Auditory rehabilitation

Auditory rehabilitation depends of the cause and the severity of the hearing loss (or deafness). Hearing losses dues to middle ear pathologies can beneficiate of medical or surgical treatments, by ossicular prostheses, if it is necessary to restore the function of the ossicles chain. In the sensorineural hearing losses, with inner ear pathology, the use of auditory aid is immediately considered. In the cases for which they are insufficient because of severity of the hearing loss or not suitable because of local non-tolerance, it is possible to use middle ear implant or cochlear implant. The indications of the auditory brainstern implants remain at this day limited to the total bilateral hearing losses due to a complete destruction of cochleae and auditory nerves. These therapeutic orientations are selected after a multidisciplinary evaluation of the deaf person, evaluation that allows the characterization of the hearing loss and its repercussion. In all the cases, the restoration of a bilateral hearing has to be done if possible, making an improvement of the speech comprehension, mainly in the noisy situations, as well as the localization of the sound sources.     

Diffusion Tensor Imaging of the Auditory Neural Pathway for Clinical Outcome of Cochlear Implantation in Pediatric Congenital Sensorineural Hearing Loss Patients

Although conventional structural MRI provides vital information in the evaluation of congenital sensorineural hearing loss (SNHL), it is relatively insensitive to white matter microstructure. Our objective was to evaluate possible changes in microstructure of the auditory pathway in children with congenital sensorineural hearing loss (SNHL), and the possible distinction between good and poor outcome of cochlear implantation (CI) patients by using diffusion tensor imaging (DTI). Twenty-four patients with congenital SNHL and 20 healthy controls underwent conventional MRI and DTI examination using a 1.5T MR scanner. The DTI metrics of fractional anisotropy (FA) and mean diffusivity (MD) of six regions of interest (ROIs) positioned along the auditory pathway—the trapezoid body, superior olivary nucleus, inferior colliculus, medial geniculate body, auditory radiation and white matter of Heschl''s gyrus—was measured in all subjects. Among the 24 patients, 8 patients with a categorie of auditory performance (CAP) score over 6 were classified into the good outcome group, and 16 patients with a CAP score below 6 were classified into the poor outcome group. A significant decrease was observed in FA values while MD values remained unchanged at the six ROIs of SNHL patients compared with healthy controls. Compared to good outcome subjects, poor outcome subjects displayed decreased FA values at all of the ROIs. No changes were observed in MD values. Correlation analyses only revealed strong correlations between FA values and CAP scores, and strong correlations between CAP scores and age at implant were also found. No correlations of FA values with age at implant were observed. Our results show that preoperative DTI can be used to evaluate microstructural alterations in the auditory pathway that are not detectable by conventional MR imaging, and may play an important role in evaluating the outcome of CI. Early cochlear implantation might be more effectively to restore hearing in SNHL patients.     

常染色体显性遗传非综合征型耳聋致病基因定位研究

耳聋具有高度的遗传异质性, 迄今已定位了51个常染色体显性遗传非综合征型耳聋(autosomal dominant non-syndromic sensorineural hearing loss, DFNA)基因位点, 20个DFNA相关基因被克隆.文章收集了一个DFNA巨大家系, 家系中有血缘关系的家族成员共170人, 对73名家族成员进行了详细的病史调查、全身检查和耳科学检查, 提示39人有不同程度的迟发性感音神经性听力下降, 未见前庭及其他系统的异常.应用ABI公司382个常染色体微卫星多态标记进行全基因组扫描连锁分析, 将该家系致聋基因定位于14q12-13处D14S1021-D14S70之间约7.6 cM (3.18 Mb)的区域, 最大LOD值为6.69 (D14S1040), 与已知DFNA9位点有4.7 cM (2.57 Mb)的重叠区, DFNA9致病基因COCH位于重叠区域内.下一步拟进行COCH基因的突变筛查, 以揭示该家系耳聋的分子致病机制.     

