Microglia induce auditory dysfunction after status epilepticus in mice.

Auditory dysfunction and increased neuronal activity in the auditory pathways have been reported in patients with temporal lobe epilepsy, but the cellular mechanisms involved are unknown. Here, we report that microglia play a role in the disinhibition of auditory pathways after status epilepticus in mice. We found that neuronal activity in the auditory pathways, including the primary auditory cortex and the medial geniculate body (MGB), was increased and auditory discrimination was impaired after status epilepticus. We further demonstrated that microglia reduced inhibitory synapses on MGB relay neurons over an 8-week period after status epilepticus, resulting in auditory pathway hyperactivity. In addition, we found that local removal of microglia from the MGB attenuated the increase in c-Fos+ relay neurons and improved auditory discrimination. These findings reveal that thalamic microglia are involved in auditory dysfunction in epilepsy.

Hearing dysfunction heralds an increase in non-motor burden and a worse quality of life in Parkinson's disease: new insights from non-motor spectrum.

BACKGROUND: Sensorial non-motor symptoms (NMSs) in Parkinson's disease (PD) still lack appropriate investigation in clinical practice. This study aimed to assess if and to what extent auditory dysfunction is associated with other NMSs in PD and its impact on patient's quality of life (QoL). METHODS: We selected patients with idiopathic PD, without other concomitant neurological diseases, dementia, or diagnosis of any audiological/vestibular disease. Demographic and clinical data were collected. Patients underwent otoscopic examination, audiological testing with pure tone audiometry (PTA) and distortion product otoacoustic emissions (DPOAEs) and completed Non-Motor Symptoms Scale (NMSS) and Parkinson's Disease Questionnaires-39 (PDQ-39). ANCOVA and partial correlation analysis have been used for statistical analysis. RESULTS: 60 patients were enrolled and completed PTA and DPOAEs. 32 patients with hearing impairment (HI), assessed by PTA, (hearing threshold ≥ 25 dB) showed similar disease duration, motor impairment, and staging, compared to patients without HI, but higher scores both in NMSS and in PDQ-39, except for cardiovascular (CV), gastrointestinal (GI), urogenital (U) and sexual function (SF) of NMSS. In addition, DPOAEs showed a significant correlation with higher scores both in NMSS and PDQ-39, except for CV, SF, GI, U and perceptual problem subdomains of NMSS. CONCLUSION: This study demonstrated that PD patients with HI have a greater burden of NMS and lower related QoL and functioning. Our results highlight the importance to reconsider HI as a NMS, in parallel with the others. HI evaluation, even in asymptomatic patients, may reveal a wider pathology with a worse QoL.

Neuroprotective Effect of Valproic Acid on Salicylate-Induced Tinnitus.

High-dose salicylate induces temporary moderate hearing loss and the perception of a high-pitched tinnitus in humans and animals. Previous studies demonstrated that high doses of salicylate increase N-methyl-d-aspartate (NMDA) receptor levels, resulting in a rise in Ca2+ influx and induction of excitotoxicity. Glutamate excitotoxicity is associated with failure in the maintenance of calcium homeostasis, mitochondrial dysfunction, and production of reactive oxygen species (ROS). Valproic acid (VPA) is widely used for the management of bipolar disorder, epilepsy, and migraine headaches, and is known to regulate NMDA receptor activity. In this study, we examined the beneficial effects of VPA in a salicylate-induced tinnitus model in vitro and in vivo. Cells were pretreated with VPA followed by salicylate treatment. The expression levels of NMDA receptor subunit NR2B, phosphorylated cAMP response element-binding protein-an apoptosis marker, and intracellular levels of ROS were measured using several biochemical techniques. We observed increased expression of NR2B and its related genes TNFα and ARC, increased intracellular ROS levels, and induced expression of cleaved caspase-3. These salicylate-induced changes were attenuated in the neuronal cell line SH-SY5Y and rat cortical neurons after VPA pretreatment. Together, these results provide evidence of the beneficial effects of VPA in a salicylate-induced temporary hearing loss and tinnitus model.

