoretical assumptions and approaches, the significance of hearing loss in tinnitus generation is not questioned. Thus, several attempts have been made to explain pathophysiology mechanisms of tinnitus in patients with normal hearing ability particularly using otoacoustic emissions (OAEs). Several studies have revealed that TEOAEs and DPOAEs can be used as a tool to detect early hearing loss before it can be diagnosed by PTA13-15. The contradict findings from previous research motivates researchers to find alternative theories to explain tinnitus mechanisms in tinnitus patients with normal hearing thresholds. This study investigated 27 tinnitus subjects (42 tinnitus ears and 12 contralateral non-tinnitus ear) with normal hearing thresholds who were recruited from Welsh Hearing Institute, University Hospital of Wales. Full history taking and otoscopy examination were carried out at the beginning of the session. TEOAEs test was performed using unfiltered clicks of 80 µs duration presented in non-linear modes. The stimulus comprised of a pair of primary pure tones (f1 and f2) at a frequency ratio equal to 1.22.
The basic principle of this test is to control for "off-frequency listening" from occurring by using a broad band noise (the threshold equalising noise). This research has received the ethical approvals from the School of Applied Community and Health Studies (SACHS), University of Bristol Human Participants Ethics Committee and the South East Wales Research Ethics Committee. Initially, the left and right of DPOAE results were compared within the tinnitus and control groups. Then, the differences of overall mean DPOAE amplitude between tinnitus and control ear were compared. Various hypotheses have been put forward to explain tinnitus generation in normal hearing patients.
Decreased TEOAE amplitudes were observed in 35.7% of the tinnitus subjects with normal hearing sensitivity. A statistically significant increase in DPOAE amplitude was observed in tinnitus ears at f2 frequency of 1414 Hz. The fact that tinnitus patients with normal hearing have a significantly higher percentage of abnormal TEOAEs and a limited frequency of DPOAE than the controls may suggest that OHC dysfunction may be pivotal in tinnitus generation. In the current study, the percentage between abnormal TEOAE and DPOAE in both groups had no statistically significant difference. In the field of tinnitus, however, only two studies reported the application of TEN(HL) test in tinnitus patients with normal hearing24,25. Based on systematic review, no research on the application of TEN test in detecting acoustic neuroma has been published. No published data was found on the application of a TEN test in detecting acoustic neuroma. This study showed that subtle cochlear problem may exist in tinnitus patients before it is significantly appeared in the audiogram.
Thanks to University Hospital of Wales, UK for providing the facilities to conduct this research. This study was supported by the University of Bristol, UK and Ministry of Higher Education (MOHE) Malaysia and Universiti Kebangsaan Malaysia (UKM) as parts of the first author's PhD research.
Paper submitted to the ITJ-SGP (Publishing Management System) on February 17, 2014; and accepted on February 20, 2014.
You will receive an email whenever this article is corrected, updated, or cited in the literature. The generation of tinnitus is commonly linked with the impaired functioning of the outer hair cells (OHC) inside the cochlea.
Relation of distortion product otoacoustic emission and tinnitus in normal hearing patients: A pilot study. Impaired cochlear function correlates with the presence of tinnitus and its estimated spectral profile. Investigation of olivocochlear and middle ear muscle reflexes with contralateral suppression of DPOAEs in real time; [abstract]. Comparison of otoacoustic emissions in patients with tinnitus having normal hearing versus mild hearing loss.
Fifty subjects suffering from unilateral or bilateral tinnitus with normal hearing sensitivity or mild hearing loss were recruited. When the analyzed frequency is the same as the tinnitus frequency, the prevalence of detected DPOAE is in tinnitus ears (50.0 %).
The current definition of tinnitus is a perception of a sound in the absence of external stimulus. Damage to the outer hair cells (OHC) of the cochlea is believed to be one of the principal mechanisms of tinnitus1,3. However, it was only in 1977 that David Kemp documented OAE in a normal hearing subject that OAE measurement became possible7. The essential purpose of an OAE test is to verify cochlear status, mainly OHC functioning3.
The relationship between anxiety and depression and the risk of tinnitus has been reported as well. On the other hand, no significant heritability for tinnitus was found in the sample of 412 monozygotic and same-sex dizygotic elderly male twins in this Danish cohort; but the male sample shows that long-term exposure to occupational noise was the main risk factor for tinnitus11. Based on this test, only patients with normal hearing or with mild hearing loss were selected for this study. Normal hearing has an average smaller than 20 decibel hearing level (dB HL) and a mild hearing loss corresponds to 21-40 dB HL.
Observing the histogram of Figure 1, it was possible to identify that the most of the tinnitus was found in the higher frequencies, between 4 and 8 kHz.
So, we accept the null hypothesis (H0), which states that the no detected DPOAE is independent of tinnitus. Then, we can conclude that there are no significant differences between subjects with normal hearing and subjects with mild hearing loss, when the two groups are compared (with and without sensation of tinnitus).
