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Open AccessJournal ArticleDOI

Ringing Ears: The Neuroscience of Tinnitus

TLDR
Evidence is considered that deafferentation of tonotopically organized central auditory structures leads to increased neuron spontaneous firing rates and neural synchrony in the hearing loss region, which covers the frequency spectrum of tinnitus sounds.
Abstract
Tinnitus is a phantom sound (ringing of the ears) that affects quality of life for millions around the world and is associated in most cases with hearing impairment. This symposium will consider evidence that deafferentation of tonotopically organized central auditory structures leads to increased neuron spontaneous firing rates and neural synchrony in the hearing loss region. This region covers the frequency spectrum of tinnitus sounds, which are optimally suppressed following exposure to band-limited noise covering the same frequencies. Cross-modal compensations in subcortical structures may contribute to tinnitus and its modulation by jaw-clenching and eye movements. Yet many older individuals with impaired hearing do not have tinnitus, possibly because age-related changes in inhibitory circuits are better preserved. A brain network involving limbic and other nonauditory regions is active in tinnitus and may be driven when spectrotemporal information conveyed by the damaged ear does not match that predicted by central auditory processing.

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Citations
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Journal ArticleDOI

Tinnitus with a normal audiogram: physiological evidence for hidden hearing loss and computational model.

TL;DR: It is reported that in human subjects with tinnitus and a normal audiogram, auditory brainstem responses show a significantly reduced amplitude of the wave I potential but normal amplitudes of the more centrally generated wave V.
Journal ArticleDOI

Reversing pathological neural activity using targeted plasticity

TL;DR: Evidence is reported that reversing the brain changes responsible can eliminate the perceptual impairment in an animal model of noise-induced tinnitus and this method for restoring neural activity to normal may be applicable to a variety of neurological disorders.
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

Tinnitus: causes and clinical management

TL;DR: Assessment of patients includes a detailed case history, measurement of hearing function, quantification of tinnitus severity, and identification of causal factors, associated symptoms, and comorbidities.
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.
References
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Journal ArticleDOI

Cortical Hubs Revealed by Intrinsic Functional Connectivity: Mapping, Assessment of Stability, and Relation to Alzheimer's Disease

TL;DR: To identify regions of high connectivity in the human cerebral cortex, a computationally efficient approach was applied to map the degree of intrinsic functional connectivity across the brain and explored whether the topography of hubs could explain the pattern of vulnerability in Alzheimer's disease (AD).
Journal ArticleDOI

Homeostatic plasticity in the developing nervous system

TL;DR: Evidence is discussed from a number of systems that homeostatic synaptic plasticity is crucial for processes ranging from memory storage to activity-dependent development, and how these processes maintain stable activity states in the face of destabilizing forces is discussed.
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

The Neuroscience of Tinnitus

TL;DR: Downregulation of intracortical inhibition induced by damage to the cochlea or to auditory projection pathways highlights neural processes that underlie the sensation of phantom sound.
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