RESUMO
Testudines are a highly threatened group facing an array of stressors, including alteration of their sensory environment. Underwater noise pollution has the potential to induce hearing loss and disrupt detection of biologically important acoustic cues and signals. To examine the conditions that induce temporary threshold shifts (TTS) in hearing in the freshwater Eastern painted turtle (Chrysemys picta picta), three individuals were exposed to band limited continuous white noise (50-1000 Hz) of varying durations and amplitudes (sound exposure levels ranged from 151 to 171 dB re 1 µPa2 s). Control and post-exposure auditory thresholds were measured and compared at 400 and 600 Hz using auditory evoked potential methods. TTS occurred in all individuals at both test frequencies, with shifts of 6.1-41.4 dB. While the numbers of TTS occurrences were equal between frequencies, greater shifts were observed at 600 Hz, a frequency of higher auditory sensitivity, compared to 400 Hz. The onset of TTS occurred at 154 dB re 1 µPa2 s for 600 Hz, compared to 158 dB re 1 µPa2 s at 400 Hz. The 400-Hz onset and patterns of TTS growth and recovery were similar to those observed in previously studied Trachemys scripta elegans, suggesting TTS may be comparable across Emydidae species.
Assuntos
Estimulação Acústica , Limiar Auditivo , Tartarugas , Animais , Tartarugas/fisiologia , Fatores de Tempo , Ruído/efeitos adversos , Potenciais Evocados Auditivos/fisiologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Perda Auditiva Provocada por Ruído/etiologia , Masculino , Feminino , Audição/fisiologiaRESUMO
Objective: To explore the mechanism of noise-induced hidden hearing loss by proteomics. Methods: In October 2022, 64 SPF male C57BL/6J mice were divided into control group and noise exposure group with 32 mice in each group according to random sampling method. The noise exposure group was exposed to 100 dB sound pressure level, 2000-16000 Hz broadband noise for 2 h, and the mouse hidden hearing loss model was established. Auditory brainstem response (ABR) was used to test the change of hearing threshold of mice on the 7th day after noise exposure, the damage of basal membrane hair cells was observed by immunofluorescence, and the differentially expressed proteins in the inner ear of mice in each group were identified and analyzed by 4D-Label-free quantitative proteomics, and verified by Western blotting. The results were statistically analyzed by ANOVA and t test. Results: On the 7th day after noise exposure, there was no significant difference in hearing threshold between the control group and the noise exposure group at click and 8000 Hz acoustic stimulation (P>0.05) . The hearing threshold in the noise exposure group was significantly higher than that in the control group under 16000 Hz acoustic stimulation (P<0.05) . Confocal immunofluorescence showed that the basal membrane hair cells of cochlear tissue in noise exposure group were arranged neatly, but the relative expression of C-terminal binding protein 2 antibody of presynaptic membrane in middle gyrus and basal gyrus was significantly lower than that in control group (P<0.05) . GO enrichment analysis showed that the functions of differentially expressed proteins were mainly concentrated in membrane potential regulation, ligand-gated channel activity, and ligand-gated ion channel activity. KEGG pathway enrichment analysis showed that differentially expressed proteins were significantly enriched in phosphatidylinositol 3 kinase-protein kinase B (PI3K-Akt) signaling pathway, NOD-like receptor signaling pathway, calcium signaling pathway, etc. Western blotting showed that the expression of inositol 1, 4, 5-trisphosphate receptor 3 (Itpr3) was increased and the expression of solute carrier family 38 member 2 (Slc38a2) was decreased in the noise exposure group (P<0.05) . Conclusion: Through proteomic analysis, screening and verification of the differential expression proteins Itpr3 and Slc38a2 in the constructed mouse noise-induced hidden hearing loss model, the glutaminergic synaptic related pathways represented by Itpr3 and Slc38a2 may be involved in the occurrence of hidden hearing loss.
Assuntos
Potenciais Evocados Auditivos do Tronco Encefálico , Perda Auditiva Provocada por Ruído , Camundongos Endogâmicos C57BL , Ruído , Proteômica , Animais , Camundongos , Perda Auditiva Provocada por Ruído/metabolismo , Perda Auditiva Provocada por Ruído/fisiopatologia , Masculino , Ruído/efeitos adversos , Modelos Animais de Doenças , Limiar Auditivo , Orelha Interna/metabolismo , Perda Auditiva OcultaRESUMO
Fear and anxiety among patients are sometimes evoked in dental clinics due to the sound of dental drills. This study aimed to explore the impact of age-related hearing loss in the extended high frequency (EHF) range above 8 kHz on individuals' subjective discomfort towards dental drill noise. After measuring pure-tone audiometric thresholds at both conventional and extended high frequencies, we used a psychoacoustic approach to evaluate subjective impressions of four dental drill sound stimuli, which featured varying frequency components, in 62 participants (aged 12-67 years). We found a significant decrease in hearing sensitivity within the EHF range as age increased, with notable differences in hearing thresholds at 14 kHz between teenage and older adults exceeding 65 dB. Furthermore, significant differences were observed between younger and older (above 40 years) participants in the subjective impressions of dental drill noise, emphasizing age as a critical factor in the perception of high frequency components. Consequently, age may influence the unpleasantness of dental drilling noise. Compared to older individuals, young participants may exhibit increased fear of dental procedures owing to physiological factors. These results underscore the need for age-appropriate noise control strategies in dental clinics to mitigate anxiety and improve patient comfort.
Assuntos
Ruído , Humanos , Adulto , Pessoa de Meia-Idade , Idoso , Masculino , Feminino , Adolescente , Adulto Jovem , Criança , Ruído/efeitos adversos , Limiar Auditivo/fisiologia , Fatores Etários , Perda Auditiva Provocada por Ruído/fisiopatologia , Perda Auditiva Provocada por Ruído/etiologia , Audiometria de Tons PurosRESUMO
Understanding the complex pathologies associated with hearing loss is a significant motivation for conducting inner ear research. Lifelong exposure to loud noise, ototoxic drugs, genetic diversity, sex, and aging collectively contribute to human hearing loss. Replicating this pathology in research animals is challenging because hearing impairment has varied causes and different manifestations. A central aspect, however, is the loss of sensory hair cells and the inability of the mammalian cochlea to replace them. Researching therapeutic strategies to rekindle regenerative cochlear capacity, therefore, requires the generation of animal models in which cochlear hair cells are eliminated. This review discusses different approaches to ablate cochlear hair cells in adult mice. We inventoried the cochlear cyto- and histo-pathology caused by acoustic overstimulation, systemic and locally applied drugs, and various genetic tools. The focus is not to prescribe a perfect damage model but to highlight the limitations and advantages of existing approaches and identify areas for further refinement of damage models for use in regenerative studies.
