Onset Of Sensorineural Hearing Loss Research Articles

The value of synthetic MRI in detecting the brain changes and hearing impairment of children with sensorineural hearing loss.

Sensorineural hearing loss (SNHL) can arise from a diverse range of congenital and acquired factors. Detecting it early is pivotal for nurturing speech, language, and cognitive development in children with SNHL. In our study, we utilized synthetic magnetic resonance imaging (SyMRI) to assess alterations in both gray and white matter within the brains of children affected by SNHL. The study encompassed both children diagnosed with SNHL and a control group of children with normal hearing {1.5-month-olds (n = 52) and 3-month-olds (n = 78)}. Participants were categorized based on their auditory brainstem response (ABR) threshold, delineated into normal, mild, moderate, and severe subgroups.Clinical parameters were included and assessed the correlation with SNHL. Quantitative analysis of brain morphology was conducted using SyMRI scans, yielding data on brain segmentation and relaxation time.Through both univariate and multivariate analyses, independent factors predictive of SNHL were identified. The efficacy of the prediction model was evaluated using receiver operating characteristic (ROC) curves, with visualization facilitated through the utilization of a nomogram. It's important to note that due to the constraints of our research, we worked with a relatively small sample size. Neonatal hyperbilirubinemia (NH) and children with inner ear malformation (IEM) were associated with the onset of SNHL both at 1.5 and 3-month groups. At 3-month group, the moderate and severe subgroups exhibited elevated quantitative T1 values in the inferior colliculus (IC), lateral lemniscus (LL), and middle cerebellar peduncle (MCP) compared to the normal group. Additionally, WMV, WMF, MYF, and MYV were significantly reduced relative to the normal group. Additionally, SNHL-children with IEM had high T1 values in IC, and LL and reduced WMV, WMF, MYV and MYF values as compared with SNHL-children without IEM at 3-month group. LL-T1 and WMF were independent risk factors associated with SNHL. Consequently, a prediction model was devised based on LL-T1 and WMF. ROC for training set, validation set and external set were 0.865, 0.806, and 0.736, respectively. The integration of T1 quantitative values and brain volume segmentation offers a valuable tool for tracking brain development in children affected by SNHL and assessing the progression of the condition's severity.

Genetically Predicted Sleep Traits and Sensorineural Hearing Loss: A Mendelian Randomization Study.

Observational studies suggest a potential association between sleep characteristics, sensorineural hearing loss (SNHL), and sudden SNHL (SSNHL), but causal evidence is scarce. We sought to clarify this issue using two-sample Mendelian randomization analysis. The inverse-variance weighted (IVW) method was performed as primary analysis to assess bidirectional causal associations between sleep traits (chronotype, sleep duration, insomnia, daytime sleepiness, and snoring) and SNHL/SSNHL using publicly available Genome-Wide Association Studies summary data from two large consortia (UK Biobank and FinnGen). Sensitivity analyses, including Mendelian randomization (MR)-Egger, Mendelian randomization pleiotropy residual sum and outlier, weight median, Cochran's Q test, leave-one-out analysis, and potential pleiotropy analysis, were conducted to ensure robustness. IVW analysis found suggestive associations of morning chronotype (odds ratio [OR] = 1.08, 95% confidence interval [CI] = 1.01-1.16, p = 0.031) and daytime sleepiness (OR = 1.88, 95% CI = 1.24-2.87, p = 0.003) with SNHL onset. Additionally, morning chronotype was nominally associated with SSNHL onset using IVW method (OR = 1.37, 95% CI = 1.10-1.71, p = 0.006). However, there was no evidence for the causal effect of SNHL and SSNHL on different sleep traits (all p > 0.05). Sensitivity analysis showed that the results were stable. Within the MR limitations, morning chronotype and daytime sleepiness were underlying causal contributors to the burden of SNHL, indicating that optimal sleep might facilitate the prevention and development of SNHL. 3 Laryngoscope, 2024.

