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Alzheimer's disease (AD) is a neurodegenerative disease involving cognitive impairment and abnormalities in speech and language. Here, we examine how AD affects the fidelity of auditory feedback predictions during speaking. We focus on the phenomenon of speaking-induced suppression (SIS), the auditory cortical responses' suppression during auditory feedback processing. SIS is determined by subtracting the magnitude of auditory cortical responses during speaking from listening to playback of the same speech. Our state feedback control (SFC) model of speech motor control explains SIS as arising from the onset of auditory feedback matching a prediction of that feedback onset during speaking, a prediction that is absent during passive listening to playback of the auditory feedback. Our model hypothesizes that the auditory cortical response to auditory feedback reflects the mismatch with the prediction: small during speaking, large during listening, with the difference being SIS. Normally, during speaking, auditory feedback matches its predictions, then SIS will be large. Any reductions in SIS will indicate inaccuracy in auditory feedback prediction not matching the actual feedback. We investigated SIS in AD patients [ n  =   20; mean (SD) age, 60.77 (10.04); female (%), 55.00] and healthy controls [ n  =   12; mean (SD) age, 63.68 (6.07); female (%), 83.33] through magnetoencephalography (MEG)-based functional imaging. We found a significant reduction in SIS at ∼100 ms in AD patients compared with healthy controls (linear mixed effects model, F (1,57.5)  = 6.849, p  =   0.011). The results suggest that AD patients generate inaccurate auditory feedback predictions, contributing to abnormalities in AD speech., Competing Interests: The authors declare no competing financial interests., (Copyright © 2023 Kim et al.)

Neuromodulation treatment effect size for bothersome tinnitus may be larger and more predictable by adopting a target selection approach guided by personalized striatal networks or functional connectivity maps. Several corticostriatal mechanisms are likely to play a role in tinnitus, including the dorsal/ventral striatum and the putamen. We examined whether significant tinnitus treatment response by deep brain stimulation (DBS) of the caudate nucleus may be related to striatal network increased functional connectivity with tinnitus networks that involve the auditory cortex or ventral cerebellum. The first study was a cross-sectional 2-by-2 factorial design (tinnitus, no tinnitus; hearing loss, normal hearing, n = 68) to define cohort level abnormal functional connectivity maps using high-field 7.0 T resting-state fMRI. The second study was a pilot case-control series (n = 2) to examine whether tinnitus modulation response to caudate tail subdivision stimulation would be contingent on individual level striatal connectivity map relationships with tinnitus networks. Resting-state fMRI identified five caudate subdivisions with abnormal cohort level functional connectivity maps. Of those, two connectivity maps exhibited increased connectivity with tinnitus networks-dorsal caudate head with Heschl's gyrus and caudate tail with the ventral cerebellum. DBS of the caudate tail in the case-series responder resulted in dramatic reductions in tinnitus severity and loudness, in contrast to the nonresponder who showed no tinnitus modulation. The individual level connectivity map of the responder was in alignment with the cohort expectation connectivity map, where the caudate tail exhibited increased connectivity with tinnitus networks, whereas the nonresponder individual level connectivity map did not., (© 2021 The Authors. Human Brain Mapping published by Wiley Periodicals LLC.)

Objectives: Auditory cortical activation of the two hemispheres to monaurally presented tonal stimuli has been shown to be asynchronous in normal hearing (NH) but synchronous in the extreme case of adult-onset asymmetric hearing loss (AHL) with single-sided deafness. We addressed the wide knowledge gap between these two anchoring states of interhemispheric temporal organization. The objectives of this study were as follows: (1) to map the trajectory of interhemispheric temporal reorganization from asynchrony to synchrony using magnitude of interaural threshold difference as the independent variable in a cross-sectional study and (2) to evaluate reversibility of interhemispheric synchrony in association with hearing in noise performance by amplifying the aidable poorer ear in a repeated measures, longitudinal study., Design: The cross-sectional and longitudinal cohorts were comprised of 49 subjects (AHL; N = 21; 11 male, 10 female; mean age = 48 years) and NH (N = 28; 16 male, 12 female; mean age = 45 years). The maximum interaural threshold difference of the two cohorts spanned from 0 to 65 dB. Magnetoencephalography analyses focused on latency of the M100 peak response from auditory cortex in both hemispheres between 50 msec and 150 msec following monaural tonal stimulation at the frequency (0.5, 1, 2, 3, or 4 kHz) corresponding to the maximum and minimum interaural threshold difference for better and poorer ears separately. The longitudinal AHL cohort was drawn from three subjects in the cross-sectional AHL cohort (all male; ages 49 to 60 years; varied AHL etiologies; no amplification for at least 2 years). All longitudinal study subjects were treated by monaural amplification of the poorer ear and underwent repeated measures examination of the M100 response latency and quick speech in noise hearing in noise performance at baseline, and postamplification months 3, 6, and 12., Results: The M100 response peak latency values in the ipsilateral hemisphere lagged those in the contralateral hemisphere for all stimulation conditions. The mean (SD) interhemispheric latency difference values (ipsilateral less contralateral) to better ear stimulation for three categories of maximum interaural threshold difference were as follows: NH (≤ 10 dB)-8.6 (3.0) msec; AHL (15 to 40 dB)-3.0 (1.2) msec; AHL (≥ 45 dB)-1.4 (1.3) msec. In turn, the magnitude of difference values were used to define interhemispheric temporal organization states of asynchrony, mixed asynchrony and synchrony, and synchrony, respectively. Amplification of the poorer ear in longitudinal subjects drove interhemispheric organization change from baseline synchrony to postamplification asynchrony and hearing in noise performance improvement in those with baseline impairment over a 12-month period., Conclusions: Interhemispheric temporal organization in AHL was anchored between states of asynchrony in NH and synchrony in single-sided deafness. For asymmetry magnitudes between 15 and 40 dB, the intermediate mixed state of asynchrony and synchrony was continuous and reversible. Amplification of the poorer ear in AHL improved hearing in noise performance and restored normal temporal organization of auditory cortices in the two hemispheres. The return to normal interhemispheric asynchrony from baseline synchrony and improvement in hearing following monoaural amplification of the poorer ear evolved progressively over a 12-month period., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2021 The Authors. Ear & Hearing is published on behalf of the American Auditory Society, by Wolters Kluwer Health, Inc.)