Peripheral auditory dysfunction secondary to traumatic brain injury: a systematic review of literature.

PRIMARY OBJECTIVE: To understand the effects of non-blast-related TBI on peripheral auditory function in adults, as measured through basic and advanced audiological assessments. BACKGROUND: Despite numerous studies demonstrating hearing loss post TBI there has been no systematic investigation of the prevalence, nature and severity of peripheral hearing loss. DATA IDENTIFICATION: An English-language systematic search using MEDLINE, CINAHL, PsychINFO, PubMed and hand-searching of reference lists was conducted from 1 January 1990 to 31 October 2016. STUDY SELECTION: After independent review by the authors, 20 of 281 originally identified articles were retained. DATA EXTRACTION: Audiological findings were extracted and synthesized across studies. RESULTS: Using the Oxford Centre for Evidence Based Medicine levels of evidence (2009), 3b was the highest level of evidence within the review. Sensorineural hearing loss was the most consistent auditory deficit reported post TBI. CONCLUSION: The range and frequency of auditory dysfunction in patients with TBI remain unclear. Future research should focus on understanding the nature, frequency and change of auditory deficits over time following TBI. Knowledge in this area will provide crucial information for clinicians and facilitate the development of diagnostic and best practice guidelines which currently are lacking for the management of this patient population.

Audiometric evaluation in patients with Alzheimer's disease.

The objective of this study is to assess the validity of ASSR as a complementary diagnostic test for peripheral hearing loss by proving a significant correlation between behavioral thresholds and ASSR. The design used in this study is monocentric prospective study from November 2014 to April 2015. The setting used in this study is the ENT-Head and Neck Surgery Department and Geriatrics Department in a French Regional and University Hospital. The participants are patients over 75 years with cognitive impairment (Alzheimer's disease or mild-cognitive impairment) with a Mini-Mental State Examination score under 27/30 and without hearing aids. Exclusion criteria were: otoscopic and middle ear abnormalities, retro-cochlear lesion, other types of dementia, and central nervous system disease altering cerebral lateralization. The intervention used in this study is pure-tone audiometry, speech audiometry, dichotic listening test, and auditory steady-state responses recording. The correlations between these exams were studied with Pearson's correlation coefficient and Student's t test. Results were significant if p < 0.05. Twenty-three ears were analyzed from 12 patients. There were six women and six men with cognitive impairment, mean age 82.1 (±4.6) years, and mean MMSE score that was 21.3/30 (±5.7). The correlation between pure-tone audiometry and ASSR was significant for all frequencies: r = 0.55 (p = 0.006) for 500 Hz, r = 0.58 (p = 0.005) for 1000 Hz, r = 0.61 (p = 0.003) for 2000 Hz, and r = 0.66 (p = 0.002) for 4000 Hz. There was no significant correlation between the MMSE and the difference between ASSR and PTA on each frequency. The dichotic listening test showed a right ear advantage (50.9 %, p = 0.039). The ASSR in patients with cognitive impairment and understanding troubles is a promising complementary technique to estimate the hearing thresholds.

Baseline vestibular and auditory findings in a trial of post-concussive syndrome

Previous studies have reported high rates of auditory and vestibular-balance deficits immediately following head injury. This study uses a comprehensive battery of assessments to characterize auditory and vestibular function in 71 U.S. military service members with chronic symptoms following mild traumatic brain injury that did not resolve with traditional interventions. The majority of the study population reported hearing loss (70%) and recent vestibular symptoms (83%). Central auditory deficits were most prevalent, with 58% of participants failing the SCAN3:A screening test and 45% showing abnormal responses on auditory steady-state response testing presented at a suprathreshold intensity. Only 17% of the participants had abnormal hearing (⟩25 dB hearing loss) based on the pure-tone average. Objective vestibular testing supported significant deficits in this population, regardless of whether the participant self-reported active symptoms. Composite score on the Sensory Organization Test was lower than expected from normative data (mean 69.6 ±vestibular tests, vestibulo-ocular reflex, central auditory dysfunction, mild traumatic brain injury, post-concussive symptoms, hearing15.6). High abnormality rates were found in funduscopy torsion (58%), oculomotor assessments (49%), ocular and cervical vestibular evoked myogenic potentials (46% and 33%, respectively), and monothermal calorics (40%). It is recommended that a full peripheral and central auditory, oculomotor, and vestibular-balance evaluation be completed on military service members who have sustained head trauma.