A pH imbalance is linked to autophagic dysregulation of inner ear hair cells in Atp6v1ba-deficient zebrafish

V-ATPase is an ATP hydrolysis-driven proton pump involved in the acidification of intracellular organelles and systemic acid-base homeostasis through H+ secretion in the renal collecting ducts. V-ATPase dysfunction is associated with hereditary distal renal tubular acidosis (dRTA). ATP6V1B1 encodes the B1 subunit of V-ATPase that is integral to ATP hydrolysis and subsequent H+ transport. Patients with pathogenic ATP6V1B1 mutations often exhibit an early onset of sensorineural hearing loss. However, the mechanisms underlying this association remain unclear. We employed morpholino oligonucleotide-mediated knockdown and CRISPR/Cas9 gene editing to generate Atp6v1ba-deficient (atp6v1ba−/−) zebrafish as an ortholog model for ATP6V1B1. The atp6v1ba−/− zebrafish exhibited systemic acidosis and significantly smaller otoliths compared to wild-type siblings. Moreover, deficiency in Atp6v1ba led to degeneration of inner ear hair cells, with ultrastructural changes indicative of autophagy. Our findings indicate a critical role of ATP6V1B1 in regulating lysosomal pH and autophagy in hair cells, and the results provide insights into the pathophysiology of sensorineural hearing loss in dRTA. Furthermore, this study demonstrates that the atp6v1ba−/− zebrafish model is a valuable tool for further investigation into disease mechanisms and potential therapies for acidosis-related hearing impairment.

Usher Syndrome: A Rare Case

Usher syndrome is a rare heterogenous autosomal recessive genetic disorder with features of visual impairment due to retinitis pigmentosa and hearing loss. Other names for it include Hallgren syndrome, Usher-Hallgren syndrome, retinitis pigmentosa-dysacusis syndrome, and dystrophia retinae dysacusis syndrome.1,2 Usher syndrome represents a genetically diverse condition that involves both early onset sensorineural hearing loss and retinal pathology. While reports of disease prevalence vary, the condition has been estimated to occur in three in 100, 000 individuals.

The Importance of Mitochondrial Disease Testing in Young Adults With New Onset Sensorineural Hearing Loss.

Sensorineural hearing loss (SNHL) occurs commonly as part of mitochondriopathies and varies in severity and onset. In this study, we characterized hearing with specific consideration for hearing loss as a potential early indicator of mitochondrial disease (MD). We hypothesize that genetic testing at the earliest detection of SNHL may lead to an earlier MD diagnosis. We reviewed the clinical and audiometric data of 49 patients undergoing genetic testing for MD. One-third of individuals with molecularly confirmed MD presented with SNHL. On average, patients had hearing loss at least 10 years before genetic testing. The collective audiometric profile includes mild to moderate SNHL at lower frequencies and moderate SNHL at 2 kHz and higher frequencies. This study suggests that screening for SNHL could be an early indicator of MD. We propose that the audiometric profile for those with a MD diagnosis may have clinical triage utility.

Evaluation of Role of Prognostic Factors on Hearing Outcome in Unilateral Idiopathic Sudden Onset Sensorineural Hearing Loss

Introduction: Owing to its uncertain and multiple possible etiologies, use of multiple empirical treatment regimens and possibility of spontaneous recovery, it becomes important to look for the possible prognostic factors affecting the outcome of sudden sensorineural hearing loss (SSNHL). Material and methods: This prospective observational study was conducted with the primary aim of analyzing the role of various possible prognostic factors on the outcome of idiopathic SSNHL including demographic (Age, gender), audio-vestibular (Pre-treatment hearing loss in the affected ear, hearing in the contralateral ear, time elapse between onset of hearing loss and start of treatment, type of hearing loss in term of frequencies affected), presence of tinnitus / vertigo and Comorbidities (Diabetes, Hypothyroidism & Deranged lipid profile/ dyslipidemia). Result: The absence of vertigo and tinnitus led to better hearing outcomes while raised HbA1c levels, deranged lipids and thyroid profiles adversely affected the outcome. Conclusion: Vertigo, tinnitus, raised HbA1c levels, deranged lipids and thyroid profiles are possible negative prognostic factors. Better pretreatment hearing levels in the affected and unaffected ears prompted improved recovery.

P496: The importance of mitochondrial disease testing in young adults with new onset sensorineural hearing loss

P496: The importance of mitochondrial disease testing in young adults with new onset sensorineural hearing loss

Pathogenic mtDNA variants, in particular single large-scale mtDNA deletions, are strongly associated with post-lingual onset sensorineural hearing loss in primary mitochondrial disease.