Single-sided deafness (SSD) or profound unilateral hearing loss is the condition where the transfer of acoustic information to the brain is restricted to one ear. SSD impairment is most evident under adverse acoustic environments with overlapping interference, which burdens cognitive resources. It is known that bilateral deafness induces cross-modal brain plasticity within visual cortical areas. Here we investigate whether similar cross-modal plasticity is observed in adult-onset SSD. In SSD patients (n ​= ​29) and matched controls (n ​= ​29) we estimated voxel level resting-state power and functional connectivity in the alpha band (8-12 ​Hz) from magnetoencephalography (MEG) data. We examined both global functional connectivity (mean functional connectivity of each voxel with the rest of the brain), and seeded functional connectivity of primary auditory cortices (A1), primary visual cortices (V1) and posterior cingulate cortex (PCC) of the default mode network (DMN). Power reduction was observed in left auditory cortex. Global functional connectivity showed reduction in frontal cortices and enhancement in visual cortex. Seeded functional connectivity of auditory cortices showed reduction in temporal, frontal and occipital regions, and enhancement in parietal cortex. Interestingly, seeded functional connectivity of visual cortices showed enhancement in visual cortices, inferior parietal lobe, post-central gyrus, and the precuneus, and reduction in auditory cortex. Seeded functional connectivity of PCC showed reduction in frontal cortical regions that are part of the DMN, attention, and working memory networks. Adult-onset SSD exhibited widespread cross-modal brain plasticity involving alterations in auditory, visual, attention, working memory and default mode networks., Competing Interests: Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: To evaluate brain networks for motor control of voice production in patients with treated unilateral vocal fold paralysis (UVFP)., Study Design: Cross-sectional comparison., Methods: Nine UVFP patients treated by type I thyroplasty, and 11 control subjects were compared using magnetoencephalographic imaging to measure beta band (12-30 Hz) neural oscillations during voice production with perturbation of pitch feedback. Differences in beta band power relative to baseline were analyzed to identify cortical areas with abnormal activity within the 400 ms perturbation period and 125 ms beyond, for a total of 525 ms., Results: Whole-brain task-induced beta band activation patterns were qualitatively similar in both treated UVFP patients and healthy controls. Central vocal motor control plasticity in UVFP was expressed within constitutive components of central human communication networks identified in healthy controls. Treated UVFP patients exhibited statistically significant enhancement (P < 0.05) in beta band activity following pitch perturbation onset in left auditory cortex to 525 ms, left premotor cortex to 225 ms, and left and right frontal cortex to 525 ms., Conclusion: This study further corroborates that a peripheral motor impairment of the larynx can affect central cortical networks engaged in auditory feedback processing, vocal motor control, and judgment of voice-as-self. Future research to dissect functional relationships among constitutive cortical networks could reveal neurophysiological bases of central contributions to voice production impairment in UVFP. Those novel insights would motivate innovative treatments to improve voice production and reduce misalignment of voice-quality judgment between clinicians and patients., Level of Evidence: 3b Laryngoscope, 129:2125-2130, 2019., (© 2018 The American Laryngological, Rhinological and Otological Society, Inc.)

