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03.10.2014
Indispensable in fitting today's more advanced digital and semi-digital tinnitus masking aids. Ultra-high-frequency (UHF) external acoustic stimulation with the UltraQuiet device (UQ) has been reported to provide significant relief of severe disabling-type tinnitus. Since 1989, nuclear medicine imaging has been introduced into the discipline of tinnitology for both basic science and clinical diagnosis and treatment. Paired t-tests were used to investigate differences for both interhemispheric and intrahemispheric differences in the 12 ROI.
Behavioral responses to the presence of tinnitus were recorded and evaluated after the SIT patients had completed questionnaires regarding tinnitus intensity, severity, and annoyance [11,12,14,15].
We attempted to identify subjective tinnitus severity by use of the tinnitus severity index (TSI), which consists of five questions. When corrected for number of tests (Bonferroni correction for 12 paired t-tests), the normalized data for the interhemispheric difference in the cerebellum, left versus right, were significant (p = .003) before UHF stimulation but were not significant after stimulation. We found in all other ROI no significant difference in left versus right hemisphere in either pre- or poststimulation (p > .05). Scattergrams of the raw SUVs for individual patients showed that patients responded individually and differently to UHF stimulation.
Plots of the ratio of post- and pre-UHF stimulation showed a correlation of PET of brain activation counts with a patient's report of relief from tinnitus with UHF stimulation (see Fig. Because our sample size was small for this pilot study (six patients), we were not able to factor out the differences in SUVs on the basis of the patients' level of relief from symptoms.
The PET of brain finding of cerebellum involvement supports the hypothesis of involvement of the acoustic motor pathway in tinnitus patients (see Fig. The identification with PET of brain of metabolic alterations in multiple ROI in brain involved with tinnitus supports the concept and findings reported initially with SPECT of brain of multiple ROI other than and in addition to the auditory cortex involved in tinnitus [1]. The PET categories of response are considered to support the proposition that the application of high audio frequencies (> 10 kHz) to the skull by bone conduction may produce "masking" in frequencies corresponding specifically to the brain's resonant frequency (approximately 15 kHz) [8]. Correlation of the PET data from the six patients with the UHF audiograms revealed that the best clinical subjective report of reduction in severity (in two patients) was in the hypoactive metabolic PET category and that the UHF audiometric thresholds were 40-50 dB SPL or less in the frequency range of 10-14 kHz (see Tables 1, 2; see Figs. Attempts to correlate the subjective behavioral responses of tinnitus patients for UHF tinnitus relief included questionnaires for tinnitus intensity and annoyance and the TSI. The PET of brain data suggest that the "masking" for perception of UHF frequencies is a different mechanism from that of "masking" from classic conventional audio frequencies. The PET categories of metabolic response and their correlation with the UHF audiometric responses support the suggestion that the "masking" effect may be predominantly cortical and is reflected in cortical neural reorganization and reprogramming. In classic masking, a noise band is effective generally if it overlaps with the sound to be masked [24]. The MML alterations varied in different degrees for each of the three PET of brain metabolic categories of response (see Table 2).
Nuclear medicine imaging in general and demonstrated with PET of brain in this study provides a means to identify underlying molecular genetic and neurochemical mechanisms-individual or shared (or both)- that are involved in the masking effect of a given masking signal in attempting tinnitus relief.
This PET of brain study demonstrates the involvement of multiple ROI in the brain in tinnitus patients, not only in the auditory cortex.
Observed electrophysiological cortical changes have been linked in animal experiments to behavior [30,31]. The problem one faces with the clinical interpretation of the PET of brain data is that it is limited to six SIT patients and that the organization of the cortical auditory system is still controversial in 2004 [32]. Whether regional specialization occurs in cortical processing of a complex sound is unclear [32]. 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. INTRODUCTION: Tinnitus is considered as one of the major symptom associated with many pathologies along with its presence in individuals with normal hearing. OBJECTIVE: Study was undertaken to find the efficacy of Residual Inhibition Therapy as treatment procedure for unilateral tinnitus in individuals with normal hearing by comparing pre and post Residual Inhibition Therapy, Contra-lateral Acoustic Reflexes and Tinnitus Handicap Inventory.
MATERIALS AND METHODS: Ten subjects between the age range of 20-45 years were included for the study. RESULTS AND CONCLUSION: Statistical analysis revealed no significant difference, however, elevated contra-lateral acoustics reflexes post Residual Inhibition Therapy were seen.
Tinnitus is referred to, a sound generated by brain in the absence of acoustic stimulation due to increased neural activity1. Today, with advancing field of Audiology, treatment strategies are aimed to reduce or eliminate symptoms and distress caused by tinnitus which includes Residual Inhibition Therapy (RIT), Masking Tinnitus Retraining Therapy and Cognitive Behavioral Therapy. In support of the literature, audiological practice encounters an increasing number of tinnitus and thus, one needs to evaluate the efficacy of the treatment.
Reflexometry at 500 Hz, 1000 Hz, 2000 Hz and 4000 Hz was repeated to elicit the baseline contra-lateral acoustic reflexes pre Residual Inhibition Therapy. Statistical analysis using paired sample t test is carried out with Bonferroni's correction applied for multiple comparison between pre and post comparison of four frequency thresholds in contra-lateral reflexometry.
The present study investigated the effectiveness of RIT using a questionnaire aiming to betterment of tinnitus and contra-lateral acoustic reflexes in adult individuals. From Table 2, the Tinnitus Handicap Inventory did not show any significant changes in the scores obtained pre and post RIT.
Similarly, obtained contra-lateral reflexes pre and post RIT were compared using sample t-test. From Figure 1 we can conclude that, post RIT contra-lateral acoustic reflexes required higher intensity in comparison to pre RIT contra-lateral acoustic reflexes to elicit a reflex. From Table 3 it is evident that there is no significant difference (p > 0.05) between contra-lateral acoustic reflexes pre and post RIT (Boneferroni's correction applied for multiple comparisons). Primary aim of the study was to establish the effectiveness of RIT on subjects experiencing tinnitus. The depth and duration of residual inhibition was found to be varied from individual to individual and the peak measurement of duration of residual inhibition was 70 sec. The current study results are in support with the previous literature where the 57% of tinnitus experiencing subjects relapse in 2 minutes, 23% subjects in 2 to 4 minutes, 11% subjects in 4 to 6 minutes, 4% subjects in 6 to 8 minutes, 2% subjects in 8 to 10 minutes and 3% subjects with more than 10 minutes19. The current study used duration of 60 seconds for the presentation of target stimulus and the RIT success rate is obtained with increase in number of the target stimulus experienced to suppress tinnitus however, due to the fatigue of masking in subjects some might require longer duration of target stimulus to maintain residual inhibition12.
The poor agreement with the earlier literature could be due to differences in noise bandwidths used for the study, tinnitus pitch tuning methods, sound levels used and the various differences in the experimental details. The present study aimed at testing the effectiveness of RIT using pre and post tinnitus questionnaire response and contra-lateral acoustic reflexes. Paper submitted to the ITJ-SGP (Publishing Management System) on May 21, 2015; and accepted on June 23, 2015.
Congenital atresia of the external ears and severe tinnitus has been reported by two patients to be contralateral to the atretic ear. Our clinical experience since 1977 with tinnitus of the severe disabling type (subjective idiopathic tinnitus [SIT]) in more than 10,000 patients leads us to consider the establishment of a clinical accuracy for the diagnosis of tinnitus as the "key" to achieving tinnitus relief with therapeutic modalities now available.
The completion of a medical audiological tinnitus patient protocol (MATPP) for SIT patients, with extensive testing of the cochleovestibular system, both peripheral and central, has been recommended to establish (1) accuracy of diagnosis of tinnitus, (2) its medical significance, and (3) a rationale for treatment based on a correlation of structure and function [4-6]. Patients with congenital atresia of the external ear and SIT completed the MATPP to establish an accurate diagnosis for the clinical type of tinnitus, to identify and treat factors influencing the clinical course of the tinnitus, and to establish a rationale for attempting tinnitus relief. The patient's tinnitus was described as a noise in "spells of increased intensity of a constant rumble in the left ear," fluctuant intensity, and increasing annoyance within 1-2 months before his neurotological consultation on November 30, 2004. We informed the patient that although no cure was available for tinnitus at this time, the goals of the consultation were to attempt to establish a clinically accurate tinnitus diagnosis and the medical significance of the tinnitus and to attempt to provide tinnitus relief by medication alone or in combination with instrumentation. We recorded the left-ear tinnitus intensity reported by the patient on a tinnitus intensity index (TII) and a tinnitus annoyance index (TAI). Associated complaints included increased left-ear hearing loss, fluctuant left-ear blockage, and weight loss of approximately 20 pounds. Sudden-onset tinnitus in the left ear occurred while the patient was at work on May 5, 2004, in a standing position. Tinnitus originally was reported as an intermittent "highpitched ring" in the left ear at age 21-25 after exposure to loud music. The patient's significant history included congenital atresia of the right external ear, presence of allergies, presence of hearing loss following noise exposure (including to firearms), and reconstructive surgery to the external right ear at age 6-7 years, and hospitalization for kidney stones.
The physical examination included evaluation of the patient's general appearance and an external inspection, both of which were found to be satisfactory.
Site-of-lesion audiometry identified severe hearing loss, which was mixed and predominantly conductive, on the right. Electronystagmography (December 1, 2004) revealed no spontaneous nystagmus, positional nystagmus, or neck torsion. A computed sinusoidal harmonic rotation test (December 1, 2004) revealed left labyrinthine asymmetry, normal saccadic eye movement, and normal OFS.
QEEG (December 1, 2004) demonstrated significant electrical dysfunction in the central nervous system (CNS)(Fig. Baseline SPECT of brain findings (November 2, 2004) included bilateral parietal lobes hypoperfusion, more dominant on the right than on the left side, and bilateral mesial temporal hypoperfusion, more prominent on the right (Fig. Neuroradiology suggested findings may represent vascular deficiency as opposed to cortical atrophy.
