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Tinnitus: animal models and findings in humans.

Eggermont JJ, Roberts LE - Cell Tissue Res. (2014)

Bottom Line: Chronic tinnitus (ringing of the ears) is a medically untreatable condition that reduces quality of life for millions of individuals worldwide.Forms of neural plasticity underlie these neural changes, which include increased spontaneous activity and neural gain in deafferented central auditory structures, increased synchronous activity in these structures, alterations in the tonotopic organization of auditory cortex, and changes in network behavior in nonauditory brain regions detected by functional imaging of individuals with tinnitus and corroborated by animal investigations.Research on the molecular mechanisms that underlie neural changes in tinnitus is in its infancy and represents a frontier for investigation.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Hotchkiss Brain Institute, and Department of Psychology, University of Calgary, 2500 University Drive N.W, Calgary, AB, Canada, eggermon@ucalgary.ca.

ABSTRACT
Chronic tinnitus (ringing of the ears) is a medically untreatable condition that reduces quality of life for millions of individuals worldwide. Most cases are associated with hearing loss that may be detected by the audiogram or by more sensitive measures. Converging evidence from animal models and studies of human tinnitus sufferers indicates that, while cochlear damage is a trigger, most cases of tinnitus are not generated by irritative processes persisting in the cochlea but by changes that take place in central auditory pathways when auditory neurons lose their input from the ear. Forms of neural plasticity underlie these neural changes, which include increased spontaneous activity and neural gain in deafferented central auditory structures, increased synchronous activity in these structures, alterations in the tonotopic organization of auditory cortex, and changes in network behavior in nonauditory brain regions detected by functional imaging of individuals with tinnitus and corroborated by animal investigations. Research on the molecular mechanisms that underlie neural changes in tinnitus is in its infancy and represents a frontier for investigation.

No MeSH data available.


Related in: MedlinePlus

Psychoacoustic properties of tinnitus. a Sound frequencies judged to resemble tinnitus (Likeness Rating) and the center frequency of band pass maskers giving optimal forward suppression of tinnitus (residual Inhibition, RI Depth) track the region of audiometric threshold shift (from Roberts et al. 2008). A likeness rating of 40 denotes a sound beginning to resemble tinnitus. Sound thresholds (broken lines) are considered normal when ≤ 20 dB HL. WN RI depth after a white noise masker. b, c When audiometric notches are present, Likeness Ratings (b) and RI Depth (c) follow this principle. Two individual subjects are shown in (b) from Noreña et al. (2002) and one subject in (c) from Roberts (2007). During RI in (a) and (c, lower panel), tinnitus elimination corresponds to an RI depth of −5.0
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Fig1: Psychoacoustic properties of tinnitus. a Sound frequencies judged to resemble tinnitus (Likeness Rating) and the center frequency of band pass maskers giving optimal forward suppression of tinnitus (residual Inhibition, RI Depth) track the region of audiometric threshold shift (from Roberts et al. 2008). A likeness rating of 40 denotes a sound beginning to resemble tinnitus. Sound thresholds (broken lines) are considered normal when ≤ 20 dB HL. WN RI depth after a white noise masker. b, c When audiometric notches are present, Likeness Ratings (b) and RI Depth (c) follow this principle. Two individual subjects are shown in (b) from Noreña et al. (2002) and one subject in (c) from Roberts (2007). During RI in (a) and (c, lower panel), tinnitus elimination corresponds to an RI depth of −5.0