Age-related hearing loss: An updated and comprehensive review of the interventions.

Aging causes progressive degenerative changes in many organs, particularly the auditory system. Several attempts have been conducted to investigate preventive and therapeutic strategy/strategies for age-related auditory dysfunction, such as maintaining a healthy lifestyle through good nutrition, lower anxiety levels, and noise exposure, different pharmacological approaches, gene and cell therapy, and other strategies. However, it is not clear which approach is the best to slow down these dysfunctions because several different underlying mechanistic pathways are associated with presbycusis which eventually leads to different types of this disease. A combination of several methods is probably required, whereas the effectiveness for some people needs to be monitored. The effectiveness of treatments will not be the same for all; therefore, we may need to have a unique and personalized approach to the prevention and treatment of ARHL for each person. In addition, each method needs to specify what type of presbycusis can prevent or treat and provide complete information about the extent, duration of treatment, persistency of treatment, side effects, and whether the approach is for treatment or prevention or even both. This paper reviews the updated literature, which targets current interventions for age-related hearing loss.

Assessing Auditory and Cochlear Function in Alopecia Areata Patients: Exploring the Link to Cochlear Melanocyte Damage.

Introduction Alopecia areata (AA) is an autoimmune disorder causing hair loss, including eyebrows, eyelashes, and body hair, primarily due to melanocyte impact. Though the precise AA melanocyte hearing loss mechanisms are not fully clear, it's speculated that cochlear melanocyte inflammation could disrupt endolymph production, which is necessary for sound signal transmission. Cochlear melanocytes maintain crucial potassium ion levels, which are pivotal for hearing. The potential AA-melanocyte-hearing loss link underscores the need to monitor auditory and cochlear function and consider interventions for AA-related hearing challenges. The study aimed to assess auditory and cochlear function using OAE and audiometry measurements to correlate disease severity and duration with OAE outcomes. Materials and methods In this study, we included 32 patients diagnosed with AA; the control group consisted of 29 healthy volunteers. We collected data on the patient's age, gender, onset age, family history, and disease duration. Audiological and otological evaluations were conducted, including pure tone audiometry (PTA), speech discrimination test (SD), and otoacoustic emission (DPOAE) measurements at frequencies of 500, 1000, 2000, 4000, 6000, 8000, and 10000 Hz. The patients were divided into two groups based on age: 18-25 and over 25 years old, and all parameters were compared. To examine differences between the right and left ears, gender, and age groups, we initially tested the variables for normal distribution using the Kolmogorov-Smirnov and Shapiro-Wilk tests. An independent sample t-test was conducted to compare the means for normally distributed variables. Results There were statistical differences at the 5% significance level in the mean DPOAE values of the 1 KHz SNR and 6 KHz SNR variables. According to the Mann-Whitney U test results, a significant difference was found in the gender-based DPOAE value at 2 kHz SNR (p=0.041), which was lower in men than women. Although there were no significant differences in the audiological parameters based on age, significant differences were found in the otoacoustic emission values. Variables, including 4 kHz DP1 (p=0.049), 500 Hz SNR (p=0.045), and 1 kHz SNR (p=0.023), differed significantly between age groups, with these values being lower in patients over 25 years old. Conclusion Overall, our study contributes to the growing body of evidence supporting an association between AA and auditory dysfunction, emphasizing the need for comprehensive assessment and management of hearing-related issues in individuals with AA.

A Prospective Study of Genetic Variants in Infants with Congenital Unilateral Sensorineural Hearing Loss.

