A Review of Hyperacusis and Future Directions: Part II. Measurement, Mechanisms, and Treatment

Pienkowski, Martin; Tyler, Richard S.; Rojas-Roncancio, Eveling; Jun, Hyung Jin; Brozoski, Tom; Dauman, Nicolas; Coelho, Clarisse Simões; Andersson, Gerhard; Keiner, Andrew J.; Cacace, Anthony T.; Martin, Nora; Moore, Brian C. J.

doi:10.1044/2014_aja-13-0037

Cited by 100 publications

(94 citation statements)

References 176 publications

(138 reference statements)

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“…Regarding comorbidity, we found that hyperacusis co-occurred with several diagnoses, similar to other studies including psychiatric diagnoses,[15373839] functional somatic syndromes,[1423242526] hearing impairment,[40] and tinnitus. [7161718]…”

Section: Discussionsupporting

confidence: 87%

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Characteristics of hyperacusis in the general population

2016

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There is a need for better understanding of various characteristics in hyperacusis in the general population. The objectives of the present study were to investigate individuals in the general population with hyperacusis regarding demographics, lifestyle, perceived general health and hearing ability, hyperacusis-specific characteristics and behavior, and comorbidity. Using data from a large-scale population-based questionnaire study, we investigated individuals with physician-diagnosed (n=66) and self-reported (n=313) hyperacusis in comparison to individuals without hyperacusis (n=2995). High age, female sex, and high education were associated with hyperacusis, and that trying to avoid sound sources, being able to affect the sound environment, and having sough medical attention were common reactions and behaviors. Posttraumatic stress disorder, chronic fatigue syndrome, generalized anxiety disorder, depression, exhaustion, fibromyalgia, irritable bowel syndrome, migraine, hearing impairment, tinnitus, and back/joint/muscle disorders were comorbid with hyperacusis. The results provide ground for future study of these characteristic features being risk factors for development of hyperacusis and/or consequences of hyperacusis.

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Section: Discussionsupporting

confidence: 87%

“…[4121314] To what extent individuals with hyperacusis in the general population cope with their condition by seeking medical attention lacks documentation to the best of our knowledge.…”

Section: Introductionmentioning

confidence: 99%

Characteristics of hyperacusis in the general population

2016

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“…Intense sounds are not only perceived as painfully loud (Ades et al, 1959), but can also induce pain sensations in around the external ear (otalgia; Dominguez et al, 2006; Hebert et al, 2013; Henry et al, 2014; Kaltenbach et al, 2000; Knipper et al, 2013; McFerran and Baguley, 2007; Norena, 2011; Pienkowski et al, 2014; Tyler et al, 2014a; Van Campen et al, 1999; Westcott et al, 2013). Pain transmitting neuropeptides and receptors are present in the CN and auditory nerve (Aguilar et al, 2004; Bauer et al, 2007b; Jongkamonwiwat et al, 2003; Nguyen et al, 2014; Phansuwan-Pujito et al, 2003; Tongjaroenbuangam et al, 2006), raising the possibility that loud sounds may trigger the perception of pain through these signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

Manohar

Dahar

Adler

et al. 2016

Molecular and Cellular Neuroscience

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Severe noise-induced damage to the inner ear leads to auditory nerve fiber degeneration thereby reducing the neural input to the cochlear nucleus (CN). Paradoxically, this leads to a significant increase in spontaneous activity in the CN which has been linked to tinnitus, hyperacusis and ear pain. The biological mechanisms that lead to an increased spontaneous activity are largely unknown, but could arise from changes in glutamatergic or GABAergic neurotransmission or neuroinflammation. To test this hypothesis, we unilaterally exposed rats for 2 h to a 126 dB SPL narrow band noise centered at 12 kHz. Hearing loss measured by auditory brainstem responses exceeded 55 dB from 6 to 32 kHz. The mRNA from the exposed CN was harvested at 14 or 28 days post-exposure and qRT-PCR analysis was performed on 168 genes involved in neural inflammation, neuropathic pain and glutamatergic or GABAergic neurotransmission. Expression levels of mRNA of Slc17a6 and Gabrg3, involved in excitation and inhibition respectively, were significantly increased at 28 days post-exposure, suggesting a possible role in the CN spontaneous hyperactivity associated with tinnitus and hyperacusis. In the pain and inflammatory array, noise exposure up-regulated mRNA expression levels of four pain/inflammatory genes, Tlr2, Oprd1, Kcnq3 and Ntrk1 and decreased mRNA expression levels of two more genes, Ccl12 and Il1β. Pain/inflammatory gene expression changes via Ntrk1 signaling may induce sterile inflammation, neuropathic pain, microglial activation and migration of nerve fibers from the trigeminal nerve and cuneate and vestibular nuclei into the CN. These changes could contribute to somatic tinnitus, hyperacusis and otalgia.