Mentions: Hearing loss, resulting for instance from exposure to loud noise, is considered an important risk factor for developing tinnitus. Consequently, a history of recreational, occupational, and firearm noise exposure may all be associated with increased likelihood of acquiring tinnitus. The relationship between noise exposure and tinnitus, however, differs depending on the presence or absence of hearing impairment. Occupational noise exposure is more likely to correlate with significant tinnitus in participants with hearing impairment, while leisure-time noise exposure is more associated with increased occurrence of significant tinnitus in participants without audiometric (frequencies ≤8 kHz) hearing loss (Eggermont 2012, pp. 21–24). While this dissociation could reflect early occurring cochlear changes to which the audiogram is not sensitive (a topic discussed in “Cochlear pathology revisited: animals and humans”), it is clear that, when audiometric hearing loss is present, the frequencies reported by patients to correspond to their tinnitus are in the frequency region of threshold shift in the audiogram (Noreña et al. 2002; Roberts et al. 2008; see Fig. 1) with the dominant pitch most commonly reported for NIHL-induced tinnitus matching that of a 3-kHz tone (Penner 1980). Whether the dominant pitch of tinnitus is at the audiometric edge of hearing loss or well within the hearing loss region is still debated. The prediction of overrepresentation of edge frequencies in tonotopic maps after noise trauma, implying that tinnitus pitch would match the edge frequencies (Rauschecker 1999), could not be confirmed (Roberts et al. 2008; Pan et al. 2009). Moore and Vinay (2010) assessed whether this failure might be related to octave errors in pitch matching. Following the training of participants to avoid these errors, the mean pitch matches were close to the values of the edge frequency, with a correlation coefficient of 0.94. In contrast, Schecklmann et al. (2012) confirmed a relationship between tinnitus pitch and maximum hearing loss but not to the edge frequency, suggesting to them that tinnitus is rather a fill-in-phenomenon resulting from homeostatic mechanisms (Roberts et al. 2008) rather than a result of contrast enhancement and the audiometric edge consequent deficient lateral inhibition (Llinás et al. 2005). While these disparate findings could reflect that even in tonal tinnitus a band of frequencies may be present, they concur regardless that tinnitus frequencies are related to hearing loss. Interestingly, narrow-band maskers giving a brief post-masking suppression of tinnitus (called “residual inhibition” in the tinnitus literature, RI) do so most effectively when the center frequency of the masker is also in the hearing loss region (see Fig. 1). Overall, these results suggest that neurons tuned to frequencies in the hearing loss region do generate tinnitus, and stopping what they do suppresses it.Fig 1


Tinnitus: animal models and findings in humans.

Eggermont JJ, Roberts LE - Cell Tissue Res. (2014)

Psychoacoustic properties of tinnitus. a Sound frequencies judged to resemble tinnitus (Likeness Rating) and the center frequency of band pass maskers giving optimal forward suppression of tinnitus (residual Inhibition, RI Depth) track the region of audiometric threshold shift (from Roberts et al. 2008). A likeness rating of 40 denotes a sound beginning to resemble tinnitus. Sound thresholds (broken lines) are considered normal when ≤ 20 dB HL. WN RI depth after a white noise masker. b, c When audiometric notches are present, Likeness Ratings (b) and RI Depth (c) follow this principle. Two individual subjects are shown in (b) from Noreña et al. (2002) and one subject in (c) from Roberts (2007). During RI in (a) and (c, lower panel), tinnitus elimination corresponds to an RI depth of −5.0
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4487353&req=5