That is, rejecting the null hypothesis suggests that the alternative hypothesis may be true, which means that the undetected DPOAE could be dependent of tinnitus. Most of the authors consider the origin of tinnitus as cochlear, like lesions of the hair cells after acoustic trauma, presbycusis, sudden hearing loss, etc. According to this model the annoyance of tinnitus is determined exclusively by the limbic and autonomic nervous systems. The OAE are always associated with the behavior of OHC, their presence is an indicator of cochlear structural integrity and on the other hand their lack could indicate a cochlear lesion5. Reduction in OAE is known to follow decreased task of the stria vascularis and to follow hair cell loss16. However, these results may have been influenced by the effect of hearing loss since it is challenging to isolate the aging consequence from that.
In this study, 73.5% of DPOAE presence was found among ears with normal hearing sensitivity or mild hearing loss, without tinnitus (control group). In this paper DPOAE were anomalous in 68.4% of the tinnitus patients and in 50% of the healthy ones, showing that the study group had significantly higher prevalence of abnormal DPOAE than the control one.
It was in this frequency range that the most reduced incidence of DPOAE detected was found for both tinnitus and nontinnitus ears (Figure 2).
Some studies reported that a tinnitus patient seems to have lower DPOAE than nontinnitus patients9,22,23,25,29,31,32. In their study, the average DPOAE amplitudes for frequencies of 3003, 4004, and 5005 Hz in patients with tinnitus and proper hearing were higher than in the control group. They did not discover any statistical differences between the DPOAE amplitude of the ears with tinnitus versus the control ears, although slightly increased DPOAE amplitudes were detected for tinnitus ears. The work of the team shown the occurrence of abnormal OAEs, mainly at higher frequencies, in patients with tinnitus and with normal hearing, but no correlation was obtained concerning the range of frequencies with abnormal DPOAE level and the bandwidth of tinnitus (tonal, narrow-band, or broadband) or, in patients with tonal tinnitus, with the pitch.
The significance level increased to a significant value when the results were compared at coincident frequencies between DPOAEs and tinnitus as referred above (Table 3), suggesting that there was some correlation between the frequencies range with no detected DPOAE.
The results of the present study suggested that it is still premature to conclude that DPOAE provided an objective evidence of tinnitus, considering the number of variables at play.
Biomechanics - LAETA, INEGI, Faculdade de Engenharia da Universidade do Porto, Clinica ORL Dr. Biomechanics - LAETA, INEGI, Faculdade de Engenharia da Universidade do Porto - Porto - AC - Portugal. Otoacoustic emissions and cochlear microphonism are present, making normal function of external ciliated cells evident, while brainstem audiometry shows alterations from wave I present even with tonal threshold changed (1). Measurement of subtle auditory deficit in tinnitus patients with normal audiometric thresholds using evoked otoacoustic emissions and threshold equalizing noise tests.
The absence of hearing loss on the audiogram in this group of patients poses a serious challenge to the cochlear theories in explaining tinnitus generation in this group of patients. For many years, progress towards finding the effective treatments for tinnitus was hindered by vague understanding of its underlying pathologic mechanisms.

The association between hearing loss and tinnitus has been well documented in the previous literature2-4. Some studies found a correlation between severity of tinnitus and degree of hearing loss3,8 while others found no such correlation9.
On the other hand, clinical observations have shown that 8 to 10 per cent of tinnitus patients had normal audiometric thresholds12. It is hypothesised that outer hair cells damage results in stereocilia decoupling from the tectorial membrane, thus causing them to depolarise and subsequently resulting in tinnitus perception1.
An association of tinnitus with the changes in amplitude of TEOAEs and DPOAEs has been reported. One study by Weisz et al.24 proposed that subtle auditory abnormality may also arise from the inner hair cells (IHCs) dysfunction. The subjects who were attending the Institute from January to December 2010, were identified by an audiology physician and audiologists based in this hospital. Then, all subjects underwent basic audiological tests which include pure tone audiometry and tympanometry.
Off-frequency listening occurs when the presented stimulus is being picked up by other parts of the cochlea instead of the targeted frequency area of the cochlea. From the analysis, the parameters of the TEOAEs for tinnitus ears are not significantly different from the control ears. Since no statistically significant difference was observed between both ears, further statistical analyses were performed using combined data from both sides together.
Distribution of the number of test frequencies with abnormal DPOAE in tinnitus and control ears. Based on the chi-square analysis, tinnitus ears have a statistically significant higher percentage of abnormal DPOAEs at some frequencies, mainly at 2000 and 4000 Hz regions (Table 4).
For example, it has been postulated that the different level of functionality between OHCs and IHCs (the Jastreboff's discordant dysfunction theory) can generate an unbalanced stimulation of dorsal cochlear nucleus's cells which produces abnormal neural activity. Abnormal DPOAE amplitudes were also found in this group, particularly at high frequency regions, but in a slightly lower percentage than the TEOAE. For example, in Shiomi et al.19, the mean amplitudes of the DPOAE were significantly decreased in tinnitus patients with normal hearing than in normally hearing controls.
One possible explanation for this finding is that it may be due to OHCs hypersensitivity, as reported in some previous research.
Abnormal TEOAEs and DPOAE in the tinnitus patients also imply that they may have subtle cochlear damage that is not yet appearing on the audiogram. This finding might suggest that both tests were sensitive to detect minor OHCs dysfunction.