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“…Hyperacusis is a comorbidity in 80% of tinnitus patients (4) suggesting common pathogenic mechanisms (5). In the most severe cases, hyperacusis is described as debilitating "ear pain" (6). The response to trauma by type II afferents may relate most directly to such noxious hearing-"noxacusis," to coin a term.…”

mentioning

confidence: 99%

Unmyelinated type II afferent neurons report cochlear damage

Liu

Glowatzki

Fuchs

2015

Proc. Natl. Acad. Sci. U.S.A.

109

102

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In the mammalian cochlea, acoustic information is carried to the brain by the predominant (95%) large-diameter, myelinated type I afferents, each of which is postsynaptic to a single inner hair cell. The remaining thin, unmyelinated type II afferents extend hundreds of microns along the cochlear duct to contact many outer hair cells. Despite this extensive arbor, type II afferents are weakly activated by outer hair cell transmitter release and are insensitive to sound. Intriguingly, type II afferents remain intact in damaged regions of the cochlea. Here, we show that type II afferents are activated when outer hair cells are damaged. This response depends on both ionotropic (P2X) and metabotropic (P2Y) purinergic receptors, binding ATP released from nearby supporting cells in response to hair cell damage. Selective activation of P2Y receptors increased type II afferent excitability by the closure of KCNQ-type potassium channels, a potential mechanism for the painful hypersensitivity (that we term "noxacusis" to distinguish from hyperacusis without pain) that can accompany hearing loss. Exposure to the KCNQ channel activator retigabine suppressed the type II fiber's response to hair cell damage. Type II afferents may be the cochlea's nociceptors, prompting avoidance of further damage to the irreparable inner ear.type II cochlear afferents | ATP | acoustic trauma | hyperacusis | noxacusis T he mammalian cochlea is the most elaborate of vertebrate auditory organs. The elegantly coiled, mechanically tuned cochlear duct and functional differentiation between inner hair cells (IHCs) and outer hair cells (OHCs), afferent and efferent neuronal connections are among the features that enable the widest acoustic frequency range and most complex vocalizations among vertebrate species. This benefit, however, has been gained at a significant cost in the metabolic and mechanical vulnerability of cochlear hair cells and neurons. Loud sound progressively damages type I afferent neurons and OHCs (1). Once damaged beyond repair, these do not regenerate as they do in nonmammalian vertebrates, suggesting that protective mechanisms should exist to preserve cochlear function. Indeed, middle ear reflexes (2) and efferent inhibition of hair cells (3) can mitigate acoustic trauma to some extent. However, a more effective strategy is simply to avoid or withdraw from sources of trauma, by analogy to limb withdrawal triggered by C-fiber activation in skin.Here, we provide evidence that unmyelinated type II cochlear afferents can report cochlear trauma, a potential trigger for nocifensive behavior. Hyperactivity of type II neurons could contribute as well to the paradoxical hypersensitivity to loud sound that can accompany hearing loss, despite diminished type I afferent function. Hyperacusis is a comorbidity in 80% of tinnitus patients (4) suggesting common pathogenic mechanisms (5). In the most severe cases, hyperacusis is described as debilitating "ear pain" (6). The response to trauma by type II afferents may relate most directly to such ...

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A Review of Hyperacusis and Future Directions: Part II. Measurement, Mechanisms, and Treatment

Abstract: Hyperacusis can make life difficult in this increasingly noisy world, forcing sufferers to dramatically alter their work and social habits. We believe this is an opportune time to explore approaches to better understand and treat hyperacusis.

Cited by 100 publications

References 176 publications

Characteristics of hyperacusis in the general population

Characteristics of hyperacusis in the general population

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

Unmyelinated type II afferent neurons report cochlear damage

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