Tinnitus frequency test online hd,dokter tinus uitzending gemist aflevering 12 2014,what can i do to stop the ringing in my ears lyrics - PDF Books

Tinnitus is the perception of sound within the human ear not including the perception of sound outside the ear. Tinnitus is not a disease, but a condition that can result from a wide range of underlying causes: neurological damage multiple sclerosis, ear infections, oxidative stress, foreign objects in the ear, nasal allergies that prevent (or induce) fluid drain, wax build-up, and exposure to loud sounds. Tinnitus may be an accompaniment of sensorineural hearing loss or congenital hearing loss, or it may be observed as a side effect of certain medications (ototoxic tinnitus).
Tinnitus is the perception of sound within the ear or head, without a corresponding external stimulus for that sound. Tinnitus may be described as a buzzing, ringing, roaring, clicking, booming, hissing, whistling or cicada-like noise.
Objective tinnitus is generated by musculoskeletal and vascular structures that are in close proximity to the cochlea. Consider a review of medicines - have there been any new medicines started, including any over-the-counter medicines?
A live insect in the ear canal may produce noises that are described in a similar way to tinnitus.
Hit the tuning fork lightly on your knee, elbow or firm surface and hold the base on the patient's forehead.
A normal result is when the sound is heard again - air conduction is greater than bone conduction.
If the cause of tinnitus is found to be an underlying condition that is treatable in primary care, e.g.
Tinnitus often disturbs sleep and the tiredness that results may then compound the problem. Many people with tinnitus seek quietness in an attempt to gain relief from the noise of their tinnitus.
Distraction with day to day activities (leisure or work) and regular exercise can be effective.
The evidence to support the use of pharmacological treatments for tinnitus is inconclusive.
Thank you to Dr Ron Goodey, Otolaryngologist, Auckland for expert guidance in developing this article. 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. Claims of hearing loss can sometimes result in larger monetary settlements from insurance companies or in the proceedings of litigation.
In addition to malingering of hearing loss, individuals may complain of ear pain, hyperacusis and tinnitus. As hearing loss and tinnitus are subjective conditions, when there is a potential to gain by convincing another group of people that one has these disorders, it is common to encounter individuals claiming to have lost hearing or to have tinnitus. For hearing loss, this is a foolish undertaking, as there are abundant methods of showing that someone actually hears better than they admit. As is the case for malingering in general, inconsistency between subjective claims and objective measurements is often the key clue.
There are many simple methods of detection of an inconsistency between subjective claims of hearing loss (e.g. Another method of hearing testing that does not require cooperation is the auditory steady state response (ASSR) Attias et al, 2014. A regular audiogram was not very revealing -- often people forget that audiograms basically just test every octave -- if the ear is damaged somewhere other than the tone being tested in that octave -- the audiogram can be normal. However, a more careful audiogram that covered the frequencies around the tinnitus was abnormal. Audiograms are subjective tests, and in theory at least, someone could pretend not to hear at this frequency. From the combination of the tinnitus match, detailed and careful audiogram, and sweep OAE, it is clear that this patient has objectively confirmed inner ear damage. The complicated perception of body position and its separate parts in space is a result of analyzed and synthesized impulses by the vestibular analyzer, by both superficial and deep proprioception, and by the ocular analyzer. The aim of our investigation was to evaluate the effect of treatment with 8 mg and 16 mg of Betaserc on patients (workers in the transport system) with vascular auditory and vestibular disturbances. A detailed neurootological history was obtained by means of a questionnaire, and otological and neurological examinations were conducted in each patient.
First, with the help of Frenzel's spectacles, we evaluated spontaneous reactions, checking for spontaneous, positional, and latent nystagmus.
Figure 2 shows a decrease in complaints of vertigo (16 patients) and dizziness (14 patients) on the twentieth day in one-half of the 30 patients treated with 16 mg of Betaserc.
The frequency of attacks was lower in both treated groups, but the result was considerably better after treatment with 16 mg of Betaserc.
Regarding nystagmus reactions, the general test showed the presence of different nystagmus forms-horizontal, horizontal rotatory, and rotatory-according to the phase and nosological units. On the twentieth day of treatment with 16 mg of Betaserc, we noted an improvement in the spontaneous and, especially, the latent nystagmus symptoms.