Unexpectedly, the use of a TEN test in the current study has led us to find an acoustic neuroma in a patient. Sincere thanks to Ministry of Higher Education (MOHE), Malaysia, Universiti Kebangsaan Malaysia (UKM) and University of Bristol for providing sponsorship to pursue this PhD study.
Program Audiologi, Pusat Pengajian Sains Rehabilitasi, Fakulti Sains Kesihatan - Universiti Kebangsaan Malaysia - Kuala Lumpur - AC - Malaysia. There are evidence that non-linear mobile features of the OHC leads to OAE, through the action of myosin and actin, the elements responsible for contraction in the infrastructure of the OHC4 and the OHC active mobility seems to be the reason for the frequency selectivity and high hearing sensitivity.
Since then, an increased interest in the use of these measures to explore peripheral hearing function in unprecedented depth and detail has been noted. The study group consisted of 66 tinnitus ears and the control group of 34 ears without tinnitus.
The Post hoc comparisons using the Tuckey test indicated that the difference was present in the frequency of 3 kHz. That is, there is insufficient evidence to conclude that the absence or presence of DPOAE influences the occurrence of tinnitus when the analyzed frequency could not be the same as the tinnitus frequency.
Statistically significant differences were found in the proportion of ears with tinnitus that did not show DPOAE in relation to those without tinnitus that did not show DPOAE, as we can see in the Table 3.
Tinnitus was perceived as a sound, and the receptor organ of sound was the ear, so this leads that a significant proportion of tinnitus cases are also related with the onset of an auditory pathology, such as otitis media, acoustic trauma, sudden deafness, etc.13. A weak imbalance of neuronal activity within the auditory system, is noticed at low levels in the auditory system, and being a new signal it is enhanced by subcortical centres, transferred to the auditory cortex and perceived as a sound - tinnitus, and evaluated. DPOAE are reduced or absent when the mobility of the OHC, which is the source of OAE generation, is impaired by damage to those cells15. There are more young adults affected by tinnitus than seniors in spite of the double increase of prevalence for seniors.
Consequently, as audiometric thresholds worsen, the amplitude of the DPOAE response decreases and finally disappears19.
Ears with normal hearing or mild hearing loss in combination with tinnitus (study group) showed a lower incidence than the control group, reaching only 50% of total ears, when ears were compared at coincident frequencies between DPOAE and tinnitus (Table 3).
Based on these results, tinnitus could have not been caused by changes in OHC but seems be affected by that. In 59% of cases with normal hearing and tinnitus, the amplitude of DPOAE at almost all frequencies of tinnitus was decreased.
In that study, although hearing thresholds did not significantly differ between tinnitus and nontinnitus normal-hearing subjects, DPOAE amplitudes of tinnitus patients were significantly lower than individuals without tinnitus over 4-7 kHz range, which suggests that the decrease of DPOAE amplitudes over a limited frequency range may be associated with the occurrence of tinnitus. Others studies also shown that OAE were worse in ears of tinnitus individuals with normal hearing3,22,28,29 suggesting abnormalities of cochlear micromechanics in these ears, even without hearing loss. Together with this information, we have noticed, based on the same figure that no significant differences were found between tinnitus ears and nontinnitus ears at each test frequency, including the lower frequencies and even at higher frequencies. However, many of these studies included patients with poor hearing thresholds and with tinnitus, and this could possibly influence the results. These results were consistent with Gouviers et al.33 but not in accordance with the present study and studies referred above3,9,23-25,27,29,31 which reported lower DPOAE amplitudes in cases with tinnitus than in cases without tinnitus.
They also compared the DPOAE signal-to-noise ratio between the two groups and found that individuals with normal hearing and with tinnitus had significantly more abnormal DPOAE results than individuals with normal hearing but without tinnitus.
Furthermore significantly lower DPOAE, mainly at high test frequencies were measured in subjects with tinnitus compared to nontinnitus controls, reflecting OHC dysfunction generally in high-frequency cochlear regions.
It is noted that the audiometer and the Capella Cochlear Emission Analyzer, Madsen used only measure frequencies below 8 kHz.
A new method for the automated detection of spontaneous otoacoustic emissions embedded in noisy data.
Evidence for two discrete sources of 2f1-f2 distortion-product otoacoustic emission in rabbit. A speculation about the parallel ear asymmetries and sex differences in hearing sensitivity and otoacoustic emissions. Transient and distortion product evoked oto-acoustic emissions in normal hearing patients with and without tinnitus.
Quantitative analysis of cochlear active mechanisms in tinnitus subjects with normal hearing sensitivity: multiparametric recording of evoked otoacoustic emissions and contralateral suppression. DPOAE in estimation of the function of the cochlea in tinnitus patients with normal hearing. Comparison of auditory electrophysiological responses in normal-hearing patients with and without tinnitus.
This neural implication is also showed by absence of estapedial reflex and medial olivocochlear reflexes.
