Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus

Kaltenbach, James A.; Zhang, Jinsheng; Finlayson, Paul G.

doi:10.1016/j.heares.2005.02.013

Cited by 186 publications

(171 citation statements)

References 160 publications

(204 reference statements)

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“…This complexity, and the growing array of contributing and associated brain factors further suggest why tinnitus has not been amenable to a single treatment. Indeed, future treatment strategies may have to target multiple factors at the same time (Kaltenbach et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, tinnitus may be the consequence of such maladaptive neuroplastic brain alterations (Eggermont, 2005). Kaltenbach, Zhang, and Finlayson (2005) has even gone a step further and described tinnitus as the perceptual manifestation of plastic brain changes that result in neural hyperactivity. The quest for where neural hyperactivity may reside, how it can be identified, what initiates it, and how it is sustained, constitutes much of the driving force behind current efforts to uncover the neural basis of tinnitus.…”

Section: Neuroplasticitymentioning

confidence: 99%

“…Inner ear ototrauma can lead to increases in the levels of SA in the dorsal cochlear nucleus (DCN), the IC, and the auditory cortex (AC). These changes occur over variable time scales, may exhibit tonotopic specificity, are robust, and are sustained for long times (Kaltenbach et al, , 2005. Fig.…”

Section: Brainstem Plasticity and Tinnitusmentioning

confidence: 99%

“…Based on current understanding of DCN neuronal circuitry and its functional aspects, a model for disinhibition has been proposed (for a most recent summary see Kaltenbach et al, 2005). Briefly, there are well characterized interneurons in the DCN called granule and cartwheel cells (see Fig.…”

Section: Brainstem Plasticity and Tinnitusmentioning

confidence: 99%

“…Moreover, how bursting and synchronization can engender the percepts of tinnitus is uncertain, but they remain additional aspects of the neuroplastic response to peripheral ear insult. Kaltenbach et al (2005) discussed additional aspects of plastic changes in the DCN beginning with the up and down regulation of gene expressions capable of modulating cell excitability. These modulations relate to neurotransmission and the processes that control vesicle dynamics, changes in the function of receptors on post-synaptic membranes, and the number and species of ion channels expressed in excitable membranes.…”

Section: Brainstem Plasticity and Tinnitusmentioning

confidence: 99%

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The role of central nervous system plasticity in tinnitus

Saunders

2007

Journal of Communication Disorders

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Tinnitus is a vexing disorder of hearing characterized by sound sensations originating in the head without any external stimulation. The specific etiology of these sensations is uncertain but frequently associated with hearing loss. The "neurophysiogical" model of tinnitus has enhanced appreciation of central nervous system (CNS) contributions. The model assumes that plastic changes in the primary and non-primary auditory pathways contribute to tinnitus with the former perhaps sustaining them, and the latter contributing to perceived severity and emotionality. These plastic changes are triggered by peripheral injury, which results in new patterns of brain activity due to anatomic alterations in the connectivity of CNS neurons. These alterations may change the balance between excitatory and inhibitory brain processes, perhaps producing cascades of new neural activity flowing between brainstem and cortex in a self-sustaining manner that produces persistent perceptions of tinnitus. The bases of this model are explored with an attempt to distinguish phenomenological from mechanistic explanations.Learning outcomes-(1) Readers will learn that the variables associated with the behavioral experience of tinnitus are as complex as the biological variables. (2) Readers will understand what the concept of neuroplastic brain change means, and how it is associated with tinnitus. (3) Readers will learn that there may be no one brain location associated with tinnitus, and it may result from interactions between multiple brain areas. (4) Readers will learn how disinhibition, spontaneous activity, neural synchronization, and tonotopic reorganization may contribute to tinnitus.

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Section: Discussionmentioning

confidence: 99%

Section: Neuroplasticitymentioning

confidence: 99%

Section: Brainstem Plasticity and Tinnitusmentioning

confidence: 99%

Section: Brainstem Plasticity and Tinnitusmentioning

confidence: 99%

Section: Brainstem Plasticity and Tinnitusmentioning

confidence: 99%

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The role of central nervous system plasticity in tinnitus

Saunders

2007

Journal of Communication Disorders

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Effect of Nitrous Oxide as a Treatment for Subjective, Idiopathic, Nonpulsatile Bothersome Tinnitus

Hong

Karadaghy

Kallogjeri

et al. 2018

JAMA Otolaryngol Head Neck Surg

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Ototoxicity

Forge¹,

Taylor²,

Harpur³

2009

General, Applied and Systems Toxicology

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Ototoxicity is the process by which chemicals cause damage to the end organs of hearing (the cochlea) or balance (the vestibular system). Hearing loss is the common effect of ototoxins, although many also affect the vestibular system. Some cause temporary hearing loss (e.g. the ‘loop’ diuretics or salicylates). However, the most significant group of ototoxic agents cause death of the sensory hair cells (HCs) and permanent hearing loss, for example aminoglycoside antibiotics, cis ‐platinum and organic solvents. In mammalian species the HC losses caused by these agents are permanent because, unlike the sensory epithelia in the inner ear in birds and other nonmammalian vertebrates, there is no capacity for HC regeneration. The effects generally develop only after repeated administration, but in some cases a single administration is sufficient (e.g. trimethyltin). Drug interactions can result in much greater damage than would be expected from the single agents. Excess noise can also cause HC death and can act synergistically with ototoxic chemicals. The most characteristic pattern of damage is predominantly death of outer HCs initially at the base of the cochlea (affecting high frequency hearing). Among humans, some individuals may be genetically predisposed to ototoxic damage.

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Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus

Cited by 186 publications

References 160 publications

The role of central nervous system plasticity in tinnitus

The role of central nervous system plasticity in tinnitus

Effect of Nitrous Oxide as a Treatment for Subjective, Idiopathic, Nonpulsatile Bothersome Tinnitus

Ototoxicity

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