Tinnitus: clinical measurement

Vernon, Jack; Meikle, Mary B.

doi:10.1016/s0030-6665(02)00162-7

Cited by 100 publications

(89 citation statements)

References 9 publications

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“…Generally, our subjects rated their tinnitus to be of very high pitch, which fits well with previous observations (Vernon and Meikle, 2003). Conforming with the results of Norena et al (2002) the tinnitus spectrum was not circumscribed but usually changed from low ratings to relatively high ratings and remained elevated.…”

Section: Discussionsupporting

confidence: 92%

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: Discussionsupporting

confidence: 92%

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

et al. 2006

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“…If spontaneous hyperactivity is indeed involved in the generation of tinnitus (Brozoski et al, 2002;Kaltenbach et al, 2004;Bauer et al, 2008), then our results could indicate a beneficial effect of OC system activation on tinnitus. Our observations that the suppressive effects on spontaneous activity lasted after the stimulation had ceased, is consistent with a role for the OC system in residual inhibition, a temporary reduction of tinnitus experienced in tinnitus patients that persists for a few seconds after masking sounds are turned off (Vernon and Meikle, 2003;Roberts et al, 2008). Furthermore, activation of the OC system could be a contributory mechanism to the often beneficial effects of masking sounds on the perception of tinnitus (Jastreboff, 2007;Lugli et al, 2009), since the OC system itself can be activated by sound (Robertson and Gummer, 1985;Robertson and Winter, 1988 …”

Section: Discussionsupporting

confidence: 86%

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Mulders

Seluakumaran²,

Robertson³

2010

Journal of Neuroscience

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Animal models have demonstrated that mild hearing loss caused by acoustic trauma results in spontaneous hyperactivity in the central auditory pathways. This hyperactivity has been hypothesized to be involved in the generation of tinnitus, a phantom auditory sensation. We have recently shown that such hyperactivity, recorded in the inferior colliculus, is still dependent on cochlear neural output for some time after recovery (up to 6 weeks). We have now studied the capacity of an intrinsic efferent system, i.e., the olivocochlear system, to alter hyperactivity. This system is known to modulate cochlear neural output. Anesthetized guinea pigs were exposed to a loud sound and after 2 or 3 weeks of recovery, single-neuron recordings in inferior colliculus were made to confirm hyperactivity. Olivocochlear axons were electrically stimulated and effects on cochlear neural output and on highly spontaneous neurons in inferior colliculus were assessed. Olivocochlear stimulation suppressed spontaneous hyperactivity in the inferior colliculus. This result is in agreement with our earlier finding that hyperactivity can be modulated by altering cochlear neural output. Interestingly, the central suppression was generally much larger and longer lasting than reported previously for primary afferents. Blockade of the intracochlear effects of olivocochlear system activation eliminated some but not all of the effects observed on spontaneous activity, suggesting also a central component to the effects of stimulation. More research is needed to investigate whether these central effects of olivocochlear efferent stimulation are due to central intrinsic circuitry or to coactivation of central efferent collaterals to the cochlear nucleus.

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“…4B). The prevalence of RI in our data (some degree of RI reported by~69.5% of bilateral cases) is less than the reports by Henry and Meikle (2000) and Vernon and Meikle (2003) that RI can be demonstrated in~88% of tinnitus cases. Because RI functions were determined here, one might have expected a higher prevalence of RI in our sample.…”

Section: Ri Functionscontrasting

confidence: 87%

“…RI of longer duration has also been reported when measured for its full extent (no timeout), following 60 s of masking (twice the masker duration we used to measure RI functions). Vernon and Meikle (2003) found that 43% of patients attending a tinnitus clinic experienced RI lasting over 2 min after a noise masker was presented for 1 min at a level 10 dB above a level that masked the tinnitus.…”

Section: Ri Functionsmentioning

confidence: 99%

“…This phenomenon has come to be called "residual inhibition" (RI) in the tinnitus literature, although "post-masking suppression" (adapted from ) is more neutral with regard to its possible underlying mechanisms. It is known from foundation studies now more than 20 years old that the duration of RI is typically on the order of tens of seconds, although reports of RI lasting minutes or longer are not uncommon (Vernon and Meikle 2003). For RI to be experienced, masking sounds are presented at levels exceeding the loudness of tinnitus for at least 10 s, with RI duration increasing as a negatively accelerated function of masking duration, and approaching asymptote around 1 min with little gain thereafter (Terry et al 1983).…”

Section: Introductionmentioning

confidence: 99%

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Residual Inhibition Functions Overlap Tinnitus Spectra and the Region of Auditory Threshold Shift

Roberts

Moffat

Baumann

et al. 2008

JARO

200

215

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Animals exposed to noise trauma show augmented synchronous neural activity in tonotopically reorganized primary auditory cortex consequent on hearing loss. Diminished intracortical inhibition in the reorganized region appears to enable synchronous network activity that develops when deafferented neurons begin to respond to input via their lateral connections. In humans with tinnitus accompanied by hearing loss, this process may generate a phantom sound that is perceived in accordance with the location of the affected neurons in the cortical place map. The neural synchrony hypothesis predicts that tinnitus spectra, and heretofore unmeasured "residual inhibition functions" that relate residual tinnitus suppression to the center frequency of masking sounds, should cover the region of hearing loss in the audiogram. We confirmed these predictions in two independent cohorts totaling 90 tinnitus subjects, using computer-based tools designed to assess the psychoacoustic properties of tinnitus. Tinnitus spectra and residual inhibition functions for depth and duration increased with the amount of threshold shift over the region of hearing impairment. Residual inhibition depth was shallower when the masking sounds that were used to induce residual inhibition showed decreased correspondence with the frequency spectrum and bandwidth of the tinnitus. These findings suggest that tinnitus and its suppression in residual inhibition depend on processes that span the region of hearing impairment and not on mechanisms that enhance cortical representations for sound frequencies at the audiometric edge. Hearing thresholds measured in age-matched control subjects without tinnitus implicated hearing loss as a factor in tinnitus, although elevated thresholds alone were not sufficient to cause tinnitus.

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Tinnitus: clinical measurement

Cited by 100 publications

References 9 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

Efferent Pathways Modulate Hyperactivity in Inferior Colliculus

Residual Inhibition Functions Overlap Tinnitus Spectra and the Region of Auditory Threshold Shift

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