An MRI of the brain with gadolinium (May 10, 2004) showed none of the following: acute infarct or intracranial mass lesion, cerebellopontine angle mass or abnormal enhancement within the IAC or inner ears bilaterally, or otomastoiditis.
MRI and MRA scans (December 16, 2004) demonstrated a small area of flow gap or narrowing in the proximal portion of the straight sinus. Tinnitus was diagnosed to be predominantly of a central type in the left ear but to be subclinical in the right ear and to have a bilateral cochlear component. Additional diagnoses included an anxiety syndrome and bilateral heterochromia of the irises. Arteriovenous (AV) fistula, dural fistula, bilateral SEH, autoimmune inner-ear disease, hereditary sensorineural hearing loss, anterior internal cerebral artery (AICA) syndrome (left-sided), and cerebrovascular disease all were recommended to be ruled out.
The initial ear, nose, and throat (ENT) consultation took place 2 days later (May 8, 2004). The patient made an emergency room visit (May 9, 2004) for evaluation of recurrent and increased intensity of the rumble and with concern about left-ear hearing. Neurotological consultation and follow-up visits (November 30, 2004-December 7, 2004) clinically established the following diagnoses: tinnitus of a predominantly central type in the left ear, with a left cochlear component, and subclinical in the right ear. Neurotological recommendations (December 4, 2004) for attempting tinnitus control included general rules pertaining to diet, such as elimination of stimulants and caffeine, and use of ear protection from noise, and specific recommendations of a combined therapy via medication and instrumentation, differentiating between sensory and affect components.
For the sensory component, we recommended medication initially, followed by introduction of instrumentation. For treatment of the affect component, we recommended follow-up with neuropsychiatry and psychology for the anxiety syndrome complaint and for fear. Close observation was advised to include clinical consideration of gradual, progressive cerebrovascular disease.
Neurological followup evaluation (December 9, 2004) reported the tinnitus to be associated with "pressure pulsations" in the left head area. Neurological follow-up on January 14, 2005, reported persistent pulsation tinnitus on the left side of the patient's head.
A neurotological follow-up visit on January 25, 2005, reflected attempts of tinnitus relief from December 7, 2004, to January 25, 2005, as initially recommended and which, by cooperation between the neurologist and the patient, were completed.
The patient reported overall improvement-"water sound in back of head" gone since December 14, 2004-and described the quality of tinnitus frequency as "midrange electric motor" and "80-90% gone." Location of the tinnitus-left ear and back of the head on the right side-was significant. During telephone communication with the neurology physician (February 4, 2005), the patient reported that he was "doing OK," although concern about steroid dependence persisted in order to maintain tinnitus relief.
In a telephone communication with the neurotology physician (February 15, 2005), the patient reported tinnitus relief was being maintained.
At a follow-up visit with neurotology (March 8, 2005), the patient reported tinnitus relief of 15-20% and increasing periods of "ignoring the complaint," with associated reduction in anxiety. During telephone communications with the neurotologist (March 15, 2005-April 12, 2005), the patient reported continued increasing periods and degrees of tinnitus relief.
In telephone communication between the neurotologist and the patient (September 13, 2005), the patient reported tinnitus relief in excess of 90%, absence of any spells, occasional ear blockage prior to or accompanying the tinnitus, no imbalance, and occasional hyperacusis with tinnitus. During further telephone communication with the neurotologist (December 20, 2005), the patient reported tinnitus "rumble" relief in excess of 90%. The etiology of the symptom of tinnitus, as described at the time of and following completion of neurotological consultation (November 30, 2004-December 7, 2004), is considered to have a chiefly vascular basis, reflecting insufficiency of the anterior and posterior intracerebral circulation, and to be a predominantly "soft" sign of gradual, progressive cerebrovascular disease. The clinical history of the original tinnitus, described as an intermittent high-pitched ring in the left ear, is traced to age 21-25 and occurred after exposure to loud music (TII: best = 0 [95%] and 7 [3 days in duration after noise exposure]).
Within the limits of examination at this time, we hypothesized that the clinical course of the tinnitus as described is a reflection of a gradual alteration in the hemodynamics of the intracerebral circulation, highlighted at this time by SPECT of brain of hypoperfusion in regions of interest supplied by the right MCA.
We considered a presumptive left SEH to be clinically related to alteration in homeostatic mechanisms between the fluid compartments of the brain and inner ear, with the resultant accompanying imbalance and reported left-ear hearing loss (May 5, 2004).
Acknowledged was the clinical history of a sudden onset of the tinnitus and the clinical history of tinnitus described as an increase in left-ear ringing 3-4 years ago. We recommended SPECT of brain in an attempt to improve the accuracy of the tinnitus diagnosis, to monitor the efficacy of modalities of therapy attempting tinnitus relief, and to provide a basis for neuroprotective drug therapy. In an attempt to establish a specific vascular etiology, to exclude AV dural fistula, AV malformations, and cisternal and venous sinus anomalies, we recommended MRI, MRA, and MRV, which were reported to be essentially normal.
In summary, we considered the tinnitus complaint in the left ear (as described on November 30, 2004) and its clinical course predominantly to be a "soft" sign of CNS dysfunction, on a vascular basis, superimposed on a preexisting sensorineural hearing loss.
Is the reported SPECT of brain finding of hypoperfusion of the MCA in patients with a congenital atresia of the external ear an anomaly or a coincidence of occurrence [10-12]? We consider to be clinically significant the objective demonstration of hypoperfusion in brain areas of distribution of the MCA on the side of the congenital atretic ear in two patients. Over the long term, the inclusion of nuclear medicine imaging of brain and follow-up in cases of congenital atretic ear wherein this finding was demonstrated will determine the significance of the clinical course of cerebrovascular disease and cochleovestibular complaints in atretic and nonatretic ears. Is brain plasticity altered in the patient with a congenital atretic ear for tinnitus therapies hypothesized to occur at brain cortex [13-20]?
Electrical and air conduction UHF thresholds of hearing (10-20 kHz) in the two cases of congenital atresia of the external ear (in both the ipsilateral and contralateral ears) were greater than expected for the age of the patient.
Is the identification of a UHF sensorineural hearing loss greater than expected for the age of a patient, particularly a tinnitus patient with a congenital atresia of the external ear, a sign of predisposition to the effects of noise exposure and gradually increasing sensorineural hearing loss? Is the finding of hypoperfusion in brain areas of distribution of the MCA in congenital atresia of the external ear a predisposition or a factor (or both) in the development of SEH [27-31]? We considered the SEH and tinnitus in the contralateral ear to be a sign of the effect or presence of a vascular anomaly or an alteration in the intracerebral circulatory pattern on the side of the brain contralateral and secondary to the hypoperfusion in brain areas of the MCA in the atretic ear. The diagnosis of a delayed SEH in patients with tinnitus of the severe disabling type has been reported to be frequent and to influence the clinical course of tinnitus [27].
Clinically, the tinnitus described as a ringing in the ear contralateral to the atresia is considered a soft sign of inner-ear dysfunction. What pathology in this tinnitus patient is reflected in the action of the drugs selected for attempting tinnitus relief (i.e., specifically steroids)? In addition to therapy directed at factors identified as influencing the clinical course of the tinnitus, therapy directed to the GABA-A receptor is hypothesized to increase inhibition at the brain cortex and provide neuroprotection, with resultant increased tinnitus relief and reduction or elimination of the steroid.
What is the incidence of an autoimmune etiology in patients with sensorineural hearing loss? The clinical history of the tinnitus in association with an alteration in hearing in the nonatretic ear introduces the consideration of autoimmune inner-ear disease. What is the incidence of occurrence of objective and subjective tinnitus in the tinnitus population and, in particular, in the tinnitus patient with an atretic ear? In the patient in this report, the objective tinnitus was the rumble auscultated with the stethoscope at the left lateral neck overlying the external ear and left postauricular fold. Is the congenital atretic external ear part of a syndrome that includes the MCA and a loss in the UHFs (10-20 kHz)? SPECT of brain has demonstrated hypoperfusion in brain areas of distribution of the MCA on the side of an atretic ear. A neuroprotective drug therapy strategy targeting the GABA-A receptor (RTT-GABA), for treatment of a severe, disabling, predominantly central-type tinnitus, with a clinical diagnosis of brain cortical ischemia based on brain SPECT, resulted in significant longterm tinnitus relief. The incidence of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear in patients with congenital atresia of the external ear remains to be established. The authors gratefully express their appreciation to the Martha Entenmann Tinnitus Research Center, Inc., for support of this educational and research effort. Unfortunately you cannot use our pictures, as we do not have the copyright, but only have the right to use them on our website.
To play the media you will need to either update your browser to a recent version or update your Flash plugin. OBJECTIVE: The purpose of this study was to evaluate, by using distortion product otoacoustic emission test, the action of Ginkgo biloba extract 761, which has a known antioxidant property, as a possible otoprotective against cisplatin induced hearing loss. METHODS: This prospective study was conducted on individuals that were treated by cancer with cisplatin (CDDP) in a tertiary University center.
RESULTS: Comparisons were made between baseline measurements and those recorded after maximum cumulative CDDP dose. CONCLUSION: Ginkgo biloba extract 761 probably has antioxidant properties, and might play otoprotective effect against cisplatin ototoxicity in these patients.
Cisplatin (cis-diamminedichloroplatinum) (CDDP) is a highly effective chemotherapeutic agent that is widely used to treat a variety of soft tissue neoplasms, including ovarian, testicular, cervical, head and neck, lung and bladder cancer. The reported incidence of hearing loss associated with CDDP administration in adults ranges from 4% to 50%3.