Children with unilateral sensorineural hearing loss (uSNHL) have a high risk of speech-language delays and academic difficulties. Still, challenges remain in the diagnosis of uSNHL. With a prospective cross-sectional design, 20 infants were consecutively recruited from a universal newborn hearing screening program and invited to genetic testing. Eighteen of the subjects agreed to genetic testing, 15 subjects with OtoSCOPE® v.9 screening 224 genes, and four subjects underwent targeted testing, screening for chromosomal abnormalities or 105-137 gene mutations. The genetic results were described together with the 20 infants' previously published auditory profiles and imaging results. Genetic causes for the uSNHL were found in 28% of subjects (5/18) including CHARGE syndrome (CHD7), autosomal recessive non-syndromic hearing loss (GJB2), Townes-Brocks syndrome (SALL1), Pendred Syndrome (SLC26A4) and Chromosome 8P inverted duplication and deletion syndrome. In subjects with comorbidities (malformation of fingers, anus, brain, and heart), 100% were diagnosed with a genetic cause for uSNHL (3/3 subjects), while 13% (2/15 subjects) were diagnosed without comorbidities observed at birth (p = 0.002). Genetic testing for congenital uSNHL is currently efficient for alleged syndromes, whereas genetic variants for non-syndromic congenital uSNHL need further research.

Obstructive Sleep Apnea and Auditory Dysfunction-Does Snoring Sound Play a Role?

The objective of the study was to investigate the relationship between obstructive sleep apnea (OSA) and auditory dysfunction, and to clarify the role of snoring sounds in contributing to auditory dysfunction. A comprehensive assessment of OSA and the auditory system was performed, including overnight polysomnography, detection of the intra-ear canal snoring sound energy (SSE), pure tone average (PTA), tinnitus pitch matching, the tinnitus handicap inventory (THI), and the Epworth sleepiness scale (ESS). The patients were identified as having tinnitus if their THI score was higher than zero or their tinnitus pitches were matched to specific frequencies. The median age, body mass index, and apnea-hypopnea index score were 41 years, 26.4 kg/m2, and 29.9 events/h, respectively. Among the 50 participants, 46 (92%) had a normal PTA, and only 4 (8%) patients had mild hearing loss. There was no significant difference in PTA among OSA severities (p = 0.52). Among the 50 participants, 33 patients (66%) were identified as having tinnitus. In the tinnitus group (n = 33), the ESS score (p = 0.01) and intra-ear canal SSE of 851-1500 Hz (p = 0.04) were significantly higher than those in the non-tinnitus group (n = 17). OSA patients with a higher ESS score had a higher risk of tinnitus (odds ratio 1.22 [95% CI: 1.01-1.46]). OSA-related auditory dysfunction emerged in tinnitus rather than in hearing impairment. OSA patients with daytime sleepiness had a higher risk of tinnitus. High-frequency SSE can jeopardize cochlea and is a potential mechanism contributing to tinnitus. Detection of snoring sounds through an intra-ear canal device may be more precise in assessing acoustic trauma from snoring sounds to vulnerable auditory system and thus warrants further research.

Nitrative Stress and Auditory Dysfunction.

Nitrative stress is increasingly recognized as a critical mediator of apoptotic cell death in many pathological conditions. The accumulation of nitric oxide along with superoxide radicals leads to the generation of peroxynitrite that can eventually result in the nitration of susceptible proteins. Nitrotyrosine is widely used as a biomarker of nitrative stress and indicates oxidative damage to proteins. Ototoxic insults, such as exposure to noise and ototoxic drugs, enhance the generation of 3-nitrotyrosine in different cell types in the cochlea. Nitrated proteins can disrupt critical signaling pathways and eventually lead to apoptosis and loss of sensory receptor cells in the cochlea. Accumulating evidence shows that selective targeting of nitrative stress attenuates cellular damage. Anti-nitrative compounds, such as peroxynitrite decomposition catalysts and inducible nitric oxide synthase inhibitors, prevent nitrative stress-mediated auditory damage. However, the role of nitrative stress in acquired hearing loss and its potential significance as a promising interventional target is yet to be fully characterized. This review provides an overview of nitrative stress mechanisms, the induction of nitrative stress in the auditory tissue after ototoxic insults, and the therapeutic value of targeting nitrative stress for mitigating auditory dysfunction.

