Restoration of auditory input through the use of hearing aids has been proposed as a potentially important means of altering tinnitus among those tinnitus sufferers who experience significant sensorineural hearing loss. The connection between the individual with tinnitus and their world seldom receives attention in neurophysiological research. Deafferentation pain is also associated with hyperactivity of the somatosensory thalamus and cortex. (2007). Recent research shows that tinnitus is a disorder that originates in the brain but has its trigger in the peripheral region. Intensity discrimination thresholds were significantly increased in the tinnitus frequency range, consistent with the hypothesis that auditory nerve fiber deafferentation is associated with tinnitus. 1.
However, whilst positive feedback is present and important at a neuronal level, it is generally less pivotal than and subservient to negative feedback systems (). These data suggest that thetagamma coupling as proposed by the thalamocortical dysrhythmia model might be causally related to a conscious auditory phantom percept. Down-regulation of inhibitory neurotransmission, related to partial peripheral deafferentation, is consistently presented as partially underpinning neuronal hyperactivity seen in animal models of tinnitus. , and Mills, J. The volume changes observed may represent antecedents or consequences of tinnitus and tinnitus-associated hearing loss and also raise the possibility that small cortical volume constitutes a vulnerability factor. Understanding the cellular and network basis of this aberrant EEG state may facilitate the development of clinical intervention approaches to reduce disruption of neuronal function during cortical disease. Acoust.
Comparisons to tinnitus were also discussed, as were ideas on how to better determine underlying differences in potential mechanisms between the two conditions. 2006;222(1-2):108-114. Further processing of this sensory stimulation generates an internal representation of the outer and inner world called a percept (De Ridder et al. 6. Norena, A. J. , Micheyl, C.
, Chery-Croze, S. For example presbyacousis is characterized by hearing loss at high frequencies, noise trauma usually induces a hearing loss which is fairly specific for 4000 Hz. (2002). “Psychoacoustic characterization of the tinnitus spectrum: Implications for the underlying mechanisms of tinnitus” Audiol. Neurootol. 7, 358–369. 9.
a Prior to hearing onset, IHCs exhibit spontaneous Ca2+ action potentials (APs), which are elicited through ATP signaling (). , Hartmann, T. , Dohrmann, K. Neurologic examination was unremarkable except for bilateral, symmetric sensory-neural hearing impairment. , and Norena, A. J. (2006).
“ High-frequency tinnitus without hearing loss does not mean absence of deafferentation,” Hear. Res. 222, 108–114. 10. Yates, G. K. , Winter, I.
M. Two other groups of researchers, at close to the same time, showed that neurogenesis takes place in the olfactory bulb in the adult mammalian brain (Corotto et al., 1994; Lois and Alvarez-Buylla, 1994). Activity in the delta range was also marked in seven people in this group. “ Basilar membrane nonlinearity determines auditory nerve rate-intensity functions and cochlear dynamic range,” Hear. Res. 45, 203–219. Recent auditory brain stem response measurements in tinnitus subjects with normal audiograms indicate the presence of hidden hearing loss that manifests as reduced neural output from the cochlea at high sound intensities, and results from mice suggest a link to deafferentation of auditory nerve fibers.
As deafferentation would lead to deficits in hearing performance, the present study investigates whether tinnitus patients with normal hearing thresholds show impairment in intensity discrimination compared to an audiometrically matched control group. Intensity discrimination thresholds were significantly increased in the tinnitus frequency range, consistent with the hypothesis that auditory nerve fiber deafferentation is associated with tinnitus.