常染色体显性遗传非综合征性耳聋致病基因定位研究

耳聋具有高度的遗传异质性, 迄今已定位了51个常染色体显性遗传非综合征型耳聋(autosomal dominant non-syndromic sensorineural hearing loss, DFNA)基因位点, 20个DFNA相关基因被克隆。文章收集了一个DFNA巨大家系, 家系中有血缘关系的家族成员共170人, 对73名家族成员进行了详细的病史调查、全身检查和耳科学检查, 提示39人有不同程度的迟发性感音神经性听力下降, 未见前庭及其他系统的异常。应用ABI公司382个常染色体微卫星多态标记进行全基因组扫描连锁分析, 将该家系致聋基因定位于14q12-13处D14S1021-D14S70之间约7.6 cM (3.18 Mb)的区域, 最大LOD值为6.69 (D14S1040), 与已知DFNA9位点有4.7 cM (2.57 Mb)的重叠区, DFNA9致病基因COCH位于重叠区域内。下一步拟进行COCH基因的突变筛查, 以揭示该家系耳聋的分子致病机制。     

Photobiomodulation using low‐level 808 nm diode laser rescues cochlear synaptopathy after acoustic overexposure in rat

A certain degree of noise can cause hearing problems without a permanent change in the hearing threshold, which is called hidden hearing loss and results from partial loss of auditory synapses. Photobiomodulation (PBM) enhances neural growth and connections in the peripheral nervous systems. In this study, we assessed whether PBM could rescue cochlear synaptopathy after acoustic overexposure in rat. PBM was performed for 7 days after noise exposure. The auditory brainstem responses (ABRs) were acquired before and after noise exposure using a tone and a paired‐click stimulus. Auditory response to paired click sound with short time interval was performed to evaluate auditory temporal processing ability. In the result, hearing threshold recovered 2 weeks after noise exposure in both groups. Peak wave 1 amplitude of the ABR and ABR recovery threshold did not recover in the noise only group, whereas it fully recovered in the noise + PBM group. The number of synaptic ribbons was significantly different in the control and noise only groups, while there was no difference between the control and noise + PBM group. These results indicate that PBM rescued peak wave 1 amplitude and maintained the auditory temporal processing ability resulting from a loss of synaptic ribbons after acoustic overexposure.     

Reliability and effectiveness of screening for hearing loss in high risk neonates.

OBJECTIVE--To establish the reliability and effectiveness of screening for hearing loss by brainstem auditory evoked potential testing in high risk neonates. DESIGN--Seven year investigation of newborn babies admitted to a special care baby unit and monitored through a regional children''s audiology unit. SETTING--Special care baby unit and children''s audiology department, Belfast. SUBJECTS--405 neonates admitted to the baby unit, during 1 October 1982 to 31 March 1987. MAIN OUTCOME MEASURES--Presence of hearing impairment, type and severity of hearing impairment, mortality. RESULTS--85 children failed the screening test, 62 of whom were followed up. Five children had severe bilateral sensorineural impairment and 12 had conductive impairment requiring surgical intervention. A further 18 had severe neurological disorder detected. The sensitivity of screening was 100% and specificity was 88%. If the procedure was introduced into routine clinical practice the mean age at diagnosis for all children with severe perinatal hearing impairment would be 11 (median 1) months. The mean age at diagnosis with the health visitor screening service was 23 (19) months (difference 10 months, 95% confidence interval 6 to 16 months; p < 0.0001). CONCLUSION--Screening for hearing loss in high risk neonates is highly reliable and cost effective. It also provides valuable neurophysiological information. Routine testing of these infants would result in over half of all children with severe bilateral perinatal sensorineural hearing impairment being identified by 2 months of age. This would make an important contribution to the habilitation of this socially, emotionally, and educationally vulnerable group.     

Application of a New Genetic Deafness Microarray for Detecting Mutations in the Deaf in China

Objective

The aim of this study was to evaluate the GoldenGate microarray as a diagnostic tool and to elucidate the contribution of the genes on this array to the development of both nonsyndromic and syndromic sensorineural hearing loss in China.

Methods

We developed a microarray to detect 240 mutations underlying syndromic and nonsyndromic sensorineural hearing loss. The microarray was then used for analysis of 382 patients with nonsyndromic sensorineural hearing loss (including 15 patients with enlarged vestibular aqueduct syndrome), 21 patients with Waardenburg syndrome, and 60 unrelated controls. Subsequently, we analyzed the sensitivity, specificity, and reproducibility of this new approach after Sanger sequencing-based verification, and also determined the contribution of the genes on this array to the development of distinct hearing disorders.

