Tinnitus: Maladaptive auditory–somatosensory plasticity

Wu, Calvin; Stefanescu, Roxana A.; Martel, David T.; Shore, Susan E.

doi:10.1016/j.heares.2015.06.005

Cited by 86 publications

(92 citation statements)

References 99 publications

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“…In support of this view, in (animal) models of acoustic trauma induced tinnitus, increased spontaneous firing rates throughout the auditory system have been observed (Wang et al, 1997; Ahlf et al, 2012; Tziridis et al, 2015; Wu et al, 2016), and the DCN is the earliest processing stage in the auditory pathway in which acoustic trauma leads to tinnitus-related changes and increased spontaneous firing rates (Kaltenbach et al, 1998; Kaltenbach and Afman, 2000; Brozoski et al, 2002; Zacharek et al, 2002; Kaltenbach et al, 2004; Wu et al, 2016). The amount of this increase in spontaneous activity in the DCN has been shown to be correlated with the strength of the behavioral signs for tinnitus (Kaltenbach et al, 2004).…”

Section: Discussionmentioning

confidence: 88%

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

et al. 2016

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Subjective tinnitus is generally assumed to be a consequence of hearing loss. In animal studies it has been demonstrated that acoustic trauma induced cochlear damage can lead to behavioral signs of tinnitus. In addition it was shown that noise trauma may lead to deafferentation of cochlear inner hair cells (IHC) even in the absence of elevated hearing thresholds, and it seems conceivable that such hidden hearing loss may be sufficient to cause tinnitus. Numerous studies have indicated that tinnitus is correlated with pathologically increased spontaneous firing rates and hyperactivity of neurons along the auditory pathway. It has been proposed that this hyperactivity is the consequence of a mechanism aiming to compensate for reduced input to the auditory system by increasing central neuronal gain, a mechanism referred to as homeostatic plasticity (HP), thereby maintaining mean firing rates over longer timescales for stabilization of neuronal processing. Here we propose an alternative, new interpretation of tinnitus-related development of neuronal hyperactivity in terms of information theory. In particular, we suggest that stochastic resonance (SR) plays a key role in both short- and long-term plasticity within the auditory system and that SR is the primary cause of neuronal hyperactivity and tinnitus. We argue that following hearing loss, SR serves to lift signals above the increased neuronal thresholds, thereby partly compensating for the hearing loss. In our model, the increased amount of internal noise—which is crucial for SR to work—corresponds to neuronal hyperactivity which subsequently causes neuronal plasticity along the auditory pathway and finally may lead to the development of a phantom percept, i.e., subjective tinnitus. We demonstrate the plausibility of our hypothesis using a computational model and provide exemplary findings in human patients that are consistent with that model. Finally we discuss the observed asymmetry in human tinnitus pitch distribution as a consequence of asymmetry of the distribution of auditory nerve type I fibers along the cochlea in the context of our model.

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Section: Discussionmentioning

confidence: 88%

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

et al. 2016

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“…However, studies using a behavioral tinnitus model to examine tinnitus-related activity in the VCN after noise-exposure have yet to be performed. Thus, at present, the DCN can be considered to be the site where diminished auditory nerve input initiates hyperactivity, the first physiological hallmark of tinnitus, which is then conveyed to higher brainstem and cortical regions [46, 47]. …”

Section: Neurophysiological Alterations In Animal Models Of Tinnitusmentioning

confidence: 99%

Maladaptive plasticity in tinnitus — triggers, mechanisms and treatment

2016

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Tinnitus is a phantom auditory sensation that reduces quality of life for millions worldwide and for which there is no medical cure. Most cases are associated with hearing loss caused by the aging process or noise exposure. Because exposure to loud recreational sound is common among youthful populations, young persons are at increasing risk. Head or neck injuries can also trigger the development of tinnitus, as altered somatosensory input can affect auditory pathways and lead to tinnitus or modulate its intensity. Emotional and attentional state may play a role in tinnitus development and maintenance via top-down mechanisms. Thus, military in combat are particularly at risk due to combined hearing loss, somatosensory system disturbances and emotional stress. Neuroscience research has identified neural changes related to tinnitus that commence at the cochlear nucleus and extend to the auditory cortex and brain regions beyond. Maladaptive neural plasticity appears to underlie these neural changes, as it results in increased spontaneous firing rates and synchrony among neurons in central auditory structures that may generate the phantom percept. This review highlights the links between animal and human studies, including several therapeutic approaches that have been developed, which aim to target the neuroplastic changes underlying tinnitus.

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“…According to our model, the noise required for SR is generated within the brain and then perceived as a phantom sound. We have proposed that it corresponds to increased spontaneous neuronal firing rates in early processing stages of the auditory brain stem -a phenomenon which is frequently observed in both humans with subjective tinnitus (Wang et al, 1997;Ahlf et al, 2012;Tziridis et al, 2015;Wu et al, 2016) and animal models, where the presence of tinnitus is tested using behavioral paradigms (Gerum et al, 2019, Turner et al, 2006. Furthermore, tinnitus is assumed to be virtually always caused by some kind of either apparent (Heller 2003;König et al, 2006;Nelson & Chen 2004;Shore et al, 2016) or hidden hearing loss (Schaette & McAlpine 2011;Liberman & Liberman 2015).…”

Section: Tinnitus Developmentmentioning

confidence: 99%

The Stochastic Resonance model of auditory perception: A unified explanation of tinnitus development, Zwicker tone illusion, and residual inhibition

Schilling

Tziridis

Schulze

et al. 2020

Preprint

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Stochastic Resonance (SR) has been proposed to play a major role in auditory perception, and to maintain optimal information transmission from the cochlea to the auditory system. By this, the auditory system could adapt to changes of the auditory input at second or even subsecond timescales. In case of reduced auditory input, somatosensory projections to the dorsal cochlear nucleus would be disinhibited in order to improve hearing thresholds by means of SR. As a side effect, the increased somatosensory input corresponding to the observed tinnitus-associated neuronal hyperactivity is then perceived as tinnitus. In addition, the model can also explain transient phantom tone perceptions occurring after ear plugging, or the Zwicker tone illusion. Vice versa, the model predicts that via stimulation with acoustic noise, SR would not be needed to optimize information transmission, and hence somatosensory noise would be tuned down, resulting in a transient vanishing of tinnitus, an effect referred to as residual inhibition.

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Tinnitus: Maladaptive auditory–somatosensory plasticity

Cited by 86 publications

References 99 publications

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

Maladaptive plasticity in tinnitus — triggers, mechanisms and treatment

The Stochastic Resonance model of auditory perception: A unified explanation of tinnitus development, Zwicker tone illusion, and residual inhibition

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