We confirmed the opinion of many scientists that a larger amount of Betaserc leads more rapidly to considerable acceleration of the vestibular function recovery processes [8,9]. Complete investigation revealed decreased complaints of vertigo and dizziness (in frequency and strength of attacks) among one-half of our patients on the twentieth day of treatment with 16 mg of Betaserc. On the basis of investigations carried out, we recommend 16 mg of Betaserc three times daily in the acute phase. Recent studies have indicated that the pathophysiological basis for tinnitus may be abnormal activity in the auditory areas of the brain rather than aberrant activity in the periphery. Tinnitus is the sensation of hearing a sound when no external auditory stimulus is present [1]. A variety of tinnitus treatments have been tried, but hearing aids, maskers, drugs, and surgical interventions thus far have not been shown to be very effective [10, 11].
In general, antidepressants appear to work best for those who are depressed or anxious, who have more severe tinnitus, or who are treated for a longer time with an adequate dose of medication [13]. Recent studies have suggested that the pathophysiological basis for chronic tinnitus is neural activity in the brain rather than aberrant activity in the peripheral auditory system [17-22]. These theories suggest that overactive feedback loops in the brainstem-thalamus-auditory cortex may be the underlying mechanism of this problem. Furthermore, the perception of tinnitus has been observed to be enhanced when the person perceiving the subjective noise "attends" to it and associates it with unpleasant emotions [28]. This model for the etiology of tinnitus suggests that, though tinnitus may be triggered by events in the periphery, the mechanisms that cause tinnitus to be a persistent and annoying condition are in the brain [32,33]. Given this theoretical background, we have approached the problem of tinnitus treatment by using customized sound-more specifically, a replica of the subjective tinnitus experience-to reduce the overactive sound-processing circuits. After completion of pilot study 1, we implemented a more formalized and longer-duration protocol. We selected subjects between the ages of 20 and 60 years if they exhibited "primary tinnitus" as defined by Dr. In study 2, prior to recording of the EEG and eventrelated potentials (ERP), subjects had bilateral audiograms using adult routine clinical procedures with appropriate level of contralateral masking as needed. Study 2 subjects underwent an otoscopic examination, tympanogram, and ipsilateral acoustic reflex screening.
The perceptual experience of tinnitus was characterized in both studies using a successive approximation technique. Auditory stimulation in both studies consisted of sine waves generated by a function generator (Goldstar FG2002C; LG Precision, Seoul, South Korea). Audiograms were taken from 7 of the tinnitus subjects and 13 of the control subjects in study 1.
Most subjects indicated changes in their tinnitus perceptions very soon after beginning CST, in one case even after trying out the habituation sound for only a few minutes in the laboratory. In four of the five subjects who completed the 3 weeks of CST, hearing threshold at the frequency closest to the subject's tinnitus pitch improved by 10 dB or more (Fig.
The EEG recording procedure required the determination of hearing thresholds prior to each session. In study 1, we assessed the short-term effects of habituation on the electrophysiology by recording the N100 component from tinnitus and control subjects before and after 1 hour of CST. In study 2, comparison of the N100 responses (slope) before and after 3 weeks of CST showed a decrease in the intensity dependence in response to the 4-kHz tinnitus frequency tones (Fig.
Recent studies indicate that an altered afferent input to the auditory pathway may be the initiator of a complex sequence of events resulting in the generation of tinnitus at the central level of the auditory nervous system [17]. The hearing loss observed at the tinnitus frequencies raises the possibility that the stronger intensity dependence observed in the responses of tinnitus subjects to tinnitus frequency tones may have been caused by recruitment (abnormal loudness growth) rather than tinnitus. The observed changed intensity dependence of the auditory N100 response in tinnitus subjects in the present studies and in previously published findings [19,27,50- 52] indicate that tinnitus is accompanied by a reorganization of the tonotopic map in the auditory cortex.
Our studies on the effectiveness of CST were conducted without a placebo treatment and were not blinded. Possible conflict of interest: Authors are shareholders in Tinnitus Otosound Products, LLC, a company developing diagnostic and treatment methods for tinnitus.
It is a common, but frustrating problem for both patients and clinicians, as in many cases the cause cannot be identified and there is no single effective treatment.