Results

The sensitivity and specificity of the microarray chip were 98.73% and 98.34%, respectively. Genetic defects were identified in 61.26% of the patients with nonsyndromic sensorineural hearing loss, and 9 causative genes were identified. The molecular etiology was confirmed in 19.05% and 46.67% of the patients with Waardenburg syndrome and enlarged vestibular aqueduct syndrome, respectively.

Conclusion

Our new mutation-based microarray comprises an accurate and comprehensive genetic tool for the detection of sensorineural hearing loss. This microarray-based detection method could serve as a first-pass screening (before next-generation-sequencing screening) for deafness-causing mutations in China.     

FGF23 Deficiency Leads to Mixed Hearing Loss and Middle Ear Malformation in Mice

Fibroblast growth factor 23 (FGF23) is a circulating hormone important in phosphate homeostasis. Abnormal serum levels of FGF23 result in systemic pathologies in humans and mice, including renal phosphate wasting diseases and hyperphosphatemia. We sought to uncover the role FGF23 plays in the auditory system due to shared molecular mechanisms and genetic pathways between ear and kidney development, the critical roles multiple FGFs play in auditory development and the known hearing phenotype in mice deficient in klotho (KL), a critical co-factor for FGF23 signaling. Using functional assessments of hearing, we demonstrate that Fgf mice are profoundly deaf. Fgf mice have moderate hearing loss above 20 kHz, consistent with mixed conductive and sensorineural pathology of both middle and inner ear origin. Histology and high-voltage X-ray computed tomography of Fgf mice demonstrate dysplastic bulla and ossicles; Fgf mice have near-normal morphology. The cochleae of mutant mice appear nearly normal on gross and microscopic inspection. In wild type mice, FGF23 is ubiquitously expressed throughout the cochlea. Measurements from Fgf mice do not match the auditory phenotype of Kl ^−/− mice, suggesting that loss of FGF23 activity impacts the auditory system via mechanisms at least partially independent of KL. Given the extensive middle ear malformations and the overlap of initiation of FGF23 activity and Eustachian tube development, this work suggests a possible role for FGF23 in otitis media.     

Otoacoustic emissions at different click intensities: invariant and subject-dependent features.

A study of click-evoked otoacoustic emissions (CEOAEs) elicited at stimulation intensities from 35 to >80 dB was carried out by recurrence quantification analysis on signals from both normal and hearing-impaired subjects. In normal subjects, a clear scaling of determinism with increasing stimulation intensity was observed in the click intensity range from 41 to 59 dB. Outside that range and, in particular, above its upper end, subject-dependent features appeared in the form of different maximal levels of determinism. A comparative analysis of responses from hearing-impaired subjects with conductive hearing losses and sensorineural hearing losses suggested that the principal contributor to this behavior is the middle ear and allowed us to discriminate the two pathologies solely on the basis of CEOAEs. These observations are consistent with a simple phenomenological model of the auditory periphery in which different functional modules are sequentially recruited at increasing stimulus intensities, with a consequent rise in CEOAE coherence.     

Age-related degradation of tectorial membrane dynamics with loss of CEACAM16

Studies of genetic disorders of sensorineural hearing loss have been instrumental in delineating mechanisms that underlie the remarkable sensitivity and selectivity that are hallmarks of mammalian hearing. For example, genetic modifications of TECTA and TECTB, which are principal proteins that comprise the tectorial membrane (TM), have been shown to alter auditory thresholds and frequency tuning in ways that can be understood in terms of changes in the mechanical properties of the TM. Here, we investigate effects of genetic modification targeting CEACAM16, a third important TM protein. Loss of CEACAM16 has been recently shown to lead to progressive reductions in sensitivity. Whereas age-related hearing losses have previously been linked to changes in sensory receptor cells, the role of the TM in progressive hearing loss is largely unknown. Here, we show that TM stiffness and viscosity are significantly reduced in adult mice that lack functional CEACAM16 relative to age-matched wild-type controls. By contrast, these same mechanical properties of TMs from juvenile mice that lack functional CEACAM16 are more similar to those of wild-type mice. Thus, changes in hearing phenotype align with changes in TM material properties and can be understood in terms of the same TM wave properties that were previously used to characterize modifications of TECTA and TECTB. These results demonstrate that CEACAM16 is essential for maintaining TM mechanical and wave properties, which in turn are necessary for sustaining the remarkable sensitivity and selectivity of mammalian hearing with increasing age.     