Assuntos
Cóclea , Modelos Animais de Doenças , Células Ciliadas Auditivas , Regeneração , Animais , Células Ciliadas Auditivas/patologia , Células Ciliadas Auditivas/metabolismo , Camundongos , Cóclea/patologia , Cóclea/fisiopatologia , Humanos , Audição , Perda Auditiva Provocada por Ruído/fisiopatologia , Perda Auditiva Provocada por Ruído/patologia , Perda Auditiva/patologia , Perda Auditiva/fisiopatologia , Estimulação AcústicaRESUMO
Auditory nerve (AN) function has been hypothesized to deteriorate with age and noise exposure. Here, we perform a systematic review of published studies and find that the evidence for age-related deficits in AN function is largely consistent across the literature, but there are inconsistent findings among studies of noise exposure history. Further, evidence from animal studies suggests that the greatest deficits in AN response amplitudes are found in noise-exposed aged mice, but a test of the interaction between effects of age and noise exposure on AN function has not been conducted in humans. We report a study of our own examining differences in the response amplitude of the compound action potential N1 (CAP N1) between younger and older adults with and without a self-reported history of noise exposure in a large sample of human participants (63 younger adults 18-30 years of age, 103 older adults 50-86 years of age). CAP N1 response amplitudes were smaller in older than younger adults. Noise exposure history did not appear to predict CAP N1 response amplitudes, nor did the effect of noise exposure history interact with age. We then incorporated our results into two meta-analyses of published studies of age and noise exposure history effects on AN response amplitudes in neurotypical human samples. The meta-analyses found that age effects across studies are robust (r = -0.407), but noise exposure effects are weak (r = -0.152). We conclude that noise exposure effects may be highly variable depending on sample characteristics, study design, and statistical approach, and researchers should be cautious when interpreting results. The underlying pathology of age-related and noise-induced changes in AN function are difficult to determine in living humans, creating a need for longitudinal studies of changes in AN function across the lifespan and histological examination of the AN from temporal bones collected post-mortem.
Assuntos
Estimulação Acústica , Nervo Coclear , Ruído , Humanos , Ruído/efeitos adversos , Idoso , Nervo Coclear/fisiopatologia , Pessoa de Meia-Idade , Adulto , Idoso de 80 Anos ou mais , Fatores Etários , Adulto Jovem , Adolescente , Envelhecimento/fisiologia , Potenciais Evocados Auditivos , Perda Auditiva Provocada por Ruído/fisiopatologia , Feminino , Masculino , Animais , Potenciais de AçãoRESUMO
OBJECTIVE: To explore the changes in the cerebral microstructure of patients with noise-induced hearing loss (NIHL) using diffusion tensor imaging (DTI). METHOD: Overall, 122 patients with NIHL (mild [MP, n = 79], relatively severe patients [including moderate and severe; RSP, n = 32], and undetermined [lost to follow-up, n = 11]) and 84 healthy controls (HCs) were enrolled. All clinical data, including age, education level, hearing threshold, occupation type, noise exposure time, and some scale scores (including the Mini-Mental State Examination [MMSE], tinnitus handicap inventory [THI], and Hamilton Anxiety Scale [HAMA]), were collected and analyzed. All participants underwent T1WI3DFSPGR and DTI, and tract-based spatial statistics and region of interest (ROI) analysis were used for assessment. RESULTS: The final sample included 71 MP, 28 RSP, and 75 HCs. The HAMA scores of the three groups were significantly different (p < .05). The noise exposure times, hearing thresholds, and HAMA scores of the MP and RSP were significantly different (p < .05). The noise exposure time was positively correlated with the hearing threshold and negatively correlated with the HAMA scores (p < .05), whereas the THI scores were positively correlated with the hearing threshold (p < .05). DTI analysis showed that all DTI parameters (fractional anisotropy [FA], axial diffusivity [AD], mean diffusivity [MD], and radial diffusivity [RD]) were significantly different in the left inferior longitudinal fasciculus (ILF) and left inferior fronto-occipital fasciculus (IFOF) for the three groups (p < .05). In addition, the FA values were significantly lower in the bilateral corticospinal tract (CST), right fronto-pontine tract (FPT), right forceps major, left superior longitudinal fasciculus (temporal part) (SLF), and left cingulum (hippocampus) (C-H) of the MP and RSP than in those of the HCs (p < .05); the AD values showed diverse changes in the bilateral CST, left IFOF, right anterior thalamic radiation, right external capsule (EC), right SLF, and right superior cerebellar peduncle (SCP) of the MP and RSP relative to those of the HC (p < .05). However, there were no significant differences among the bilateral auditory cortex ROIs of the three groups (p > .05). There was a significant negative correlation between the FA and HAMA scores for the left IFOF/ILF, right FPT, left SLF, and left C-H for the three groups (p < .05). There was a significant positive correlation between the AD and HAMA scores for the left IFOF/ILF and right EC of the three groups (p < .05). There were significantly positive correlations between the RD/MD and HAMA scores in the left IFOF/ILF of the three groups (p < .05). There was a significant negative correlation between the AD in the right SCP and noise exposure time of the MP and RSP groups (p < .05). The AD, MD, and RD in the left ROI were significantly positively correlated with hearing threshold in the MP and RSP groups (p < .05), whereas FA in the right ROI was significantly positively correlated with the HAMA scores for the three groups (p < .05). CONCLUSION: The changes in the white matter (WM) microstructure may be related to hearing loss caused by noise exposure, and the WM structural abnormalities in patients with NIHL were mainly located in the syndesmotic fibers of the temporooccipital region, which affected the auditory and language pathways. This confirmed that the auditory pathways have abnormal structural connectivity in patients with NIHL.