In some cases, referral for further investigations such as MRI is required to make a specific diagnosis. Proceedings of ‘Tinnitus Discovery': Asia-Pacific Tinnitus Symposium, 11-12 Sept 2009, Auckland, New Zealand. 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. The audiology community has an immense repertoire of procedures available to it to detect such behavior. Predicting Hearing Thresholds in Occupational Noise-Induced Hearing Loss by Auditory Steady State Responses. Vestibular receptors play a main role in this complex system and determine changes both in linear and angular acceleration and in gravity strength [1-3]. Arterial hypertonia or atherosclerosis is accepted to be the most common etiopathogenic factor. The patients, all transport workers, presented with vascular pathology of the vestibular and auditory analyzer. Tonal threshold audiometry was performed using a Siemens (Copenhagen, Denmark) SD-50 audiometer.
The total number of patients treated with 16 mg of Betaserc was 30 (18 with central otoneurological syndrome and 12 with peripheral otoneurological syndrome). On day 45, substantial improvement was seen among one-third of the 20 patients treated with 8 mg of Betaserc. The otological and neurological status of all patients was normal before starting treatment. Figure 3 shows the breakdown of patients according to whether they experienced spontaneous, latent, or positional nystagmus (according to Frenzy's spectacles) and to whether they were being treated with 8 mg or 16 mg of Betaserc. Subdivision of men with spontaneous (SNy), latent (LNy), and positional nystagmus (PNy) (according to Frenzel's spectacles) during treatment with 8 mg and 16 mg of Betaserc. Better results were received after treatment with 16 mg of Betaserc, considering spontaneous and, especially, latent nystagmus symptoms. The medication is very well tolerated, has no sedative effect, and is suitable for long-term treatment of transport workers with auditory and vestibular disturbances of vascular etiology. The US Food and Drug Administration (FDA) has not approved any drugs for treatment of tinnitus, though some studies have focused on medications, including benzodiazepines [12] and antidepressants [13]. Though studies of newer medications are ongoing, the use of current drugs involves a substantial incidence of side effects that individuals wish to avoid or often find intolerable.
Functional imaging techniques have demonstrated a relationship between the intensity of tinnitus and the degree of reorganization of the primary auditory cortex.
Indeed, research from our own laboratory [27] has shown that the brain activity of tinnitus sufferers in response to sounds similar to their tinnitus is different from the response to other sounds or from the brain response to sounds of people without tinnitus. In this scenario, the person experiencing tinnitus is annoyed by the sound, thereby activating the limbic system. Subjects participated in this first experiment at different times, varying between 1 and 24 months. The THQ consists of 27 statements relating to the impact of tinnitus on an individual's life. We obtained pure-tone air and bone conduction hearing sensitivity thresholds for the standard audiometric frequencies of 250 Hz to 8 kHz in a double-walled sound suite meeting current American National Standards Institute standards for threshold air conduction and bone conduction testing. We obtained middle-ear measures using a currently calibrated, portable Grason-Stadler GS-17 acoustic immitance Middle Ear Analyzer (Grason Stadler Inc., Madison WI).
Spectrogram of a typical tinnitus habituation stimulus, showing two closely spaced narrow-band noises centered at 2,800 Hz and 3,225 Hz and a very-narrow-band noise centered at 7,417 Hz that is almost 40 dB stronger than the first two.
Data were recorded from 15 electrode sites mounted on an elastic cap and located over a variety of scalp sites (F3, Fz, F4, C3, Cz, C4, P3, Pz, P4, T3, T4, T5, T6, O1, and O2 according to the modified International 10-20 System). The intensity and duration of each stimulus were set by a specially designed programmable logarithmic amplifier that is controlled in real time by a stimulus presentation and data collection program running in ADAPT. During study 2, they were required to wear their MPEG player and listen to the customized habituation sound for 6-8 hours daily as they went about their normal activities. One of the tinnitus subjects had mild hearing loss, and three had moderate hearing loss on the right ear, whereas five had mild hearing loss, and none had moderate hearing loss on the left ear at their tinnitus frequency.
