Neuroanatomical and resting state EEG power correlates of central hearing loss in older adults.

To gain more insight into central hearing loss, we investigated the relationship between cortical thickness and surface area, speech-relevant resting state EEG power, and above-threshold auditory measures in older adults and younger controls. Twenty-three older adults and 13 younger controls were tested with an adaptive auditory test battery to measure not only traditional pure-tone thresholds, but also above individual thresholds of temporal and spectral processing. The participants' speech recognition in noise (SiN) was evaluated, and a T1-weighted MRI image obtained for each participant. We then determined the cortical thickness (CT) and mean cortical surface area (CSA) of auditory and higher speech-relevant regions of interest (ROIs) with FreeSurfer. Further, we obtained resting state EEG from all participants as well as data on the intrinsic theta and gamma power lateralization, the latter in accordance with predictions of the Asymmetric Sampling in Time hypothesis regarding speech processing (Poeppel, Speech Commun 41:245-255, 2003). Methodological steps involved the calculation of age-related differences in behavior, anatomy and EEG power lateralization, followed by multiple regressions with anatomical ROIs as predictors for auditory performance. We then determined anatomical regressors for theta and gamma lateralization, and further constructed all regressions to investigate age as a moderator variable. Behavioral results indicated that older adults performed worse in temporal and spectral auditory tasks, and in SiN, despite having normal peripheral hearing as signaled by the audiogram. These behavioral age-related distinctions were accompanied by lower CT in all ROIs, while CSA was not different between the two age groups. Age modulated the regressions specifically in right auditory areas, where a thicker cortex was associated with better auditory performance in older adults. Moreover, a thicker right supratemporal sulcus predicted more rightward theta lateralization, indicating the functional relevance of the right auditory areas in older adults. The question how age-related cortical thinning and intrinsic EEG architecture relates to central hearing loss has so far not been addressed. Here, we provide the first neuroanatomical and neurofunctional evidence that cortical thinning and lateralization of speech-relevant frequency band power relates to the extent of age-related central hearing loss in older adults. The results are discussed within the current frameworks of speech processing and aging.

Photobiomodulation by laser therapy rescued auditory neuropathy induced by ouabain.

Auditory neuropathy is a hearing disorder caused by impaired auditory nerve function. The lack of information about the pathophysiology of this disease limits early diagnosis and further treatment. Laser therapy is a novel approach to enhance nerve growth or induce axonal regeneration. We induced auditory neural degeneration sparing the sensory epithelium with local ouabain application in an animal model and observed the rescue effect of photobiomodulation (PBM), showing recovered auditory function and favorable histologic outcome. Hearing was evaluated using the auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). Seven days after ouabain application, the animals were sacrificed to evaluate the morphological changes. DPOAE change was not observed in all groups after ouabain application indicating no changes of outer hair cell function. Ouabain application increased the ABR thresholds increase, while the use of ouabain plus laser produced lower threshold compared to the ouabain group. Hematoxylin and Eosin staining of cochlea mid-modiolar sections in animals treated with ouabain showed damaged spiral ganglion cells, neurofilaments, and post synaptic puncta. Ouabain plus laser group showed higher number of spiral ganglion cells, higher density of neurofilaments, and higher number post synaptic puncta counts compared with ouabain application group. Short-term application of ouabain caused spiral ganglion cell damage while sparing the inner and outer hair cells in gerbils. Photobiomodulation alleviated the hearing loss caused by ouabain induced auditory neuropathy. The results indicate the possible role of photobiomodulation therapy for inner ear diseases accompanied by spiral ganglion degeneration.

Mutation of Foxo3 causes adult onset auditory neuropathy and alters cochlear synapse architecture in mice.

Auditory neuropathy is a form of hearing loss in which cochlear inner hair cells fail to correctly encode or transmit acoustic information to the brain. Few genes have been implicated in the adult-onset form of this disease. Here we show that mice lacking the transcription factor Foxo3 have adult onset hearing loss with the hallmark characteristics of auditory neuropathy, namely, elevated auditory thresholds combined with normal outer hair cell function. Using histological techniques, we demonstrate that Foxo3-dependent hearing loss is not due to a loss of cochlear hair cells or spiral ganglion neurons, both of which normally express Foxo3. Moreover, Foxo3-knock-out (KO) inner hair cells do not display reductions in numbers of synapses. Instead, we find that there are subtle structural changes in and surrounding inner hair cells. Confocal microscopy in conjunction with 3D modeling and quantitative analysis show that synaptic localization is altered in Foxo3-KO mice and Myo7a immunoreactivity is reduced. TEM demonstrates apparent afferent degeneration. Strikingly, acoustic stimulation promotes Foxo3 nuclear localization in vivo, implying a connection between cochlear activity and synaptic function maintenance. Together, these findings support a new role for the canonical damage response factor Foxo3 in contributing to the maintenance of auditory synaptic transmission.

Cortical thickness in congenital amusia: when less is better than more.

Congenital amusia (or tone deafness) is a lifelong disorder characterized by impairments in the perception and production of music. A previous voxel-based morphometry (VBM) study revealed that amusic individuals had reduced white matter in the right inferior frontal gyrus (IFG) relative to musically intact controls (Hyde et al., 2006). However, this VBM study also revealed associated increases in gray matter in the same right IFG region of amusics. The objective of the present study was to better understand this morphological brain anomaly by way of cortical thickness measures that provide a more specific measure of cortical morphology relative to VBM. We found that amusic subjects (n = 21) have thicker cortex in the right IFG and the right auditory cortex relative to musically intact controls (n = 26). These cortical thickness differences suggest the presence of cortical malformations in the amusic brain, such as abnormal neuronal migration, that may have compromised the normal development of a right frontotemporal pathway.

The relation among hearing loss, sensory cell loss and tuning characteristics in the chinchilla.

Evoked-potential tuning curves were obtained on over 150 chinchillas before and after acoustic overstimulation in order to relate the effects of changes in frequency selectivity to sensory cell loss over a wide range of hearing loss. Pre- and post-exposure measures of auditory thresholds and masked thresholds (simultaneous tone-on-tone paradigm) were obtained in each animal at 0.5, 1.0, 2.0, 4.0, 8.0 and 11.2 kHz, using the auditory evoked potential recorded from the inferior colliculus. Three tuning curve variables (Q10dB, low-frequency slope and high-frequency slope) were compared to the amount of noise-induced permanent threshold shift and to the percent sensory cell loss produced by a variety of noise exposures. Based upon large sample averages, frequencies showing permanent threshold shifts in excess of 10 dB also showed statistically significant differences between pre- and post-exposure measures of all three tuning curve variables. Shifts of less than 10 dB were not accompanied by statistically significant changes in the tuning curve variables. The percentage of outer hair cell loss, and percentage change in tuning curve characteristics showed systematic and parallel increases as threshold shifts increased at all probe tone frequencies except 8.0 and 11.2 kHz. In general, the results were consistent in showing that there is a systematic change in the variables which define the quality of tuning as hearing loss progressively increases and that these changes are clearly related to outer hair cell losses.