Fig1: Psychoacoustic properties of tinnitus. a Sound frequencies judged to resemble tinnitus (Likeness Rating) and the center frequency of band pass maskers giving optimal forward suppression of tinnitus (residual Inhibition, RI Depth) track the region of audiometric threshold shift (from Roberts et al. 2008). A likeness rating of 40 denotes a sound beginning to resemble tinnitus. Sound thresholds (broken lines) are considered normal when ≤ 20 dB HL. WN RI depth after a white noise masker. b, c When audiometric notches are present, Likeness Ratings (b) and RI Depth (c) follow this principle. Two individual subjects are shown in (b) from Noreña et al. (2002) and one subject in (c) from Roberts (2007). During RI in (a) and (c, lower panel), tinnitus elimination corresponds to an RI depth of −5.0
Mentions: Hearing loss, resulting for instance from exposure to loud noise, is considered an important risk factor for developing tinnitus. Consequently, a history of recreational, occupational, and firearm noise exposure may all be associated with increased likelihood of acquiring tinnitus. The relationship between noise exposure and tinnitus, however, differs depending on the presence or absence of hearing impairment. Occupational noise exposure is more likely to correlate with significant tinnitus in participants with hearing impairment, while leisure-time noise exposure is more associated with increased occurrence of significant tinnitus in participants without audiometric (frequencies ≤8 kHz) hearing loss (Eggermont 2012, pp. 21–24). While this dissociation could reflect early occurring cochlear changes to which the audiogram is not sensitive (a topic discussed in “Cochlear pathology revisited: animals and humans”), it is clear that, when audiometric hearing loss is present, the frequencies reported by patients to correspond to their tinnitus are in the frequency region of threshold shift in the audiogram (Noreña et al. 2002; Roberts et al. 2008; see Fig. 1) with the dominant pitch most commonly reported for NIHL-induced tinnitus matching that of a 3-kHz tone (Penner 1980). Whether the dominant pitch of tinnitus is at the audiometric edge of hearing loss or well within the hearing loss region is still debated. The prediction of overrepresentation of edge frequencies in tonotopic maps after noise trauma, implying that tinnitus pitch would match the edge frequencies (Rauschecker 1999), could not be confirmed (Roberts et al. 2008; Pan et al. 2009). Moore and Vinay (2010) assessed whether this failure might be related to octave errors in pitch matching. Following the training of participants to avoid these errors, the mean pitch matches were close to the values of the edge frequency, with a correlation coefficient of 0.94. In contrast, Schecklmann et al. (2012) confirmed a relationship between tinnitus pitch and maximum hearing loss but not to the edge frequency, suggesting to them that tinnitus is rather a fill-in-phenomenon resulting from homeostatic mechanisms (Roberts et al. 2008) rather than a result of contrast enhancement and the audiometric edge consequent deficient lateral inhibition (Llinás et al. 2005). While these disparate findings could reflect that even in tonal tinnitus a band of frequencies may be present, they concur regardless that tinnitus frequencies are related to hearing loss. Interestingly, narrow-band maskers giving a brief post-masking suppression of tinnitus (called “residual inhibition” in the tinnitus literature, RI) do so most effectively when the center frequency of the masker is also in the hearing loss region (see Fig. 1). Overall, these results suggest that neurons tuned to frequencies in the hearing loss region do generate tinnitus, and stopping what they do suppresses it.Fig 1

Bottom Line: Chronic tinnitus (ringing of the ears) is a medically untreatable condition that reduces quality of life for millions of individuals worldwide.Forms of neural plasticity underlie these neural changes, which include increased spontaneous activity and neural gain in deafferented central auditory structures, increased synchronous activity in these structures, alterations in the tonotopic organization of auditory cortex, and changes in network behavior in nonauditory brain regions detected by functional imaging of individuals with tinnitus and corroborated by animal investigations.Research on the molecular mechanisms that underlie neural changes in tinnitus is in its infancy and represents a frontier for investigation.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Pharmacology, Hotchkiss Brain Institute, and Department of Psychology, University of Calgary, 2500 University Drive N.W, Calgary, AB, Canada, eggermon@ucalgary.ca.

ABSTRACT
Chronic tinnitus (ringing of the ears) is a medically untreatable condition that reduces quality of life for millions of individuals worldwide. Most cases are associated with hearing loss that may be detected by the audiogram or by more sensitive measures. Converging evidence from animal models and studies of human tinnitus sufferers indicates that, while cochlear damage is a trigger, most cases of tinnitus are not generated by irritative processes persisting in the cochlea but by changes that take place in central auditory pathways when auditory neurons lose their input from the ear. Forms of neural plasticity underlie these neural changes, which include increased spontaneous activity and neural gain in deafferented central auditory structures, increased synchronous activity in these structures, alterations in the tonotopic organization of auditory cortex, and changes in network behavior in nonauditory brain regions detected by functional imaging of individuals with tinnitus and corroborated by animal investigations. Research on the molecular mechanisms that underlie neural changes in tinnitus is in its infancy and represents a frontier for investigation.

No MeSH data available.


Related in: MedlinePlus