Generally, they thought that their tinnitus was much more bearable when the habituation sound was present and that the tinnitus was less bothersome at other times. Changes in four tinnitus subjects' hearing levels at the tinnitus frequency during habituation training. This provided records of the tinnitus subjects' hearing thresholds at their tinnitus frequency. For the tinnitus patients, the habituation sound was the one used in habituation training, and the stimuli used for recording the N100 component were 1,000-Hz tones and the tinnitus frequency tones. N100 intensity dependence in response to A) tinnitus frequency (4000 Hz) and B) control frequency (1000 Hz). Responses to 4-Hz tinnitus frequency tones A) before versus after customized sound therapy and B) tinnitus versus control. The results of our two studies indicate that CST aimed at this central dysfunction can reduce chronic tinnitus quickly and safely.
However, the reduced intensity dependence observed in responses to 2,000-Hz tones, one octave below the tinnitus frequency, is opposite to the effect of recruitment and thus not attributed to it.
The main correlate of this reorganization in our studies was the enhanced contrast between responses to tinnitus frequency and tones approximately one octave lower than the perceived tinnitus pitch. In-ear earphones, whose sound enters directly into the ear canal without any opportunity to be deflected or absorbed elsewhere, are a common cause of tinnitus when volume is set beyond moderate levels.
As tinnitus is usually a subjective phenomenon, it is difficult to measure using objective tests, such as by comparison with noise of known frequency and intensity, as in an audiometric test. 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. We purposefully limit the information on this page, but it isn't difficult to detect malingering. Pathological changes in functioning of the aforementioned systems cause vertigo [4], dizziness, a sensation of floating, noise in the ears, and balance disorders. Sensory structures, being highly differential, are more vulnerable to ischemia than are other nerve structures [5,6]. In the central ear, it improves histaminergic neurotransmission by blocking presynapsis H3 receptors, it increases histamine release in synapses, and it normalizes the exciting processes in vestibular nuclei of the medulla oblongata [7]. The otoneurological investigation was conducted before and on the twentieth and the forty-fifth days of treatment in the Department of Neurology and Neurootology of the National Multiprofile Transport Hospital, King Boris III, Sofia.
Examination of the vestibular system was directed at both spontaneous and provoked reactions. The total number of patients treated with 8 mg of Betaserc was 20 (12 with central otoneurological syndrome and 8 with peripheral otoneurological syndrome).
Complaints of vertigo remained in 6.7% of the 16 vertigo patients receiving 16 mg of Betaserc, as compared to 20% of the 11 vertigo patients treated with 8 mg of Betaserc. No pathological change was found after tonal audiometry; the results were within normal limits (hearing decrease of 5-10 dB, mainly for the high-frequency zone) for those older than 36 years.
On the twentieth day after treatment, the percentage of patients with values of less than 1.50 (within normal limits) was increased by 40% (12 patients) in those treated with 16 mg of Betaserc and by 20% (4 patients) when treated with 8 mg of Betaserc.
Also, the symmetry of reaction was considerably improved after above-threshold provocation, mainly in terms of duration, slow-phase speed, and amplitude. However, such reorganization can be reversed through training-induced changes in the response pattern of cortical neurons.
However, tinnitus sensations can be constant, loud, and annoying to the point that the sufferer is emotionally affected by this sensation. Finally, psychotherapy for tinnitus does help some, but it is aimed at mitigating the psychological effects of the problem rather than the sound itself. This suggests that aberrant activity exists in the sound-processing circuits for sounds that the tinnitus sufferer hears.
A feedback mechanism under control of the limbic system is assumed to give rise to an increased generation of tinnitus-related activity [29,30].
These studies support the idea that tinnitusrelated neuronal activity is confined to certain isofrequency regions of the auditory cortex.
We describe two studies: an initial pilot study (study 1) and one with a more formalized protocol (study 2). We first required tinnitus subjects to complete the Tinnitus Handicap Questionnaire (THQ) [44], and subsequently we audiometrically evaluated all subjects and recorded their EEGs. Susan Gold, MS, CCC-A, of the University of Maryland Medical Center, Tinnitus and Hyperacusis Clinic. It contains three subscales relating to mental health, hearing, and attitude toward tinnitus [44].