Temporal Characteristics of Azimuthally Moving Sound Source Localization in Patients with Mild and Moderate Sensorineural Hearing Loss

Journal of Evolutionary Biochemistry and Physiology - The work is devoted to investigation of the auditory motion localization in patients with sensorineural hearing loss (SNHL). Minimal time to...     

Sensorineural hearing loss as evidenced by the auditory brainstem response following prenatal cocaine exposure in the Long-Evans rat

Prenatal cocaine exposure has been associated with a variety of adverse neurological effects. Three recent studies found evidence that prenatal cocaine exposure is associated with abnormal auditory electrophysiology, suggesting abnormal processing of auditory information. The present study used the auditory brainstem response to evaluate the effects of prenatal cocaine exposure on hearing in an animal model (Long-Evans rat). We report that prenatal cocaine exposure can cause elevated ABR thresholds and latency-intensity curves consistent with a recruitment-type sensorineural hearing loss.     

Melanin precursors prevent premature age-related and noise-induced hearing loss in albino mice

Strial melanocytes are required for normal development and correct functioning of the cochlea. Hearing deficits have been reported in albino individuals from different species, although melanin appears to be not essential for normal auditory function. We have analyzed the auditory brainstem responses (ABR) of two transgenic mice: YRT2, carrying the entire mouse tyrosinase (Tyr) gene expression-domain and undistinguishable from wild-type pigmented animals; and TyrTH, non-pigmented but ectopically expressing tyrosine hydroxylase (Th) in melanocytes, which generate the precursor metabolite, L-DOPA, but not melanin. We show that young albino mice present a higher prevalence of profound sensorineural deafness and a poorer recovery of auditory thresholds after noise-exposure than transgenic mice. Hearing loss was associated with absence of cochlear melanin or its precursor metabolites and latencies of the central auditory pathway were unaltered. In summary, albino mice show impaired hearing responses during ageing and after noise damage when compared to YRT2 and TyrTH transgenic mice, which do not show the albino-associated ABR alterations. These results demonstrate that melanin precursors, such as L-DOPA, have a protective role in the mammalian cochlea in age-related and noise-induced hearing loss.     

Discrimination task reveals differences in neural bases of tinnitus and hearing impairment

We investigated auditory perception and cognitive processing in individuals with chronic tinnitus or hearing loss using functional magnetic resonance imaging (fMRI). Our participants belonged to one of three groups: bilateral hearing loss and tinnitus (TIN), bilateral hearing loss without tinnitus (HL), and normal hearing without tinnitus (NH). We employed pure tones and frequency-modulated sweeps as stimuli in two tasks: passive listening and active discrimination. All subjects had normal hearing through 2 kHz and all stimuli were low-pass filtered at 2 kHz so that all participants could hear them equally well. Performance was similar among all three groups for the discrimination task. In all participants, a distributed set of brain regions including the primary and non-primary auditory cortices showed greater response for both tasks compared to rest. Comparing the groups directly, we found decreased activation in the parietal and frontal lobes in the participants with tinnitus compared to the HL group and decreased response in the frontal lobes relative to the NH group. Additionally, the HL subjects exhibited increased response in the anterior cingulate relative to the NH group. Our results suggest that a differential engagement of a putative auditory attention and short-term memory network, comprising regions in the frontal, parietal and temporal cortices and the anterior cingulate, may represent a key difference in the neural bases of chronic tinnitus accompanied by hearing loss relative to hearing loss alone.     

Delayed detection of congenital hearing loss in high risk infants.

OBJECTIVE--To examine the methods used to investigate children at high risk of congenital hearing impairment, and to see whether the introduction of evoked response audiometry has reduced the mean age at which hearing loss is identified. DESIGN--Clinicians who notified children to the national congenital rubella surveillance programme were asked retrospectively to complete a questionnaire examining the methods used to identify hearing impairment and the age at testing in two consecutive five year cohorts. The presence or absence of hearing loss was confirmed by obtaining the results of audiometric evaluations and, whenever possible, a recent pure tone audiogram. SETTING--The United Kingdom. PATIENTS--Children notified to the national congenital rubella surveillance programme and born in 1978-87 in whom IgM specific for rubella was detected shortly after birth. MAIN OUTCOME MEASURES--The age at which hearing loss was identified and the degree of loss in decibels at 250, 500, 1000, 2000, and 4000 Hz measured by pure tone audiometry. RESULTS--61 (52%) Of 117 children born in 1978-82 had a hearing impairment of 40 dB or greater in both ears. The mean loss was 93 dB. In the following five years 75 (47%) of 159 children had impaired hearing, their mean loss being 96 dB. The age at which the hearing loss was confirmed decreased from 11.6 to 9.8 months as a result of earlier auditory evoked response testing. Nevertheless, only eight (13%) of the children with hearing impairment born in 1978-82 and 16 (21%) of those born in 1983-7 had these tests performed in the first six months of life. CONCLUSIONS--Unacceptable delays in identifying hearing loss occurred in this high risk group because of failure to arrange auditory evoked response testing in early infancy. Evoked response audiometry is sensitive and specific and should be undertaken within the first few months of life for all infants known to be at risk of sensorineural hearing loss.     

