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Advances in the neurobiology of hearing disorders: recent developments regarding the basis of tinnitus and hyperacusis

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TLDR
Novel studies confirm the involvement of peripheral de Afferentation for tinnitus and hyperacusis, but suggest that the disorder results from different brain responses to different degrees of deafferentation: while tinnitis may arise as a failure of the brain to adapt to deprived peripheral input, hyperacusIS may result from an 'over-adaptive' increase in response gain.
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This article is published in Progress in Neurobiology.The article was published on 2013-12-01 and is currently open access. It has received 257 citations till now. The article focuses on the topics: Hyperacusis & Noise-induced hearing loss.

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Citations
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Journal ArticleDOI

The Nervous System

Lord Brain
- 01 Feb 1963 - 
TL;DR: Experimental NeurologyBy Prof. Paul Glees.
Journal ArticleDOI

Synaptopathy in the noise-exposed and aging cochlea: Primary neural degeneration in acquired sensorineural hearing loss

TL;DR: The research suggests that primary neural degeneration is an important contributor to the perceptual handicap in SNHL, and in cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from spiral ganglion neurons and re-establishment of their peripheral synapses.
Journal ArticleDOI

Cochlear synaptopathy in acquired sensorineural hearing loss:Manifestations and mechanisms

TL;DR: Work described here will review structural and functional manifestations of this cochlear synaptopathy and will consider possible mechanisms underlying its appearance and progression in ears with and without traditional 'hearing loss' arising from several common causes in humans.
Journal ArticleDOI

Toward a Differential Diagnosis of Hidden Hearing Loss in Humans.

TL;DR: The results suggest that the SP/AP ratio may be useful in the diagnosis of “hidden hearing loss” and that, as suggested by animal models, the noise-induced loss of cochlear nerve synapses leads to deficits in hearing abilities in difficult listening situations, despite the presence of normal thresholds at standard audiometric frequencies.
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Aging after Noise Exposure: Acceleration of Cochlear Synaptopathy in “Recovered” Ears

TL;DR: Interactions between noise and aging may require an acute synaptopathy, but a single synaptopathic exposure can accelerate cochlear aging.
References
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Journal ArticleDOI

Adding Insult to Injury: Cochlear Nerve Degeneration after “Temporary” Noise-Induced Hearing Loss

TL;DR: It is shown that acoustic overexposures causing moderate, but completely reversible, threshold elevation leave cochlear sensory cells intact, but cause acute loss of afferent nerve terminals and delayed degeneration of the co chlear nerve.
Book

Current Estimates from the National Health Interview Survey, 1991

TL;DR: This report on the 1988 civilian noninstitutionalized population residing in the US presents estimates of acute conditions episodes of persons injured restriction in activity limitation of activity due to chronic conditions prevalence of chronic conditions respondent-assessed health status and the use of medical services.
Journal ArticleDOI

Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression

TL;DR: Because the MPFC and related limbic structures provide forebrain modulation over visceral control structures in the hypothalamus and brainstem, their dysfunction can account for the disturbances in autonomic regulation and neuroendocrine responses that are associated with mood disorders.
Journal ArticleDOI

The Nervous System

Lord Brain
- 01 Feb 1963 - 
TL;DR: Experimental NeurologyBy Prof. Paul Glees.
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