Auditory Deficits Research Articles

Computational Synaptic Modeling of Pitch and Duration Mismatch Negativity in First-Episode Psychosis Reveals Selective Dysfunction of the N-Methyl-D-Aspartate Receptor.

Mismatch negativity (MMN) to pitch (pMMN) and to duration (dMMN) deviant stimuli is significantly more attenuated in long-term psychotic illness compared to first-episode psychosis (FEP). It was recently shown that source-modeling of magnetically recorded MMN increases the detection of left auditory cortex MMN deficits in FEP, and that computational circuit modeling of electrically recorded MMN also reveals left-hemisphere auditory cortex abnormalities. Computational modeling using dynamic causal modeling (DCM) can also be used to infer synaptic activity from EEG-based scalp recordings. We measured pMMN and dMMN with EEG from 26 FEP and 26 matched healthy controls (HCs) and used a DCM conductance-based neural mass model including α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, N-methyl-D-Aspartate (NMDA), and Gamma-aminobutyric acid receptors to identify any changes in effective connectivity and receptor rate constants in FEP. We modeled MMN sources in bilateral A1, superior temporal gyrus, and inferior frontal gyrus (IFG). No model parameters distinguished groups for pMMN. For dMMN, reduced NMDA receptor activity in right IFG in FEP was detected. This finding is in line with literature of prefrontal NMDA receptor hypofunction in chronic schizophrenia and suggests impaired NMDA-induced synaptic plasticity may be present at psychosis onset where scalp dMMN is only moderately reduced. To the best of our knowledge, this is the first report of impaired NMDA receptor activity in FEP found through computational modeling of dMMN and shows the potential of DCM to non-invasively reveal synaptic-level abnormalities that underly subtle functional auditory processing deficits in early psychosis.

Contribution of the serotonergic system to developmental brain abnormalities in autism spectrum disorder.

This review highlights a key role of the serotonergic system in brain development and in distortions of normal brain development in early stages of fetal life resulting in cascades of abnormalities, including defects of neurogenesis, neuronal migration, neuronal growth, differentiation, and arborization, as well as defective neuronal circuit formation in the cortex, subcortical structures, brainstem, and cerebellum of autistic subjects. In autism, defects in regulation of neuronal growth are the most frequent and ubiquitous developmental changes associated with impaired neuron differentiation, smaller size, distorted shape, loss of spatial orientation, and distortion of cortex organization. Common developmental defects of the brain in autism include multiregional focal dysplastic changes contributing to local neuronal circuit distortion, epileptogenic activity, and epilepsy. There is a discrepancy between more than 500 reports demonstrating the contribution of the serotonergic system to autism's behavioral anomalies, highlighted by lack of studies of autistic subjects' brainstem raphe nuclei, the center of brain serotonergic innervation, and of the contribution of the serotonergic system to the diagnostic features of autism spectrum disorder (ASD). Discovery of severe fetal brainstem auditory system neuronal deficits and other anomalies leading to a spectrum of hearing deficits contributing to a cascade of behavioral alterations, including deficits of social and verbal communication in individuals with autism, is another argument to intensify postmortem studies of the type and topography of, and the severity of developmental defects in raphe nuclei and their contribution to abnormal brain development and to the broad spectrum of functional deficits and comorbid conditions in ASD.