Assuntos
Imagem de Tensor de Difusão , Perda Auditiva Provocada por Ruído , Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Perda Auditiva Provocada por Ruído/patologia , Perda Auditiva Provocada por Ruído/diagnóstico por imagem , Perda Auditiva Provocada por Ruído/fisiopatologia , Substância Branca/diagnóstico por imagem , Substância Branca/patologia , Substância Branca/fisiopatologia , Encéfalo/diagnóstico por imagem , Encéfalo/patologia , Encéfalo/fisiopatologiaRESUMO
Cochlear synaptopathy, a form of cochlear deafferentation, has been demonstrated in a number of animal species, including non-human primates. Both age and noise exposure contribute to synaptopathy in animal models, indicating that it may be a common type of auditory dysfunction in humans. Temporal bone and auditory physiological data suggest that age and occupational/military noise exposure also lead to synaptopathy in humans. The predicted perceptual consequences of synaptopathy include tinnitus, hyperacusis, and difficulty with speech-in-noise perception. However, confirming the perceptual impacts of this form of cochlear deafferentation presents a particular challenge because synaptopathy can only be confirmed through post-mortem temporal bone analysis and auditory perception is difficult to evaluate in animals. Animal data suggest that deafferentation leads to increased central gain, signs of tinnitus and abnormal loudness perception, and deficits in temporal processing and signal-in-noise detection. If equivalent changes occur in humans following deafferentation, this would be expected to increase the likelihood of developing tinnitus, hyperacusis, and difficulty with speech-in-noise perception. Physiological data from humans is consistent with the hypothesis that deafferentation is associated with increased central gain and a greater likelihood of tinnitus perception, while human data on the relationship between deafferentation and hyperacusis is extremely limited. Many human studies have investigated the relationship between physiological correlates of deafferentation and difficulty with speech-in-noise perception, with mixed findings. A non-linear relationship between deafferentation and speech perception may have contributed to the mixed results. When differences in sample characteristics and study measurements are considered, the findings may be more consistent.
Assuntos
Cóclea , Percepção da Fala , Zumbido , Humanos , Cóclea/fisiopatologia , Zumbido/fisiopatologia , Zumbido/diagnóstico , Animais , Percepção da Fala/fisiologia , Hiperacusia/fisiopatologia , Ruído/efeitos adversos , Percepção Auditiva/fisiologia , Sinapses/fisiologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Perda Auditiva Provocada por Ruído/diagnóstico , Percepção SonoraRESUMO
Following adult-onset hearing impairment, crossmodal plasticity can occur within various sensory cortices, often characterized by increased neural responses to visual stimulation in not only the auditory cortex, but also in the visual and audiovisual cortices. In the present study, we used an established model of loud noise exposure in rats to examine, for the first time, whether the crossmodal plasticity in the audiovisual cortex that occurs following a relatively mild degree of hearing loss emerges solely from altered intracortical processing or if thalamocortical changes also contribute to the crossmodal effects. Using a combination of an established pharmacological 'cortical silencing' protocol and current source density analysis of the laminar activity recorded across the layers of the audiovisual cortex (i.e., the lateral extrastriate visual cortex, V2L), we observed layer-specific changes post-silencing in the strength of the residual visual, but not auditory, input in the noise exposed rats with mild hearing loss compared to rats with normal hearing. Furthermore, based on a comparison of the laminar profiles pre- versus post-silencing in both groups, we can conclude that noise exposure caused a re-allocation of the strength of visual inputs across the layers of the V2L cortex, including enhanced visual-evoked activity in the granular layer; findings consistent with thalamocortical plasticity. Finally, we confirmed that audiovisual integration within the V2L cortex depends on intact processing within intracortical circuits, and that this form of multisensory processing is vulnerable to disruption by noise-induced hearing loss. Ultimately, the present study furthers our understanding of the contribution of intracortical and thalamocortical processing to crossmodal plasticity as well as to audiovisual integration under both normal and mildly-impaired hearing conditions.
Assuntos
Estimulação Acústica , Córtex Auditivo , Modelos Animais de Doenças , Potenciais Evocados Visuais , Plasticidade Neuronal , Estimulação Luminosa , Córtex Visual , Animais , Córtex Visual/fisiopatologia , Córtex Auditivo/fisiopatologia , Masculino , Perda Auditiva Provocada por Ruído/fisiopatologia , Percepção Visual , Percepção Auditiva , Ruído/efeitos adversos , Potenciais Evocados Auditivos , Ratos , Audição , Ratos Sprague-DawleyRESUMO
Homeostatic plasticity, the ability of neurons to maintain their averaged activity constant around a set point value, is thought to account for the central hyperactivity after hearing loss. Here, we investigated the putative role of GABAergic neurotransmission in this mechanism after a noise-induced hearing loss larger than 50 dB in high frequencies in guinea pigs. The effect of GABAergic inhibition is linked to the normal functioning of K + -Cl- co-transporter isoform 2 (KCC2) which maintains a low intracellular concentration of chloride. The expression of membrane KCC2 were investigated before and after noise trauma in the ventral and dorsal cochlear nucleus (VCN and DCN, respectively) and in the inferior colliculus (IC). Moreover, the effect of gabazine (GBZ), a GABA antagonist, was also studied on the neural activity in IC. We show that KCC2 is downregulated in VCN, DCN and IC 3 days after noise trauma, and in DCN and IC 30 days after the trauma. As expected, GBZ application in the IC of control animals resulted in an increase of spontaneous and stimulus-evoked activity. In the noise exposed animals, on the other hand, GBZ application decreased the stimulus-evoked activity in IC neurons. The functional implications of these central changes are discussed.