In this retrospective cohort study of 193 consecutive subjects with primary mitochondrial disease (PMD) seen at the Children's Hospital of Philadelphia Mitochondrial Medicine Frontier Program, we assessed prevalence, severity, and time of onset of sensorineural hearing loss (SNHL) for PMD cases with different genetic etiologies. Subjects were grouped by genetic diagnosis: mitochondrial DNA (mtDNA) pathogenic variants, single large-scale mtDNA deletions (SLSMD), or nuclear DNA (nDNA) pathogenic variants. SNHL was audiometrically confirmed in 27% of PMD subjects (20% in mtDNA pathogenic variants, 58% in SLSMD and 25% in nDNA pathogenic variants). SLSMD had the highest odds ratio for SNHL. SNHL onset was post-lingual in 79% of PMD cases, interestingly including all cases with mtDNA pathogenic variants and SLSMD, which was significantly different from PMD cases caused by nDNA pathogenic variants. SNHL onset during school age was predominant in this patient population. Regular audiologic assessment is important for PMD patients, and PMD of mtDNA etiology should be considered as a differential diagnosis in pediatric patients and young adults with post-lingual SNHL onset, particularly in the setting of multi-system clinical involvement. Pathogenic mtDNA variants and SLSMD are less likely etiologies in subjects with congenital, pre-lingual onset SNHL.

The Absence of Permanent Sensorineural Hearing Loss in a Cohort of Children with SARS-CoV-2 Infection and the Importance of Performing the Audiological "Work-Up".

Currently, the novel coronavirus (SARS-CoV-2) causes an acute respiratory illness named COVID-19 and is a controversial risk factor for hearing loss (HL). Herein, we aim to describe the associated symptoms and to evaluate hearing function in the COVID-19 pediatric population. A retrospective cross-sectional observational study was carried out on 37 children who contracted COVID-19 infection with no previous audio-vestibular disorders. Clinical data on the infections were collected, and an audiological assessment of all affected children was performed by using different diagnostic protocols according to their age. Fever, upper respiratory and gastrointestinal manifestations were common presentations of infection. Audiological function was normal in 30 (81.08%) children, while 7 children showed an increased hearing threshold: 6 (16.21%) had transient conductive hearing loss (CHL) due to middle ear effusion and normalized at the follow-up and 1 had sensorineural hearing loss (SNHL). A single child was affected by bilateral SNHL (2.7%); however, he underwent a complete audiological work-up leading to a diagnosis of genetic HL due to a MYO6 gene mutation which is causative of progressive or late onset SNHL. HL needs to be considered among the manifestations of COVID-19 in children, nevertheless, we found cases of transient CHL. The onset of HL during or following COVID-19 infection does not eliminate the indication for maintaining audiological surveillance and audiological work-ups, including genetic diagnosis, to avoid the risk of mistaking other causes of HL.

Clinical Impact of Genetic Diagnosis of Sensorineural Hearing Loss in Adults.

Adult genetic sensorineural hearing loss (SNHL) may be underestimated. The diagnosis of genetic hearing loss is challenging, given its extreme genetic and phenotypic heterogeneity, particularly in adulthood. This study evaluated the utility of next-generation sequencing (NGS) in the etiological diagnosis of adult-onset SNHL. Adults (>16 yr old) with SNHL were recruited at the Otolaryngology Department at Marqués de Valdecilla University Hospital (Spain). Environmental factors, acoustic trauma, endolymphatic hydrops, and age-related hearing loss were excluding criteria. An NGS gene panel was used, including 196 genes (OTOgenics v3) or 229 genes (OTOgenics v4) related to syndromic and nonsyndromic hearing loss. Sixty-five patients were included in the study (average age at the onset of SNHL, 41 yr). Fifteen pathogenic/likely pathogenic variants considered to be causative were found in 15 patients (23% diagnostic yield) in TECTA (4), KCNQ4 (3), GJB2 (2), ACTG1 (1), COL2A1 (1), COCH (1), COCH/COL2A1 (1), STRC (1), and ABHD12 (1). Three patients had syndromic associations (20% of patients with genetic diagnosis) that had not been previously diagnosed (two Stickler type I and one polyneuropathy, hearing loss, ataxia, retinitis pigmentosa, cataract syndrome). Seven variants of unknown significance were found in COL11A1 (1), GSMDE (2), DNTM1 (1), SOX10 (1), EYA4 (1), and TECTA (1). NGS gene panels can provide diagnostic yields greater than 20% for adult SNHL, with a significant proportion of variant of unknown significance that could potentially contribute to increasing diagnostic output. Identifying a genetic cause enables genetic counseling, provides prognostic information and can reveal unrecognized syndromes contributing to an accurate management of their associated manifestations.

Depletion of CD4 and CD8 T Cells Reduces Acute Disease and Is Not Associated with Hearing Loss in ML29-Infected STAT1-/- Mice.

Lassa virus (LASV) is a zoonotic virus endemic to western Africa that can cause a potentially lethal and hemorrhagic disease, Lassa fever (LF). Survivors suffer a myriad of sequelae, most notably sudden onset sensorineural hearing loss (SNHL), the mechanism of which remains unclear. Unfortunately, studies aiming to identify the mechanism of these sequelae are limited due to the biosafety level 4 (BSL4) requirements of LASV itself. ML29, a reassortant virus proposed as an experimental vaccine candidate against LASV, is potentially an ideal surrogate model of LF in STAT1-/- mice due to similar phenotype in these animals. We intended to better characterize ML29 pathogenesis and potential sequelae in this animal model. Our results indicate that while both CD4 and CD8 T cells are responsible for acute disease in ML29 infection, ML29 induces significant hearing loss in a mechanism independent of either CD4 or CD8 T cells. We believe that this model could provide valuable information for viral-associated hearing loss in general.

Characteristics of patients with sudden onset sensorineural hearing loss: observational study

<p class="abstract"><strong>Background:</strong> Sudden sensorineural hearing loss (SNHL) is considered as acute onset hearing disturbance characterized by hearing loss of greater than 30 decibels.</p><p class="abstract"><strong>Methods:</strong> This retrospective research included data from 83 hospitalized patients (92 ears) and was conducted in a regional multidisciplinary children's medical centre between January 2014 and December 2019. We performed examinations of the eardrum as well as cranial nerves.</p><p class="abstract"><strong>Results:</strong> Among the 92 ears with SNHL, 8 ears (8.7%) in age group of 2-18 years, 33 ears (35.9%) in the group of 19-30 years, 30 (32.6%) and 21 ears (22.8%) represented the age groups of 31-65 and those aged over 65 years respectively. Hearing loss in 5 ears (5,4%) was rated as light, in 7 ears (7.6%) as moderate, in 14 ears (15.2%) as severe, and 66 ears (71.7%) out of the 92 had profound degree of hearing loss. Early treatment of SNHL was positive predictive factor for recovery (OR=2.54, 95% CI 1.09-5.91, p=0.03). The presence of tinnitus was also strongly linked with better recovery outcomes while not significantly associated (OR=2.59, 95% CI 0.91-7.37, p=0.07).</p><p class="abstract"><strong>Conclusions:</strong> In the course of our research, we found that 11.9% of patients made a full recovery, while the total recovery rate was 42.3%. Positive prognostic markers for hearing recovery were early treatment and a strong trend was observed with the presence of tinnitus.</p>

1010 Audit of Acute Management of Sudden Onset Sensorineural Hearing Loss and Streamlining of Local Management Pathway

Abstract Aim Sudden onset sensorineural hearing loss (SSNHL) presents infrequently to ENT services in Aberdeen Royal Infirmary. Although ENT UK guidelines are in place for the management of SSNHL, the practicalities of organising these cases within our department can be challenging to junior staff leading to variation in time to review and timings of intervention. We Aimed to assessed current local practice in comparison compare it to national ENT UK guidelines Method Retrospective audit of 6 months data set recording management pathway of patients presenting with SSNHL to Rapid Access Clinic of Royal Aberdeen Infirmary Hospital. Electronic patient records were searched for: time of referral, duration of symptoms, times to first ENT review, intervention and audiogram, and timings and management during subsequent reviews. Results Seven patients meeting the inclusion criteria were identified and included in the audit. Average times from referral were calculated including time from referral to intervention (1.47 days), from referral to first ENT review (3.82 days), from referral to first audiogram (4.43 says). Average time from presentation to starting oral steroids was very efficient of just 0.33 days and average time from symptom onset to oral steroids initiation was 7.5 days suggesting late patient presentation. Conclusions The data gather helped our department to reinforce management pathway of SSNHL as per ENT UK guidelines and improved the way urgent audiograms are organised in the hospital. It also emphasised the importance of performing tuning fork test to determine the nature of hearing loss when audiogram is not immediately available.