근원적 인지 메커니즘을 통한 난독증 탐구

Objectives The purpose of this paper is to identify dyslexia among various types of learning disabilities, explain its manifestation mechanism, and demonstrate it clinically.
 Methods This paper shows that through the fundamental cognitive mechanism, not only can the characteristics of dyslexia be understood in the most fundamental, essential, and holistic way, but also a better understanding of how dyslexia is fundamentally manifested. For clinical proof, non-verbal intelligence test (K-CTONI-2), Korean version of Children's Visual Perception Development Test (K-DTVP-3), the Korean Reading Test (KOLRA), and speech hearing test were administered to 7 elementary school students who continued to experience difficulties despite receiving reading education.
 Results Dyslexia begins with an excessively imbalanced structure of the brain's large visual and small auditory cognitive spaces. Due to the imbalance between the two cognitive spaces, visual acuity and visual memory appear strong, while auditory acuity and auditory memory appear weak, resulting in auditory internal attention deficit, which is the most important cognitive condition for language development. Auditory internal attention deficit in turn interferes with auditory information processing, resulting in serious difficulties in written language development and various symptoms observed in dyslexic children. The test results showed a low auditory function score compared to a high visual function score.
 Conclusions Dyslexia occurs due to functional defects in hierarchical cognitive processes such as auditory sensation, memory, and thought processing caused by an imbalance between the brain's small auditory cognitive space and large visual cognitive space. This paper presents directions for effective dyslexia treatment based on research results.

Auditory brainstem responses are resistant to pharmacological modulation in Sprague Dawley wild-type and Neurexin1α knockout rats

Sensory processing in the auditory brainstem can be studied with auditory brainstem responses (ABRs) across species. There is, however, a limited understanding of ABRs as tools to assess the effect of pharmacological interventions. Therefore, we set out to understand how pharmacological agents that target key transmitter systems of the auditory brainstem circuitry affect ABRs in rats. Given previous studies, demonstrating that Nrxn1α KO Sprague Dawley rats show substantial auditory processing deficits and altered sensitivity to GABAergic modulators, we used both Nrxn1α KO and wild-type littermates in our study. First, we probed how different commonly used anesthetics (isoflurane, ketamine/xylazine, medetomidine) affect ABRs. In the next step, we assessed the effects of different pharmacological compounds (diazepam, gaboxadol, retigabine, nicotine, baclofen, and bitopertin) either under isoflurane or medetomidine anesthesia. We found that under our experimental conditions, ABRs are largely unaffected by diverse pharmacological modulation. Significant modulation was observed with (i) nicotine, affecting the late ABRs components at 90 dB stimulus intensity under isoflurane anesthesia in both genotypes and (ii) retigabine, showing a slight decrease in late ABRs deflections at 80 dB stimulus intensity, mainly in isoflurane anesthetized Nrxn1α KO rats. Our study suggests that ABRs in anesthetized rats are resistant to a wide range of pharmacological modulators, which has important implications for the applicability of ABRs to study auditory brainstem physiology.

Treatment approaches of central auditory processing deficit

Treatment approaches of central auditory processing deficit

Aberrant thalamocortical connectivity and shifts between the resting state and task state in patients with schizophrenia.

Prominent pathological hypotheses for schizophrenia include auditory processing deficits and dysconnectivity within cerebral networks. However, most neuroimaging studies have focused on impairments in either resting-state or task-related functional connectivity in patients with schizophrenia. The aims of our study were to examine (1) blood oxygen level-dependent (BOLD) signals during auditory steady-state response (ASSR) tasks, (2) functional connectivity during the resting-state and ASSR tasks and (3) state shifts between the resting-state and ASSR tasks in patients with schizophrenia. To reduce the functional consequences of scanner noise, we employed resting-state and sparse sampling auditory fMRI paradigms in 25 schizophrenia patients and 25 healthy controls. Auditory stimuli were binaural click trains at frequencies of 20, 30, 40 and 80 Hz. Based on the detected ASSR-evoked BOLD signals, we examined the functional connectivity between the thalamus and bilateral auditory cortex during both the resting state and ASSR task state, as well as their alterations. The schizophrenia group exhibited significantly diminished BOLD signals in the bilateral auditory cortex and thalamus during the 80 Hz ASSR task (corrected p < 0.05). We observed a significant inverse relationship between the resting state and ASSR task state in altered functional connectivity within the thalamo-auditory network in schizophrenia patients. Specifically, our findings demonstrated stronger functional connectivity in the resting state (p < 0.004) and reduced functional connectivity during the ASSR task (p = 0.048), which was mediated by abnormal state shifts, within the schizophrenia group. These results highlight the presence of abnormal thalamocortical connectivity associated with deficits in the shift between resting and task states in patients with schizophrenia.