Assuntos
Perda Auditiva Provocada por Ruído , Cotransportadores de K e Cl- , Simportadores , Ácido gama-Aminobutírico , Animais , Simportadores/metabolismo , Simportadores/antagonistas & inibidores , Cobaias , Perda Auditiva Provocada por Ruído/metabolismo , Perda Auditiva Provocada por Ruído/fisiopatologia , Ácido gama-Aminobutírico/metabolismo , Masculino , Núcleo Coclear/metabolismo , Piridazinas/farmacologia , Neurônios/metabolismoRESUMO
INTRODUCTION: Auditory injuries induced by repeated exposures to blasts reduce the operational performance capability and the life quality of military personnel. The treatment for blast-induced progressive hearing damage is lacking. We have recently investigated the therapeutic function of liraglutide, a glucagon-like peptide-1 receptor agonist, to mitigate blast-induced hearing damage in the animal model of chinchilla, under different blast intensities, wearing earplugs (EPs) or not during blasts, and drug-treatment plan. The goal of this study was to investigate the therapeutical function of liraglutide by comparing the results obtained under different conditions. MATERIALS AND METHODS: Previous studies on chinchillas from two under-blast ear conditions (EP/open), two blast plans (G1: 6 blasts at 3-5 psi or G2:3 blasts at 15-25 psi), and three treatment plans (blast control, pre-blast drug treatment, and post-blast drug treatment) were summarized. The auditory brainstem response (ABR), distortion product otoacoustic emission (DPOAE), and middle latency response (MLR) recorded within 14 days after the blasts were used. Statistical analysis was performed to evaluate the effect of liraglutide under different conditions. RESULTS: ABR threshold shifts indicated that the conditions of the EP and open ears were substantially different. Results from EP chinchillas indicated that the pre-blast treatment reduced the acute ABR threshold elevation on the day of blasts, and the significance of such an effect increased with the blast level. Liraglutide-treated open chinchillas showed lower ABR threshold shifts at the later stage of the experiment regardless of the blast levels. The DPOAE was less damaged after G2 blasts compared to G1 when pre-blast liraglutide was administrated. Lower post-blast MLR amplitudes were observed in the pre-blast treatment groups. CONCLUSIONS: This study indicated that the liraglutide mitigated the blast-induced auditory injuries. In EP ears, the pre-blast administration of liraglutide reduced the severity of blast-induced acute damage in ears with EP protection, especially under G2. In animals with open ears, the effect of liraglutide on the restoration of hearing increased with time. The liraglutide potentially benefits post-blast hearing through multiple approaches with different mechanics.
Assuntos
Traumatismos por Explosões , Chinchila , Modelos Animais de Doenças , Liraglutida , Animais , Liraglutida/farmacologia , Liraglutida/uso terapêutico , Traumatismos por Explosões/complicações , Traumatismos por Explosões/tratamento farmacológico , Traumatismos por Explosões/fisiopatologia , Perda Auditiva Provocada por Ruído/tratamento farmacológico , Perda Auditiva Provocada por Ruído/fisiopatologia , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Emissões Otoacústicas Espontâneas/efeitos dos fármacos , Emissões Otoacústicas Espontâneas/fisiologiaRESUMO
Musicians are at risk of hearing loss and tinnitus due to regular exposure to high levels of noise. This level of risk may have been underestimated previously since damage to the auditory system, such as cochlear synaptopathy, may not be easily detectable using standard clinical measures. Most previous research investigating hearing loss in musicians has involved cross-sectional study designs that may capture only a snapshot of hearing health in relation to noise exposure. The aim of this study was to investigate the effects of cumulative noise exposure on behavioural, electrophysiological, and self-report indices of hearing damage in early-career musicians and non-musicians with normal hearing over a 2-year period. Participants completed an annual test battery consisting of pure tone audiometry, extended high-frequency hearing thresholds, distortion product otoacoustic emissions (DPOAEs), speech perception in noise, auditory brainstem responses, and self-report measures of tinnitus, hyperacusis, and hearing in background noise. Participants also completed the Noise Exposure Structured Interview to estimate cumulative noise exposure across the study period. Linear mixed models assessed changes over time. The longitudinal analysis comprised 64 early-career musicians (female n = 34; age range at T0 = 18-26 years) and 30 non-musicians (female n = 20; age range at T0 = 18-27 years). There were few longitudinal changes as a result of musicianship. Small improvements over time in some measures may be attributable to a practice/test-retest effect. Some measures (e.g., DPOAE indices of outer hair cell function) were associated with noise exposure at each time point, but did not show a significant change over time. A small proportion of participants reported a worsening of their tinnitus symptoms, which participants attributed to noise exposure, or not using hearing protection. Future longitudinal studies should attempt to capture the effects of noise exposure over a longer period, taken at several time points, for a precise measure of how hearing changes over time. Hearing conservation programmes for "at risk" individuals should closely monitor DPOAEs to detect early signs of noise-induced hearing loss when audiometric thresholds are clinically normal.
Assuntos
Audiometria de Tons Puros , Limiar Auditivo , Potenciais Evocados Auditivos do Tronco Encefálico , Perda Auditiva Provocada por Ruído , Audição , Música , Exposição Ocupacional , Emissões Otoacústicas Espontâneas , Autorrelato , Zumbido , Humanos , Feminino , Perda Auditiva Provocada por Ruído/fisiopatologia , Perda Auditiva Provocada por Ruído/diagnóstico , Perda Auditiva Provocada por Ruído/etiologia , Adulto , Zumbido/diagnóstico , Zumbido/fisiopatologia , Zumbido/etiologia , Estudos Longitudinais , Masculino , Adulto Jovem , Adolescente , Exposição Ocupacional/efeitos adversos , Percepção da Fala , Hiperacusia/fisiopatologia , Hiperacusia/diagnóstico , Hiperacusia/etiologia , Ruído/efeitos adversos , Fatores de Tempo , Ruído Ocupacional/efeitos adversos , Doenças Profissionais/diagnóstico , Doenças Profissionais/fisiopatologia , Doenças Profissionais/etiologia , Fatores de Risco , Estimulação Acústica , Modelos LinearesRESUMO
INTRODUCCIÓN: Recientes investigaciones mencionan que, debido a los altos niveles de ruidos, el 75% de los habitantes en las ciudades industrializadas padecen algún tipo de deficiencia auditiva. La audiometría de alta frecuencia es un examen complementario importante para detectar tempranamente la pérdida de audición. OBJETIVO: Determinar la utilidad diagnóstica de la audiometría de alta frecuencia en la detección temprana de la hipoacusia en sujetos expuestos a ruido recreacional. MATERIAL Y MÉTODO: Estudio analítico de corte transversal. Se evaluaron 87 estudiantes de fonoaudiología. Se aplicó una audiometría convencional y de alta frecuencia mediante audiómetro clínico. RESULTADOS: La audiometría de alta frecuencia presenta una sensibilidad del 100%, especificidad del 64,60%. El valor predictivo (+) es de 14,70%, mientras que el valor predictivo (-) es del 100%. La razón de verosimilitud (+) es de 2,28, y para la razón de verosimilitud (-) es de 0,0. CONCLUSIÓN: La audiometría de alta frecuencia puede ser utilizada para monitorizar la audición de los sujetos, comprobando que efectivamente los umbrales auditivos de alta frecuencia se encuentren dentro de rangos normales. Lo anterior, dado por sus valores de sensibilidad, valor predictivo negativo, razón de verosimilitud negativa y por el aumento entre la probabilidad preprueba y posprueba.