The CDDP interacts with cochlear tissue and generates reactive oxygen species (ROS) such as superoxide anion. Ultrastructural examination of human temporal bones has shown that the primary site of the CDDP ototoxicity is the outer hair cells (OHCs) of the basal and middle turns of the cochlea. Although the treatment with this drug is often effective, serious side-effects such as nausea, nephrotoxicity, neurotoxicity and ototoxicity occur often. Considerable data indicate that distortion product otoacoustic emissions (DPOAEs) can provide information regarding the functional status of OHCs6,7. Gingko biloba extract 761 (GBE 761) is a known extract with antioxidant effects that might prevent the ototoxic effects of cisplatin. We performed the present study in attempting to clarify the role of GBE 761 in the preventing OHCs damage caused by CDDP therapy in patients treated for cancer by means of DPOAEs. This study was submitted and approved by the ethic committee on human beings research at the University of Brasilia - Brazil and the patients signed an informed authorization term in order to be included in the research protocol. Patients were sent to oncologic treatment from the regional public hospitals and were approached to follow this protocol as they signed the consent permition. The study group (SG) was composed by 8 subjects undergoing to CDDP treatment for cancer and GBE 761 (120 mg twice a day) and the control group (CG) was formed by 7 individuals that received CDDP also for cancer treatment and placebo (twice a day).
The placebo was very similar to the GBE 761 and so the researchers and the patients could not tell one from the other and did not know the pills allocated for each patient. Pure tone audiometry (PTA), impedance audiometry and DPOAEs tests were performed just previously to the beginning of CDDP treatment in sG and CG.
PTA thresholds were considered normal if less than 25 dB as referred by Silman and Silverman in 199717. DPOAEs were recorded by using a Scout biologic equipment from bio-logic systems® with the patient sitting in a silent room. When we compared the initial amplitude of the signal of DPOEs, regarding the 90 and 10 percentiles, before the total cumulative dose in the CG (Figure 3A) with the post cumulative dose we found a statistical significant difference for 8 KHz frequency (p = 0.04, t-Student Test) (Figure 3C).
Cisplatin therapy is a well known treatment for cancer and the side effects include: gastrointestinal toxicity, neurotoxicity, nephrotoxicity and ototoxicity.
It was not uncommon to find loss in higher frequencies; nonetheless, continuous administration of this agent increases loss, and other frequencies are altered. In the present study we employed DPOAE test that is recognized as a fast, non-invasive and reliable method to follow early cochlear changes.
Clinical studies showed that ototoxic effect of CDDP depended on total dose administered in all sessions. For these reasons it is rational to search for new protective drugs that might ameliorate CDDP therapy toxic effects in order to become it well tolerated to the patients suffering from cancer23.
The most part of the clinical studies are concentrated in the early diagnostic methods to detect ototoxicity in subjects using CDDP.
To our knowledge, this is the first study with patients undergoing to CDDP anti-cancer therapy and GBE 761.
One of the proposed mechanisms for its beneficial pharmacologic effect is its potent antioxidant action24,25. These findings were supported by OHC preservation by GBE 761 in animals models demonstrated by scanning electron microscopy as compared with the marked OHC loss observed in animals receiving CDDP and no protection drug12,13. Our findings suggest that GBE 761 could protect against CDDP induced ototoxicity in this preliminary clinical trial and are consistent with a Japanese study which showed that a standardized GBE 761 administered 90 minutes before administration of CDDP could ameliorate drug-induced auditory threshold shifts and could protect renal function without any attenuation of the anticancer effect of CDDP in Fisher rats33. The combined activity of all the EGB 761 components is required for optimal therapeutic action32. By the other hand, CDDP ototoxicity affects different individuals in a widely variable manner. Other studies allocating more patients should be addressed in order to minimize the bias of the individual predisposition to the toxic effects of CDDP in the auditory system and chemoprotective role of EGB 761. CDDP induced hearing loss might continue to develop days after the interruption of CDDP administration. GBE 761 at 240 mg a day showed some otoprotection effect against CDDP induced OHCs damage evaluated by DPOAE. Paper submitted to the RBCMS-SGP (Publishing Management System) on November 16, 2015; and accepted on January 21, 2016. Ultra-High-Frequency Acoustic Stimulation and Tinnitus Control: A Positron Emission Tomography Study . For basic science, nuclear medicine imaging attempts to understand and identify underlying mechanisms of tinnitus production and translational neuroscience for establishing structure and functional relationships of brain and ear and to identify its underlying molecular genetic neurochemistry [1-4]. The nuclear medicine imaging technique of positron emission tomography (PET) was included in a study protocol for 6 patients randomly selected from a cohort of 15 patients with tinnitus of the severe disabling type (SIT). Furthermore, it was employed to monitor what, if any, alteration in brain metabolism occurred in brain regions of interest (ROI) selected for data analysis and to correlate the PET data with parameters of subjective hearing, balance, behavior, and electrophysiological responses of the cochlear vestibular system, both peripheral and central. All 15 patients had completed the medical-audiological tinnitus patient protocol and the outcomes questionnaires [11,12,16,17]. The final PET of brain imaging was completed within 5 minutes of the last UHF therapy (n = 5) and within 12 hours (n = 1).
Anatomical tissue images were generated, and standard circular ROI were created for each patient in the study.
Ultra-high-frequency air conduction audiograms (right ear) and correlated with positron emission tomography (PET) of brain metabolic categories: hypermetabolic (hyper), hypometabolic (hypo), and mixed metabolic (mixed).
Ultra-high-frequency air conduction audiograms (left ear) and correlated with positron emission tomography (PET) of brain metabolic categories: hypermetabolic (hyper), hypometabolic (hypo), and mixed metabolic (mixed).
The test is easily administered, is brief, has clearly defined categories, and is simple for patients to answer. The number marked for each question is viewed individually and then scored for all five answers. Ratio of before and after positron emission tomography (PET) metabolic standard uptake values in selected regions of interest (right and left frontal, right and left temporal, right and left parietal, right and left auditory, right and left thalamus, right and left cerebellum).
For all patients, the left cerebellum prior to UHF stimulation showed more activity in the left side than the right. Intrahemispheric recordings showed no significant difference in pre- versus poststimulation (p > .05) uncorrected for Bonferroni. When they were tested as a group with the paired t-test, the difference in responses cancelled out and were not significant. Positive associations were established among the PET of brain metabolic categories of response, UHF audiograms, minimal masking levels, and subjective reports of UHF efficacy for tinnitus relief (see Table 2).
Two patients reported no significant change in their tinnitus 1 week after stimulation but good relief 8 weeks after. The greatest shifts in MMLs were seen in the two patients in the hypoactive PET category, with the maximal shift indicating a 45-dB reduction.
The outcome correlated with the PET of brain metabolic category of hypoactivity and UHF audiometric thresholds of at least 40-50 dB SPL and in the frequency range of 10-14 kHz (see Table 2).
The three metabolic categories of brain PET- hyperactivity, hypoactivity, and mixed activity (see Fig. Reorganization of the auditory cortex in tinnitus patients has demonstrated an expansion in the tinnitus frequency area (more than doubled in size), with a suggestion of lower-frequency expansion below the expected frequency subsequent to the hearing loss [20].
The mechanism of detecting bone- and fluid-conducted ultrasound is likely related to a single demodulating system. Ultrasonic masking has been reported to suppress audio thresholds in the 8- to 12.5-kHz range by 2-29 dB [21,22]. The outcome in the one patient in the mixed category is considered to support the clinical significance of the correlation of the brain PET of brain metabolic categories and the UHF audiogram.
The integrity of the brain cortex is critical for plastic changes involving neural reprogramming and neural reorganization.
The results of the behavioral correlation have been reported for the total cohort (N = 15) [11-15].
The masking phenomenon of the auditory system is conceived to have different generators at different levels of the ascending and descending auditory system, with involvement of different and multiple neurotransmitter systems. The role of brain demodulation for sound perception and attempted tinnitus relief is suggested to be unique for UHF and introduces concepts new to that of classic acoustic masking [24]. We consider a predominantly cortical effect to be supported by the lack of correlation of the PET of brain metabolic categories of response and the Feldmann masking curves (see Table 2). An exception is the case of upward spread of masking when a low tone at a certain intensity can mask a tone much higher in frequency. Similarly, our experience with attempting electrical suppression for tinnitus relief suggested that "electrical masking" was different from classic acoustic masking at 250 Hz - 8 kHz.
A preliminary report of the application of magnetoencephalography to try to establish electrophysiological evidence of classic acoustic masking has reported involvement of the temporal lobe [26]. Whether the metabolic function in these ROI, as demonstrated with PET of brain, reflects the tinnitus signal or that of the UHF stimulus or both remains for future investigation. The role of the auditory cortex in auditory space mapping occurs in the process of identification [27].
The transition between the two is hypothesized to occur in a final common pathway for tinnitus. The PET of brain data of this study contribute to basic science questions in systems neuroscience of the structure of the neural code [33]. Imaging goes beyond investigations of the cortical auditory syst em with electrophysiological recordings.
It is suggested that the PET results may reflect an anteriorly directed "what" pathway of the sensory stimulus and a posteriorly directed "where" pathway-both of which may have application for auditory processing.
Scientific Computing Center at Downstate Medical Center-State University of New York, Brooklyn, New York. 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.
With varied cause and mechanism of its generation and increase in number of individuals with complaint of tinnitus, rehabilitation becomes crucial for Audiologists. Even though small sample size made it hard to conclude on the effectiveness of Residual Inhibition Therapy as treatment of tinnitus, elevated contralateral acoustic reflexes post Residual Inhibition Therapy pay way for further advanced studies on the same. It is considered to be an auditory phantom sensation experienced by 10-15 persons out of general population2. RIT is referred to the auditory stimulation that results in temporary suppression of tinnitus6.
Thus, the study was designed to know the effectiveness of RIT by comparing pre RIT contra-lateral acoustic reflexes to post RIT contra-lateral acoustic reflexes in normal hearing subjects experiencing continuous tinnitus unilaterally. The study protocol was approved by the Institutional Ethical Committee Board at Nitte Institute of Speech and Hearing, Mangalore. Subjects answered a questionnaire developed by five experienced Audiologists to rule out nature of complaint. For this, obtained questionnaire score and contra-lateral acoustic reflexes were measured at octave frequencies between 500 Hz and 4000 Hz were compared. Bonferroni's correction was applied for multiple comparison between pre and post comparison of four frequency thresholds.