A Prospective Study of Etiology and Auditory Profiles in Infants with Congenital Unilateral Sensorineural Hearing Loss.

Congenital unilateral sensorineural hearing loss (uSNHL) is associated with speech-language delays and academic difficulties. Yet, controversy exists in the choice of diagnosis and intervention methods. A cross-sectional prospective design was used to study hearing loss cause in twenty infants with congenital uSNHL consecutively recruited from a universal neonatal hearing-screening program. All normal-hearing ears showed ≤20 dB nHL auditory brainstem response (ABR) thresholds (ABRthrs). The impaired ear median ABRthr was 55 dB nHL, where 40% had no recordable ABRthr. None of the subjects tested positive for congenital cytomegalovirus (CMV) infection. Fourteen subjects agreed to participate in magnetic resonance imaging (MRI). Malformations were common for all degrees of uSNHL and found in 64% of all scans. Half of the MRIs demonstrated cochlear nerve aplasia or severe hypoplasia and 29% showed inner ear malformations. Impaired ear and normal-hearing ear ABR input/output functions on a group level for subjects with ABRthrs < 90 dB nHL were parallel shifted. A significant difference in interaural acoustic reflex thresholds (ARTs) existed. In congenital uSNHL, MRI is powerful in finding a possible hearing loss cause, while congenital CMV infection may be relatively uncommon. ABRs and ARTs indicated an absence of loudness recruitment, with implications for further research on hearing devices.

Auditory Dysfunction in Animal Models of Autism Spectrum Disorder.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder mainly characterized by social-communication impairments, repetitive behaviors and altered sensory perception. Auditory hypersensitivity is the most common sensory-perceptual abnormality in ASD, however, its underlying neurobiological mechanisms remain elusive. Consistently with reports in ASD patients, animal models for ASD present sensory-perception alterations, including auditory processing impairments. Here we review the current knowledge regarding auditory dysfunction in rodent models of ASD, exploring both shared and distinct features among them, mechanistic and molecular underpinnings, and potential therapeutic approaches. Overall, auditory dysfunction in ASD models seems to arise from impaired central processing. Depending on the model, impairments may arise at different steps along the auditory pathway, from auditory brainstem up to the auditory cortex. Common defects found across models encompass atypical tonotopicity in different regions of the auditory pathway, temporal and spectral processing impairments and histological differences. Imbalance between excitation and inhibition (E/I imbalance) is one of the most well-supported mechanisms explaining the auditory phenotype in the ASD models studied so far and seems to be linked to alterations in GABAergic signaling. Such E/I imbalance may have a large impact on the development of the auditory pathway, influencing the establishment of connections responsible for normal sound processing.

Blast Exposure Causes Long-Term Degeneration of Neuronal Cytoskeletal Elements in the Cochlear Nucleus: A Potential Mechanism for Chronic Auditory Dysfunctions.

Blast-induced auditory dysfunctions including tinnitus are the most prevalent disabilities in service members returning from recent combat operations. Most of the previous studies were focused on the effect of blast exposure on the peripheral auditory system and not much on the central auditory signal-processing regions in the brain. In the current study, we have exposed rats to single and tightly coupled repeated blasts and examined the degeneration of neuronal cytoskeletal elements using silver staining in the central auditory signal-processing regions in the brain at 24 h, 14 days, 1 month, 6 months, and 1 year. The brain regions evaluated include cochlear nucleus, lateral lemniscus, inferior colliculus, medial geniculate nucleus, and auditory cortex. The results obtained indicated that a significant increase in degeneration of neuronal cytoskeletal elements was observed only in the left and right cochlear nucleus. A significant increase in degeneration of neuronal cytoskeletal elements was observed in the cochlear nucleus at 24 h and persisted through 1 year, suggesting acute and chronic neuronal degeneration after blast exposure. No statistically significant differences were observed between single and repeated blasts. The localized degeneration of neuronal cytoskeletal elements in the cochlear nucleus suggests that the damage could be caused by transmission of blast shockwaves/noise through the ear canal and that use of suitable ear protection devices can protect against acute and chronic central auditory signal processing defects including tinnitus after blast exposure.