Only one patient was found with a positive TEN test result, who was confirmed by Magnetic Resonance Imaging to have acoustic neuroma on the affected ear. The last half of the twentieth century saw considerable advances in our understanding of tinnitus from both physiological and psychological perspectives. It has been generally accepted that any severe damage along the auditory system may lead to a certain degree of hearing loss, which is generally associated with tinnitus5,6. Moreover, the incidence of tinnitus in patients with sensorineural hearing loss varies widely across studies. These observations may have several indications, such as hearing loss is not necessary in tinnitus generation, pure tone audiogram does not always indicate auditory damage, tinnitus may be a primary symptom of diseases that are only diagnosed after the occurrence of hearing loss, or several mechanisms exist in a group of patients. The different functionality of outer and inner hair cells can also cause imbalanced activity in the dorsal cochlear nucleus which in turn causes changes at higher levels of the auditory system that may be perceived as tinnitus1. In some studies, lower amplitude of TEOAEs13,16 or DPOAEs13,17-19 have been observed in tinnitus patients compared to in non-tinnitus controls.
All participants had no history or current external and middle ear problem, noise exposure and psychiatric problem. In this experiment, a 2f1 - f2 distortion product was used because of its established clinical value. This off frequency listening occurs when the targeted area of inner hair cells or neurons are not functioning well and is referred to as a dead region27.
In this case (Subject RX), the TEN (HL) test revealed that dead regions might exist at 1.5, 3 and 4 kHz on the left ear (Table 7).
Since all the subjects in this study had normal hearing, the decrease in the TEOAE and DPOAE finding may possibly be considered as the effect of cochlear dysfunction of the cochlear active mechanism, which is related to OAE generation. Frequency analysis also showed that a significant decrease in DPOAE amplitude was mainly at the f2 frequency of 4000 to 7000 kHz. Therefore, the hearing status of these patients should be monitored for possibility of developing hearing loss later in life.
Previous research has clearly demonstrated that OAE may be used to reveal subclinical OHCs damage in audiometrically normal ears13-15. Apart from difficulty hearing in background noise, she did not have any other classical symptoms of acoustic neuroma such as balance problem or poor speech discrimination scores.
Firstly, it implies that a TEN test may offer a quick, inexpensive and non-invasive method for retrocochlear screening. In their study, they found 7 out of 8 auditory neuropathy patients with abnormal TEN test results.
The finding also supported the possible clinical advantage of the TEN test as a screening tool for retrocochlear problem. Risk factors for tinnitus in a population of older adults: the blue mountains hearing study. Characteristics of tinnitus and etiology of associated hearing loss: a study of 123 patients.
The more the worse: the grade of noise-induced hearing loss associates with the severity of tinnitus. Tinnitus with normal hearing sensitivity: extended high-frequency audiometry and auditory-nerve brain-stem-evoked responses. The effect of the number of averaged responses on the measurement of transiently evoked otoacoustic emissions in newborns. Dead regions in the cochlea: diagnosis, perceptual consequences, and implications for the fitting of hearing aids.
Tinnitus and 2f1-f2 distortion product otoacoustic emissions following salicylate overdose.
Ten(HL)-test results and psychophysical tuning curves for subjects with auditory neuropathy. All subjects had thresholds below 25 dBHL at frequencies 250–8,000 Hz, tympanogram type A and normal acoustic reflex thresholds. Objective: The objective of the investigation was to study the features of Distortion product OtoAcoustic emissions (DPOAE) in a group of tinnitus patients with normal hearing and to find out whether there is any difference in DPOAE findings in the tinnitus patients with normal hearing and in persons with normal hearing with no complaint of tinnitus. According to different reports, 85-96% of patients with tinnitus present with some levels of hearing loss and only 8-10% have normal hearing. The tinnitus effects depend on the degree of stimulation of the autonomic and limbic nervous systems and not on the activation level in the auditory pathways1.
The presence of OAE is a strong evidence of cochlear structural integrity and their lack could indicate a cochlear lesion due the link with OHC activity5. The two pure tone stimuli that induce DPOAE have two different frequencies f1 and f2, identified as primary frequencies.
They were recruited from one Clinic that was approved by the relevant research ethics committee and all the individuals who participated in the study signed the Informed Consent Form. To verify the differences between the tinnitus ears (study group) and ears without the sensation of tinnitus (control group) in regards to DPOAE, the ANOVA test was used. The current theory on tinnitus generation is based upon Jastreboff's "neurophysiological model"1,14 and postulates that tinnitus is a consequence of a modified neural activity in the central auditory system consequential to a peripheral damage in the auditory structures. In the majority of the cases, the continued presence of tinnitus combined without any situation associated results in habituation of the reaction to the tinnitus signal1. Some previous studies demonstrated that DPOAE incidence greatly differed depending on age16 gender and hearing level. Cilento et al.16 shown that women lose DPOAE amplitude from age and hearing losses, with men loosing more amplitude than women. As the results show, no significant differences were found between the two groups in respect of gender, age or auditory acuity (Table 1).
