Multi-modal deep learning for joint prediction of otitis media and diagnostic difficulty.

Objectives: In this study, we propose a diagnostic model for automatic detection of otitis media based on combined input of otoscopy images and wideband tympanometry measurements. Methods: We present a neural network-based model for the joint prediction of otitis media and diagnostic difficulty. We use the subclassifications acute otitis media and otitis media with effusion. The proposed approach is based on deep metric learning, and we compare this with the performance of a standard multi-task network. Results: The proposed deep metric approach shows good performance on both tasks, and we show that the multi-modal input increases the performance for both classification and difficulty estimation compared to the models trained on the modalities separately. An accuracy of 86.5% is achieved for the classification task, and a Kendall rank correlation coefficient of 0.45 is achieved for difficulty estimation, corresponding to a correct ranking of 72.6% of the cases. Conclusion: This study demonstrates the strengths of a multi-modal diagnostic tool using both otoscopy images and wideband tympanometry measurements for the diagnosis of otitis media. Furthermore, we show that deep metric learning improves the performance of the models.

A Deep Learning Approach for Detecting Otitis Media From Wideband Tympanometry Measurements.

OBJECTIVE: In this study, wepropose an automatic diagnostic algorithm for detecting otitis media based on wideband tympanometry measurements. METHODS: We develop a convolutional neural network for classification of otitis media based on the analysis of the wideband tympanogram. Saliency maps are computed to gain insight into the decision process of the convolutional neural network. