ABSTRACT
RESUMO Objetivo Identificar as definições fisiopatológicas adotadas pelos estudos que investigaram a "sinaptopatia coclear" (SC) e "perda auditiva oculta" (PAO). Estratégia de pesquisa Utilizou-se a combinação de unitermos "Auditory Synaptopathy" or "Neuronal Synaptopathy" or "Hidden Hearing Loss" com "etiology" or "causality" or "diagnosis" nas bases de dados EMBASE, Pubmed (MEDLINE), CINAHL (EBSCO) e Web of Science. Critérios de seleção Incluiu-se estudos que investigaram a SC ou PAO em humanos com procedimentos comportamentais e/ou eletrofisiológicos. Análise dos dados Realizou-se a análise e extração de dados quanto a terminologia, definição e população estudada. Resultados Foram incluídos 49 artigos. Destes, 61,2% utilizaram a terminologia SC, 34,7% ambos os termos e 4,1% utilizaram PAO. As condições mais estudadas foram exposição ao ruído e zumbido. Conclusão A terminologia SC foi empregada na maioria dos estudos, com referência ao processo fisiopatológico de desaferenciação entre as fibras do nervo coclear e as células ciliadas internas
ABSTRACT Purpose To identify the pathophysiological definitions adopted by studies investigating "cochlear synaptopathy" (CS) and "hidden hearing loss" (HHL). Research strategies The combination of keywords "Auditory Synaptopathy" or "Neuronal Synaptopathy" or "Hidden Hearing Loss" with "etiology" or "causality" or "diagnosis" was used in the databases EMBASE, Pubmed (MEDLINE), CINAHL (EBSCO), and Web of Science. Selection criteria Studies that investigated CS or HHL in humans using behavioral and/or electrophysiological procedures were included. Data analysis Data analysis and extraction were performed with regard to terminology, definitions, and population. Results 49 articles were included. Of these, 61.2% used the CS terminology, 34.7% used both terms, and 4.1% used HHL. The most-studied conditions were exposure to noise and tinnitus. Conclusion CS terminology was used in most studies, referring to the pathophysiological process of deafferentiation between the cochlear nerve fibers and inner hair cells.
ABSTRACT
Objective: Contribute to clarifying the existence of subclinical hearing deficits associated with aging. Design: In this work, we study and compare the auditory perceptual and electrophysiological performance of normal-hearing young and adult subjects (tonal audiometry, high-frequency tone threshold, a triplet of digits in noise, and click-evoked auditory brainstem response). Study sample: 45 normal hearing volunteers were evaluated and divided into two groups according to age. 27 subjects were included in the "young group" (mean 22.1 years), and 18 subjects (mean 42.22 years) were included in the "adult group." Results: In the perceptual tests, the adult group presented significantly worse tonal thresholds in the high frequencies (12 and 16 kHz) and worse performance in the digit triplet tests in noise. In the electrophysiological test using the auditory brainstem response technique, the adult group presented significantly lower I and V wave amplitudes and higher V wave latencies at the supra-threshold level. At the threshold level, we observed a significantly higher latency in wave V in the adult group. In addition, in the partial correlation analysis, controlling for the hearing level, we observed a relationship (negative) between age and speech in noise performance and high-frequency thresholds. No significant association was observed between age and the auditory brainstem response. Conclusion: The results are compatible with subclinical hearing loss associated with aging.
ABSTRACT
In animal models, prolonged exposure (2 h) to high-level noise causes an irreparable damage to the synapses between the inner hair cells and auditory nerve fibers within the cochlea. Nevertheless, this injury does not necessarily alter the hearing threshold. Similar findings have been observed as part of typical aging in animals. This type of cochlear synaptopathy, popularly called "hidden hearing loss," has been a significant issue in neuroscience research and clinical audiology scientists. The results obtained in different investigations are inconclusive in their diagnosis and suggest new strategies for both prognosis and treatment of cochlear synaptopathy. Here we review the major physiological findings regarding cochlear synaptopathy in animals and humans and discuss mathematical models. We also analyze the potential impact of these results on clinical practice and therapeutic options.
Subject(s)
Cochlea/pathology , Hearing/physiology , Noise/adverse effects , Synapses/physiology , Synaptic Transmission/physiology , Animals , Disease Models, Animal , HumansABSTRACT
"Growing old" is the most common cause of hearing loss. Age-related hearing loss (ARHL) (presbycusis) first affects the ability to understand speech in background noise, even when auditory thresholds in quiet are normal. It has been suggested that cochlear denervation ("synaptopathy") is an early contributor to age-related auditory decline. In the present work, we characterized age-related cochlear synaptic degeneration and hair cell loss in mice with enhanced α9α10 cholinergic nicotinic receptors gating kinetics ("gain of function" nAChRs). These mediate inhibitory olivocochlear feedback through the activation of associated calcium-gated potassium channels. Cochlear function was assessed via distortion product otoacoustic emissions and auditory brainstem responses. Cochlear structure was characterized in immunolabeled organ of Corti whole mounts using confocal microscopy to quantify hair cells, auditory neurons, presynaptic ribbons, and postsynaptic glutamate receptors. Aged wild-type mice had elevated acoustic thresholds and synaptic loss. Afferent synapses were lost from inner hair cells throughout the aged cochlea, together with some loss of outer hair cells. In contrast, cochlear structure and function were preserved in aged mice with gain-of-function nAChRs that provide enhanced olivocochlear inhibition, suggesting that efferent feedback is important for long-term maintenance of inner ear function. Our work provides evidence that olivocochlear-mediated resistance to presbycusis-ARHL occurs via the α9α10 nAChR complexes on outer hair cells. Thus, enhancement of the medial olivocochlear system could be a viable strategy to prevent age-related hearing loss.