Qasem et al.3 tried to compare cochlear OHC function between 48 normal hearing patients, half with tinnitus and the other half without tinnitus. It can be concluded that the reduced number of ears with detected DPOAE at high frequencies was probably related to other reason than tinnitus. Hearing loss is usually associated with reduced DPOAE amplitude, making difficult to conclude whether the perceived reduction in DPOAE amplitude was associated to tinnitus alone or instead was just due to the hearing loss. Their clarification would be the different levels of higher auditory pathways to the dysfunction of the OHC. More commonly, various studies have shown that sensorineural hearing loss plays an important role in tinnitus generation. Therefore, the absence of hearing loss on the audiogram in this group poses a serious challenge to the aforementioned theories in explaining tinnitus generation in tinnitus patients with normal hearing. In the study, they investigated the inner hair cells functions in 11 chronic tinnitus patients with normal hearing thresholds using Threshold Equalising Noise (TEN) test and found 8 of them with possible inner hair cells problems. The results were presented as a distortion-product audiogram i.e the amplitude of the 2f1 - f2 DPOAE was plotted against the f2 from 1000 to 6169 Hz.
The broad band noise is designed to produce almost equal masked thresholds over a wide frequency range, for listeners with normal hearing and hearing impairment but without dead regions28. The abnormal TEOAEs in the tinnitus group were present for 1 and 4 kHz mostly, while in the control group, the abnormalities were mostly at 4 kHz. A t-test revealed that with regard to mean amplitude of TEOAE for tinnitus ears, there were no statistically significant differences for all frequencies tested (p > 0.05). Later, the mean amplitude of DPOAE for tinnitus and control ears against the corresponding f2 was compared. From 20 tinnitus patients with abnormal OAEs, 13 of them exhibit either failed TEOAE or DPOAE results. According to this theory, discordant dysfunction can occur without affecting the audiometric hearing thresholds when the OHCs are partially damaged and where the IHCs are intact. Stated differently, abnormal or poor OAE results may be the indicator of subtle cochlear damage before the abnormality affects hearing sensitivity and appears on the audiogram. Thus, the similar findings indicate that DPOAE measurement can offer a frequency specific measurement for the detection of subtle localised cochlear damage even before affecting pure tone thresholds34.
The high percentage of TEOAE abnormality at 4 kHz for the control ears may suggest that the hearing status of these participants also needs to be monitored.
Nonetheless, only the difference between numbers of abnormal TEOAE in tinnitus and control ears reached a statistically significant level. The former study suggested that tinnitus generation in their group of participants may be due to the effect of deafferentation of the neuron.
Secondly, tinnitus patients may have a serious problem that triggers the tinnitus perception despite having normal hearing thresholds and normal OAE test results.
Patients with auditory neuropathy are known to have problems with transmission of the auditory signal to the brain, thus abnormal TEN test results in this group of patients were assumed to be due to the neuron dysfunction.
However, more research needs to be carried out in this area in order to support the current finding. In this last group, the isolated presence of tinnitus indicates that it may be an initial first symptom of diseases that are only diagnosed after the onset of hearing loss. The chi-square test for independence was used to discover if there was a relationship between DPOAE with the two groups. It is well known that hearing thresholds are minor in adult men than in women and that thresholds get worse with age in both genders. They found significant decreases in the DPOAE amplitudes over the following frequencies ranges 750-6000 Hz in all tinnitus patients compared to nontinnitus, although hearing threshold levels did not shown significant differences differ between both groups.
Other studies reported increased DPOAE amplitude33,34 but again, the involved subjects in these studies presented differences in the hearing thresholds, what does not clarify if the irregularities in DPOAE are due to the expansion of tinnitus or due to the hearing losses32. We would agree with Jastreboff, who indicated that the levels of the auditory pathway may be involved in the creation of tinnitus, but, in the majority of cases, the cause is probably at the OHC level1.
What occurs on hearing system, on these cases can precede, in many years, the appearing of peripheral neuropathy.
Evidence showed a higher incidence of tinnitus patients with sensorineural hearing loss compared with conductive hearing loss7.

In addition, not all individuals with hearing loss experience tinnitus, and not all tinnitus patients have hearing loss. While the theories seem cannot fit in this minority group, evidence obtained from this group may have huge implication for a better tinnitus mechanisms understanding as well as assist in developing and shaping tinnitus management. The studies reported that tinnitus subjects were found to have increased TEOAEs20,21 or DPOAEs22,23 compared with non-tinnitus counterparts. Thabet25 attempted to replicated the earlier study by investigating 20 normally hearing unilateral tinnitus patients with TEN test and TEOAE. The presence of DP amplitude was accepted as valid when the signal to + 2 SD noise floor ratio exceeded 3 dB and the absolute DPOAE amplitude was at least - 10 dB SPL at each individual f2. Table 2 shows the normal and abnormal TEOAEs at each frequency tested in both the tinnitus and control group.
Generally, an independent t-test showed no statistically significant differences observed between tinnitus and control ears at all frequencies except for frequency 1414, 4757, 5187 and 6169 Hz (Table 5). Meanwhile, from 16 control ears with abnormal OAEs, 10 ears exhibit either failed TEOAE or DPOAE results. The ABR showed absent wave V at 70 dBnHL in the left ear and normal ABR waveforms in the right ear, which were correlated with the TEN test results, suggesting of abnormal neural function. Therefore, in this current study, we sought to determine whether the measurement of TEOAE and DPOAE may reveal subtle cochlear abnormality in tinnitus patients with normal audiometric thresholds. Although the difference between numbers of abnormal DPOAE in tinnitus and control ears failed to reach a significant level, mean amplitude of tinnitus ears at frequency region of 2000 and 4000 Hz were statistically significantly lower than the control ears. They suggested that it could be the result of reduced afferent input to the central auditory system due to cochlear lesion, thus resulting in a decreased OHC efferent activity and ultimately leading to OHC hypersensitivity.
TEOAE measurement stimulates the whole basilar membrane of the cochlear, which means it gives more global information.
Furthermore, dead regions normally exist in those who have hearing thresholds of 60 dB HL and above28.
In other words, even though dead regions normally exist in patients with hearing loss of more than 55 dBHL, normal hearing people can also have a 'dead region' which may be due to retrocochlear abnormality. Similarly, the abnormal result in Subject RX in the current study may also be because of the problem in neurons rather than in the inner hair cells.
MRI revealed a large vestibular schwannoma in the left cerebello-pontine angle which was compressiong the brainstem and cisternal portion of the VIIIth cranial nerve.This study showed that subtle cochlear problem may exist in tinnitus patients before it is significantly appeared in the audiogram. The subject group consisted of 16 ears of patients, in which 6 subjects were having tinnitus in both ears while 4 subjects were having tinnitus only in one ear. The origin of tinnitus in this group is still more obscure than in those with concomitant hearing loss. Several DPOAE components could be recorded, but the one that has been thoroughly studied in humans is 2 f1-f2 DPOAE8.
This implies that the decrease of DPOAE amplitudes may be related to the occurrence of tinnitus. Hyperbilirubinemia, premature conditon, anoxia are also considered risky situations to hearing neuropathy development, especially to the cases of prelingual (2,3).
Jastreboff & Jastreboff11 reported that about 27% of totally deaf patients do not have tinnitus, whereas 20% of normal hearing people have tinnitus. This is because the results obtained from this special group may directly related to the tinnitus perception, but not to the concomitant hearing loss.
The test was performed in a sound treated room where the ambient noise was maintained between 20 to 40 dB A. The difference between the two groups is highly significant at frequencies of 1, 1.5 and 2 kHz, but not at 3 and 4 kHz. The decrease in DPOAEs amplitude over a limited frequency range in DP-gram found in tinnitus patients with normal hearing may be a susceptible area representing minor cochlear pathology. Similarly, a more recent study by Sztuka et al.35 attributed the increase in DPOAE amplitude in tinnitus patients with normal hearing as a result of increased motility of the OHCs due to decreased neural activity in the auditory nerve. Conversely, the number of abnormal DPOAE in tinnitus ears was not statistically significantly different from the controls.
They found that outer hair cells damage (assessed by TEOAE) was more common in normally hearing tinnitus patients than inner hair cells damage.
In this case, the positive TEN (HL) results may not be due to inner hair cells damage but maybe because of poor processing efficiency that is associated with neural problems due to compression of large vestibular schwannoma on the VIIIth nerve38. However, caution should be taken in interpreting the TEN test results as 10 dB-above-thresholds criteria is just a binary criteria that means passing or failing the TEN test, but does not mean dead or not dead. All subjects were aged between 20 to 60 years with complaint of tinnitus with audiometrically normal hearing. Therefore, OAE is a phenomenon that may appear in normal hearing ears or even in ears with mild hearing loss. DPOAE are believed to be the fast, objective, consistent and reproductible measure of the physiological integrity of the OHC of the cochlea. All analyses were performed using the statistical software SPSS version 20.0 (SPSS Inc, Chicago, IL, USA). It can be assumed that the role of sensorineural hearing loss as a tinnitus generator is complex and the mechanism of tinnitus may rely on the presence of other contributing factors such as damage to specific hair cells or the auditory nerve fibers.
This appears to support the hypothesis that a reinforced mechanical distortion is generated by cochlear hyperactivity that can be the source of the tinnitus. DPOAE is more frequency specific and thus is expected to be more sensitive in detecting subclinical abnormality in cochlear function over TEOAE. Their finding supports the theory that outer hair cells abnormality may be an important factor in the tinnitus mechanism37. For this reason, more research needs to be carried out on the clinical benefit of the TEN test before applying this method clinically. There was significant difference regarding prevalence abnormal TEOAE and DPOAE between study group and control group. Control group was comprised of 16 audiometrically normal hearing ears of persons who were age and gender matched with the subject groups and had no complaint of tinnitus.
If the OHC of the human cochlea are to be involved in the generation of tinnitus, testing of otoacoustic emissions (OAEs) could provide a reliable means of recording OHC dysfunction.
These phenomena can be recorded in almost all normal ears, and are known to be reduced or absent in ears with hearing loss.
By contrast, in other cases, TEOAE and DPOAE results showed poor or absent emissions in tinnitus patients with sensorineural hearing loss, even in those ears with normal hearing16,19,36.
In this current study, the result may possibly be due to subtle cochlear abnormality also existing in non-tinnitus participants with normal hearing.
However, results from both studies may be more compelling if they included a retrocochlear test. There was relationship between dysfunction of outer hair cells and tinnitus in subjects with normal hearing.