The Additional Burden of Auditory Processing Skill “Deficits” for a Young Person with Multiple Exceptionalities: A Case Study of a Twice-Exceptional Student

ABSTRACT This article reports on the findings of a qualitative case study exploring the auditory skill “deficits” of a twice-exceptional male student who had multiple exceptionalities, including deficits in auditory processing skills, which contributed to learning issues and social connection difficulties in unique ways. Auditory skill deficits are an under-researched area in the field of gifted education, yet these are requisite skills necessary for learning in school. For this case study, auditory deficits were related to phonological processing, auditory sequential memory, lowered auditory recall abilities, and weaknesses in auditory analysis skills. The role that these auditory skill deficits played in the educational experiences of this young person is explored. Findings suggest that the presentation and impact of auditory processing deficits is very individual.

Dissociating reading and auditory comprehension in persons with aphasia.

Language comprehension is often affected in individuals with post-stroke aphasia. However, deficits in auditory comprehension are not fully correlated with deficits in reading comprehension and the mechanisms underlying this dissociation remain unclear. This distinction is important for understanding language mechanisms, predicting long-term impairments and future development of treatment interventions. Using comprehensive auditory and reading measures from a large cohort of individuals with aphasia, we evaluated the relationship between aphasia type and reading comprehension impairments, the relationship between auditory versus reading comprehension deficits and the crucial neuroanatomy supporting the dissociation between post-stroke reading and auditory deficits. Scores from the Western Aphasia Battery-Revised from 70 participants with aphasia after a left-hemisphere stroke were utilized to evaluate both reading and auditory comprehension of linguistically equivalent stimuli. Repeated-measures and univariate ANOVA were used to assess the relationship between auditory comprehension and aphasia types and correlations were employed to test the relationship between reading and auditory comprehension deficits. Lesion-symptom mapping was used to determine the dissociation of crucial brain structures supporting reading comprehension deficits controlling for auditory deficits and vice versa. Participants with Broca's or global aphasia had the worst performance on reading comprehension. Auditory comprehension explained 26% of the variance in reading comprehension for sentence completion and 44% for following sequential commands. Controlling for auditory comprehension, worse reading comprehension performance was independently associated with damage to the inferior temporal gyrus, fusiform gyrus, posterior inferior temporal gyrus, inferior occipital gyrus, lingual gyrus and posterior thalamic radiation. Auditory and reading comprehension are only partly correlated in aphasia. Reading is an integral part of daily life and directly associated with quality of life and functional outcomes. This study demonstrated that reading performance is directly related to lesioned areas in the boundaries between visual association regions and ventral stream language areas. This behavioural and neuroanatomical dissociation provides information about the neurobiology of language and mechanisms for potential future treatment interventions.

Predicting self-reported hearing problems using suprathreshold auditory processing and cognitive measures

Measures typically included in standard audiometric test batteries often fail to correlate with self-reported auditory complaints. This is especially common for patients with normal- or near-normal-hearing sensitivity, like those who are aging or have a history of traumatic brain injury (TBI). This discrepancy likely stems from the use of measures that are not sensitive to auditory or cognitive processing deficits underlying patient complaints, which limits effective clinical assessment and management. Recent work has focused on making common laboratory-based measures more clinically accessible using a tablet-based app called PART. The goal of the current study was to identify PART measures that better reflect patient complaints. Data was collected from adults with (n = 37) or without (n = 36) a history of TBI that were matched in age and hearing sensitivity. Regression modeling was used to determine relationships between self-reported auditory difficulties and measures of auditory processing and cognition, including spectrotemporal modulation detection, frequency modulation detection, spatial release from masking, and the Auditory Visual Divided Attention Task (AVDAT). Items from the Concussion Symptom Subtype Inventory were used to measure self-reported auditory complaints. Results contribute to a better understanding of processing difficulties that underly auditory complaints in those with and without TBI.

Twenty Years of Blast-Induced Neurotrauma: Current State of Knowledge.