However there is no significant difference between the pre and post RIT contra- lateral acoustic reflexes. For this, pre and post RIT questionnaire response and contra-lateral acoustic reflexes were compared. This variation may be due to quieter level of stimulus intensity and lesser duration of narrow band noise played to the subjects which were required to influence the tinnitus triggering system. Explanation on subject's response to RIT after the target sound ends is with the start of silent phase of 20 to 35 seconds, followed by 30 to 35 seconds in which the tinnitus sound gradually recovers back. RIT has approved good effectiveness when the pitch of the tinnitus is matched with the target sound presented to suppress tinnitus15 however; in the present study we used narrowband noise of the nearing experienced tinnitus frequency.
Also, sample size used is small which can significantly influence the effectiveness of RIT.
Contra-lateral acoustics reflex thresholds obtained post therapy state is relatively higher than the pre therapy state, however, Tinnitus Handicap Inventory scores showed not much improvement. Lectutrer, Nitte Institute of Speech and Hearing, Mangalore University, Approved by Rehabilitation Council of India.
Intern (BASLP), Nitte Institute of Speech and Hearing, Mangalore University, Approved by Rehabilitation Council of India. The use of the nuclear medicine imaging technique of single-photon emission computed tomography (SPECT) of brain has demonstrated hypoperfusion in brain areas supplied by the middle cerebral artery on the side of the atretic ear.
Multifactorial elements influence the clinical course of SIT and attempts for establishing tinnitus relief [1-3]. We present these findings to support previous recommendations of extensive cochleovestibular and brain function testing to be completed in SIT patients.
As far as we can determine, these findings, highlighted by brain SPECT, have not previously been reported in patients with congenital atresia of the external ear. Also demonstrated were memory interference and increased tinnitus intensity reported with increasing left-ear blockage. The TII at that time was reported as best (0; 95%) and worst (7) for 3 days after noise exposure.
Ocular examination revealed symmetrical eyelids, clear conjunctivae, heterochromic irises, and equally reactive pupils without sign of spontaneous labyrinthine irritation. SPECT of brain: bilateral parietal lobes hypoperfusion, more dominant on the right than on the left side, and bilateral mesial temporal hypoperfusion, more prominent on the right. Sinusitis was seen bilaterally, although it was more pronounced in the maxillary than the ethmoid sinus. A partial obstruction in this area was suspected, although artifact may have accounted for this finding. Hearing loss was mixed moderate-severe and predominantly of the conductive type in the right ear and of a mild sensorineural type in the left, with a bilateral cochlear component and involvement of the central auditory pathways bilaterally (see Fig. An objective tinnitus and presumptive secondary endolymphatic hydrops (SEH) was diagnosed in the left ear. SPECT of brain (December 2, 2004) reported hypoperfusion in regions of interest in brain consistent with distribution of the right MCA (see Fig. The diagnoses included atypical left-ear tinnitus, congenital right-ear deafness, structural anatomy of the seventh and eighth nerve complexes to be normal right as reported on the MRI obtained on May 10, 2004. Instrumentation recommendations were deferred pending tinnitus relief results and would include (if necessary) a trial tinnitus masker and UHF acoustic stimulation and external electrical stimulation and tinnitus retraining therapy. Follow-up with an internist was recommended to maintain stable blood pressure and to complete a metabolic battery with appropriate treatment as necessary. We further advised that the patient consider Klonopin use if no medical contraindication existed.
Progression complaints of hearing loss, tinnitus, vertigo, and ear blockage, alone and or in combination, were to be clinically considered a "soft" sign of gradual, progressive CNS disease. We hypothesized this original tinnitus to have been clinically predominantly a cochlear type before May 2004 and considered it to have become since age 21-25 years subclinical in the left ear. We further conjectured a resultant ischemia at brain cortex with noisy spells at the brain cortex owing to left cortical activation and a cochlear tone (as previously outlined), reflecting activation of a subclinical left-ear tinnitus, due to possible interference in AICA blood flow to the left cochlea.
Alteration in aeration of the middle ears secondary to Eustachian tube dysfunction or SEH (or both) identified in the left ear may result in fluctuation in hearing or progressive sensorineural hearing loss (or both). The hearing in the left ear has been stable clinically and confirmed by audiometric testing since November 30, 2004, and when the patient was last seen (September 13, 2005). When seen in initial neurotological consultation (November 30, 2004), the ear blockage had been predominantly located in the left ear and clinically related to left inner-ear SEH. The report of interference in memory 3 months before November 30, 2004, was considered significant. The report of SPECT perfusion asymmetries in the brain was the basis for recommending a neuroprotective receptor-targeted therapy directed at the GABA-A receptor, in an attempt to treat a presumptive ischemia of the affected cortical areas.
We considered the medical significance of the tinnitus symptom to be gradual, progressive cerebrovascular disease. What is the incidence of the hypoperfusion in brain areas of distribution of the MCA in patients with a congenital atresia of the external ear?
Follow-up nuclear medicine imaging studies in the atretic ear population with and without tinnitus will determine its incidence of occurrence. Nuclear medicine positron emission tomography imaging of brain before and after UHF stimulation revealed a correlation of metabolism of brain at the cortex, with residual neuronal function in the 10- to 20-kHz range of hearing [25]. Additional considerations to explain differences in UHF thresholds include exposure to loud noise and a hereditary sensorineural hearing loss. Follow-up studies by hearing conservation programs in general and specifically for the population of tinnitus patients with a congenital atresia of the external ear will provide answers to this question.
It is considered to be a reflection of the SEH: the result of failure to reestablish "normal" homeostatic mechanisms controlling the hemodynamics of the intracerebral vascular and spinal fluid systems in response to hypoperfusion in the areas of distribution of the right MCA.
Within the limits of examination and supported by blood testing, we did not identify any evidence of autoimmune inner-ear disease. Correlation of the findings of the neurotological workup with extensive testing of the cochleovestibular system (both central and peripheral and objective testing of CNS metabolic and electrophysiological responses) provided for accuracy of the tinnitus diagnosis and a rationale for achieving significant tinnitus relief. The medical significance of an objective and subjective tinnitus of the severe disabling type, as demonstrated with SPECT of brain, may be a soft sign of gradual, progressive cerebrovascular disease.
We suggest that the findings of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear and hearing UHF thresholds in the ear contralateral to the atresia are part of a syndrome in patients with congenital atresia of the external ear.
The only condition is that you provide a direct link to the specific article you use on the page where you quote us. The chemopreventive effect of Ginkgo biloba extract 761 against cisplatin ototoxicity: a pilot study.
This prospective and double blinded study was conducted on individuals that were to begin cisplatin treatment in a tertiary university center. Both groups were instructed to ingest the either placebo or Ginkgo biloba extract 761 before the first cisplatin dose. Some audiometric studies have reported elevated hearing thresholds in 75-100% of patients treated with CDDP3,4. However, if ultra-high frequency audiometry is used, the incidence of threshold changes may be as great as 100%1,5. Cochlear tissues from animals receiving ototoxic doses of cisplatin were depleted of glutathione and antioxidant enzymes1. These side effects interfere with the treatment and often force the reduction of the dose, frequency and duration of the CDDP therapy2. With evidence that CDDP preferentially affects OHCs function, it is possible to believe that DPOAEs would change with CDDP treatment8-11.
GBE 761 was found to eliminate free oxygen radicals and therefore it might block oxidative stress and the hair cells apoptosis12,13.
The general selection criteria were: Age 18 years and older, no previous history of middle and inner ear diseases, no previous treatment with CDDP, normal audiometric and impedance audiometric tests as well as normal DPOAEs in the range of frequencies studied.
Although a dose-response relationship is not established, 240 mg day GBE seems to show a higher rate of treatment response than other doses of GBE14. The individuals were required to intake either placebo or GBE 761 two hours before the first CDDP dose and to keep the dosage during the whole CDDP treatment. Normal tympanogram type A and presence of ipsi and contralateral stapedial reflex were the normal parameters for impedance audiometry. The average of the amplitude of the signals were calculated and used for comparisons between the groups.
The results of the groups were compared by U-ManWhitney, Kruskal Wallis and t Student test by employing. Kruskal Wallis test was used to investigate the differences between the groups of cumulative doses of CDDP. There was no statistically significant difference (p > 0.05) between the groups according to the age and the analysis of the amplitude of the signal in the pre-treatment evaluation in all frequencies.
In patients of SG, GBE 761 did not interfere with the antitumor activity of CDDP as registred by the patients records. In our study we tested the protective effect of GBE 761 in the OHCs of human beings by means of DPOAE record.
Just a few studies were designed to evaluate the chemoprotective drugs against CDDP ototoxicity.
The ototoxicity is reported to be due to superoxide products formation that leads to the OHCs apoptosis. Studies have shown the in vitro and in vivo protective effects of GBE 761 against oxidative stress25,26, and these are closely related to its ability to scavenge free radicals, such as superoxide anion, hydroxyl, and peroxyl radicals27,28. In this study we attempted to investigate whether GBE 761 had otoprotective effect against CDDP ototoxic effect in the OHCs. Our data offer evidence supporting the potential benefits of the antioxidant GBE 761 in CDDP chemotherapy in the preservation of hearing in humans for the first time.
Further studies with long term follow up including more patients should be addressed in order to clarify the long term effects of GBE 761 on hearing preservation and antitumor properties. Further studies with more patients and long term follow up may reveal optimal dosing, administration via and potential clinical usefulness of GBE 761 as a chemoprotective agent against CDDP ototoxicity.
Kose K, Doğan P Lipoperoxidation induced by hydrogen peroxide in human erythrocyte membranes. Wong A, Dukic-Stefanovic S, Gasic-Milenkovic J, Schinzel R, Wiesinger H, Riederer P, et al. Clinically, nuclear medicine imaging attempts to correlate structure and function, to identify conditions associated with tinnitus, to improve the accuracy of the diagnosis of the tinnitus symptom, and to monitor the efficacy of therapeutic modalities focused on tinnitus relief [5,6]. Attempts were made to establish the efficacy of UHF for tinnitus relief both short-term (1 week) and long-term (8 weeks). Selection of the ROI for PET of brain analysis was based on a clinical experience with single-photon emission computed tomography (SPECT) of brain, ongoing since 1989 at Downstate Medical Center-State University of New York.
