Translabyrinthine nerve section: effect on tinnitus

Barrs, David M.; Brackmann, Derald E.

doi:10.1017/s1755146300090648

Cited by 29 publications

(18 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Peripheral-dependent tinnitus should be abolished by cochlear nerve section, and indeed cochlear nerve section can lead to tinnitus suppression (Barrs and Brackmann 1984;House and Brackmann 1981;Pulec 1995;Silverstein et al 1986). As most tinnitus subjects have relatively good hearing (Pan et al 2009;Sereda et al 2011) with functional IHCs and consequently residual spontaneous firing in the cochlear nerve, the peripheral-dependent tinnitus may be a relatively prevalent form of tinnitus.…”

Section: Implications For Understanding Tinnitus Mechanisms and Tinnimentioning

confidence: 99%

“…Centralized tinnitus should be unaffected by cochlear nerve section, and indeed cochlear nerve section is sometimes inefficient to suppress tinnitus (Barrs and Brackmann 1984;House and Brackmann 1981;Pulec 1995;Silverstein et al 1986). However, ECES with positive current has been shown to suppress tinnitus in subjects with severe hearing loss and chronic tinnitus (Cazals et al 1978).…”

Section: Implications For Understanding Tinnitus Mechanisms and Tinnimentioning

confidence: 99%

See 1 more Smart Citation

Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation

Noreña

Mulders

Robertson

2015

Journal of Neurophysiology

View full text Add to dashboard Cite

Noreña AJ, Mulders WH, Robertson D. Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation. J Neurophysiol 113: 132-143, 2015. First published October 8, 2014 doi:10.1152/jn.00580.2014.-Studies on animals have shown that noise-induced hearing loss is followed by an increase of spontaneous firing at several stages of the central auditory system. This central hyperactivity has been suggested to underpin the perception of tinnitus. It was shown that decreasing cochlear activity can abolish the noise-induced central hyperactivity. This latter result further suggests that an approach consisting of reducing cochlear activity may provide a therapeutic avenue for tinnitus. In this context, extra-cochlear electric stimulation (ECES) may be a good candidate to modulate cochlear activity and suppress tinnitus. Indeed, it has been shown that a positive current applied at the round window reduces cochlear nerve activity and can suppress tinnitus reliably in tinnitus subjects. The present study investigates whether ECES with a positive current can abolish the noise-induced central hyperactivity, i.e., the putative tinnitus-related activity. Spontaneous and stimulus-evoked neural activity before, during and after ECES was assessed from single-unit recordings in the inferior colliculus of anesthetized guinea pigs. We found that ECES with positive current significantly decreases the spontaneous firing rate of neurons with high characteristic frequencies, whereas negative current produces the opposite effect. The effects of the ECES are absent or even reversed for neurons with low characteristic frequencies. Importantly, ECES with positive current had only a marginal effect on thresholds and tone-induced activity of collicular neurons, suggesting that the main action of positive current is to modulate the spontaneous firing. Overall, cochlear electrical stimulation may be a viable approach for suppressing some forms of (peripheral-dependent) tinnitus.

show abstract

Section: Implications For Understanding Tinnitus Mechanisms and Tinnimentioning

confidence: 99%

Section: Implications For Understanding Tinnitus Mechanisms and Tinnimentioning

confidence: 99%

Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation

Noreña

Mulders

Robertson

2015

Journal of Neurophysiology

View full text Add to dashboard Cite

show abstract

“…Despite its simple origins, the mechanisms underlying the phantom perception remain elusive (1)(2)(3)(4)(5). Although often arising from peripheral hearing loss, tinnitus persists after auditory nerve transection or lesions of the cochlear nucleus, suggesting the involvement of more central mechanisms (6,7). Recent studies revealed that abnormal auditory cortex activation and cortical map reorganization are correlated with the occurrence and severity of tinnitus in patients and model animals (8)(9)(10)(11)(12).…”

