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Threshold Shift (threshold + shift)

Distribution by Scientific Domains

Medical Sciences	90%

Selected Abstracts

Chronologic Changes of Nitric Oxide Concentration in the Cochlear Lateral Wall and Its Role in Noise-Induced Permanent Threshold Shift

THE LARYNGOSCOPE, Issue 5 2008
Yuh-Shyang Chen MD
Abstract Objective: The objective of this study was to investigate the chronologic changes of nitric oxide (NO) concentration in the cochlear lateral wall and to explore its possible role in permanent threshold shift (PTS) after intense noise exposure. Materials and Methods: Seventeen guinea pigs were subjected to a single continuous exposure to broadband white noise at 105 ± 2 dB sound pressure level (SPL) for 40 hours and were divided into four groups according to various postnoise recovery periods. Another 12 guinea pigs were not exposed to noise and served as controls. The hearing status of all animals was evaluated with auditory brainstem responses (ABR) evoked by condensation "click" sounds. ABR were recorded both prior to noise exposure and immediately before killing the animal. After death, NO concentration in the cochlear lateral wall was directly measured with an NO/ozone chemiluminescence technique. Results: An approximately 1.7-fold increase in NO concentration was observed immediately postnoise exposure, which persisted for up to 28 days. The threshold of ABR elevation (mean, 30 dB SPL) peaked immediately after cessation of noise exposure and gradually resolved to a PTS (mean, 14.5 dB SPL) 56 days after noise exposure when NO concentration had returned to its prenoise exposure level. Conclusion: Noise-induced threshold shift, which resolved to a mild PTS, can be partially attributed to NO elevation in the cochlear lateral wall. Our results revealed a nonlinear correlation between ABR recovery and depletion of NO, indicating that the mechanisms of NO changes in the cochlear lateral wall may be more complicated than previously conceived and that other pathophysiologic mechanisms may also play important roles in noise-induced PTS. [source]

Diameter of the Cochlear Nerve in Endolymphatic Hydrops: Implications for the Etiology of Hearing Loss in Ménière's Disease,

THE LARYNGOSCOPE, Issue 9 2005
Cliff A. Megerian MD
Abstract Objective/Hypothesis: Endolymphatic hydrops (ELH) is an important histopathological hallmark of Ménière's disease. Experimental data from human temporal bones as well as animal models of the disorder have generally failed to determine the mechanism by which ELH or related pathology causes hearing loss. Hair cell and spiral ganglion cell counts in both human and animal case studies have not, for the most part, shown severe enough deterioration to explain associated severe sensorineural hearing loss. However a limited number of detailed ultrastructural studies have demonstrated significant reductions in dendritic innervation densities, raising the possibility that neurotoxicity plays an important role in the pathology of Ménière's disease (MD) as well as experimental endolymphatic hydrops (ELH). This study tests the hypothesis that neurotoxicity is an important primary mediator of injury to the hydropic ear and is reflected in measurable deterioration of the cochlear nerve in the animal model of ELH. This study also explores the previously presented hypothesis that cochlear injury in ELH is mediated through the actions of nitric oxide (NO) by evaluating whether hearing loss or various measures of cochlear damage can be ameliorated by administration of an agent that limits excess production of NO. Study Design: Part one of the project involves the surgical induction of endolymphatic hydrops and correlation of long term hearing loss with histological parameters of ELH severity as well as cochlear nerve and eighth cranial nerve diameter measurements. In part two, aminoguanidine is administered orally to a separate set of hydropic animals in an attempt to limit cochlear injury presumably mediated by NO. Methods: Guinea pigs are subjected to surgical induction of unilateral endolymphatic hydrops after establishing baseline ABR thresholds at 2, 4, 8, 16, and 32 kHz. Threshold shifts are established prior to sacrifice at 4 to 6 months and temporal bones processed for light microscopy. Measurements of cochlear nerve and eighth cranial nerve maximal diameters as well as average maximal diameters are carried out and correlated to hearing loss and a semi-quantitative measure of hydrops severity. The identical experiments are carried out in animals treated with aminoguanidine, an inhibitor of inducible nitric oxide synthase. Results: The mean maximal diameter (n = 14) of the hydropic cochlear nerve was significantly reduced (432.14 ± 43.18 vs. 479.28 ± 49.22 microns, P = .0025) as compared to the control nerve. This was also seen in measures of the eighth cranial nerve (855.71 ± 108.82 vs. 929 ± 81.53 microns, P = 0.0003). Correlation studies failed to show correlation between hydrops severity and a cochlear nerve deterioration index (r = -0.0614, P = .8348). Similarly, hearing loss severity failed to correlate with cochlear nerve deterioration (r = 0.1300, P = .6577). There was a significant correlation between hearing loss and hydrops severity (r = 0.6148, P = .0193). Aminoguanidine treated animals (n = 5) also sustained nerve deterioration to the same degree as non-treated animals and there appeared to be no protective effect (at the dosage administered) against ELH related hearing loss, hydrops formation, or nerve deterioration. Conclusion: ELH results in significant deterioration of cochlear nerve and eighth cranial nerve maximal diameters in the guinea pig model. These findings are in accord with previous studies which detected ultrastructural evidence of dendritic damage and indicate that neural injury is of sufficient severity to result in light microscopic evidence of cochlear nerve and eighth cranial nerve deterioration. These data support the concept that the principle pathological insult in ELH is a form of neurotoxicity, especially in light of previous studies which indicate relative preservation of hair cells at similar points in time. The lack of correlation between the severity of hydrops and nerve deterioration suggests that nerve deterioration is independent of hydrops severity. [source]