We used a Macio MA-41 portable audiometer (Maico Diagnostics, Eden Prairie MN) with a current calibration sticker for the pure-tone testing. In response to the subjects' statements, sounds were synthesized using highprecision, general-purpose sound synthesis software. Auditory stimuli of five different intensities were presented through insert earphones (Eartone 3A transducers with Earl link foam eartips; Cabot Safety Co, Indianapolis IN). The intensity of the habituation sound was set by the individual so that the tinnitus perception was slightly louder than the habituation sound. The hearing tests in study 2 (Table 1) showed mostly normal hearing in both tinnitus and control subjects at 1 kHz and 2 kHz.
For CST to be effective, the stimulus has to be audible but must not be so loud as to mask the tinnitus itself. However, in one case, a 10-dB improvement in one ear was offset by a 10-dB decrement in the other ear.
For control subjects, the stimuli used for recording the N100 component were 1,000-Hz and 4,000-Hz tones. Note that tinnitus subjects showed slightly higher slopes to their tinnitus tones than to the controls' 1,000-Hz tone, both before and after habituation. Furthermore, the intensity dependence of the control 2-kHz tones (approximately one octave below the tinnitus frequency) was also significantly decreased in tinnitus subjects. This tinnitus suppression may reflect aspects of "residual inhibition" (RI), though distinct mechanisms may be involved as well. Rather, we attribute this effect on intensity dependence to lateral inhibition caused by the tinnitus-related activity in auditory cortex. After 3 weeks of CST, the intensity dependence of responses to tinnitus frequency tones was decreased, rendering the responses to tinnitus frequency tones more similar to responses from normal subjects to tones in the same frequency range. However, to conceive of a placebo condition that is truly blinded is difficult, because CST subjects have to undergo the sound-matching process to create their own habituation stimulus.
Transient reduction of tinnitus intensity is marked by concomitant reductions of delta band power. Changes in spontaneous neural activity immediately after an acoustic trauma: Implications for neural correlates of tinnitus. Tinnitus sensitization: Sensory and psychophysiological aspects of a new pathway of acquired centralization of chronic tinnitus. Tinnitus dyssynchrony-synchrony theory: A translational concept for diagnosis and treatment. Dynamical properties of a plastic neural network model for tinnitus therapy and inhibition of oscillation using noise stimulus. Experimental-neuromodeling framework for understanding auditory object processing: Integrating data across multiple scales. ADAPT (Analog Data Acquisition and Processing Tools)-a software system for PC-compatible computers, designed to be used in neuro- and psychophysiological experiments, and for analysis and monitoring of various parameters of human spontaneous and event related brain potentials. Residual inhibition functions in relation to tinnitus spectra and auditory threshold shift. It is important to identify people who are hearing genuine sounds generated within the body (objective tinnitus) or have some other underlying treatable condition. 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? Someone who claims to be deaf on audiometry, but has normal OAE tests, is likely to be pretending. The main symptom in neurootological clinical practice - vestibular vertigo - is common among disturbances of cerebral hemodynamics and the blood supply of peripheral and stem parts of the vestibular analyzer. During the investigation, patients were given either only 16 mg of Betaserc three times daily or 8 mg of Betaserc three times daily, as those with arterial hypertonia underwent simultaneous antihypertensive treatment. Vertigo and dizziness were the main symptoms of patients with otoneurological disease, and the symptoms often were accompanied by noise in the ears, hearing decrease, and balance disorders. Complaints of dizziness remained in 10% of the 14 dizziness patients treated with 16 mg of Betaserc, as compared to 25% of the 9 dizziness patients treated with 8 mg of Betaserc.
These data correlate with the results of above-threshold provocation, objectified by electronystagmography (Fig.
As compared to static body changes, better results were registered in kinetic changes on the twentieth day of treatment with 16 mg of Betaserc. Arterial pressure was not influenced during treatment with either 8 mg or 16 mg of Betaserc. Results of coordinating and statokinetic tests were also improved after treatment of patients with 16 mg of Betaserc, as better results were achieved in body kinetic indices.
We address this problem by using customized sounds that reproduce the subjective experience to reduce overactive auditory circuits.