mentioning

confidence: 99%

Homeostatic plasticity drives tinnitus perception in an animal model

Yang

Weiner

Zhang

et al. 2011

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

247

242

View full text Add to dashboard Cite

Hearing loss often results in tinnitus and auditory cortical map changes, leading to the prevailing view that the phantom perception is associated with cortical reorganization. However, we show here that tinnitus is mediated by a cortical area lacking map reorganization. High-frequency hearing loss results in two distinct cortical regions: a sensory-deprived region characterized by a decrease in inhibitory synaptic transmission and a normal hearing region showing increases in inhibitory and excitatory transmission and map reorganization. Hearing-lesioned animals displayed tinnitus with a pitch in the hearing loss range. Furthermore, drugs that enhance inhibition, but not those that reduce excitation, reversibly eliminated the tinnitus behavior. These results suggest that sensory deprivation-induced homeostatic down-regulation of inhibitory synapses may contribute to tinnitus perception. Enhancing sensory input through map reorganization may plausibly alleviate phantom sensation.innitus, the perception of sounds in the absence of acoustic stimuli, often occurs as the result of hearing loss. Despite its simple origins, the mechanisms underlying the phantom perception remain elusive (1-5). Although often arising from peripheral hearing loss, tinnitus persists after auditory nerve transection or lesions of the cochlear nucleus, suggesting the involvement of more central mechanisms (6, 7). Recent studies revealed that abnormal auditory cortex activation and cortical map reorganization are correlated with the occurrence and severity of tinnitus in patients and model animals (8-12). Hearing loss normally associated with tinnitus leads to altered spontaneous activity and map reorganization, both of which are prevented if the trauma is followed by enriched acoustic experience (13-16). These findings suggest that cortical map reorganization may cause abnormal cortical activity and tinnitus, and prevention and reversal of such reorganization could alleviate tinnitus symptoms (5,16,17).Although Hebbian plasticity is believed to be the primary mediator of long-term map reorganization, non-Hebbian homeostatic plasticity may also be activated by altered sensory input (18,19). Cochlear ablation, for example, weakens inhibitory synapses and strengthens excitatory synapses, resulting in enhanced neuronal excitability in auditory cortex (20). These effects could potentially lead to elevated spontaneous cortical activity and tinnitus (21,22). Because map reorganization generally increases sensory-driven activity in the previously sensorydeprived neurons, it may attenuate or reverse homeostatic up-regulation of neuronal excitability, thereby reducing or eliminating tinnitus.In this study, we investigated hearing loss-induced cortical map reorganization, synaptic plasticity and tinnitus behaviors. We found that high-frequency hearing loss differentially alters synaptic transmissions in two zones of primary auditory cortex (AI) that represent the hearing-loss vs. normal-hearing frequency ranges. In the low-characteristic frequency (CF...

show abstract

“…Moreover, tinnitus is largely prevalent in subjects with profound hearing loss [Quaranta et al, 2004;Baguley and Atlas, 2007], where cochlear nerve activity is likely very low or absent [Hartmann et al, 1984;Shepherd and Javel, 1997]. Finally, while cochlear nerve section can abolish tinnitus in some cases, tinnitus can remain in other cases [House and Brackmann, 1981;Barrs and Brackmann, 1984;Pulec, 1995]. Altogether, these results argue for a causal role necessarily played by the auditory centres for generating the tinnitus-related activity, at least in some subtypes of tinnitus.…”

Section: Central Tinnitusmentioning

confidence: 99%

Revisiting the Cochlear and Central Mechanisms of Tinnitus and Therapeutic Approaches

Noreña¹

2015

Audiol Neurotol

102

View full text Add to dashboard Cite

This short review aims at revisiting some of the putative mechanisms of tinnitus. Cochlear-type tinnitus is suggested to result from aberrant activity generated before or at the cochlear nerve level. It is proposed that outer hair cells, through their role in regulating the endocochlear potential, can contribute to the enhancement of cochlear spontaneous activity. This hypothesis is attractive as it provides a possible explanation for cochlear tinnitus of different aetiologies, such as tinnitus produced by acute noise trauma, intense low-frequency sounds, middle-ear dysfunction or temporomandibular joint disorders. Other mechanisms, namely an excitatory drift in the operating point of the inner hair cells and activation of NMDA receptors, are also briefly reported. Central-type tinnitus is supposed to result from aberrant activity generated in auditory centres, i.e. in these patients, the tinnitus-related activity does not pre-exist in the cochlear nerve. A reduction in cochlear activity due to hearing loss is suggested to produce tinnitus-related plastic changes, namely cortical reorganisation, thalamic neuron hyperpolarisation, facilitation of non-auditory inputs and/or increase in central gain. These central changes can be associated with abnormal patterns of spontaneous activity in the auditory pathway, i.e. hyperactivity, hypersynchrony and/or oscillating activity. Therapeutic approaches aimed at reducing cochlear activity and/or tinnitus-related central changes are discussed.

show abstract

Translabyrinthine nerve section: effect on tinnitus

Cited by 29 publications

References 8 publications

Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation

Suppression of putative tinnitus-related activity by extra-cochlear electrical stimulation

Homeostatic plasticity drives tinnitus perception in an animal model

Revisiting the Cochlear and Central Mechanisms of Tinnitus and Therapeutic Approaches

Contact Info

Product

Resources

About