Objectives: To evaluate differences in vocal motor control and central auditory processing between treated unilateral vocal fold paralysis (UVFP) and healthy control cohorts., Study Design: Cross-sectional., Methods: Ten UVFP study patients treated by type I thyroplasty with stable voices were compared to 12 control subjects for vocal motor control using a pitch perturbation response task and central auditory processing performance using a battery of complex sound intelligibility assays that included adverse temporal and noise conditions. Standard clinical evaluations of voice production and peripheral audiometric sensitivity were performed., Results: Vocal motor control was impaired in treated UVFP. The UVFP cohort exhibited a 32.5% reduction in the instantaneous, subconscious compensatory response to pitch feedback perturbation in the interval between 150 ms and 550 ms following onset (P < 0.0001, linear mixed effects model). This impairment cannot simply be ascribed to vocal motor capacity insufficiency in the UVFP cohort because both cohorts demonstrated comparable functional capacity to perform the vocal motor task. The UVFP cohort also showed greater propensity for central auditory processing impairment (P < 0.05), notably for temporal compression and added noise challenges., Conclusion: Combined central vocal motor control and auditory processing impairments in treated UVFP highlight reciprocal interdependency of sensory and motor systems. This pilot study suggests that peripheral motor impairment of the larynx can degrade central auditory processing, which in turn may contribute to vocal motor control impairment. A more complete restoration communicative function in UVFP will require deeper understanding of sensory, motor, and sensorimotor aspects of the human communication loop., Level of Evidence: 3b Laryngoscope, 129:2112-2117, 2019., (© 2018 The American Laryngological, Rhinological and Otological Society, Inc.)

Objectives/hypothesis: To evaluate spatial plasticity of the auditory cortex in single-sided deafness (SSD)., Study Design: Cross-sectional study comparing a cohort with adult-onset, idiopathic SSD to a cohort with normal hearing., Methods: Demographic, audiometric, magnetoencephalographic imaging, and magnetic resonance imaging data were collected for 13 SSD adult subjects and 13 normal-hearing controls. Locations of peak activation corresponding to the M100 response in auditory cortices ipsilateral and contralateral to tonal stimuli (0.5 kHz and 4 kHz) were extracted from advanced biomagnetic source imaging analyses. Spatial extent of frequency representation across the 0.5 kHz to 4 kHz zone was computed for the two hemispheres., Results: Spatial separation distance between peak locations for 0.5 kHz and 4 kHz stimuli in SSD showed increased activation spread distance in the hemisphere contralateral to the only hearing ear and decreased distance in the ipsilateral hemisphere. In contrast, normal hearing controls had nearly the same activation spread distance in the two hemispheres for ipsilateral and contralateral inputs. The difference between interhemispheric activation spread distance in SSD is significantly increased to 6.5 mm, when compared to 1.7 mm in normal controls (P < .05)., Conclusions: Loss of unilateral peripheral input in SSD is associated with spatial reorganization of the auditory cortex in both hemispheres. This change in central auditory functional organization may in turn lead to higher order hearing deficits that rely on interhemispheric processing. Hearing optimization in the only hearing ear may require remediation of both spatial and temporal central auditory changes in SSD., Level of Evidence: NA Laryngoscope, 126:2785-2791, 2016., (© 2016 The American Laryngological, Rhinological and Otological Society, Inc.)

Hypothesis: To refine and extend the knowledge on cortical plasticity in single-sided deafness (SSD) by assessing magnetoencephalographic imaging in a well-defined group of subjects., Background: SSD causes difficulties with directional hearing, signal extraction in noise, and multispeaker identification and separation. In SSD, the ipsilateral auditory cortex is never powerfully driven by sound, which may lead to plastic change and contribute to higher-order psychoacoustic dysfunction beyond loss of a peripheral sound sensor., Study Design: A cross-sectional study on 12 subjects with long-term, adult-onset, nontraumatic SSD and 12 normal-hearing controls was conducted using magnetoencephalographic imaging, magnetic resonance imaging, and validated hearing instruments. Pure-tone stimuli at five frequencies were presented to each hearing ear individually. M100 activation peak times of the ipsilateral and contralateral auditory cortices were analyzed., Results: Controls showed an M100 interhemispheric mean latency difference of 6.6 milliseconds. In contrast, subjects with SSD exhibited a mean of 1.7 milliseconds. This loss of interhemispheric latency difference was statistically significant (p < 0.05, analysis of variance with repeated measures). SSD subjects confirmed degraded hearing function on both Hearing Handicap Inventory for Adults (p < 0.001) and Speech, Spatial, and Qualities of Hearing Scale instruments (p < 0.001)., Conclusion: SSD disrupts M100 latency difference between the two hemispheres to sound stimulation. This finding may represent maladaptive temporal cortical plasticity because of loss of a peripheral sensor. Based on this premise, a new generation of neurophysiologically inspired auditory treatments to correct or mitigate central consequences of SSD may be considered to optimize hearing in individuals with only one functional ear.