EP183: Functional assessment of a novel POU4F3 missense variant

The POU-domain family of transcription factors have a wide variety of functions and are critical regulators of many developmental processes. They are characterized by a common bipartite DNA-binding structure with POU-specific and POU-homeodomain subdomains, joined by an unstructured linkage region. Both subdomains are required for high affinity DNA binding of POU transcription factors. The POU4F3 gene has been found to be essential for inner-ear hair cell maintenance and is associated with autosomal-dominant nonsyndromic hearing loss with variable age of onset. Here we describe an individual with a novel heterozygous missense variant in POU4F3 exhibiting bilateral childhood onset sensorineural hearing loss. The proband’s mother also exhibited hearing loss. Functional assessment of this variant was performed to determine the impact on protein localization, and familial segregation studies were performed to better understand the pathogenicity of this variant. The proband underwent exome sequencing (ES) which revealed a maternally inherited missense variant in POU4F3 (NM_002700.2, c.856A>G, p.(Lys286Glu)). Family members were subsequently given audiograms and tested for this variant. To functionally assess the variant HA-tagged wild-type and mutant POU4F3 were expressed by using the mammalian expression vector pcDNA3.1 and transfected in Hek293 cells. To determine the subcellular localization of the HA-tagged wild-type and mutant POU4F3, transiently transfected cells were fixed with 4% paraformaldehyde, incubated with primary anti-HA and secondary goat-anti-mouse Alexa488-labelled antibodies. Images were taken with a fluorescence microscope and processed using ImageJ. To determine the number of cells expressing POU4F3 outside the nucleus, slides were blinded and 100 cells of each transfected mutant were scored; each construct was transfected in duplicate. Audiograms revealed that one of the proband’s brothers had mild hearing loss, while the other was unaffected. Familial variant testing then showed that the affected brother is heterozygous for the POU4F3 variant while the unaffected brother does not harbor the variant. The mother was previously shown to have hearing loss, and the variant was maternally inherited. Functional assessment of the variant demonstrated that it results in significant mis-localization from the nucleus to the cytoplasm compared to wild type controls (p value: 0.009). This affect was more significant than positive controls included in the analysis. The proband’s variant is not reported in population databases and is predicted to be deleterious by REVEL (0.89) and CADD (27.7). This variant was clinically classified as a VUS, with the following criteria applied: PM2+PP3. This variant falls within the homeodomain of the protein, which is required for DNA binding of POU transcription factors. Pathogenic missense variants in POU4F3 have previously been shown to disrupt the nuclear localization of the protein, so this was assessed in cells expressing the p.(Lys286Glu) variant. The proband’s variant was found to result in significant mis-localization of POU4F3 to the cytoplasm, suggesting an impact on the protein function. Finally, the variant was found to segregate with hearing loss in the proband’s mother and affected brother, allowing us to apply PP1 criteria based on the ClinGen hearing loss evaluation guidelines. Taken together these data are suggestive that this variant is causative for the proband, however this remains a VUS.

Usher syndrome type IV: clinically and molecularly confirmed by novel ARSG variants

Usher syndrome (USH) is an autosomal recessively inherited disease characterized by sensorineural hearing loss (SNHL) and retinitis pigmentosa (RP) with or without vestibular dysfunction. It is highly heterogeneous both clinically and genetically. Recently, variants in the arylsulfatase G (ARSG) gene have been reported to underlie USH type IV. This distinct type of USH is characterized by late-onset RP with predominantly pericentral and macular changes, and late onset SNHL without vestibular dysfunction. In this study, we describe the USH type IV phenotype in three unrelated subjects. We identified three novel pathogenic variants, two novel likely pathogenic variants, and one previously described pathogenic variant in ARSG. Functional experiments indicated a loss of sulfatase activity of the mutant proteins. Our findings confirm that ARSG variants cause the newly defined USH type IV and support the proposed extension of the phenotypic USH classification.

Dual-Specificity Phosphatase 1 (DUSP1) Has a Central Role in Redox Homeostasis and Inflammation in the Mouse Cochlea.

