Cortical reorganization in patients with high frequency cochlear hearing loss

Dietrich, Volker; Nieschalk, Matthias; Stoll, Wolfgang; Rajan, Ramesh; Pantev, Christo

doi:10.1016/s0378-5955(01)00282-9

Cited by 149 publications

(100 citation statements)

References 22 publications

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“…Because of the spread of excitation low to high frequencies, we assume however that the low frequency lesion edge is the more important one. Previous studies (Dietrich et al, 2001;Weisz et al, 2005a) have used normal clinical audiograms to define a lesion-edge (always determined as the audiometric edge). This might prove to be insufficient.…”

Section: Discussionmentioning

confidence: 99%

High-frequency tinnitus without hearing loss does not mean absence of deafferentation

et al. 2006

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A broad consensus within the neuroscience of tinnitus holds that this audiologic condition is triggered by central deafferentation, mostly due to cochlear damage. The absence of audiometrically detectable hearing loss however poses a challenge to this rather generalizing assumption. The aim of this study was therefore to scrutinize cochlear functioning in a sample of tinnitus subjects audiometrically matched to a normal hearing control group. Two tests were applied: the Threshold Equalizing Noise (TEN) test and a pitch scaling task. To perform well on both tasks relatively normal functioning of inner hair cells is a requirement. In the TEN test the tinnitus group revealed a circumscribed increment of thresholds partially overlapping with the tinnitus spectrum. Abnormal slopes were observed in the pitch scaling task which indicated that tinnitus subjects, when presented with a high-frequency stimulus, relied heavily on input derived from lower-frequency inner hair cells (off-frequency listening). In total both results argue for the presence of a deafferentation also in tinnitus subjects with audiometrically normal thresholds and therefore favour the deafferentation assumption posed by most neuroscientific theories.

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Section: Discussionmentioning

confidence: 99%

High-frequency tinnitus without hearing loss does not mean absence of deafferentation

et al. 2006

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“…It also increases the distance between the response to the tone at the lesion edge and a control tone within the region of normal hearing. Using MEG, Dietrich et al (2001) examined eight patients with highfrequency hearing loss, seven of whom also complained of TI. For each patient, tone bursts were presented at the lesion-edge frequency and two control frequencies within normal hearing.…”

Section: Human Neuroimaging Studiesmentioning

confidence: 99%

“…Similar to the previous study by Dietrich et al (2001), the response to a lesion-edge frequency was compared to that for a control frequency chosen within the range of normal hearing. In contrast however, in the TI group the N1m response was significantly enhanced for the control tone rather than the tone at the audiometric edge.…”

Section: Human Neuroimaging Studiesmentioning

confidence: 99%

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

2009

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In this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power. AbstractIn this review, we highlight the contribution of advances in human neuroimaging to the current understanding of central mechanisms underpinning tinnitus and explain how interpretations of neuroimaging data have been guided by animal models. The primary motivation for studying the neural subtrates of tinnitus in humans has been to demonstrate objectively its representation in the central auditory system and to develop a better understanding of its diverse pathophysiology and of the functional interplay between sensory, cognitive and affective systems. The ultimate goal of neuroimaging is to identify subtypes of tinnitus in order to better inform treatment strategies. The three neural mechanisms considered in this review may provide a basis for TI classification. While human neuroimaging evidence strongly implicates the central auditory system and emotional centres in TI, evidence for the precise contribution from the three mechanisms is unclear because the data are somewhat inconsistent. We consider a number of methodological issues limiting the field of human neuroimaging and recommend approaches to overcome potential inconsistency in results arising from poorly matched participants, lack of appropriate controls and low statistical power.

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“…Immediate and protracted changes in auditory pathway functions have also been observed in studies on magnetoencephalography (MEG) [71][72][73][74][75]. These studies indicate that humans can undergo similar SSNHL-induced brain plasticity as that observed in animal studies.…”

Section: Neuroplasticity-targeted Interventions In Human Modelsmentioning

confidence: 66%

Neuroplasticity-targeted Intervention for Idiopathic Sudden Sensorineural Hearing Loss: A New Therapeutic Direction

2017

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Cortical reorganization in patients with high frequency cochlear hearing loss

Cited by 149 publications

References 22 publications

High-frequency tinnitus without hearing loss does not mean absence of deafferentation

High-frequency tinnitus without hearing loss does not mean absence of deafferentation

The mechanisms of tinnitus: Perspectives from human functional neuroimaging

Neuroplasticity-targeted Intervention for Idiopathic Sudden Sensorineural Hearing Loss: A New Therapeutic Direction

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