Chronic sound sensations of tinnitus affect approximately 17% of the general US population [1-3], or approximately 44 million people, and approximately 33% of the elderly [4]. In one study, tinnitus subjects with depression treated with nortriptyline had decreased depression levels, functional disability, and tinnitus loudness [15,16]. We have hypothesized that mechanisms of lateral inhibition in the auditory areas of the brain act to confine the activity, driving the tinnitus sound perception to regions representing specific frequencies in the central auditory cortex and increasing the contrast between tinnitus-related activity in these regions and spontaneous activity in adjacent regions. The increased perception can then lead to increased annoyance, completing a positive feedback cycle that will render tinnitus persistent and annoying. Moreover, it has been shown that the changes in the size of the tonotopic map in the auditory cortex can be induced by training [35]. The rationale behind the use of white noise is to generate a decreased signal-to-noise ratio between the tinnitus-related neuronal activity and random background activity in the auditory system. Customized sound therapy (CST) involves an initial session with a sound specialist, during which a "customized" sound is created for each individual and closely mimics the subjective tinnitus. Primary-tinnitus subjects are those presenting to the otology clinic with a main complaint of tinnitus, regardless of type and degree of hearing sensitivity. The audiometer has standard Telephonic THD-39 earphones with MX-41-AR ear cushions (Audiometrics, Oceanside CA) and a standard Radioear B-71 bone vibrator (Radioear Corp., New Eagle PA). We obtained initial baseline auditory brainstem response and auditory middle latency responses for each subject using a currently calibrated and certified electrically safe Biologic Brain Atlas (Advanced Biologic Corp., Toronto, Quebec, Canada) evoked potential machine with ER-3 insert earphones. The tinnitus sound is synthesized according to the description provided by the subjects using the program "pcmusic" [46].
Experience from study 1 indicated that subjects had difficulty in distinguishing the continuous habituation sound from their tinnitus. At 4 kHz, four of eight tinnitus subjects had mild or moderate hearing loss in their right ear, and five of eight subjects had mild hearing loss in their left ear. Therefore, the intensity settings that tinnitus subjects used on their noise generator gave an estimate of the loudness of the tinnitus. Some subjects reported changes in the sound quality of their tinnitus, so that their habituation sound was no longer a match for their tinnitus perception. Nonetheless, they were carried out under defined conditions so that changes in the measurements reflected changes in hearing threshold. Both tinnitus and the recruitment due to hearing loss may have influenced the intensity dependence of the N100 response to tinnitus frequency tones. RI is the temporary suppression of tinnitus that occurs after the offset of an appropriate masking stimulus [48,49]. The main difference between tinnitus sufferers and controls manifested itself in the response to tones one octave below the tinnitus frequency (2 kHz in our studies). Consequently, all study subjects will know whether they are being habituated to a sound mimicking their tinnitus or to a "placebo" sound. 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 led us to use the medicine Betaserc (betahistine dihydrochloride), which has both peripheral and central effects and brings to normal the imbalance in the vestibular system. The results of the respective treatment of patients with balance disorders, hearing decrease, and noise in the ears are nearly identical.
The results of two preliminary studies indicate that customized sound therapy (CST*) aimed at this central dysfunction reduces tinnitus quickly and safely.
Of this group, estimates project that some 10- 12 million individuals will experience tinnitus problems sufficiently serious to seek professional help [5,6]. Shulman and Goldstein [24] interpreted these as changes in the congruence or dyssynchrony in cortical regions in the auditory and frontal cortices. This leads to increased tinnitus perception and to what most tinnitus sufferers hear-a tone or group of tones, as opposed to cacophonous noise containing all frequencies.
In short, individuals experiencing tinnitus unintentionally condition themselves to aggravate tinnitus through negative reinforcement. Taken together, these findings suggest that the observed tinnitus-related changes in the organization of the auditory cortex are the result of the involuntary learning process described earlier.
This background activity is achieved by introducing a quasirandom, stimulus-related signal in all of the parallel, tonotopic channels of the auditory system.
