Comparison of Auditory Brainstem Response Results in Normal-Hearing Patients With and Without Tinnitus

Kehrle, Helga Moura; Granjeiro, Ronaldo Campos; Sampaio, André Luiz Lopes; Bezerra, Roberta Lemos; Almeida, Vanessa Furtado de; Oliveira, Carlos Augusto Costa Pires de

doi:10.1001/archotol.134.6.647

Cited by 71 publications

(69 citation statements)

References 16 publications

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“…They are in agreement with previous reports of the following in tinnitus subjects: elevated V/I amplitude ratio (Kehrle et al 2008;Schaette and McAlpine 2011), elevated wave III amplitude (Attias et al 1996), and reduced wave I amplitude (Attias et al 1993;Schaette and McAlpine 2011). An absence of reduction in wave III of tinnitus subjects (Attias et al 1993) or wave V (Attias et al 1993; Schaette and McAlpine 2011), despite reduced wave I, has also been reported, which is tantamount to enhanced activity given the reduction in wave I (as discussed above).…”

Section: Comparison To Previous Abr Studies Of Tinnitussupporting

confidence: 93%

“…Although an earlier study by Attias et al (1993), also on subjects with highfrequency hearing loss, stated that there were no differences in ABR between tinnitus subjects and nontinnitus controls, the reported mean ABR amplitudes showed a clear trend toward reduced wave I. Kehrle et al (2008), comparing tinnitus and non-tinnitus subjects with clinically normal thresholds, reported an enhanced V/I amplitude ratio in tinnitus subjects. While they did not report whether the enhanced amplitude ratio arose from a reduction in wave I, an elevation in wave V or, a combination of both, the earlier data of Attias et al (1993) and recent report of Schaette and McAlpine (2011) indicate that reduced wave I was a factor.…”

Section: Introductionmentioning

confidence: 81%

“…Attias et al (1993Attias et al ( , 1996 doubted the trends in their data, which have now been confirmed. Kehrle et al (2008) offered no direct interpretation. Shaette and McAlpine used a dorsal cochlear nucleus (DCN) model to interpret their finding of a V/I amplitude elevation despite evidence that the DCN and its output pathways make little or no contribution to the ABR (Gardi et al 1979;Achor and Starr 1980;Fullerton and Kiang 1990;Melcher et al 1996b).…”

Section: Comparison To Previous Abr Studies Of Tinnitusmentioning

confidence: 99%

“…Notably, previous studies that examined ABR wave amplitudes (as opposed to only latencies) and also controlled for hearing sensitivity already provide indications that wave I may be reduced and subsequent waves elevated in human subjects with tinnitus (Attias et al 1993;Attias et al 1996;Kehrle et al 2008;Schaette and McAlpine 2011). Attias et al (1996) reported greater wave III amplitude in tinnitus subjects with high-frequency hearing loss compared with threshold-, sex-, and age-matched control subjects without tinnitus.…”

Section: Introductionmentioning

confidence: 99%

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Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Herrmann

Levine

et al. 2012

JARO

205

202

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Numerous studies have demonstrated elevated spontaneous and sound-evoked brainstem activity in animal models of tinnitus, but data on brainstem function in people with this common clinical condition are sparse. Here, auditory nerve and brainstem function in response to sound was assessed via auditory brainstem responses (ABR) in humans with tinnitus and without. Tinnitus subjects showed reduced wave I amplitude (indicating reduced auditory nerve activity) but enhanced wave V (reflecting elevated input to the inferior colliculi) compared with non-tinnitus subjects matched in age, sex, and puretone threshold. The transformation from reduced peripheral activity to central hyperactivity in the tinnitus group was especially apparent in the V/I and III/I amplitude ratios. Compared with a third cohort of younger, non-tinnitus subjects, both tinnitus, and matched, non-tinnitus groups showed elevated thresholds above 4 kHz and reduced wave I amplitude, indicating that the differences between tinnitus and matched non-tinnitus subjects occurred against a backdrop of shared peripheral dysfunction that, while not tinnitus specific, cannot be discounted as a factor in tinnitus development. Animal lesion and human neuroanatomical data combine to indicate that waves III and V in humans reflect activity in a pathway originating in the ventral cochlear nucleus (VCN) and with spherical bushy cells (SBC) in particular. We conclude that the elevated III/I and V/I amplitude ratios in tinnitus subjects reflect disproportionately high activity in the SBC pathway for a given amount of peripheral input. The results imply a role for the VCN in tinnitus and suggest the SBC pathway as a target for tinnitus treatment.

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Section: Comparison To Previous Abr Studies Of Tinnitussupporting

confidence: 93%

Section: Introductionmentioning

confidence: 81%

Section: Comparison To Previous Abr Studies Of Tinnitusmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Brainstem Auditory Evoked Potentials Suggest a Role for the Ventral Cochlear Nucleus in Tinnitus

Herrmann

Levine

et al. 2012

JARO

205

202

View full text Add to dashboard Cite

show abstract

“…In a study involving normal-hearing individuals, the authors concluded that the wave I extension and other BAEP wave delays are compatible with peripheral auditory lesions and can reflect hearing loss in ultra-high frequencies 21 -which were not assessed in the present study. In sensorineural hearing loss there can be an extension of wave I and its subsequent components, or reduction of the I-V interval, as well as wave I being absent, according to the level of loss.…”

Section: Discussioncontrasting

confidence: 56%