Physiological costs of the hearing due to noise exposure, additional physical stress, and combined exposure to alcohol and cigarette smoke

HUMAN FACTORS AND ERGONOMICS IN MANUFACTURING & SERVICE INDUSTRIES, Issue 3 2002
H. Strasser
In 2 studies, each with 5 test series, physiological costs of the hearing due to legally tolerable noise exposures of 94 dB (A) for 1 hr have been measured audiometrically. The temporary threshold shifts (TTS) and their restitution time, as well as cardiovascular responses in work-related heart rate increases, of 10 and 8 subjects (Ss), respectively, could be shown to be modulated by additional physical stress and combined exposure to alcohol (Study 1) and cigarette smoke (Study 2). Moderate dynamic muscle work (50 W) administered via a bicycle ergometer either immediately after noise, or simultaneous to the noise exposure, significantly reduced restitution time as well as the integrated restitution temporary threshold shift (IRTTS). A physical stress to 100 W,which exceeded the endurance level when demanded simultaneously to the noise exposure,did not show any favorable effects. However, if the same physical stress succeeded the noise exposure, and when it was interrupted several times for the audiometric measurements, it also brought about significant accelerations of the restitution processes. Some reductions in physiological costs of the hearing were found due to an intervening alcohol consumption (blood alcohol concentration , 0.08%) prior to the noise exposure and a simultaneous physical load of 50 W. Smoking 10 cigarettes instead of the consumption of alcohol was associated with a reduced TTS, but a prolonged restitution time. IRTTS as total physiological costs of the most unfavorable combination of noise, simultaneous high physical workload, and preceding smoke exposure was increased. The results of the test series with cigarette smoke,probably due to the small group of just 8 Ss and the counteracting effects of the agents carbon monoxide (CO) and nicotine,were not statistically significant, but these exposures were associated with a substantial activation of the cardiovascular system. Significant heart rate increases are evidence that CO and nicotine must not be neglected as influential factors in the context of physiological costs that the organism, and especially the hearing, has to pay for noise exposures. © 2002 Wiley Periodicals, Inc. [source]

Chronologic Changes of Nitric Oxide Concentration in the Cochlear Lateral Wall and Its Role in Noise-Induced Permanent Threshold Shift