Blast-induced neurotrauma (BINT) is an important injury paradigm of neurotrauma research. This short communication summarizes the current knowledge of BINT. We divide the BINT research into several broad categories-blast wave generation in laboratory, biomechanics, pathology, behavioral outcomes, repetitive blast in animal models, and clinical and neuroimaging investigations in humans. Publications from 2000 to 2023 in each subdomain were considered. The analysis of the literature has brought out salient aspects. Primary blast waves can be simulated reasonably in a laboratory using carefully designed shock tubes. Various biomechanics-based theories of BINT have been proposed; each of these theories may contribute to BINT by generating a unique biomechanical signature. The injury thresholds for BINT are in the nascent stages. Thresholds for rodents are reasonably established, but such thresholds (guided by primary blast data) are unavailable in humans. Single blast exposure animal studies suggest dose-dependent neuronal pathologies predominantly initiated by blood-brain barrier permeability and oxidative stress. The pathologies were typically reversible, with dose-dependent recovery times. Behavioral changes in animals include anxiety, auditory and recognition memory deficits, and fear conditioning. The repetitive blast exposure manifests similar pathologies in animals, however, at lower blast overpressures. White matter irregularities and cortical volume and thickness alterations have been observed in neuroimaging investigations of military personnel exposed to blast. Behavioral changes in human cohorts include sleep disorders, poor motor skills, cognitive dysfunction, depression, and anxiety. Overall, this article provides a concise synopsis of current understanding, consensus, controversies, and potential future directions.

Examining the Use and Benefits of Low-/Mild-Gain Hearing Aids in Service Members with Normal Hearing Thresholds and Self-Reported Hearing Difficulties.

Low- (or mild-) gain hearing aids (LGHAs) are increasingly considered for individuals with normal peripheral hearing but significant self-reported hearing difficulties (SHDs). This study assesses the benefits of LGHAs as a management option for individuals with normal hearing thresholds (NHTs) and SHDs, comparing LGHA use and benefit to individuals with non-significant hearing difficulties (NHDs) and those with peripheral hearing loss. Questionnaires addressing hearing aid usage, benefit, hearing difficulties, and tinnitus were administered to 186 individuals who self-identified as hearing aid users in a sample of 6652 service members who were receiving their annual hearing tests. Participants were divided into SHD and NHD groups based on the normative cutoff of the Tinnitus and Hearing Survey-Hearing Subscale (THS-H), and into hearing impairment (HI) and NHT based on their audiometric air-conduction thresholds. Individuals with SHDs and NHTs reported higher LGHA usage and benefit than individuals with NHDs and NHTs. Comparable use and benefit were noted between groups with SHDs regardless of peripheral hearing loss status. The findings support LGHAs as a suitable management option for individuals with NHTs and SHDs, as indicated by hearing aid use and benefit. Quantifying the level of perceived auditory processing deficits (i.e., SHDs), notably with the THS-H, enhances sensitivity in identifying those who may benefit the most from this treatment option.

Low gain hearing aids use and benefit: A viable management option for those with hearing sensitivity within the normal range

Low (or mild) gain hearing aids (LGHAs) are increasingly considered for individuals with normal peripheral hearing but self-reported auditory complaints. The Tinnitus and Hearing Survey-Hearing Subscale (THS-H) offers a normative cutoff, aiding identification of significant self-reported hearing difficulties (SHD). This research assesses the benefits of LGHAs as a management option for individuals with normal hearing sensitivity and significant SHD, comparing LGHA use and benefit to individuals without SHD and those with peripheral hearing loss. 186 participants across four groups, including those with or without SHD and peripheral hearing loss were recruited. Participants completed questionnaires that addressed hearing aid usage, benefit, SHD and tinnitus. Individuals with significant SHD and hearing sensitivity within the normal range (NHT) reported higher LGHA usage and benefit than individuals with normal hearing difficulties (NHD) and NHT. Comparable use and benefit were noted between groups with significant SHD regardless of peripheral hearing loss status. The findings support LGHAs as a suitable management option for individuals with NHT and SHD, as indicated by hearing aid use and benefit. Quantifying the level of perceived auditory processing deficits (i.e., SHD), notably with the THS-H, enhances sensitivity in identifying those who may benefit from this management option.