INTRODUCTION: Recent research mentions that, due to the high noise levels, 75% of the habitants in industrialized cities suffer from some type of hearing impairment. High frequency audiometry is an important complementary test to detect early hearing loss. AIM: To determine the diagnostic utility of high frequency audiometry in the early detection of hearing loss in subjects exposed to recreational noise. MATERIAL AND METHODS: Study analytical type and cross section. 87 speech therapy students were evaluated. A conventional and high frequency audiometry was applied, using a clinical audiometer. RESULTS: High frequency audiometry has a sensitivity of 100%, specificity of 64,60%. The predictive value (+) is 14,70%, while the predictive value (-) is 100%. The likelihood ratio (+) is 2,28, and for the likelihood ratio (-) it is 0,0. CONCLUSION: High frequency audiometry can be used to monitor the hearing of the subjects, checking that effectively the high frequency hearing thresholds are within normal ranges. The above, given by their values of sensitivity, negative predictive value, negative likelihood ratio and the increase between the pre-test probability and the posttest probability.
Assuntos
Humanos , Masculino , Feminino , Adolescente , Adulto Jovem , Recreação , Audiometria/métodos , Perda Auditiva Provocada por Ruído/diagnóstico , Valores de Referência , Limiar Auditivo , Estudantes , Estudos Transversais , Valor Preditivo dos Testes , Sensibilidade e Especificidade , Diagnóstico Precoce , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/fisiopatologiaRESUMO
RESUMO Objetivo Analisar a percepção e o conhecimento dos profissionais de saúde que atuam na rede de Atenção Primária à Saúde do Município de Curitiba - Paraná sobre a notificação compulsória da Perda Auditiva Induzida pelo Ruído (PAIR) no, Sistema de Informação de Agravos de Notificação (SINAN). Método Utilizando como método o estudo transversal na cidade de Curitiba, analisando a percepção e o conhecimento dos profissionais de saúde que atuam na rede de Atenção Primária à Saúde do Município de Curitiba sobre a notificação compulsória da PAIR no SINAN. Aplicou-se ainda um questionário semiaberto em profissionais de saúde da atenção básica sobre conhecimento sobre a PAIR e sua notificação. Resultados Dos profissionais da atenção básica, 50% eram médicos com faixa etária de 26 a 30 anos. Dentre os profissionais, 56,2% relataram estarem preparados para identificar problemas de saúde relacionados ao trabalho, porém apenas 43,7% sentem-se aptos a identificar casos de PAIR. Entre as facilidades na notificação, relataram descentralização da assistência à saúde próxima à residência do usuário, encaminhamento para referência em medicina do trabalho e prontuário eletrônico na UBS; como dificuldades, relataram a não formação específica em saúde do trabalhador e falta de capacitação, tempo reduzido para consultas e receio. Conclusão os profissionais de saúde conhecem as características e sentem-se aptos para identificar os casos de PAIR, mas ainda não notificam os casos suspeitos de PAIR e não percebem a Saúde do Trabalhador como um programa institucionalizado fazendo parte do serviço.
ABSTRACT Objective The article aims to analyze the perception and knowledge of health professionals working in primary health care networks in the Municipality of Curitiba – Paraná, regarding the compulsory notification of Induced Hearing Loss Noise (NIHL) in the National Notifiable Diseases Information System (SINAN). Methods We performed a transversal cohort study in Curitiba, analyzing perception and knowledge of health professionals working in the primary health care networks in the Municipality of Curitiba, regarding the compulsory notification of NIHL in SINAN, from 2007 to 2014, featuring the reported cases and exploring the situational analysis of the NIHL notification, through a questionnaire and a structured news conference. Results The primary care professionals’ survey showed that 50% were doctors and the predominant age group was 26-30 years, with 56.2% reported as being able to identify health problems related to work, but only 43.7% feel able to identify cases of NIHL. Conclusion It was found that health professionals know the features and feel able to identify cases of NIHL, but still do not report suspected NIHL cases and do not consider occupational health an institutionalized program that is part of the service.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoal de Saúde/classificação , Perda Auditiva Provocada por Ruído/diagnóstico , Ruído Ocupacional , Doenças Profissionais/diagnóstico , Percepção , Atenção Primária à Saúde , Fatores Socioeconômicos , População Urbana , Brasil , Conhecimentos, Atitudes e Prática em Saúde , Estudos Transversais , Inquéritos e Questionários , Notificação de Doenças , Perda Auditiva Provocada por Ruído/fisiopatologia , Pessoa de Meia-Idade , Doenças Profissionais/fisiopatologiaRESUMO
INTRODUCTION: The clinical evaluation of subjects with occupational noise exposure has been difficult due to the discrepancy between auditory complaints and auditory test results. This study aimed to evaluate the contralateral acoustic reflex thresholds of workers exposed to high levels of noise, and to compare these results to the subjects' auditory complaints.METHODS: This clinical retrospective study evaluated 364 workers between 1998 and 2005; their contralateral acoustic reflexes were compared to auditory complaints, age, and noise exposure time by chi-squared, Fisher's, and Spearman's tests.RESULTS: The workers' age ranged from 18 to 50 years (mean = 39.6), and noise exposure time from one to 38 years (mean = 17.3). We found that 15.1% (55) of the workers had bilateral hearing loss, 38.5% (140) had bilateral tinnitus, 52.8% (192) had abnormal sensitivity to loud sounds, and 47.2% (172) had speech recognition impairment. The variables hearing loss, speech recognition impairment, tinnitus, age group, and noise exposure time did not show relationship with acoustic reflex thresholds; however, all complaints demonstrated a statistically significant relationship with Metz recruitment at 3000 and 4000 Hz bilaterally.CONCLUSION: There was no significance relationship between auditory complaints and acoustic reflexes.