Olivocochlear Activity and Temporary Threshold Shift-Susceptibility in Humans

THE LARYNGOSCOPE, Issue 11 2005
W Wagner MD
Abstract Study Objectives: Animal studies (guinea pig, cat, chinchilla) have shown that activity of the medial olivocochlear efferents can exert noise-protective effects on the cochlea. It is not yet known whether such effects are also existent in humans. Olivocochlear activity can be estimated indirectly by contralateral suppression (CS) of otoacoustic emissions (OAE). Material and Methods: We measured Input/Output functions of distortion products of OAE (DPOAE), with and without contralateral acoustic stimulation by white noise, in 94 normal hearing young male subjects. Seven stimuli with L2 between 20 and 60 dB SPL and L1 = 39 dB + 0.4 L2 ("scissor paradigm") were used at f2 = 2, 3, 4, 5, and 6 kHz. The measurement was repeated 2 weeks later. In 83 subjects of the same group, pure tone audiometry was registered before and 6 minutes after shooting exercises to evaluate individual susceptibility to develop a temporary threshold shift (TTS). Results: Test-retest repeatability of CS was generally good. CS averaged 0.98 dB SPL (SD 1.19 dB, median 0.56 dB). As expected, CS was greatest at low stimulus levels (median 1.06 dB at L2 = 20 dB, as compared with 0.33 dB at L2 = 60 dB). The smallest average CS was found at 4 kHz, and the greatest CS appeared at 2 kHz. A TTS occurred in 7 of 83 (8.5%) subjects. Statistical analysis did not reveal any correlation between the amount of CS and individual TTS susceptibility. Conclusions and Outlook: 1) Measurement of CS of DPOAE using an extensive measurement paradigm revealed good test-retest repeatability, confirming the reliability of this audiologic tool. 2) CS of DPOAE does not predict individual susceptibility to mild TTS induced by impulse noise in humans. Possible explanations for the missing association are discussed. Future perspectives include longitudinal studies to further elucidate the association between medial olivocochlear bundle-activity and permanent threshold shift in humans. The goal is to develop a diagnostic tool for the prediction of individual noise vulnerability in humans, thereby preventing noise-induced hearing loss. [source]

Enhancing Intrinsic Cochlear Stress Defenses to Reduce Noise-Induced Hearing Loss,,§

THE LARYNGOSCOPE, Issue 9 2002
Richard D. Kopke COL MC USA
Abstract Objectives/Hypothesis Oxidative stress plays a substantial role in the genesis of noise-induced cochlear injury that causes permanent hearing loss. We present the results of three different approaches to enhance intrinsic cochlear defense mechanisms against oxidative stress. This article explores, through the following set of hypotheses, some of the postulated causes of noise-induced cochlear oxidative stress (NICOS) and how noise-induced cochlear damage may be reduced pharmacologically. 1) NICOS is in part related to defects in mitochondrial bioenergetics and biogenesis. Therefore, NICOS can be reduced by acetyl-L carnitine (ALCAR), an endogenous mitochondrial membrane compound that helps maintain mitochondrial bioenergetics and biogenesis in the face of oxidative stress. 2) A contributing factor in NICOS injury is glutamate excitotoxicity, which can be reduced by antagonizing the action of cochlear N -methyl-D-aspartate (NMDA) receptors using carbamathione, which acts as a glutamate antagonist. 3) Noise-induced hearing loss (NIHL) may be characterized as a cochlear-reduced glutathione (GSH) deficiency state; therefore, strategies to enhance cochlear GSH levels may reduce noise-induced cochlear injury. The objective of this study was to document the reduction in noise-induced hearing and hair cell loss, following application of ALCAR, carbamathione, and a GSH repletion drug D-methionine (MET), to a model of noise-induced hearing loss. Study Design This was a prospective, blinded observer study using the above-listed agents as modulators of the noise-induced cochlear injury response in the species chinchilla laniger. Methods Adult chinchilla laniger had baseline-hearing thresholds determined by auditory brainstem response (ABR) recording. The animals then received injections of saline or saline plus active experimental compound starting before and continuing after a 6-hour 105 dB SPL continuous 4-kHz octave band noise exposure. ABRs were obtained immediately after noise exposure and weekly for 3 weeks. After euthanization, cochlear hair cell counts were obtained and analyzed. Results ALCAR administration reduced noise-induced threshold shifts. Three weeks after noise exposure, no threshold shift at 2 to 4 kHz and <10 dB threshold shifts were seen at 6 to 8 kHz in ALCAR-treated animals compared with 30 to 35 dB in control animals. ALCAR treatment reduced both inner and outer hair cell loss. OHC loss averaged <10% for the 4- to 10-kHz region in ALCAR-treated animals and 60% in saline-injected-noise-exposed control animals. Noise-induced threshold shifts were also reduced in carbamathione-treated animals. At 3 weeks, threshold shifts averaged 15 dB or less at all frequencies in treated animals and 30 to 35 dB in control animals. Averaged OHC losses were 30% to 40% in carbamathione-treated animals and 60% in control animals. IHC losses were 5% in the 4- to 10-kHz region in treated animals and 10% to 20% in control animals. MET administration reduced noise-induced threshold shifts. ANOVA revealed a significant difference (P <.001). Mean OHC and IHC losses were also significantly reduced (P <.001). Conclusions These data lend further support to the growing body of evidence that oxidative stress, generated in part by glutamate excitotoxicity, impaired mitochondrial function and GSH depletion causes cochlear injury induced by noise. Enhancing the cellular oxidative stress defense pathways in the cochlea eliminates noise-induced cochlear injury. The data also suggest strategies for therapeutic intervention to reduce NIHL clinically. [source]