Voice perception as a bridge between psychoacoustics and speech intelligibility

While clinical assessments of speech intelligibility focus on the reception of phonetic to lexical cues by a listener, in natural situations, speech also contains cues that inform the listener about the identity of the talker, or their emotional state. These indexical cues contribute to the access of phonetic information, either through talker normalisation, or by promoting the segregation of competing talkers. They can also directly affect the interpretation of the lexical content, e.g., through prosody. In other words, indexical cues play a crucial role in everyday communication. Yet, they are rarely considered in clinical evaluations of hearing impairment. Through various studies involving child and adult hearing aid and cochlear implant users, it appears that some voice cues are more affected by hearing loss than others, and this could have consequences on the development and remediation strategies. These studies also highlight the central role that voice perception study could play in connecting psychoacoustics to communication sciences. As voice literally carries the linguistic information in speech, it sits at the forefront of auditory processing. The mechanisms underpinning hearing loss thus tend to directly affect the neural representations of voice properties. As voice manipulation technologies are becoming more precise and more widely available, new opportunities arise to link peripheral auditory deficits to speech processing difficulties in populations with impaired hearing.

Allosteric Activation of α7 Nicotinic Acetylcholine Receptors by Novel 2-Arylamino-thiazole-5-carboxylic Acid Amide Derivatives for the Improvement of Cognitive Deficits in Mice.

Enhancing α7 nAChR function serves as a therapeutic strategy for cognitive disorders. Here, we report the synthesis and evaluation of 2-arylamino-thiazole-5-carboxylic acid amide derivatives 6-9 that as positive allosteric modulators (PAMs) activate human α7 nAChR current expressed in Xenopus ooctyes. Among the 4-amino derivatives, a representative atypical type I PAM 6p exhibits potent activation of α7 current with an EC50 of 1.3 μM and the maximum activation effect on the current over 48-fold in the presence of acetylcholine (100 μM). The structure-activity relationship (SAR) analysis reveals that the 4-amino group is crucial for the allosteric activation of α7 currents by compound 6p as the substitution of 4-methyl group results in its conversion to compound 7b (EC50 = 2.1 μM; max effect: 58-fold) characterized as a typical type I PAM. Furthermore, both 6p and 7b are able to rescue auditory gating deficits in mouse schizophrenia-like model of acoustic startle prepulse inhibition.

Neurotopographical Transformations: Dissecting Cortical Reconfigurations in Auditory Deprivation.

Within the intricate matrices of cognitive neuroscience, auditory deprivation acts as a catalyst, propelling a cascade of neuroanatomical adjustments that have, until now, been suboptimally articulated in extant literature. Addressing this gap, our study harnesses high-resolution 3 T MRI modalities to unveil the multifaceted cortical transformations that emerge in tandem with congenital auditory deficits. We conducted a rigorous cortical surface analysis on a cohort of 90 congenitally deaf individuals, systematically compared with 90 normoacoustic controls. Our sample encompassed both male and female participants, ensuring a gender-inclusive perspective in our analysis. Expected alterations within prototypical auditory domains were evident, but our findings transcended these regions, spotlighting modifications dispersed across a gamut of cortical and subcortical structures, thereby epitomizing the cerebral adaptive dynamics to sensory voids. Crucially, the study's innovative methodology integrated two pivotal variables: the duration of auditory deprivation and the extent of sign language immersion. By intersecting these metrics with structural changes, our analysis unveiled nuanced layers of cortical reconfigurations, elucidating a more granulated understanding of neural plasticity. This intersectional approach bestows a unique advantage, allowing for a discerning exploration into how varying durations of sensory experience and alternative communication modalities modulate the brain's morphological terrain. In encapsulating the synergy of neuroimaging finesse and incisive scientific rigor, this research not only broadens the current understanding of adaptive neural mechanisms but also paves the way for tailored therapeutic strategies, finely attuned to individual auditory histories and communicative repertoires.