噪声所致听力损失现象的物种差异及可能生理机制研究进展

噪声广泛存在于人和动物的生活环境中,从无脊椎动物到哺乳动物乃至人类,都会受到噪声的负面影响.强烈的噪声会损伤听觉系统的结构和功能,引起噪声性听力损失(noise-induced hearing loss,NIHL).本文对噪声性听力损失的类型、影响因素、噪声所致不同程度听力损失形成的可能机制进行了总结,发现NIHL主要与突触结构肿胀、谷氨酸引起的可逆兴奋性中毒以及活性氧引起的氧化应激、细胞凋亡、带状体损伤、α激动型鸟嘌呤核苷酸结合蛋白(guanine nucleotide binding protein alpha stimulating,GNAS)基因的mRNA及其上游lncRNA Sept7的表达量上调等因素有关.比较噪声暴露后不同物种听力损失情况的差异,发现鱼类和鸟类由于具有毛细胞再生能力而能够较快从听力损伤中恢复,啮齿类较容易受到噪声影响,而回声定位鲸类噪声暴露后的暂时性听觉阈移较小,非常有趣的是回声定位蝙蝠在噪声高强度暴露后未表现出暂时性听觉阈移的现象.上述结论提示,对不同物种的比较生理研究可深入揭示NIHL机制,并为听力保护以及噪声所致的听力损伤后修复等提供理论参考.     

Establishment of Mouse Model of MYH9 Disorders: Heterozygous R702C Mutation Provokes Macrothrombocytopenia with Leukocyte Inclusion Bodies,Renal Glomerulosclerosis and Hearing Disability

Nonmuscle myosin heavy chain IIA (NMMHCIIA) encoded by MYH9 is associated with autosomal dominantly inherited diseases called MYH9 disorders. MYH9 disorders are characterized by macrothrombocytopenia and very characteristic inclusion bodies in granulocytes. MYH9 disorders frequently cause nephritis, sensorineural hearing disability and cataracts. One of the most common and deleterious mutations causing these disorders is the R702C missense mutation.We generated knock-in mice expressing the Myh9 R702C mutation. R702C knock-in hetero mice (R702C+/− mice) showed macrothrombocytopenia. We studied megakaryopoiesis of cultured fetal liver cells of R702C+/− mice and found that proplatelet formation was impaired: the number of proplatelet tips was decreased, proplatelet size was increased, and proplatelet shafts were short and enlarged. Although granulocyte inclusion bodies were not visible by May–Grünwald Giemsa staining, immunofluorescence analysis indicated that NMMHCIIA proteins aggregated and accumulated in the granulocyte cytoplasm.In other organs, R702C+/− mice displayed albuminuria which increased with age. Renal pathology examination revealed glomerulosclerosis. Sensory hearing loss was indicated by lowered auditory brainstem response.These findings indicate that Myh9 R702C knock-in mice mirror features of human MYH9 disorders arising from the R702C mutation.     

Risk of Sudden Sensorineural Hearing Loss in Patients with Common Preexisting Sensorineural Hearing Impairment: A Population-Based Study in Taiwan

Objective

The role of preexisting sensorineural hearing impairment on the risk for sudden sensorineural hearing loss (SSHL) is still unclear. In this study, we aimed to assess the risk of SSHL in patients with common preexisting sensorineural hearing impairment using population-based data.