All emission data were attenuation-corrected using standard 68- germanium transmission algorithms.
Data for each patient were paired, using each patient as his or her own control to eliminate baseline differences.
Patients were instructed to mark the degree of interference caused by the tinnitus for sleep, concentration, work performance, communication, and understanding. PET of brain metabolic categories: hypermetabolic (hyper), hypometabolic (hypo), and mixed metabolic (mixed).
After UHF stimulation, only one patient still showed greater activity in the left cerebellum, one showed no difference, and three now showed greater activity in the right cerebellum versus the left side. No association of response was established between PET of brain metabolic categories of response and the conventional, classic audiogram and tinnitus annoyance [11-15]. All six patients reported some degree of tinnitus relief either at 1 week or 8 weeks after stimulation. The subjective responses reported as "fair" at the conclusion of 1 and 8 weeks of stimulation by three tinnitus patients correlated with PET of brain metabolic categories of hyperactivity and audiometric thresholds greater than 40-50 dB SPL in the frequency range of 10-14 kHz (see Table 2).
All six PET tinnitus patients reported a degree of tinnitus relief either at 1 week or 8 weeks after stimulation.
None of the six SIT patient who completed the PET of brain study reported an increase in tinnitus or a subjective loss of hearing. Owing to the small sample size, we were not able to separate the patients into groups on the basis of their level of relief from tinnitus and to determine whether a significant difference could be detected in their individual PET recordings. The maximum ultrasonographic masking effect was reported in a 12.5- to 16-kHz range and less for frequencies higher and lower than the resonance peak characteristic for a resonance phenomenon [8].
Furthermore, the remaining two metabolic categories correlated with the residual neuronal function as revealed in the UHF audiograms and the reported tinnitus relief. The Feldmann masking curves are clinically considered to reflect a masking response, predominantly in the cochlea, of residual functioning neurons at the basilar membrane between the frequencies of 250 Hz and 8 kHz. In our study, MMLs were reduced across the audiometric range (250 Hz-8 kHz), varying individually by degree. Brain demodulation results in neural reprogramming and reorganization at a cortical level in multiple areas of cortex, which, when successful, masks the tinnitus and is reported by tinnitus patients as tinnitus relief [8,9]. The PET of brain data support the view that the function of the auditory cortex is dynamic and not stable. Again, the question arises: If residual central nervous system cortical damage exists in a particular tinnitus patient, how may it influence cortical reorganization and response to UHF stimulation or to other modalities attempting tinnitus relief? We suggest that the integrity of this pathway influences not only the individual response to a sensation but the behavioral response. The PET of brain metabolic categories of response in this study contribute to an understanding of this issue. The symptom of tinnitus and sensory disorders requires a synergy between electrophysiology and nuclear medicine imaging to correlate and identify findings for understanding underlying mechanisms and neurochemistry involved in brain structure and function.
The activation of different cortical areas is reported to have behavioral consequences of reversibly inactivating different cortical areas [30,31]. This study reinforces the need not only for bottom-up but for top-down imaging studies in SIT patients.
GABAA - Benzodiazepine-chloride receptor-targeted therapy for tinnitus control: Preliminary report.
Rapid task-related plasticity of spectrotemporal receptive fields in primary auditory cortex.
Architectonics of the human cerebral cortex and transmitter receptor fingerprints: Reconciling functional neuroanatomy and neurochemistry. Architectonics and cortical connections of the upper bank of the superior temporal sulcus in the rhesus monkey: An analysis in the tangential plane.
Dual streams of auditory afferents target multiple domains in the primate prefrontal cortex. Optical imaging of intrinsic signals in ferret auditory cortex: Responses to narrow band sound stimuli. An Investigation into the Functional Anatomy of the Ferret Auditory Cortex Using Optical Imaging and Multielectrode Recordings. 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.
Transient and distortion product evoked oto-acoustic emissions in normal hearing patients with and without tinnitus.
DPOAE in estimation of the function of the cochlea in tinnitus patients with normal hearing.
Tinnitus and 2f1-f2 distortion product otoacoustic emissions following salicylate overdose.
Ten(HL)-test results and psychophysical tuning curves for subjects with auditory neuropathy.
The Pre Residual Inhibition Therapy, contra-lateral acoustic reflexes and Tinnitus Handicap Inventory scores were compared to post Residual Inhibition Therapy, contra-lateral acoustic reflexes and Tinnitus Handicap Inventory scores. Use of this treatment has shown 90% of the subjects with tinnitus relief and 10% with modification in tinnitus with minimal reliefs7. Questions in the questionnaire probed to know the onset (sudden or gradual), progression (static or progressive), nature of the tinnitus (intermittent, continuous), ear experiencing tinnitus (right, left or both ears) and duration of tinnitus persistence. Thresholds of each subject were found out using both air conduction and bone conduction mode.
Four individuals reported of reduction in tinnitus loudness, 3 reported of complete termination of tinnitus and 3 reported of no change in the tinnitus. The influence of masking level that deepens the residual inhibition as it goes above the level required to mask tinnitus17 or due to the impedance offered by the cochlear dead region even in normal hearing individuals with tinnitus18 could have yield poorer results.
Similarly, the literature reports that few subjects experience increase in the tinnitus loudness than the decrement which lasts for a duration less than one minute20.
Residual inhibition will be effective with longer exposure to target stimulus and subjects who experience no residual inhibition in the initial stages may experience it after regular exposure to target sound21. Residual inhibition functions overlap tinnitus spectra and the region of auditory threshold shift.
Evaluation and Selection of Maskers and Other Devices Used in the Treatment of Tinnitus and Hyperacusis.
Ultrahigh-frequency audiometry (UHFA) has revealed a bilateral loss of hearing greater than expected for the age of affected patients. The clinical course of two cases of congenital atresia of the external ear and tinnitus supports this clinical experience.
In addition, the patient experienced an occasional perception of "water rushing" 4-5 days after a reduction in the rumble intensity and a "ring" in the left ear. The patient reported an increased frequency of occurrence within the last 3-4 years and an increased intensity (average TII, 3) after left-ear rumble. A review of symptoms revealed anxiety, memory interference of 3 months' duration, and kidney stone. During otoscopic examination, the external leftear canal was found to be satisfactory, whereas signs of reconstructive external right-ear surgery and right external canal atresia were seen. Among the tuning-fork evaluations, the Weber test showed right lateralization, whereas the Rinne test was positive on the left and negative on the right. Rightsided gaze testing showed a right-beating nystagmus with ocular fixation suppression (OFS), downward gaze testing resulted in vertical up-beating nystagmus with OFS, and left-sided gaze testing revealed dysrhythmia with no OFS. We considered magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA) for further evaluation. A Diamox stress test could differentiate between the two but was deferred due to allergy to sulfa.
An audiometric test (May 8, 2004) reported no response in the right ear but left-ear hearing within normal limits for language and speech and a mild sensorineural hearing loss at 4 kHz. Intramuscular Decadron (10 mg) and continued Medrol Dosepak and Ativan (1 mg) for anxiety were recommended. Hearing loss in the right ear was predominantly mixed and involved a cochlear component, whereas there was a predominantly cochlear-type hearing loss in the left ear within normal limits for language and speech (see Fig.
A neuroprotective drug protocol was recommended of a receptor-targeted therapy, gabapentin (100-mg tablet in one dose to be titrated based on the TII), and clonazepam (Klonopin, 25 mg at bedtime), if not medically contraindicated, the dose to be titrated based on the TAI.
Any deterioration in the patient's condition was to be assessed by an internist, a neurologist, or an ENT specialist, and should include audiometry in an attempt to maintain hearing. Neuroradiological follow-up including CT scan of the temporal bones confirmed right external-ear canal atresia, a dilated right IAC, and a normal left temporal bone. The complaint of ear blockage was reduced in the left ear, and no vertigo or balance complaint remained. The rumble sound was objectively auscultated over the left external ear (November 30, 2004).
We further hypothesized that a cerebrovascular factor, gradual in onset, "triggered" the subclinical left-ear tinnitus to manifest itself as spells of noise at the brain cortex, located in the head, and as a "tone" in the left-ear cochlea.
Alteration in underlying homeostatic mechanisms maintaining normal function of the fluid compartments of the blood-brain and bloodlabyrinth barriers are hypothesized to have contributed to the left-ear SEH. The UHFA findings of a loss of hearing greater than expected for the age of the patient may be a reflection not only of noise exposure in the past but, more significantly, together with the heterochromia of the irises, of a hereditary sensorineural hearing loss. To be considered at this time was a left-ear AICA syndrome associated with gradual, progressive cerebrovascular disease.
Recommendations included replacing the antiseizure medication topiramate (Topamax) with gabapentin (Neurontin) in combination with clonazepam (Klonopin).
We advised the patient to enter into this decision-making process if the tinnitus complaint persisted and the significance of the tinnitus complaint outweighed the incidence of potential complications of angiography.
Accurate tinnitus diagnosis by inclusion of peripheral and central tests of cochleovestibular function or dysfunction combined with tests of brain function (SPECT, QEEG) provided a rationale for tinnitus treatment that resulted in significant tinnitus relief, maintenance of hearing, and control of balance.
Specifically, brain plasticity at the cortex was most effective with UHF acoustic stimulation when the integrity of the brain at the cortex was intact and the residual neuronal function in the 10- to 14-kHz range of hearing did not exceed audiometric thresholds (30-40 dB).
