Multiple Indices of the ‘Bounce’ Phenomenon Obtained from the Same Human Ears

Drexl, Markus; Überfuhr, Margarete Anna; Weddell, Thomas; Lukashkin, Andrei N.; Wiegrebe, Lutz; Krause, Eike; Gürkov, Robert

doi:10.1007/s10162-013-0424-x

Cited by 16 publications

(18 citation statements)

References 52 publications

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“…Although the distribution appeared bimodal for NH participants and rather normally distributed in MD patients, the null hypothesis stating that the two subgroups were from equal distributions could not be rejected (two-sample Kolmogorov–Smirnov test; p -value = 0.86). Both subgroups had a tendency to select noises with a negative spectral tilt, which corresponds to previous reports from the literature (16–18, 23, 30). …”

Section: Resultssupporting

confidence: 89%

“…Matching stimuli were adjusted after offset of the LF exposure, on average within 68.7 ± 32.5 s (mean ± SD, N = 28). This suggests that most NH participants concluded the matching while still hearing the transient tinnitus, which lasts about 90 s on average (30). …”

Section: Resultsmentioning

confidence: 99%

“…In NH participants, each trial was started with LF-sound exposure to one ear, thereby inducing a transient tinnitus percept in the exposed ear (see Figure 1A). Since the transient tinnitus lasted only for about 90 s after LF exposure (30), NH participants were allowed to restart the LF stimulus playback if necessary. As tinnitus was a unilateral symptom in both groups, matching stimuli were presented to the contralateral, unaffected ear (see Figures 1A,B).…”

Section: Methodsmentioning

confidence: 99%

“…The time course and relative loudness of the transient tinnitus percept were characterized with psychophysical studies (26, 30), but tinnitus pitch has not been systematically described with psychophysical measures yet. This study employed a tinnitus-matching procedure to quantify and compare tinnitus percepts in MD patients and normal-hearing (NH) participants after exposure to intense LF sound.…”

Section: Introductionmentioning

confidence: 99%

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Tinnitus in Normal-Hearing Participants after Exposure to Intense Low-Frequency Sound and in Ménière’s Disease Patients

et al. 2017

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Tinnitus is one of the three classical symptoms of Ménière’s disease (MD), an inner ear disease that is often accompanied by endolymphatic hydrops. Previous studies indicate that tinnitus in MD patients is dominated by low frequencies, whereas tinnitus in non-hydropic pathologies is typically higher in frequency. Tinnitus of rather low-frequency (LF) quality was also reported to occur for about 90 s in normal-hearing participants after presentation of intense, LF sound (120 dB SPL, 30 Hz, 90 s). LF sound has been demonstrated to also cause temporary endolymphatic hydrops in animal models. Here, we quantify tinnitus in two study groups with chronic (MD patients) and presumably transient endolymphatic hydrops (normal-hearing participants after LF exposure) with a psychophysical procedure. Participants matched their tinnitus either with a pure tone of adjustable frequency and level or with a noise of adjustable spectral shape and level. Sensation levels of matching stimuli were lower for MD patients (mean: 8 dB SL) than for normal-hearing participants (mean: 15 dB SL). Transient tinnitus after LF-exposure occurred in all normal-hearing participants (N = 28). About half of the normal-hearing participants matched noise to their tinnitus, the other half chose a pure tone with frequencies below 2 kHz. MD patients matched their tinnitus with either high-frequency pure tones, mainly above 3 kHz, or with a noise. Despite a significant proportion of MD patients matching low-pass (roaring) noises to their tinnitus, the range of matched stimuli was more heterogeneous than previous data suggested. We propose that in those participants with noise-like tinnitus, the percept is probably generated by increased spontaneous activity of auditory nerve fibers with a broad range of characteristic frequencies, due to an impaired ion balance in the cochlea. For tonal tinnitus, additional mechanisms are conceivable: focal hair cell loss can result in decreased auditory nerve firing and a central auditory overcompensation. Also, normal-hearing participants after LF-exposure experience alterations in spontaneous otoacoustic emissions, which may contribute to a transient tonal tinnitus.