DPOAE would be convenient for understanding tinnitus by evaluating the cochlea, especially the OHC, since they allow the analysis of a great spectrum of frequencies, providing a detailed analysis of almost all the cochlea9. This one is responsible for post-lingual Hearing Neuropathy conditions, of dominante autossomic heredity, on chromosome area 13q14-21 in an American family (9). The TEN test appears to be a potential non-invasive and quick test of inner hair cells function. The mean pure tone audiometric thresholds of tinnitus and control groups are shown in Table 1.
The tumour was compressing the brainstem and cisternal portion of the VIIIth cranial nerve. These variations can be explained by postulating that it is most likely to reflect different cochlear mechanisms underlying tinnitus generation due to different cochlear pathological changes in tinnitus ears37. The result of the current study is consistent with Thabet's study in which only one subject was found with a dead region, on the left ear. DPOAEs can be recorded with better reliability at higher frequencies than transient evoked OAE. Nonetheless, it is too early to make a conclusion based on the aforementioned two studies on tinnitus. An independent t-test revealed that there was no significant difference in hearing thresholds between tinnitus patients and controls at all frequencies except at 6 and 8 kHz.
Thus, the variability of findings in this study may possibly be because of different mechanisms existing in the normally hearing tinnitus patients.
According to Jastreboff37 however, there are different levels of dysfunction from the OHC up to the higher auditory pathways. Result and conclusion: It was observed that the amplitudes of DPOAE were significantly lower in tinnitus patients than that of persons without complaint of tinnitus, at a frequency of 1281-1560, 5120-6250, 7243-8837 Hz, which imply that decrease of DPOAEs amplitudes may be related to the presence of tinnitus. At that time, she was 2 years old and had brainstem audiometry done from other institution which pointed presence of bilateral profound sensorineural deafness and also indicated device adaptation of sonorous amplification. At both these frequencies, tinnitus patients had significantly higher thresholds than control individuals.
He hypothesised that in some patients, though the level of dysfunction is undetectable by TEOAE, it may be sufficient to produce tinnitus. PMPH-USA, Shelton12.Ami M, Abdullah A, Awang MA, Liyab B, Saim L (2008) Relation of distortion product otoacoustic emission with tinnitus. The family denied pre, peri and neonatal antecedents and believed the child reacted to strong intensity sounds.
Therefore, this study aimed to investigate subtle cochlear abnormality in tinnitus patients with normal hearing thresholds using evoked OAEs (TEOAEs and DPOAEs) and TEN test. Contrarily, in some, the level of abnormality is detectable but not enough to trigger tinnitus. The girl presented herself as shy during the examination and did not show any reaction to sounds.
Therefore, Jastreboff's hypothesis is a possible explanation as to why not all hearing loss patients present with tinnitus, and not all tinnitus patients present with hearing loss. Korean J Aerosp Environ Med 16(1):9–1414.Chery-Croze S, Moulin A, Collet L, Morgon A (1994) Is the test of medial efferent system function a relevant investigation in tinnitus?
In our institution, the protocol of evaluation is composed by audiometric exam, by brainstem audiometry and by otoacoustic emissions, and appoitment with neuropediatrician and genetic evaluation.A new audiometry showed bilateral profound sensorineural hearing loss, with absence of estapedial reflex and tympanometric curve type A in both ears.
At the beginning of the study, random selection of patients with tinnitus of different age groups and both gender was done during the period of 6 months (January 2012 to June 2012). Brainstem audiometry was done with dense and less dense clicks and, with frequency of stimuli of 3, 19.3 and 50 stimuli per second.
Study group Consisted of 10 patients, aged ranges between 20 and 65 years complaining of tinnitus with audiometrically normal hearing, among them six were having bilateral and four were having unilateral tinnitus (n: 12 + 4 = 16). No wave was identified on higher intensity and there was no response alteration in relation to changing on stimulus frequency, therefore, with alteration of clicks, equal images occured on the record, typical feature of cochlear microphinism, up to 4 msec to left and up to 2 msec to right (1). Control group Consisted of 16 normal hearing individuals without tinnitus with pure tone average <25 dBHL in the better ear. Otoacoustic emissions by distortion product (2) and transient (3) were bilateral and normal, what confirms hearing neuropathy diagnosis.
Recording was done from 16 ears of the selected patients with tinnitus (the study group) and 16 ears of audiometrically normal hearing individuals without tinnitus (the control group).
Because of hearing neuropathy condition, DNA of the patient was submitted to SSCP technique (Single Strand Conformation Polymorphism), with the purpose of screening mutations on diverse exons of OTOF gene. The migration standard of exon 15 was altered and the sequency of the same exon showed the patient has a deletion of 16 base pairs, among nucleotides 1552-1567 (1552-1567del16).The girl is under phonotherapy focusing oral language. During therapeutical process, sonorous amplification devices with digital technology were adapted. In the beginning, it was done tests with monoaural amplifications with variations of tested ears (10), however the girl presented better performance with binaural adaptation. In relation to functinal use of hearing, she recognizes everyday sounds and can detect speech only in quiet situations; she more attentive to orofacial reading and vocalizes having few entonation variations, though with communicative intentions.
There are some differences in the mean DPOAE amplitude levels between the study and the control groups.