Stress-activated protein kinases (SAPK) are associated with sensorineural hearing loss (SNHL) of multiple etiologies. Their activity is tightly regulated by dual-specificity phosphatase 1 (DUSP1), whose loss of function leads to sustained SAPK activation. Dusp1 gene knockout in mice accelerates SNHL progression and triggers inflammation, redox imbalance and hair cell (HC) death. To better understand the link between inflammation and redox imbalance, we analyzed the cochlear transcriptome in Dusp1−/− mice. RNA sequencing analysis (GSE176114) indicated that Dusp1−/− cochleae can be defined by a distinct profile of key cellular expression programs, including genes of the inflammatory response and glutathione (GSH) metabolism. To dissociate the two components, we treated Dusp1−/− mice with N-acetylcysteine, and hearing was followed-up longitudinally by auditory brainstem response recordings. A combination of immunofluorescence, Western blotting, enzymatic activity, GSH levels measurements and RT-qPCR techniques were used. N-acetylcysteine treatment delayed the onset of SNHL and mitigated cochlear damage, with fewer TUNEL+ HC and lower numbers of spiral ganglion neurons with p-H2AX foci. N-acetylcysteine not only improved the redox balance in Dusp1−/− mice but also inhibited cytokine production and reduced macrophage recruitment. Our data point to a critical role for DUSP1 in controlling the cross-talk between oxidative stress and inflammation.

Hearing loss in a post COVID-19 patient

<p class="abstract">With the advent of COVID-19 pandemic, there has been a myriad of long-term complications in post-COVID patients. In these patients, one of the rare but dreaded symptoms reported is sudden onset sensorineural hearing loss (SNHL) that has been reported mostly during active infection. We followed up with these patients in our outpatient department and came across one patient of SNHL. We conducted a literature search in PubMed and Google Scholar but couldn’t come across any such care report from India. We are hereby reporting the first case of SNHL in a post-hospitalised COVID-19 from India presenting after 3 months of hospital discharge, with no history prior otologic illness, intake of ototoxic drugs or any head injury. Post-COVID patients can present with weird symptoms including hearing loss apart from other commonly reported post COVID 19 sequelae.</p>

High level of IgE in acute low-tone sensorineural hearing loss: A predictor for recurrence and Meniere Disease transformation

BackgroundAutoimmunity may play an important role in sudden onset sensorineural hearing loss. However, little is known about the relationship between immunoglobulin E (IgE) and acute low-tone sensorinerual hearing loss (ALHL). ObjectivesTo investigate the relationship between IgE level and endolymphatic hydrops and outcomes of ALHL. MethodsA total of 242 subjects with sudden onset hearing loss, including 115 with ALHL and 127 with idiopathic sudden sensorineural hearing loss (ISSHL), were included in this study. Peripheral venous blood samples of 242 subjects were collected for detection. Clinical data, IgE level, and distribution of allergens were compared between the ALHL and ISSHL groups. The ALHL group received an electrocochleogram (ECochG) test and a follow-up in the outpatient unit or by telephone to evaluate outcomes. ResultsCompared to the values in the ISSHL group, a significantly younger onset age (42.30±14.33 years old), higher female onset proportion (72/115, 62.61%), increased total IgE level (median: 66.47, interquartile range: 24.56, 180.96, IU/mL) and specific IgE level (median: 9.42, interquartile range: 1.42, 22.23 IU/mL) were noted in the ALHL group. A clear difference in allergen distribution was noted between the ALHL and ISSHL groups (p=.001). Total IgE and specific IgE levels were factors that contributed to the SP/AP ratio in the electrocochleogram (ECochG) (R2=0.413) in ALHL group. Finally, during the follow-up (17.61±3.46 months) for the ALHL group, 37 subjects recurred, and 17 subjects developed Meniere Disease. In the ROC curve for ALHL recurrence, the area under the curve (AUC) of total IgE was 0.709 and that of specific IgE was 0.679. For MD transformation, the AUC of total IgE was 0.736 and that of specific IgE was 0.716. ConclusionsHigh IgE levels correlated with an enhanced SP/AP ratio in ALHL. High IgE levels could be used as a predictor of ALHL recurrence and MD transformation.

Comparative Study of high-resolution T2-weighted turbo spin echo sequence and postcontrast three-dimensional volumetric T1-weighted sequence in evaluation of acute onset sensorineural hearing loss

Comparative Study of high-resolution T2-weighted turbo spin echo sequence and postcontrast three-dimensional volumetric T1-weighted sequence in evaluation of acute onset sensorineural hearing loss

Comparative Study of high-resolution T2-weighted turbo spin echo sequence and postcontrast three-dimensional volumetric T1-weighted sequence in evaluation of acute onset sensorineural hearing loss

Comparative Study of high-resolution T2-weighted turbo spin echo sequence and postcontrast three-dimensional volumetric T1-weighted sequence in evaluation of acute onset sensorineural hearing loss