Asymmetry in Cortical Thickness of the Heschl's Gyrus in Unilateral Ear Canal Atresia.

Unilateral congenital conductive hearing impairment in ear canal atresia leads to atrophy of the gray matter of the contralateral primary auditory cortex or changes in asymmetry pattern if left untreated in childhood. Unilateral ear canal atresia with associated severe conductive hearing loss results in deteriorated sound localization and difficulties in understanding of speech in a noisy environment. Cortical atrophy in the Heschl's gyrus has been reported in acquired sensorineural hearing loss but has not been studied in unilateral conductive hearing loss. We obtained T1w and T2w FLAIR MRI data from 17 subjects with unilateral congenital ear canal atresia and 17 matched controls. Gray matter volume and thickness were measured in the Heschl's gyrus using Freesurfer. In unilateral congenital ear canal atresia, Heschl's gyrus exhibited cortical thickness asymmetry (right thicker than left, corrected p = 0.0012, mean difference 0.25 mm), while controls had symmetric findings. Gray matter volume and total thickness did not differ from controls with normal hearing. We observed cortical thickness asymmetry in congenital unilateral ear canal atresia but no evidence of contralateral cortex atrophy. Further research is needed to understand the implications of this asymmetry on central auditory processing deficits.

Design and methodology for a proof of mechanism study of individualized neuronavigated continuous Theta burst stimulation for auditory processing in adolescents with autism spectrum disorder.

It has been suggested that aberrant excitation/inhibition (E/I) balance and dysfunctional structure and function of relevant brain networks may underlie the symptoms of autism spectrum disorder (ASD). However, the nomological network linking these constructs to quantifiable measures and mechanistically relating these constructs to behavioral symptoms of ASD is lacking. Herein we describe a within-subject, controlled, proof-of-mechanism study investigating the pathophysiology of auditory/language processing in adolescents with ASD. We utilize neurophysiological and neuroimaging techniques including magnetic resonance spectroscopy (MRS), diffusion-weighted imaging (DWI), functional magnetic resonance imaging (fMRI), and magnetoencephalography (MEG) metrics of language network structure and function. Additionally, we apply a single, individually targeted session of continuous theta burst stimulation (cTBS) as an experimental probe of the impact of perturbation of the system on these neurophysiological and neuroimaging outcomes. MRS, fMRI, and MEG measures are evaluated at baseline and immediately prior to and following cTBS over the posterior superior temporal cortex (pSTC), a region involved in auditory and language processing deficits in ASD. Also, behavioral measures of ASD and language processing and DWI measures of auditory/language network structures are obtained at baseline to characterize the relationship between the neuroimaging and neurophysiological measures and baseline symptom presentation. We hypothesize that local gamma-aminobutyric acid (GABA) and glutamate concentrations (measured with MRS), and structural and functional activity and network connectivity (measured with DWI and fMRI), will significantly predict MEG indices of auditory/language processing and behavioral deficits in ASD. Furthermore, a single session of cTBS over left pSTC is hypothesized to lead to significant, acute changes in local glutamate and GABA concentration, functional activity and network connectivity, and MEG indices of auditory/language processing. We have completed the pilot phase of the study (n=20 Healthy Volunteer adults) and have begun enrollment for the main phase with adolescents with ASD (n=86; age 14-17). If successful, this study will establish a nomological network linking local E/I balance measures to functional and structural connectivity within relevant brain networks, ultimately connecting them to ASD symptoms. Furthermore, this study will inform future therapeutic trials using cTBS to treat the symptoms of ASD.

Demyelination and Na+ Channel Redistribution Underlie Auditory and Vestibular Dysfunction in PMP22-Null Mice.