INTRODUÇÃO: A avaliação clínico-ocupacional de trabalhadores expostos a ruído é dificultada pela discrepância entre queixas auditivas e resultados dos exames audiológicos. Este estudo pretende avaliar limiares dos reflexos estapedianos contralaterais em sujeitos expostos a níveis elevados de pressão sonora, relacionando-os com queixas auditivas.MÉTODO: Estudo clínico retrospectivo que analisou 364 trabalhadores e seus limiares de reflexos estapedianos contralaterais, relacionado-os com queixas auditivas, idades e tempos de exposição ao ruído.RESULTADOS: Dos trabalhadores avaliados, com idades de 18 a 50 anos (média 39,6) e tempos de exposição entre um e 38 anos (média 17,3); 15,1% (55) tinham queixa de perda auditiva bilateral, 38,5% (140) zumbidos bilaterais, 52,8% (192) irritação ao ouvir sons intensos e 47,2% (172) dificuldades para reconhecer a fala. As variáveis: perda auditiva, dificuldade para reconhecimento da fala, zumbidos, faixa etária e tempo de exposição ao ruído não se relacionaram significativamente com limiares dos reflexos estapedianos, mas todas as queixas apresentaram relação estatisticamente significante com o recrutamento de Metz nas frequências de 3000 e 4000 Hz, bilateralmente.CONCLUSÃO: Não houve relações significativas entre limiares dos reflexos estapedianos e queixas auditivas.
Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Limiar Auditivo/fisiologia , Perda Auditiva Provocada por Ruído/diagnóstico , Ruído Ocupacional/efeitos adversos , Exposição Ocupacional/efeitos adversos , Reflexo Acústico/fisiologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Estudos Retrospectivos , Fatores de TempoRESUMO
INTRODUCTION: Auditory conditioning consists of the pre-exposure to low levels of a potential harmful agent to protect against a subsequent harmful presentation. OBJECTIVE: To confirm if conditioning with an agent different from the used to cause the trauma can also be effective. METHOD: Experimental study with 17 guinea pigs divided as follows: group Som: exposed to 85 dB broadband noise centered at 4 kHz, 30 minutes a day for 10 consecutive days; group Cont: intramuscular administration of gentamicin 160 mg/kg a day for 10 consecutive days; group Expt: conditioned with noise similarly to group Som and, after each noise presentation, received gentamicin similarly to group Cont. The animals were evaluated by distortion product otoacoustic emissions (DPOAEs), brainstem auditory evoked potentials (BAEPs) and scanning electron microscopy. RESULTS: The animals that were conditioned with noise did not show any protective effect compared to the ones that received only the ototoxic gentamicin administration. This lack of protection was observed functionally and morphologically. CONCLUSION: Conditioning with 85 dB broadband noise, 30 min a day for 10 consecutive days does not protect against an ototoxic gentamicin administration of 160 mg/kg a day for 10 consecutive days in the guinea pig. .
INTRODUÇÃO: O condicionamento auditivo consiste da pré-exposição de um agente lesivo em baixos níveis para proteger contra uma posterior apresentação lesiva. OBJETIVO: Confirmar se o condicionamento com um agente diferente do utilizado para causar o trauma pode ser efetivo. MÉTODO: Estudo experimental com 17 cobaias albinas divididas como a seguir- grupo Som: exposto a um ruído branco de 85 dB centrado em 4 kHz, 30 minutos por dia, por 10 dias consecutivos; grupo Cont: administração intramuscular de gentamicina 160 mg/kg por dia, por 10 dias consecutivos; grupo Expt: condicionado com ruído como o grupo Som. Após cada exposição ao ruído, recebeu gentamicina similarmente ao grupo Cont. Os animais foram avaliados por emissões otoacústicas produto de distorção (EOAPDs), potencial evocado auditivo de tronco encefálico (PEATE) e microscopia eletrônica de varredura (MEV). RESULTADOS: Os animais que foram condicionados com ruído não mostraram qualquer efeito protetor quando comparados com os que receberam apenas a gentamicina em doses ototóxicas. Esta ausência de proteção foi observada tanto funcionalmente quanto morfologicamente. CONCLUSÃO: Os autores concluíram que o condicionamento com ruído branco a 85 dB por 30 minutos, por dia por 10 dias consecutivos, não protege contra uma administração de gentamicina 160 mg/kg/dia, por 10 dias consecutivos. .