Electric acoustic stimulation of the auditory system: experience and results of ten patients using MED-EL's M and FlexEAS electrodes

CLINICAL OTOLARYNGOLOGY, Issue 3 2010
A. Lee
Clin. Otolaryngol. 2010, 35, 190,197 Objective:, To evaluate the hearing preservation rate and speech perception scores in patients with profound high frequency hearing loss and acoustically aidable low frequency hearing, managed with the MED-EL electric acoustic stimulation system referenced to the insertion depth of the electrode array. Study design:, Retrospective data analysis. Participants and setting:, Ten patients implanted at the Auditory Implant Centre, Guy's and St Thomas's Hospital, London, UK. Main outcome measures:, Pure tone audiometry, speech perception tests and electrode insertion depth angle. Results:, Postoperatively, functional hearing preservation allowing electric acoustic stimulation was achieved in eight patients and total preservation of residual hearing in five patients with follow-up periods of more than 12 months. Three of four (75%) patients with an insertion depth of >360° had a threshold shift of >25 dB, and all four patients had a threshold shift of >10 dB. All patients with total hearing preservation had the electrode inserted up to 360° at maximum. Overall, speech perception outcomes increased significantly and hearing impairment was significantly reduced after electric acoustic stimulation or electric stimulation alone as compared with the preoperative scores. Conclusion:, Electric acoustic stimulation provides significant benefit to individuals with profound high frequency hearing loss. Studies with larger number of patients are needed to establish the optimal electrode insertion angle as well as to further analyse the benefit of electric acoustic stimulation. [source]

Hearing loss among Ohio farm youth: A comparison to a national sample

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 3 2009
Katherine M. Renick MS
Abstract Background Hearing loss is prevalent among adults in the farming community, with some evidence it begins in childhood. Our objective was to compare hearing thresholds of Ohio farm youth to published data on national norms. Methods Baseline data were collected on youth (n,=,212) in 1994,1996 with follow-up (n,=,132) in 2003,2004 including pure-tone air conduction thresholds at 0.5, 1, 2, 3, 4, 6, and 8 kHz. Results When compared to nationally-representative data, study youth had a higher prevalence of hearing loss. The high-frequency range was most affected, particularly at 6 kHz where nearly 50% of the farm youth exhibited some degree of hearing loss at baseline testing. The prevalence of noise-induced threshold shifts, characterized by an audiometric notch, was nearly twice that of the national sample. Conclusions These data suggest that hearing loss, which is common among adult farmers, may be problematic for farm youth as well. Am. J. Ind. Med. 52:233,239, 2009. © 2008 Wiley-Liss, Inc. [source]