For the future, routine hearing testing, including establishment of UHF audiometric thresholds in all patients with congenital atresia of the external ear, will provide an answer to the question of whether this observation is special for patients with congenital atresia of the external ear and will assist in the determination of its medical significance for hearing conservation in general. It is considered clinically significant that the diagnosis of a secondary (delayed) endolymphatic hydrops was identified in two cases of congenital atresia of the external ear, in the tinnitus ear contralateral to the side of the atresia. We recommend conducting a complete evaluation of the cochleovestibular system, both peripheral and central, including nuclear medicine imaging (SPECT of brain, UHFA, and QEEG), in an MATPP for SIT patients to improve the accuracy of the tinnitus diagnosis, to provide a rationale for treatment, and to monitor the clinical course of the tinnitus complaint.
As far as we know, the finding of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear has not been previously reported. GABA-A-benzodiazepine- chloride receptor-targeted therapy for tinnitus control: Preliminary report. This is particularly problematic in patients receiving CDDP with risk factors that increase the risk for ototoxicity that include: younger age, larger cumulative doses, pre-existing hearing loss, nephrologic disease and irradiation of the brain or skull base3,4. The ototoxic effect in adults is characterized by irreversible, progressive, bilateral high-frequency sensorineural hearing loss associated with tinnitus5. Inhibition of antioxidant enzyme activity by cisplatin can allow ROS, such as superoxide and hydrogen peroxide, and toxic lipid peroxides to increase within the cochlea. Changes in spiral ganglion cells have also been reported in the basal turn, where OHCs damage is most extensive.
To our knowledge, by now, there are no studies in humans dealing with the antioxidant properties of GBE 761 in preventing OHCs injuries in patients undergoing to CDDP therapy.
These patients were selected for CDDP treatment based on their oncologic treatment indication at the oncologic clinic at the University of Brasilia Hospital and Hospital de Base in Brasilia, Brazil. GBE 761 can have effects within a short period of time (ie, within 1 to 3 hours from the intake)16. T student test was used for the study of the normality parameters according to percentiles 10 and 90 in the SG and CG. However, there was a statistical significant difference between the CG and SG after CDDP treatment for the frequency of 8 KHz (p = 0.03) (Figure 1). This might be in agreement to the fact that GBE 761 has been shown to possess proapoptotic activity against malignant neoplasms19. Our patients were followed up to 90 days and it is possible that the deposit effect of CDDP in the body could not be evaluated among our patients because of the short term follow up period. Animal studies attempting to investigate the protective effect of GBE 761 against CDDP therapy used doses of CDDP that sometimes could not be compared to doses used clinically12,13.
GBE 761 is a dietary supplement derived from the deciduous tree, Ginkgo biloba, considered to be the world's oldest living tree species, which contains unique chemical substances unknown in other living things13.
Furthermore, GBE 761 also inhibits lipid peroxidation reactions and enhances antioxidant enzyme activities12. It would be highly advantageous to identify genetic variants that predispose to CDDP ototoxicity in order to minimize the risk to susceptible subgroups. Changes in otoacoustic emissions and auditory brain stem response after cis-platinum exposure in gerbils. Effects of cis-platinum chemotherapy on otoacoustic emissions: the development of an objective screening protocol. Evoked otoacoustic emissions--an approach for monitoring cisplatin induced ototoxicity in children. Characteristics and risk factors of cisplatin-induced ototoxicity in testicular cancer patients detected by distortion product otoacoustic emission.
Cis-dichlorodiammineplatinum (II) (NSC-119875): hearing loss and other toxic effects in rhesus monkeys. Early changes in auditory function as a result of platinum chemotherapy: use of extended high-frequency audiometry and evoked distortion product otoacoustic emissions. From laboratory to clinic: a large scale study of distortion product otoacoustic emissions in ears with normal hearing and ears with hearing loss. Ginkgo biloba extract (EGb 761) induces apoptosis by the activation of caspase-3 in oral cavity cancer cells. Ginkgo biloba extract protects brain neurons against oxidative stress induced by hydrogen peroxide. Superoxide anion scavenging effect and superoxide dismutase activity of Ginkgo biloba extract.
Role of nitric oxide in blood-brain barrier permeability, brain edema and cell damage following hyperthermic brain injury. Anti-inflammatory antioxidants attenuate the expression of inducible nitric oxide synthase mediated by advanced glycation endproducts in murine microglia. Experimental studies of the protective effect of Ginkgo biloba extract (GBE) on cisplatin-induced toxicity in rats. This clinical experience has revealed perfusion asymmetries in multiple regions of brain, highlighted by the frontal, temporal, medial-temporal, and parietal lobes and the cerebellum (A.M.
All patients were scanned at 1 hour after intravenous administration of a standard 10-mCi dose of fluorine-18-2-deoxyfluoroglucose (18F-FDG).
For each ROI, interhemispheric counts were subjected to analysis for both pre- and post-UHF stimulation. A rating scale of 0-7 points was used, in which 0 represents no interference and 7 signifies extreme interference.
The two patients who reported no significant change in their tinnitus 1 week after stimulation reported a fair degree of relief at 8 weeks after stimulation. Two of the six reported no significant change at 1 week after stimulation but moderate relief at 8 weeks after.
The principle factor is not the relative energy but its relationship to the fundamental frequency of the forced brain in motion [8]. The category of metabolic hyperactive brain PET in tinnitus patients (n = 3) is clinically considered to reflect a reduced number of residual neurons in the UHF range of 10-20 kHz; they require more acoustic energy for activation and therefore reflect as a metabolic hyperactivity at brain cortex.
This finding is similar to our clinical experience with tinnitus acoustic masking attempting tinnitus relief and the hearing aid recommendation for attempting improvement in hearing and tinnitus relief [16]. Homeostatic synaptic stability is considered crucial for activity-dependent stabilization of the neural circuits [28]. Are the PET of brain metabolic categories of tinnitus relief the behavioral response of SIT patients and thus do they reflect the neuronal reorganization at brain auditory cortex and associated ROI in brain that has actively tuned itself to a newly acquired stimulus (UHF I UQ)?
Investigations have placed emphasis on the correlation between auditory signals and speech processing in acoustic processing. Tinnitus provides a unique opportunity to understand an aberrant sensory stimulus and its behavioral consequences. Presented at the Twenty-First Annual Meeting of the Association for Research in Otolaryngology, St.
Presented at the Neurootological and Equilibriometric Society meeting, March 24, 2004, Bad Kissingen, Germany.
Presented at the Neurootological and Equilibriometric Society meeting, March 24,2004, Bad Kissingen, Germany. Presented at Charles University, Department of Otolaryngology, Prague, Czech Republic, March 28, 2004.
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. However, few postulated etiologies can be attributed to age, exposure to loud noise, earwax blockage, air bone changes, Meniere's disease, tempro-mandibular joint disorders, head or neck injuries, acoustic neuroma, etc.
Literature has also reported the experience of residual inhibition in more than 8 out of 10 persons with tinnitus8 and reduction in tinnitus loudness by 39%9. Total ten subjects with a complaint of tinnitus persisting for more than two weeks were recruited.
The insignificant result to the success of RIT can be attributed to the influence of identification level of tinnitus expertise, the inability to match the tinnitus exactly due to overlapping of tinnitus frequency in some subjects and the effect of RIT lasting for few seconds or minutes8. However, only 54% subjects experienced complete silence in total 46 subjects with tinnitus and who underwent.
Proceedings of the Vth International Tinnitus Seminar; 1995 July 12-15, Portland, Oregon, USA. Oregon: Oregon Hearing Research Center, Department of Otolaryngology, Oregon Health & Science. Quantitative electroencephalography (QEEG) has shown a significant central nervous system electrical dysfunction correlated with the SPECT of brain findings. A sensation of "vertigo" of approximately 24-hour duration described as a "drunk feeling" followed the rumble sensation.
Clinically, an ischemia was presumed to be present based on our past SPECT of brain experiences with tinnitus patients of the severe disabling type [10]. Physical examination was consistent with the diagnosis of chronic vasomotor rhinosinusitis, chronic catarrhal otitis media, and Eustachian tube dysfunction on the left. The patient reported an improvement, which included elimination of the vertigo and left-ear blockage and a reduction in the tinnitus intensity. Initial neurological recommendations included continuation of the steroids in a tapered dosage and a trial of Topamax and verapamil if the tinnitus complaint persisted or recurred. The patient reported no associated complaint of hearing loss, vertigo, ear blockage, nausea, headache, drowsiness, or blurring of vision. Our advice was to follow the neurological recommendation of Mobic, 7.5 mg bid, to assist in prednisone reduction, which was reported by the patient to be effective.
The clinical history of spells of this tinnitus, which are influenced by steroids, is considered to be mainly cortical in location.
We considered both auditory percepts to be a clinical reflection of altered hemodynamics in cerebrovascular circulation.
Normal Eustachian tube function control has been maintained with decongestant nasal steroid spray.
We recommended neurological consultation follow-up to establish the neurological significance of these complaints and correlation with SPECT results, MRI reports, and central cochleovestibular test findings.
The MRA results (December 16, 2004) showed a small area of flow gap or narrowing in the proximal portion of the straight sinus, leading to suspicion of a partial obstruction or artifact in this area. Clinically, such tinnitus patients reported tinnitus relief as most effective and demonstrated hypometabolism at the cortex. The diagnosis of SEH was supported by the subjective complaint of ear blockage in the tinnitus ear and its reduction with diuretic therapy. A maintenance dose of Klonopin and a gradually increasing dosage of the antiseizure drug gabapentin replaced the Topamax. Presented at the Thirty-First Congress of the Neurootological and Equilibriometric Society, Bad Kissingen, Germany, March 24-27, 2004. Proceedings of the Fifth International Symposium on Meniere's Disease and Inner Ear Homeostasis Disorders. One inch of ice in 3 days !!!It wasreal windy most of the day and I spent more time in the EskimoQuick Fish 3.The two holes in the shelter provided some steady action for perch and bluegills.
The degree of hearing loss seems to be associated with cumulative dose, method of administration, previous cranial radiation, and age of the patient, with younger and older patients more commonly affected5. According to them, GBE 761 exhibited half lives ranging from 2 to 4 hours and activity levels with peak at 1.5 to 3 hours in animal and human models. However, it was sufficient to show some ototoxic effect since it usually appears during the first days of the drug administration. It has been observed that hearing loss may occur even after several days after CDDP administration21,22. The route of administration of CDDP (e.g subcutaneous, intraperitoneal and intramuscular) differs markedly from the humans.