Assuntos
Animais , Cobaias , Estimulação Acústica/métodos , Cóclea/efeitos dos fármacos , Gentamicinas/toxicidade , Perda Auditiva Provocada por Ruído/prevenção & controle , Adaptação Fisiológica/fisiologia , Limiar Auditivo/efeitos dos fármacos , Limiar Auditivo/fisiologia , Cóclea/ultraestrutura , Potenciais Evocados Auditivos do Tronco Encefálico/efeitos dos fármacos , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Microscopia Eletrônica de Varredura , Emissões Otoacústicas Espontâneas/efeitos dos fármacos , Emissões Otoacústicas Espontâneas/fisiologia , Fatores de TempoRESUMO
Studies carried out by Brainstem Evoked Auditory Potentials (BEAP) in Noise-Induced Hearing Loss (NIHL) workers show different results in relation to neuronal involvement, not involving bus drivers as study object. AIM: to use BEAP in a prospective case/control clinical study to check whether or not there is neural auditory pathway involvement in bus drivers with NIHL. MATERIALS AND METHODS: we selected 50 bus drivers between 27 and 40 years with mild to moderate NIHL, and 20 individuals between 29 and 40 years with normal hearing and without prior history of noise exposure. BEAP tests were carried out and the traces were analyzed. RESULTS: in the NIHL group, the auditory thresholds in 3, 4 and 6 kHz were significantly higher in the left ear. In the NIHL group, potentials PI, PIII and/or PV were not present in a small number of the individuals; we observed a statistically significant increase in PI, PIII and PV absolute latencies, (LIP) LIP I-III interpeak latencies, bilaterally and LIP I-V in the left ear. CONCLUSION: in the NIHL group, besides sensorial injury, changes in BEAP latencies suggest an early functional injury of the first auditory pathway afferent neuron.
Estudos realizados com os Potenciais Auditivos Evocados de Tronco Encefálico (PEATE) em trabalhadores com Perda Auditiva Induzida pelo Ruído (PAIR) apresentam resultados díspares em relação ao comprometimento neuronal, além de não contemplar motoristas de ônibus como objeto de estudo. OBJETIVO: Avaliar pelo PEATE, em estudo clínico de série caso/controle, prospectivo, se há comprometimento das vias auditivas neurais em motoristas de ônibus com PAIR. MATERIAL E MÉTODO: Foram selecionados 50 motoristas de ônibus entre 27 e 40 anos portadores de PAIR leve a moderada; e 20 sujeitos entre 29 e 40 anos com audibilidade normal e sem antecedentes de exposição a ruído. Os PEATEs foram realizados e os traçados analisados. RESULTADOS: No grupo PAIR, os limiares auditivos em 3, 4 e 6 kHz foram significativamente maiores na orelha esquerda. No grupo PAIR, os potenciais PI, PIII e/ou PV foram ausentes em uma pequena parcela; foi observado prolongamento estatisticamente significante das latências absolutas de PI, PIII e PV, das latências interpicos (LIP) LIP I-III, bilateralmente e da LIP I-V na orelha esquerda. CONCLUSÃO: No grupo PAIR, além da lesão sensorial, as modificações das latências do PEATE sugerem lesão funcional do primeiro neurônio aferente da via auditiva, de forma precoce.
Assuntos
Adulto , Humanos , Masculino , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Ruído Ocupacional/efeitos adversos , Ruído dos Transportes/efeitos adversos , Doenças Profissionais/fisiopatologia , Condução de Veículo , Estudos de Casos e Controles , Perda Auditiva Provocada por Ruído/etiologia , Doenças Profissionais/etiologia , Estudos ProspectivosRESUMO
TEMA: entre os fatores que podem causar alterações auditivas em adultos estão a idade e a exposição ao ruído. Estes fatores são considerados aditivos, pois seus efeitos causam danos nas células ciliadas do órgão de Corti. OBJETIVO: verificar se a exposição ao ruído ocupacional é um risco importante para as alterações auditivas em adultos na faixa etária de 50 a 70 anos, além do desgaste auditivo próprio do fator idade. MÉTODO: foram estudados (estudo coorte histórico) os audiogramas de 71 homens, de 50 a 70 anos, divididos em 2 grupos (Grupo 1 com histórico de exposição ocupacional ao ruído e Grupo 2 sem histórico de exposição ao ruído) para comparar-se os perfis auditivos. RESULTADOS: os grupos não apresentam diferenças significativas em relação à idade (p = 0,321) e há predomínio (48) de sujeitos entre 50 e 55 anos de idade,14 sujeitos com audição normal bilateral e os demais com perda auditiva neurossensorial. Encontrou-se associação entre ruído e alteração auditiva, com diferenças significativas entre os grupos para os limiares auditivos a partir de 3000Hz, sendo que no Grupo 1 estes foram piores (p < 0,05). CONCLUSÃO: os limiares auditivos dos sujeitos com idade entre 50 e 70 anos estão piores no grupo exposto ao ruído. O ruído é um fator de risco maior do que a idade nas alterações auditivas neurossensoriais
BACKGROUND: age and exposure to noise are among the factors that may cause hearing loss in adults. Both of these factors are considered additives once their combined effects can cause damage to the hair cells of the organ of Corti. AIM: to verify whether the exposure to occupational noise is an important risk factor for hearing disorders in adults with ages between 50 to 70 years, besides the auditory deterioration caused by age. METHOD: the audiograms of 71 men with ages ranging between 50 to 70 years were studied (cohort study), with the participants being divided in 2 groups (Group 1 with occupational exposure to noise and Group 2 without the exposure to noise) in order to compare their auditory profiles. RESULTS: the groups do not present significant differences regarding age (p = 0.321), with most of the participants with ages between 50 and 55 years (48); 14 subjects presented normal bilateral hearing thresholds and all of the others presented neurossensorial hearing loss. An association between noise and hearing disorders was found, with significant differences between the groups for auditory thresholds above 3000Hz, with Group 1 presenting worse results (p < 0.05). CONCLUSION: the auditory thresholds of individuals with ages between 50 and 70 years are worse for the group that is exposed to noise. Noise is a higher risk factor than age when considering neurossensorial hearing losses
Assuntos
Idoso , Humanos , Masculino , Pessoa de Meia-Idade , Envelhecimento/fisiologia , Limiar Auditivo/fisiologia , Perda Auditiva Provocada por Ruído/etiologia , Doenças Profissionais/etiologia , Exposição Ocupacional/efeitos adversos , Fatores Etários , Estudos de Coortes , Perda Auditiva Provocada por Ruído/fisiopatologia , Doenças Profissionais/prevenção & controle , Fatores de Risco , Estresse FisiológicoRESUMO
Entre las causas de pérdida de audición, la hipoacusia neurosensorial inducida por ruido es uno de los problemas más comunes a los que se enfrenta el otorrinolaringologo y el médico general y con no muy buenas expectativas para el paciente.Se estima que un tercio de la población mundial padece algún grado de sordera o pérdida auditiva causada por la exposición a sonidos de alta intensidad.La exposición a ruidos tiene efectos más importantes de los que podamos pensar, ya que la incapacidad para la comunicación personal reduce la calidad de vida del ser humano y su socialización, representa además un alto costo económico y afecta a la sociedad entera.Aunque tradicionalmente se sabe que la fuente más común de ruido se encuentra en los lugares de trabajo, cada vez más podemos encontrarlos en la casa, en los espacios de recreación, oficinas, escuelas, etc. y esto provoca que ahora todos los miembros de la sociedad estén siendo afectados sin importar, edad o sexo.