This is followed by a period of several weeks to months during which the individual listens to the customized sound for several hours every day while going about normal daily activities. On a separate day, subjects' tinnitus sound experiences were characterized and recorded on an MP3 sound player. Behavioral loudness discomfort levels (LDLs) were also recorded at each frequency in both ears using pulsed pure tones with a 200-msec duration and 50% duty cycle. Auditory brainstem response and auditory middle-latency response two-channel recordings followed clinical recording and analysis parameters outlined in Ferraro's Laboratory Exercises in Auditory Evoked Potentials [45]. In an iterative process, the resulting sound was played back to the subjects, who responded with suggested adjustments, such as altering the pitch, number of components, balance, or quality of the synthetic sound. Within each series, 80 stimuli of different intensities, for a total of 400 stimuli, were presented in random order and at intervals varying randomly between 1 and 3 seconds. Hence, to help individuals compare the loudness of their tinnitus to that of the habituation sound, we instructed them to use the pulsed version of their customized sound. Conversely, only 2 of 12 control subjects had mild or moderate hearing loss in their left ear, and only 1 of 12 control subjects had moderate hearing loss in the right ear. Though most subjects did not keep a detailed log of the volume settings on their MP3 players, clearly the volume setting required for the habituation sound to be just audible over the subject's internal tinnitus perception decreased over time, in one case so much that the subject exhausted the available intensity settings and the stimulus had to be resynthesized at a lower intensity. When a new habituation sound mimicking the changed tinnitus perception was synthesized, the subjects reported the CST to be as effective as before. The first threshold measured was set to 0 dB normalized hearing level (nHL), and all other measurements were plotted with reference to it. Because CST caused a lowering of the subjects' hearing thresholds at frequencies near their perceived tinnitus pitch, these results reflect an effect of CST, regardless of whether the observed change is caused by a decrease of tinnitus-related neuronal activity or decreased recruitment due to lowered hearing thresholds. Some participants in this study described immediate relief, effects on the THQ, and changes in hearing threshold within 3 weeks. The change in the EEG pattern induced by CST manifests in responses to the tinnitus frequency. However, to assess the efficacy of CST in a crossover trial with comparable therapies might be possible, as that study design would not require a placebo condition and blinding.
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.
Considering the duration, slow-phase speed, amplitude, and organization of nystagmus, symmetry of reaction is considerably improved after above-threshold provocation and 45 days treatment with 16 mg of Betaserc. Participants described immediate relief, showed changes on the Tinnitus Handicap Questionnaire, and reported changes in hearing threshold within 3 weeks. Approximately 20% suffer to a degree that their quality of life and productivity are impaired [7]. Similarly, magnetoencephalography (MEG) studies [25] have reported increased gamma-band activity in a resting condition in individuals with tinnitus. Shulman [31] demonstrated the changes in cortical and limbic regions in tinnitus subjects as compared to controls and hypothesized a final common pathway for tinnitus. Because training-induced changes in the response pattern of cortical neurons can be reversed by habituation, we hypothesize that habituation will ameliorate tinnitus.
TRT is available currently, but it is expensive, time-consuming, of long duration, and only incompletely effective. Furthermore, subjects' tinnitus had to be present all the time with constant sound quality.
We instructed each subject to push the signal button when an increasing continuous pulsed pure tone reached a subjective loudness level that represented initial annoyance.
The evoked potential recording protocols sequentially programmed into the Brain Atlas were the same for each subject. In response to these suggestions, we modified the sound description file and repeated the process until the subjects reported that the synthesized sound matched their subjective tinnitus experience well. The EEG was amplified by 10,000 and band-pass filtered between 0.01 and 100 Hz at 3 dB down. This facilitated the determination of the requisite intensity, at which point they could switch over to the continuous sound for the habituation itself.
After 1 hour of habituation, the hearing threshold at the tinnitus frequency was lowered by as much as 15 dB nHL.
Observations from one subject indicate that most of the tinnitus relief is gained during the first 4-8 weeks of CST. However, the contrast between responses to tinnitus frequency tones and tones one octave below the tinnitus frequency was not changed after 3 weeks of CST. 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? We also saw changes in the intensity dependence of the auditory N100 in tinnitus patients, supporting the idea that tinnitus reflects a reorganization of tonotopic maps in the auditory cortex. This translates to between 2% and 3% of the population whose lives are adversely affected by tinnitus [8,9]. Studies in experimental animals and humans have suggested that tinnitus is associated with a synchronized hyperactivity in the auditory cortex and proposed that the underlying pathophysiological mechanism is thalamocortical dysrhythmia. More precise methods of habituation have been suggested by computational models of tinnitus [37-41]; for a review, see Husain, [42,43]. This external sound appears to calm the internal overactive circuits and is not associated with annoyance and anxiety.
