Ringing Ears: The Neuroscience of Tinnitus
Larry E. Roberts,Jos J. Eggermont,Donald M. Caspary,Susan E. Shore,Jennifer R. Melcher,James A. Kaltenbach +5 more
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.read more
Citations
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Tinnitus with a normal audiogram: physiological evidence for hidden hearing loss and computational model.
Roland Schaette,David McAlpine +1 more
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
Jonathan Riley,Jonathan D. Seale,William A. Vrana,Jai Shetake,Sindhu P. Sudanagunta,Michael S. Borland,Michael P. Kilgard +6 more
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.
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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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Randy L. Buckner,Jorge Sepulcre,Tanveer Talukdar,Fenna M. Krienen,Hesheng Liu,Trey Hedden,Jessica R. Andrews-Hanna,Reisa A. Sperling,Keith A. Johnson +8 more
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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.