The free radical scavenging activity of GBE 761 is comparable to that of other known antioxidants such as vitamins A and C, as well as the tripeptide GSH29. The most important limitation of our study and the data analysis was the size of our sample. Comparison of the antioxidant effect of Ginkgo biloba extract (EGb 761) with those of water-soluble and lipid-soluble antioxidants. Group 1 patients received stimulation twice weekly for 2 weeks, were deprived of stimulation for 2 weeks, and then received stimulation twice weekly for 3 weeks for a total of 10 sessions. A score of 1-2 on any question indicates a grade of mild severity, whereas 0 indicates no interference for a given question category. No patient reported tinnitus as worse either at 1 or 8 weeks after stimulation (see Table 2).
In other words, a latency in the subjective report of tinnitus relief was identified in these two patients at the end of 8 weeks of UHF external acoustic stimulation (see Table 2; Fig. The PET of brain findings support the results of an interneuronal network activation in tinnitus patients as reported in previous SPECT of brain imaging studies [1-6,18].
This finding supports the clinical experience that treatment options differentiate between what is recommended for the sensory and affect components of the symptom of tinnitus [17]. Furthermore, that classic conventional acoustic stimulation (250 H z - 8 kHz) is different from the "masking" achieved with UHF masking. Of course, UHF is not masking in the sense that it is not applied simultaneously in MML testing. The auditory cortex constantly responds with a reorganization response to an experience for a sensory task to receive relevant stimuli [29,30]. Is the variation in the reported degree of tinnitus relief in the ROI a clinical reflection of a sensory-affect transformation of an aberrant auditory sensory stimulus hypothesized to occur in a final common pathway not only for the aberrant auditory stimulus tinnitus but for all sensations? Also to be considered are recent reports that coding and transmission of information by neural ensembles involve complex temporal dynamics that characterize cortical function. The ROI identified suggest that areas other than that of the auditory cortex have to be investigated in all tinnitus patients using different modalities of therapy and techniques. Integrating such reports with results of nuclear imaging studies in severely disabled tinnitus patients is necessary. Nuclear medicine brain imaging provides a basis for asking the right questions that may contribute to understanding the final common pathway for tinnitus and the ultimate improvement in the clinical diagnosis and treatment methods not only for tinnitus but for all sensory phenomena. 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. In contrast to the reasons behind tinnitus3 quoted normal hearing individuals with presence of tinnitus. In air conduction testing, frequencies 250 Hz, 500 Hz, 1000 Hz, 2000 Hz, 4000 Hz and 8000 Hz were checked. On obtaining baseline, frequency specific narrowband noise was delivered to the ear experiencing tinnitus for duration of 60 sec. Studies have reported that presence of any phobia related to tinnitus or any negative thought about tinnitus will lead to slow desensitization of tinnitus. Follow-up report of three subjects in the literature study has shown no change in tinnitus even after exposure to target stimulus for a run of 2 to 3 weeks RIT15.
The annoyance included interference in communication, concentration, performance, and participation in social activities. A screening test revealed mixed moderate-severe right-sided hearing loss and mild left sensorineural hearing loss.
Cranial nerve examination showed the eighth cranial nerve on both sides to be abnormal and the remaining nerves normal. The GABA-A receptor, with its inhibitory activity in brain function, exerts a neuroprotective action [8,11]. MRI of the IACs and brain (May 10, 2004) demonstrated no cerebellopontine or IAC angle tumor and no mass, otomastoiditis, acute infarct, or intracranial mass lesion. The air conduction UHFA identified thresholds of sensorineural hearing loss greater than expected for the age of the patient (Fig. We also recommended discussion with a neurologist of an angiogram to rule out AV malformation or dural fistula if the tinnitus complaint persisted or progressed.
The subjective tinnitus described as an occasional ringing is thought to be mostly cochlear in location. The complaint of ear blockage will be recurrent in this patient, and accurate diagnosis will determine the selection of treatment. Also recommended was that complaints of progressing or deteriorating hearing loss, tinnitus, vertigo, and ear blockage, alone or in combination, be followed up by repeat ENT and neurological consultation in an attempt to maintain hearing and to maximize attempts at tinnitus relief.
We hypothesized that the original left-ear bruit was an objective tinnitus found on auscultation, reflecting predominance of the left vascular drainage. The etiology of the SEH (delayed) in both cases of congenital atresia of the external ear is considered to be cerebrovascular. Many with tinnitus also complain of hyperacusis.Affects quality of lifeBritish studies paint a similar picture of a problem affecting millions of people. Futhermore, there is not linearity increase of the GBE 761 responses according to the increase of dosage. The subjects were followed up weekly so the researcher could supervise the oral intake of either pills in the two groups. A DPOAE was considered to be present if its level was > 8dB above that of the related noise floor.
GBE 761 also can scavenge nitric oxide and inhibit its production by nitric oxide synthase (NOS)30,31. First, the study was conducted using a small sample (30 ears), as are most ototoxicity studies and many other biological datasets.
We strongly recommend long term evaluation of the hearing in the patients undergoing to CDDP antineoplastic therapy as well as GBE 761 otoprotective effects. Group 2 patients received stimulation twice weekly for 3 weeks, were deprived of stimulation for 2 weeks, and then received stimulation twice weekly for 3 weeks, for a total of 12 sessions. The one patient in the PET of brain mixed metabolic category reported tinnitus relief as a reduction in annoyance.
When oscillation of neurons is coherent rather than noise, the result is a "normal" flow of information [33]. 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. As opposed to the traditional paradigm-tinnitus as an ear disease, today, tinnitus is accepted as a brain disorder4.
This suppression of tinnitus provides brief relief which lets victims to exert some control over the trouble. Subjects with mild to moderate severity (score ranging from 18 to 56) were considered for the study.
However, in bone conduction testing, frequencies 250 Hz, 500 Hz, 1000 Hz, 2000 Hz, and 4000 Hz were checked.
This explains the part of neuro-physiological model, where annoyance or displeasure although not strongly evoked stimulate limbic and autonomic systems producing intrusive and aversive emotions and reducing the quality of life. Completion of the medical audiological tinnitus patient protocol, including SPECT of brain, UHFA, and QEEG, accurately established the clinical tinnitus diagnosis of predominantly a central-type tinnitus, a clinical hypothesis that the medical significance of the tinnitus is a "soft" sign of cerebrovascular disease, and provided a rationale for treatment directed to a presumed ischemia of brain based on a receptor-targeted therapy targeted to the GABA-A receptor, resulting in significant tinnitus relief. Steroid therapy and a low-sodium diet received prior to November 30, 2004, resulted in a reduction of spells of the rumble. The findings of SPECT of brain in areas of distribution of the MCA were the basis for recommending various tests. Factors that are identified in the clinical history and can influence (and have influenced) the clinical course of the ringing tinnitus included fluctuation in bilateral aeration of the middle ears, SEH identified in the left ear, noise exposure, and stress. We considered this vascular hypothesis to be supported by the central cochleovestibular test findings (auditory brainstem response, QEEG), the SPECT of brain report (December 2, 2004), and the clinical response of the patient to treatment with steroids and antiseizure medication.
Close attention by patient and ENT specialists will improve the ability to maintain hearing and balance.
In addition, the alteration in the hemodynamics of the cere-brovascular circulation has been hypothesized also to involve the AICA, a long-term effect that may include SEH.
The introduction of Mobic-a nonsteroidal antiinflammatory agent, on a neurologist's recommendation-in combination with gabapentin and Klonopin, was accompanied by elimination of the steroid and an increase in and maintenance of long-term tinnitus relief. One of the clearest snapshots of tinnitus in England was provided by The National Study of Hearing in a study carried out by the MRC Institute of Hearing Research.
The death lull kicked in around1230 and fishing picked back up again at 3pm.I landed the usual residents of the lake-- a few trout, afew nice crappies, perch and gills. Distortion product otoacoustic emissions were recorded before the first cisplatin cycle, 30, 60 and 90 days after the treatment. It is possible if we had tested the patients longer after, other frequencies might become affected. Therefore we decided to perform this clinical trial in order to test the otoprotective effect of GBE 761 against CDDP toxic effects in the humans OHCs. Analysis of performance of drugs in small samples might be impacted by the idiosyncratic nature of the sample and there is always the risk of overfitting the data making the results less generalizable. Group 3 patients received stimulation twice weekly for 4 weeks, were deprived of stimulation for 1 week, and then received stimulation twice weekly for 3 weeks for a total of 14 sessions. We noted a consistency in the report of tinnitus relief for severity mostly in the hypoactive metabolic brain PET category (see Figs. In our study, the absence of random activity in the ROI of brain suggests a coherence in oscillation at brain cortex that is variable, as reflected in the metabolic categories of PET of brain.
Our PET study reinforces the need for future studies that go beyond investigation of the primary auditory cortex for auditory processing of the tinnitus signal but also of that of modalities of therapy attempting tinnitus relief [1-5,18]. 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. Tinnitus can be rated as mild to catastrophic level thereby having severe effects on social and emotional status, poor job performances, relationships and social functioning5.
Possible reasons for tinnitus suppression are stated as temporary desensitization by brain on exposure to tinnitus matched frequency noise11 and influence of overlapping central mechanism12. This inventory helped to rate the severity of tinnitus and to know its severity on day today life.
Recruitment of the subject for further testing asked for threshold ranging from -10 to 25dBHL. Post first sitting with a time gap of 1-2 minutes, contra-lateral acoustic reflexes were retested. The created negative feelings to a person cannot be treated purely by only audiological help. The goal of the patient for this consultation was to obtain information about the tinnitus complaint, to obtain tinnitus relief, to identify the medical significance of the tinnitus, to maintain hearing in the left ear in view of right hearing loss associated with congenital atresia in the right external ear, and a concern for the need for long-term prednisone therapy. On nasal assessment, mild right septal deviation and mild right-to-left hypertrophy of the turbinates were seen. UHF electrical-acoustic testing revealed sensorineural hearing loss greater than expected for the age of the patient (Fig. Computed tomography (CT) scan of temporal bones (January 7, 2005) revealed right external canal atresia but no CT abnormality of the right bony labyrinth.