Subjects were initially interviewed at the Otolaryngology Clinic to ensure that they met all exclusionary criteria.
The LDL was repeated at each standard test frequency to determine whether the initial level was stable or adjusted upward. We required subjects to document the time during which the sound player was used and the intensity settings. Over several weeks of habituation training, we observed hearing thresholds at the tinnitus frequency to decrease by as much as 25 dB nHL.
After this initial period, apparently wearing the sound device regularly is unnecessary, and the experience with this one subject indicates that using the habituation sound occasionally as needed may be sufficient. Therefore, whether longer CST treatments can completely reverse the cortical reorganization associated with tinnitus remains to be seen. The main correlate of this reorganization was the enhanced contrast between responses to the perceived tinnitus pitch and tones approximately one octave lower. Estimates anticipate that the number of serious tinnitus cases will increase significantly over the next few years.
Hence, decreased auditory stimulation results in decreased firing rate and decreased lateral inhibition. These models explain how a decreased auditory input resulting from a peripheral hearing deficit can give rise to a specific tinnitus pitch. One contained a pulsed version of the subjects' tinnitus sound (250-msec pulse duration, 50% duty cycle), and the other was a 180-sec-long continuous sound.
For stimulus presentation and data acquisition and analysis, the ADAPT scientific software [47] was used. 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.
After 3 weeks of CST, the intensity dependence to the tinnitus pitch decreased, making these responses more similar to those from normal subjects responding to tones in the same frequency.
When the tinnitus sound itself is used as a habituation stimulus, Langner's model predicts that the tinnitus should disappear. Directive counseling would tend to draw the individual's attention to the tinnitus, whereas habituation is designed to draw attention away from the tinnitus. We recorded responses to pure-tone sounds at and below the tinnitus frequency before and after the 1-hour habituation treatment. Two subjects dropped out after reporting strange sounds from their MP3 player that seemed to make their tinnitus worse. We then downloaded the digitized sound into a small portable digital sound playback device (MPEG-player). The underlying rationale for CST is to draw subjects' attention away from their tinnitus, and reports indicate that though subjects readily perceive their tinnitus and the habituation sound if they choose to, CST helps them to ignore their tinnitus. The value of this test would be to identify such individuals and provide treatment before they become symptomatic for hyperacusis. This model also assumes that the limbic system is a necessary component for stabilizing the tinnitus perception. In one case, the cause of the disturbing sounds was a defective MP3 player; in the other case, the disturbing sounds were caused by an artifact in the conversion of the digitized sound from the WAV to the MP3 file format.
The time needed for this successive approximation procedure varied, depending on the subjects' ability to describe their subjective experience of tinnitus and on their ability to characterize differences between the tinnitus they experience and the sounds being synthesized by the computer. Directive counseling in connection with CST might actually be counterproductive because it might remind subjects of the annoyance associated with untreated tinnitus and thereby draw their attention to their tinnitus rather than away from it.
On the basis of these models, we propose to use a frequency-specific or "custom-made" sound similar to an individual's tinnitus for habituation purposes. Halfway through the training period, we scheduled a second session to characterize the tinnitus sound to ensure that the stimulus still matched the subjects' tinnitus perception.
In one case, data were excluded because the subject did not wear the MP3 player for the requisite time and was not present for the follow-up examination owing to scheduling conflicts. Because it produces effects after only a few weeks of treatment without involving directive counseling or requiring frequent regular visits to health care professionals, CST is expected to provide quick and lasting relief from tinnitus at relatively low cost. We conjecture that using a customized sound and mimicking the tinnitus as closely as possible should be highly efficient in reducing the perception of tinnitus.
After 3 weeks, all subjects underwent a second EEG and audiological assessment and a final clinical evaluation. Before beginning CST, we required subjects to confirm that the habituation sound matched their tinnitus during two or more sessions separated by at least a week. Further, though adding a replica of the annoying sound that tinnitus patients experience would appear to be even more annoying, the method of playing the replica at the same volume as the experienced sound minimizes any discomfort. Adjustments to the stimulus were needed for some subjects after CST had progressed a few weeks. It seemed clear that this was owing to changes in the characteristics of the tinnitus itself rather than a mismatch in the initial sounds.



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