Auditory Agnosia for Environmental Sounds in Alzheimer's Disease: Not Hearing and Not Listening?

Auditory agnosia for environmental sounds (AES) is an example of central auditory dysfunction. It is presumed to be independent of language deficits and in presence of normal hearing. We undertook a detailed neuropsychological assessment including environmental sound naming and recognition in 34 clinically mild Alzheimer's disease (AD) patients and 29 age-matched healthy control subjects. In patients with AD, audiometry was performed to assess the impact on test performance, and in normal controls the Hearing Handicap Inventory for the Elderly - Screening Version to exclude more than mild hearing loss. We adapted a validated environmental sound battery and found near perfect scores in controls. We found that environmental sound agnosia is common in mild AD. We found a statistically significant difference in mean pure tone audiometry in the best ear between patients with and those patients without naming deficits of 11.3 dB (p = 0.010) and of 14.7 dB (p = 0.000) between those with and without recognition deficits. Statistical significance remained after correcting for age, aphasia, Mini-Mental State Examination score, and working memory. Slight and moderate peripheral hearing loss increases the odds ratio of recognition deficits by 13.75 (confidence interval 2.3-81.5) compared to normal hearing patients. We did not find evidence for different forms of AES. This work suggests that an interaction between peripheral hearing loss and AD pathology produces problems with environmental sound recognition. It confirms that the relationship between hearing and dementia is complex but also suggests that interventions to prevent and treat hearing loss could have an effect on AD in its clinical expression.

Repetitive transcranial magnetic stimulation in traumatic brain injury: Evidence from animal and human studies.

We provide here the first systematic review on the studies dealing with repetitive transcranial magnetic stimulation (rTMS) for traumatic brain injury (TBI) in animals and humans. Several experimental studies in animal models have explored with promising results the use of rTMS to enhance neuroprotection and recovery after TBI. However, there are surprisingly few studies that have obtained substantial evidence regarding effects of rTMS in humans with TBI, many of them are case reports investigating the heterogeneous conditions linked to TBI. The most studies have investigated the effects of rTMS in subjects with post-traumatic depression and variable effects have been observed. rTMS has been proposed as an experimental approach for the treatment of disorders of consciousness (DOC), but in subjects with TBI therapeutic effects on DOC have also been variously documented. Beneficial effects have been reported in subjects with cognitive/emotional disturbances and auditory dysfunction (tinnitus and hallucinations), although the results are somewhat conflicting. rTMS applied over the left prefrontal cortex may relieve, at least transiently, post-traumatic headache. Isolated rTMS studies have been performed in TBI patients with motor impairment, chronic dizziness or pain. Especially whether provided in combination, rTMS and neurorehabilitation may be synergistic in the potential to translate experimental findings in the clinical practice. In order to reach definitive conclusions, well-designed randomized controlled studies with larger patient samples, improved design and optimized rTMS setup, are warranted to verify and corroborate the initial promising findings.

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss.

Acquired hearing loss is caused by complex interactions of multiple environmental risk factors, such as elevated levels of lead and noise, which are prevalent in urban communities. This study delineates the mechanism underlying lead-induced auditory dysfunction and its potential interaction with noise exposure. Young-adult C57BL/6 mice were exposed to: 1) control conditions; 2) 2 mM lead acetate in drinking water for 28 days; 3) 90 dB broadband noise 2 h/day for two weeks; and 4) both lead and noise. Blood lead levels were measured by inductively coupled plasma mass spectrometry analysis (ICP-MS) lead-induced cochlear oxidative stress signaling was assessed using targeted gene arrays, and the hearing thresholds were assessed by recording auditory brainstem responses. Chronic lead exposure downregulated cochlear Sod1, Gpx1, and Gstk1, which encode critical antioxidant enzymes, and upregulated ApoE, Hspa1a, Ercc2, Prnp, Ccl5, and Sqstm1, which are indicative of cellular apoptosis. Isolated exposure to lead or noise induced 8-12 dB and 11-25 dB shifts in hearing thresholds, respectively. Combined exposure induced 18-30 dB shifts, which was significantly higher than that observed with isolated exposures. This study suggests that chronic exposure to lead induces cochlear oxidative stress and potentiates noise-induced hearing impairment, possibly through parallel pathways.