Assuntos
Humanos , Masculino , Feminino , Surdez/terapia , Perda Auditiva Provocada por Ruído/fisiopatologia , Perda Auditiva Neurossensorial/diagnóstico , Perda Auditiva Provocada por Ruído/terapiaRESUMO
OBJETIVO: Analisar as características clínicas e audiométricas da disacusia sensórioneural ocupacional por ruído de acordo com a faixa etária e o tempo de exposição em anos. MÉTODO: Foram estudados retrospectivamente 222 pacientes portadores de disacusia sensórioneural ocupacional decorrente da exposição ao ruído no ambiente de trabalho, correlacionando-se as queixas clínicas auditivas, alterações de limiar audiométrico nas freqüências de 250Hz a 8000Hz, índices de discriminação vocal com a faixa etária e o tempo de exposição. Como grupo controle, utilizou-se os limiares audiométricos de uma população de mesma média etária, sem antecedentes mórbidos de doença auditiva, conforme preconiza a norma ISO 1999 (1990). O grupo foi dividido em subgrupos, tendo-se analisado três décadas de exposição. RESULTADOS: Verificamos que a queixa clínica de hipoacusia aumenta de acordo com a faixa etária e o tempo de exposição, enquanto que a freqüência da queixa tinnitus mantém-se constante. Os Limiares audiométricos na segunda década de exposição apresentam variações que dependem da faixa etária analisada. As várias curvas audiométricas realizadas são paralelas entre si, mas não-horizontais, sendo que os piores limiares foram encontrados nas freqüências agudas de 3000Hz a 8000Hz, como conseqüência clínica e fisiopatológica do acometimento mais acentuado das áreas basais da cóclea. A discriminação vocal também mostrou-se pior de acordo com o aumento das faixa etária e do tempo de exposição. CONCLUSÃO: Indivíduos portadores de disacusia sensórioneural por ruído ocupacional apresentam alterações audiométricas, características que variam de acordo com a faixa etária e o tempo de exposição. Estas características definidas e resumidas nas curvas audiométricas obtidas podem constituir padrão de comparação, avaliação e controle de outras populações também expostas.
Assuntos
Humanos , Masculino , Adulto , Pessoa de Meia-Idade , Perda Auditiva Provocada por Ruído/fisiopatologia , Doenças Profissionais/fisiopatologia , Fatores de Tempo , Estudos Retrospectivos , Fatores Etários , Perda Auditiva Provocada por Ruído/diagnóstico , Perda Auditiva Provocada por Ruído/epidemiologia , Testes Auditivos , Doenças Profissionais/diagnóstico , Doenças Profissionais/epidemiologiaRESUMO
Introdução: A deficiência auditiva pode ser conseqüência de exposições a ruídos e/ou agentes ototóxicos. É importante que se reconheça a potencialidade de outros agentes e sua possível interação com o ruído sobre a saúde auditiva dos trabalhadores. Objetivo: Traçar o perfil epidemiológico e audiológico das empresas atendidas pelo Serviço Social da Indústria de Santa Catarina SESI/ SC na cidade de Brusque. Metodologia: estudo exploratório, transversal, incluindo todos os exames audiológicos registrados no banco de dados do programa Winaudio® 6.0 da Unidade de Operações Sociais de Brusque. Resultados: Mais de 81 por cento dos trabalhadores referiram estar expostos ao ruído. O uso de protetor auricular foi referido por 66,6 por cento. A prevalência de perda auditiva foi de 24,7 . O tipo de perda mais prevalente foi o bilateral, com 17,1 por cento. A perda auditiva à esquerda foi 62 por cento maior que a perda auditiva à direita (RP=1,62; p<0,001). Da mesma forma, o rebaixamento dos limiares de 250Hz, 6000Hz e/ou 8000Hz à esquerda foi mais prevalente que à direita. Conclusões: A opinião dos trabalhadores sobre a própria audição tem um baixo valor preditivo para diagnóstico de perda auditiva. A perda auditiva ainda é pouco percebida e não causa desconforto social, interferindo pouco na qualidade de vida do indivíduo. Os sintomas clínicos iniciais da disacusia sensório-neural ocupacional por ruído não são detectados pelo trabalhador.
Introduction: Hearing deficiency may be a consequence of exposure to noises and/or ototoxic agents. It is important to recognize the potentiality of other agents and their possible interaction with noise on the workers hearing health. Aim: To outline the epidemiological and audilogical profile of workers cared for at the Social Service of the Industry of Santa Catarina (SESI/SC) in the municipality of Brusque. Methods: This is an exploratory transversal study of all the audiological tests registered in the databank of the Winaudio® 6.0 program of the Social Operations Unity of Brusque. Results: More than 91 percent of the workers reported being exposed to noise. The use of ear protection was reported by 66.6 percent. The prevalence of hearing loss was 24.7 percent. The most prevalent type of loss was the bilateral, in 17.1 percent of the cases. Hearing loss on the left ear was 62 percent greater than hearing loss on the right ear (RP=1.62; p<0.001). Similarly, the downgrading in thresholds of 250Hz, 6000Hz and/or 8000Hz on the left was more prevalent than on the right. Conclusions: Workers self-reports on their hearing have a low predictive value for the diagnosis of hearing loss. Hearing loss still goes unnoticed and does not cause much social discomfort, interfering little in the quality of life of the individual. The early clinical symptoms of occupational sensory-neural dysacousia due to noise are not detected by the workers.