She also attends special school for children with hearing impairment and has been easily learning body language. Transient otoacoustic emission present at left and right.DISCUSSIONA precocious or prelingual hearing neuropathy was always related to risky situations of perinatal period, such as premature conditon, hyperbilirubinemia and anoxia (2,3). So, it is believed that the chances of not diagnosing hearing neuropathy by newborn hearing screening with otoacoustic emissions were minor, since it is recommended the use of otoacoustic emissions and brainstem audiometry for risky children.
Therefore, description of several cases of prelingual, in families without history of motor or sensitive peripheral neural implications (4,11), or even, cases as we have described, without neonatal or family deafness history, bring out the hypothesis of genetic origin to non-syndromic hearing neuropathy.MADDEN et al, 2002 (12) question that before several non-syndromic family cases, a genetic predisposition to bilirubin intolerance, where lower levels to hearing loss, could cause neural change on these people. The determination of a specific gene, when changed, that would lead to hearing neuropathy only occurred in 2003 when VARGA et al (6) identified four mutations of OTOF gene in four Spaniard families. Since then, our patients with hearing neuropathy have been submitted to mutation researchs of OTOF gene with the purpose of determining the importance and frequency of such mutation on these cases.We found in the same patient a deletion of 16 base pairs, among nucleotides 1552-1567 (1552-1567del16).
This deletion causes the appearing of a stop codon of tranlation on the next exon, which means that translated proteic product is shorter.As it is said that mutations on OTOF gene cause deafness of recessive heredity, it is expected the patient to be a carrier of a second mutation on the same gene, which was not identified yet because sequencing study of the remaining gene is still in process. Tinnitus in turn, which is an unpleasant sound, may act as a noise which resulted in a decrease of the DPOAEs amplitudes due to increase in the internal ear noises heard by the patients as ringing noises. As these patients might not present history that means risk to deafness and otoacoustic emissions are the method to newborn hearing screening, many cases can be left without diagnosis. This noise is one of the factors that result either in the absence or decrease in DPOAEs amplitudes. The exact number determination of hearing neuropathies caused by such mutations will make us rethink of newborn hearing screening procedures.Another point involving this diagnosis refers to the development of hearing ability from eletroacoustic devices. In the presence of these results, tinnitus masker could be a good solution for the relief of annoyance resulted from tinnitus. The results of the use of sonorous amplification device and cochlear implantation are questionable (2) and although the girl is making progress with the use of amplification, it has been slow and with difficulties.In relation to cochlear implantation, results depend on lesion location. Here, we would like to focus one more fact that a decrease of the DPOAE amplitude is not only a result of a cochlear insult. The closer of hearing nerve, the worse it is the implant advantage; the closer of internal ciliated cells, the better prognosis will be (12). It is impossible to determine this location before surgery and many authors have been recommended brainstem implantation when cochlear implants are not positive (14). Efferent innervation of OHC is by the olivo cochlear neural pathway which is comprised of efferent neurons that travel from the superior olivary complex in the brainstem to cochlear hair cells.
With all these varieties of results and agreeing with the literature (12), we have chosen primarely by the use of individual sonorous amplification.Therefore, the function of OTOF gene is to codify otoferlin enzyme which works on membrane fusion on synaptic vesicle of internal ciliated cells, providing stimulus conduction.
Measurements of efferent effects on OAEs have been made with efferent activity evoked by brainstem shocks or by sound in the opposite ear. So, patients with hearing neuropathy by mutation of this gene probably has located alteration on ICC and because of it, cochlear implantation can be more successful. Various investigations have supported the conclusion that medial olivo cochlear system activity turns down the gain of the cochlear amplifier.
Because of this diagnosis and of little advantage of hearing aid, we are sending the girl to a cochlear implantation program.FINAL CONSIDERATIONSThe discovery of OTOF gene mutations as main cause of hearing neuropathy brings out two important clinical implications.
The first is related to the diagnosis, as patients do not present visible risks to deafness, taking the chance not to be previously detected.
DPOAE suppression is greatest when using contralateral stimulation tones close to primary tone f2. The second is related to treatment, as lesion location is on internal ciliated cells, so recommendation of cochlear implant should be considered.BIBLIOGRAPHY1. However, in our present study, we successfully determined a statistically significant difference in three frequencies out of eight total tested frequencies.
More information can be obtained using a larger sample size which will add to the knowledge about the possible link of OHC functioning and tinnitus. Thus, it can be hypothesized that there is an association between tinnitus and reduced cochlear OHC activity which indicate that the OHC of the cochlea are involved in the generation of tinnitus. However, studies with larger patient series would be required in order to strengthen the hypothesis. Achados audiologicos em criancas com hiperbilirrubinemia neonatal: um enfoque na neuropatia auditiva.
Sao Paulo, 2002, (Dissertacao de Mestrado - Pontificia Universidade Catolica de Sao Paulo).4. Non-syndromic recessive auditory neurophaty is the result of mutations in the otoferlin (OTOF) gene.
Yasunaga S, Grati M, Cohen-Salmon M, El-Amraouni A, Mustapha M, Salem N, El -Zir E, Loiselet J, Petit C.A mutation in OTOF, encoding otoferlin, a FER-1-like protein, causes DFNB9, a nonsyndromic form of deafness.

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