Altered expression of peripheral myelin protein 22 (PMP22) results in demyelinating peripheral neuropathy. PMP22 exhibits a highly restricted tissue distribution with marked expression in the myelinating Schwann cells of peripheral nerves. Auditory and vestibular Schwann cells and the afferent neurons also express PMP22, suggesting a unique role in hearing and balancing. Indeed, neuropathic patients diagnosed with PMP22-linked hereditary neuropathies often present with auditory and balance deficits, an understudied clinical complication. To investigate the mechanism by which abnormal expression of PMP22 may cause auditory and vestibular deficits, we studied gene-targeted PMP22-null mice. PMP22-null mice exhibit an unsteady gait, have difficulty maintaining balance, and live for only ∼3-5 weeks relative to unaffected littermates. Histological analysis of the inner ear revealed reduced auditory and vestibular afferent nerve myelination and profound Na+ channel redistribution without PMP22. Yet, Na+ current density was unaltered, in stark contrast to increased K+ current density. Atypical postsynaptic densities and a range of neuronal abnormalities in the organ of Corti were also identified. Analyses of auditory brainstem responses (ABRs) and vestibular sensory-evoked potential (VsEP) revealed that PMP22-null mice had auditory and vestibular hypofunction. These results demonstrate that PMP22 is required for hearing and balance, and the protein is indispensable for the formation and maintenance of myelin in the peripheral arm of the eighth nerve. Our findings indicate that myelin abnormalities and altered signal propagation in the peripheral arm of the auditory nerve are likely causes of auditory deficits in patients with PMP22-linked neuropathies.

Alterations of resting-state functional network connectivity in patients with noise-induced hearing loss: A study based on independent component analysis.

Functional reorganization is a response to auditory deficits or deprivation, and less is known about the overall brain network alterations involving resting-state networks (RSNs) and multiple functional networks in patients with occupational noise-induced hearing loss (NIHL). So this study evaluated resting-state functional network connectivity (FNC) alterations in occupational NIHL using an independent component analysis (ICA). In total, 79 mild NIHL patients (MP), 32 relatively severe NIHL patients (RSP), and 84 age- and education- matched healthy controls (HC) were recruited. All subjects were tested using the Mini-mental State Examination scale, the tinnitus Handicap Inventory scale, the Hamilton Anxiety scale (HAMA) and scanned by T1-3DFSPGR, resting-state functional magnetic resonance imaging sequence in 3.0 T and analysed by the ICA. Seven RSNs were identified, compared with the HC, the MP showed increased FNC within the executive control network (ECN) and enhanced FNC within the default mode network (DMN) and the visual network (VN); compared with the HC, the RSP showed decreased FNC within the ECN and auditory network (AUN), DMN and VN; no significant changes in FNC were found in the MP compared with the RSP. Furthermore, the correlation analysis between the noise exposure time and hearing loss level, HAMA were both negative, and there were no significant correlations between the abnormal RSNs and the hearing level, noise exposure time and HAMA. These findings indicate that different degrees of NIHL involve different alterations in RSNs connectivity and may reveal the neural mechanisms related to emotion-related features and functional abnormalities following long-term NIHL.

Variability in auditory processing performance is associated with reading difficulties rather than with history of otitis media.

The nature and cause of auditory processing deficits in dyslexic individuals have been debated for decades. Auditory processing deficits were argued to be the first step in a causal chain of difficulties, leading to difficulties in speech perception and thereby phonological processing and literacy difficulties. More recently, it has been argued that auditory processing difficulties may not be causally related to language and literacy difficulties. This study compares two groups who have phonological processing impairments for different reasons: dyslexia and a history of otitis media (OM). We compared their discrimination thresholds and response variability to chronological age- and reading age-matched controls, across three auditory processing tasks: frequency discrimination, rise-time discrimination and speech perception. Dyslexic children showed raised frequency discrimination thresholds in comparison with age-matched controls but did not differ from reading age-matched controls or individuals with a history of OM. There were no group differences on speech perception or rise-time tasks. For the dyslexic children, there was an association between phonological awareness and frequency discrimination response variability, but no association with thresholds. These findings are not consistent with a 'causal chain' explanation but could be accounted for within a multiple deficits view of literacy difficulties.