Methods

A population-based case-control study design was used to analyze claims data between January 2001 and December 2011 obtained from the Taiwan National Health Insurance Research Database. The cases consisted of 514 patients with SSHL and the controls were frequency matched to 2,570 cases by sex, 10-year age group, and year of index date. Common sensorineural hearing impairments were retrospectively assessed in the cases and controls. Associations between sensorineural hearing impairment and risk of SSHL were evaluated using unconditional univariate and multivariate logistic regression analyses.

Results

The mean age for the 3,084 study subjects was 53.1 years (standard deviation, S.D. = 15.6). Of the 514 cases, 49 (9.5%) had sensorineural hearing impairment while only 44 (1.7%) of the 2,570 controls had the same condition. Univariate logistic regression analyses indicated that preexisting sensorineural hearing impairment was significantly associated with SSHL (odds ratio, OR = 6.05, p < 0.001). Other comorbidities including hypertension, diabetes mellitus, and hyperlipidemia also showed significant associations with SSHL. Similar results were obtained when the association between SSHL and sensorineural hearing impairment was adjusted with either all the covariates (adjusted OR = 6.22, p < 0.001) or with only those selected using a backward elimination procedure (adjusted OR = 6.20, p < 0.001).

Conclusions

Results from this population-based case-control study revealed that common sensorineural hearing impairment might be a novel risk factor for SSHL.     

Mosquito bioacoustics: Auditory processing in <Emphasis Type="Italic">Culex pipiens pipiens</Emphasis> L. Males (Diptera,Culicidae) during flight simulation

As a part of mating behavior, male mosquitoes detect and locate females by listening to the sound of their wingbeats. Up to date, the auditory physiological properties in mosquitoes were studied in steady preparations. However, the sensory organs of a flying insect are affected by strong vibrations caused by its own flight muscles and wings. This influence can sufficiently modify the perception due to the nonlinear characteristics of the receptor cells. The aim of this study was to demonstrate the effect of flight conditions on the functioning of Johnston’s organs (hearing organs) in the male mosquitoes Culex pipiens pipiens L. To simulate the flight conditions, a small amount of air around the mosquito was oscillated at 500 Hz along the dorso-ventral axis. These air oscillations affected the pinnate antennae of the mosquito, causing vibration of the antennal flagellum which, in turn, was transmitted to and sensed by Johnston’s organ. Along with the flight simulation, the mosquito was stimulated by low-amplitude sinusoidal auditory signals of different frequencies. The responses were recorded from neurons using glass microelectrodes. The auditory responses contained two rhythms of amplitude modulation which were produced due to nonlinear processes in the receptors: the first rhythm had the difference frequency of flight simulation and the stimulus; the second rhythm corresponded to the beating of heterodyne frequencies. As compared to the steady-state conditions, an additional optimum of auditory sensitivity at 540–640 Hz (the so-called image channel) was shown to appear during flight simulation. This optimum corresponds to the second harmonic of the conspecific female sound. An improvement of sensitivity by 7 dB (2.2-fold) was also observed at the main optimum (220–320 Hz). We conclude that the mechanical influence of locomotor movements not only produces noise but can also improve the sensitivity of the sensory system or even add new properties.     

甲基强的松龙治疗2型糖尿病合并突发性感音神经聋的临床疗效研究

目的:观察甲基强的松龙治疗2型糖尿病合并突发性感音神经聋患者的治疗效果。方法:本研究共纳入2018年1月至2020年10月期间于深圳大学附属华南医院内分泌科、耳鼻喉科住院治疗的60例合并单侧突发性感音神经聋的成人2型糖尿病患者,按照随机数字表法分为治疗组(n=30)和对照组(n=30)。两组患者均给予营养神经、胰岛素降糖和高压氧治疗,治疗组给予甲基强的松龙静脉滴注3日后,减少甲基强的松龙剂量继续治疗4天,两组总疗程为14天。观察两组患者治疗后听力障碍改善情况,两组患者分别于治疗开始前、治疗1周后、治疗2周后分别测定纯音听阈均值(PTA)、听性脑干反应(ABR)以评估治疗效果。结果:治疗2周后治疗组听力障碍分级优于对照组(P<0.05);治疗2周后,治疗组的PTA和70dB、80dB、90dB声波刺激ABR指标均优于对照组(P<0.05)。结论:甲基强的松龙联合营养神经、降糖和高压氧等综合治疗,可有效提高2型糖尿病合并突发性感音神经聋患者的听力,值得临床推广应用。