Impaired speech perception in noise with a normal audiogram: No evidence for cochlear synaptopathy and no relation to lifetime noise exposure.

In rodents, noise exposure can destroy synapses between inner hair cells and auditory nerve fibers ("cochlear synaptopathy") without causing hair cell loss. Noise-induced cochlear synaptopathy usually leaves cochlear thresholds unaltered, but is associated with long-term reductions in auditory brainstem response (ABR) amplitudes at medium-to-high sound levels. This pathophysiology has been suggested to degrade speech perception in noise (SPiN), perhaps explaining why SPiN ability varies so widely among audiometrically normal humans. The present study is the first to test for evidence of cochlear synaptopathy in humans with significant SPiN impairment. Individuals were recruited on the basis of self-reported SPiN difficulties and normal pure tone audiometric thresholds. Performance on a listening task identified a subset with "verified" SPiN impairment. This group was matched with controls on the basis of age, sex, and audiometric thresholds up to 14 kHz. ABRs and envelope-following responses (EFRs) were recorded at high stimulus levels, yielding both raw amplitude measures and within-subject difference measures. Past exposure to high sound levels was assessed by detailed structured interview. Impaired SPiN was not associated with greater lifetime noise exposure, nor with any electrophysiological measure. It is conceivable that retrospective self-report cannot reliably capture noise exposure, and that ABRs and EFRs offer limited sensitivity to synaptopathy in humans. Nevertheless, the results do not support the notion that noise-induced synaptopathy is a significant etiology of SPiN impairment with normal audiometric thresholds. It may be that synaptopathy alone does not have significant perceptual consequences, or is not widespread in humans with normal audiograms.

The Application of the International Classification of Functioning, Disability and Health to Functional Auditory Consequences of Mild Traumatic Brain Injury.

This article reviews the auditory consequences of mild traumatic brain injury (mTBI) within the context of the International Classification of Functioning, Disability and Health (ICF). Because of growing awareness of mTBI as a public health concern and the diverse and heterogeneous nature of the individual consequences, it is important to provide audiologists and other health care providers with a better understanding of potential implications in the assessment of levels of function and disability for individual interdisciplinary remediation planning. In consideration of body structures and function, the mechanisms of injury that may result in peripheral or central auditory dysfunction in mTBI are reviewed, along with a broader scope of effects of injury to the brain. The activity limitations and participation restrictions that may affect assessment and management in the context of an individual's personal factors and their environment are considered. Finally, a review of management strategies for mTBI from an audiological perspective as part of a multidisciplinary team is included.

[Hearing loss and Alzheimer's disease]. / Déficit auditif et maladie d'Alzheimer.

Recent studies suggest that subjects with hearing loss are more likely to develop Alzheimer's disease. Hearing loss can be consecutive to presbycusis and/or to central auditory dysfunction. Standard audiometric measures (pure tone and speech intelligibility) allow the diagnosis of presbycusis. However, to demonstrate central auditory dysfunction, specific audiometric tests are needed such as noisy and/or dichotic tests. Actually, no consensus exists to investigate hearing loss in people with Alzheimer's disease though hearing loss may be an early manifestation of Alzheimer's disease. Until now, investigations and clinical procedure related to the diagnosis of Alzheimer's disease ignored the hearing ability of the patient. However, the major part of care management and investigations implies the patient's communication ability with the caregivers. Hearing loss may be one of the most unrecognized deficit in subjects with Alzheimer's disease. Auditory rehabilitation could benefit to the patient in order to lessen cognitive decline, but this must be investigated during longitudinal studies in order to clearly demonstrate their efficiency.