A follow-up neurological visit (July 9, 2004) reported the trial of verapamil for 2-3 days to be associated with an increased tinnitus intensity and was stopped by the patient. The neurotological workup and particularly the SPECT of brain identified significant bilateral perfusion asymmetries, greater on the right than on the left (see Fig. The extensive medical evaluation, to the limits of examina tion, has excluded coagulopathy and autoimmune disease.
Paradoxically, the "dependence" on the steroid for tinnitus relief may have been a sign of a steroid toxicity related to increasing stress before and during the initial course of the tinnitus.
The CG and SG subjects received either placebo that were pills manufactured by pharmaceutic laboratory of Hospital Regional da Asa Norte in Brasilia and or GBE 761 is a standardized GB extract manufactured by pharmaceutical standards by Dr.
Cumulative distribution responses from normal and abnormal ears according to 90 and 10 percentiles were employed for the result analysis. The purpose of the present study was to examine the efficacy of the standardized GBE 761 in protecting against CDDP-induced ototoxicity in humans by means of DPOAE test.
The same analysis was performed on the intrahemispheric recordings, comparing each ROI before and after UHF stimulation. Follow-up was conducted for 1 week (short-term) and 8 weeks (longterm) after therapy had ceased. UHF could activate the olivary system, changing the afferent output of the cochlea, or plasticity in neural responses could change from the thalamus through the cortex [9,10]. 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.
Thus, the purpose of this study was to gain information on the effectiveness of Residual Inhibition Therapy as a treatment of tinnitus in normal hearing subjects experiencing tinnitus unilaterally and hence the study was undertaken.
Subjects experiencing continuous tinnitus with static nature for two weeks unilaterally were shortlisted. Secondly, Immittance Audiometry (Tympanometry and Reflexometry) using calibrated Interacoustic AT (235) Immittance Audiometer with probe tone of 226 Hz was used to know the integrity of tympanic membrane and middle ear status. The obtained pre contra-lateral acoustic reflexes and post contra-lateral acoustic reflexes were compared to each other to get the effect of RIT on contra-lateral acoustic reflexes.
As far as we can determine, these findings, highlighted by the brain SPECT, have not previously been reported in patients with congenital atresia of the external ear. A dilated right internal auditory canal (IAC) showed no enhancing mass, but the right demonstrated abnormal pinna with calcifications. 4), highlighted by the perfusion asymmetry in regions of interest in brain areas of distribution of the right MCA. The affect component is complex and reflective of the frustration of patients with the complaint of tinnitus and fear of loss of hearing in the left nonatretic ear. Control of the foregoing factors highlighted by control of blood pressure is considered to provide an increased prognosis to maintain hearing and balance and tinnitus relief. The study showed that:10 percent of British adults have experienced spontaneous tinnitus lasting more than five minutes. 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. Type 'A' tympanogram with present ipsi-lateral and contra-lateral acoustic reflexes were considered.
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. Thirdly, Distortion Product Oto-acoustic Emission (DPOAE) was carried out using GSI Audera to rule out normal outer hair cell functioning.
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. Auscultation of the left ear side overlying the external auditory meatus and in the postauricular fold discovered a bruit (November 30, 2004). 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.
Plenty ofpanfish with a few perch hitting the 9-inch mark and a crappie thatwas almost 10 inches.I caught trout sporadically throughout the day, ending with 9.
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.
Teddy told me the lake is completed covered and the ice might be about 1 inch orso.Teddy has patrolled and lived next toAntietam Lakealmostall his life and he knows the lake. There isplenty of rainfall predicted for that area.Most of the fish sitting in the estuary should be entering the river as I type this. Anglers tend to give you space, the scenery is beautiful and the Osprey's always put on a show. Wednesday was spent in the upper fly zone and wasslow in the morning but pretty consistent in the afternoon. Ialso landed a smallmouth bass, a few small brown trout, afew small rainbows (steelhead smolts ?), a fallfishand a baby AtlanticSalmon. The Mohawk egg pattern accounted for many smaller fish and the salmon sized Light Spruce fly produced a few hookups. Last years--One Day Trip-- hot fly,Olive bugger with White marabou tail and redcrystal flash also received plenty of attention and did account for 2 fish. The guyI was fishing withused plenty of flies with smaller bucktail flies doing most of the damage. He didhook-up with a few fish while usingmy Death Stonefly, landing one nice Coho.I can tell you this---the next few weeks will provide some serious action. There are fish in the system at this moment and with the water release at 1800 CFS and the rain. The pool we were fishing was loaded with suckers and chubs and I did see a few trout and a couple of nice sized smallmouth bass. Any questions as to what to tie, just shoot me an email or use the Contact 2Bonthewater page. All that cold water coming from a quarry and the creek itself in that area is near lifeless.
The bridge is now being painted a Hunter Green color.Most of the creeks in the OleyValley are really low. Even with the rain, the creeks remain very low.A I have a trip scheduled to the Salmon River planned inlate September thanks to Jack. Without Jack's kindness and awesomeness, I would not be going salmon fishing.A I have startedtyingflies for the upcoming salmon trip. Zoe competed in a National Beauty pageant and won honorable mention in the beauty competition (FYI -- Zoe wears no make-up, fake hairor fake teethand she competes in the natural division--she is my little girl and I would never DRESS HER UP like all those crazy folks you see on TV).
We dressed as fishermen, answered a question about each other and then Zoe did some fly casting on stage. Zoe was crowned Little Queen when she won the Pennsylvania state pageant back in 2006 while competing in a Sunburst pageant. There are plenty of out of the way smaller streams that are teeming with Smallmouths, Carp and a variety of Panfish.
Perkiomen Creek -- air temp 89 degrees, checked the temperature at two spots, temps were 70 and 69 degrees -- Taken between 415-425 pmA Manatawny Creek -- air temp was 88 degrees, checked the temperature at three spots, temps were 76 degrees at Red Covered Bridge, 74 degrees above TIKI bar and 76 degrees below the Rt.
This heatwave has made most ofthe local trout streams too warm to fishfor the catch and release angler. Maiden Creek below Ontelaunee Lake should provide anglers with some fishthat are willing to bite. You can find Carp, Smallmouth Bass, Largemouth Bassand a wide assortment of panfish to keep you busy. Take some cold water with you !!!Your best way to keep the water cool is to freeze a bottle or two of water the night before you head out. As the day heats up, the water bottles will slowly melt, leaving you with nice cold waterto drink throughout the day. I fished for 30-minutes on Manatawny and landed 2 wild browns on a tan caddis dry fly in the area where the water temp was 68 degrees. Temperature wise, if it is 90 degrees outside, pretty sure most, if not all of the local trout waters will be at 70 degrees or higher. We don't wantto kill the trout.The trout that survive through the summer will offerus great fishing in the fall. I have not made a trip to the Schuylkill River as of yet, but I'd bet the house that the smallie action should be pretty darn good. You can also takeyour watercraft outbefore Epler atCross Keys Road or at Muhlenburg Township park which is below the PFBC Epler Access. There is little room to fish, unless you don't mind walking the shoreline that is covered with all types of vegetation, including Poison Ivy.
Pleny of fish to be caught in this body of water, that is if you can get to them.A Manatawny Creek fished OK.
This stretch used to provide some very nice smallmouth action, but the last few trips here have been poor.
Switched to a spent spinner pattern and hooked up twice--snapped one off and landed a nice stocker brown. The water is up from recent rains inthe valley, but the stream was clear and in perfect condition. The Schuylkill River and a few tribs shouldprovide any cat or carp angler with a few bites each nite.
Channel catfish prefer dead baits andsmaller live bait, while the Flatheads prefer larger live bait. Carp will eatsmaller live bait including minnows andcrayfish along with the standard fare of homemade MUSH bait or whole kernel corn.The bottom line is--It doesn't really matter what bait you areusing. But, by now it was pitch black and it was raining pretty good and thelightning made it look like the 4th of July came early.I managed to land 2 fish on my emerger pattern androll 2 other trout.
Started out at the mouth of Sacony Creek but there was some serious bridge work going on, so I left after a few casts. Caught some nice bluegills, onebrown trout, pumpkinseeds, green sunfish, agolden shiner and I almost hooked into a very nice largemouth bass.
Kids and water mean plenty of noise,lots of splashing and lots offun.Normally, 750pm is about the timethe sulphurs start popping off. I saw some Iso's and huge stoneflies coming off and flying around.I caught a trophy Bluegill, no kidding check out the picture, almost 9 inches. I left my headlamp in the truck so I had to walkout before it got too dark and miss the potential spinner fall.
I then drove to another stretch of the crick and hooked up a few times fishing a brown spent spinner. I lost them at the bank.A Fish the mornings with a brown or white spent spinner and you might get a few takes on the surface. My favorite is a "John's Spring Creek Pupa" tied in size 18 and 20 (Trout Flies of The East--page 93).
I caught two brookies on a CDC sulphur dry fly and the rest of the fish were caught with nymphs. What an amazing fish, especially on a 2 wt bamboo fly rod with a fly reel that is dated to the 1930's or 1940's. What a specimen.He looked like a submarine swimming in the water !!My first impression of the leviathan is that it was a wild fish. Tonights fishing provided a mixed bag of fish, a few smallwild brown trout, along with a few stocker browns, stockerrainbows and the brook trout. I topped it all off with a visit to Ted's house to show off the bamboo fly rod and talk shop.
It was about 40 degrees and raining.I didroll a larger fish on a midge, but aside from that, it was a very slow night. Cast down and across and hop the flies upoff the bottom with quick upward lifts of the fly rod.The fish would really strike hard.
I still have not figured out whyone day I will catch all browns, one day I will catch all rainbows and some days, you will catch a little of everything.



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