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Section: Resultssupporting

confidence: 89%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Tinnitus in Normal-Hearing Participants after Exposure to Intense Low-Frequency Sound and in Ménière’s Disease Patients

et al. 2017

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“…Intense low-frequency sound presented for about 1 min is known to generate a form of low-frequency ('roaring noise') tinnitus [Patuzzi and Wareing, 2002;Drexl et al, 2014]. The intense low-frequency sound is supposed to shift the operating point of MET channels toward the hyperpolarising side of the transfer function, which could lead to an increase in EP.…”

Section: Peripheral or Cochlear Tinnitusmentioning

confidence: 99%

Revisiting the Cochlear and Central Mechanisms of Tinnitus and Therapeutic Approaches

Noreña¹

2015

Audiol Neurotol

102

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This short review aims at revisiting some of the putative mechanisms of tinnitus. Cochlear-type tinnitus is suggested to result from aberrant activity generated before or at the cochlear nerve level. It is proposed that outer hair cells, through their role in regulating the endocochlear potential, can contribute to the enhancement of cochlear spontaneous activity. This hypothesis is attractive as it provides a possible explanation for cochlear tinnitus of different aetiologies, such as tinnitus produced by acute noise trauma, intense low-frequency sounds, middle-ear dysfunction or temporomandibular joint disorders. Other mechanisms, namely an excitatory drift in the operating point of the inner hair cells and activation of NMDA receptors, are also briefly reported. Central-type tinnitus is supposed to result from aberrant activity generated in auditory centres, i.e. in these patients, the tinnitus-related activity does not pre-exist in the cochlear nerve. A reduction in cochlear activity due to hearing loss is suggested to produce tinnitus-related plastic changes, namely cortical reorganisation, thalamic neuron hyperpolarisation, facilitation of non-auditory inputs and/or increase in central gain. These central changes can be associated with abnormal patterns of spontaneous activity in the auditory pathway, i.e. hyperactivity, hypersynchrony and/or oscillating activity. Therapeutic approaches aimed at reducing cochlear activity and/or tinnitus-related central changes are discussed.

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Responses of the Human Inner Ear to Low-Frequency Sound

Drexl

Krause

Gürkov

et al. 2016

Advances in Experimental Medicine and Biology

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The perceptual insensitivity to low frequency (LF) sound in humans has led to an underestimation of the physiological impact of LF exposure on the inner ear. It is known, however, that intense, LF sound causes cyclic changes of indicators of inner ear function after LF stimulus offset, for which the term "Bounce" phenomenon has been coined.Here, we show that the mechanical amplification of hair cells (OHCs) is significantly affected after the presentation of LF sound. First, we show the Bounce phenomenon in slow level changes of quadratic, but not cubic, distortion product otoacoustic emissions (DPOAEs). Second, Bouncing in response to LF sound is seen in slow, oscillating frequency and correlated level changes of spontaneous otoacoustic emissions (SOAEs). Surprisingly, LF sound can induce new SOAEs which can persist for tens of seconds. Further, we show that the Bounce persists under free-field conditions, i.e. without an in-ear probe occluding the auditory meatus. Finally, we show that the Bounce is affected by contralateral acoustic stimulation synchronised to the ipsilateral LF sound. These findings clearly demonstrate that the origin of the Bounce lies in the modulation of cochlear amplifier gain. We conclude that activity changes of OHCs are the source of the Bounce, most likely caused by a temporary disturbance of OHC calcium homeostasis. In the light of these findings, the effects of long-duration, anthropogenic LF sound on the human inner ear require further research.

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Multiple Indices of the ‘Bounce’ Phenomenon Obtained from the Same Human Ears

Cited by 16 publications

References 52 publications

Tinnitus in Normal-Hearing Participants after Exposure to Intense Low-Frequency Sound and in Ménière’s Disease Patients

Tinnitus in Normal-Hearing Participants after Exposure to Intense Low-Frequency Sound and in Ménière’s Disease Patients

Revisiting the Cochlear and Central Mechanisms of Tinnitus and Therapeutic Approaches

Responses of the Human Inner Ear to Low-Frequency Sound

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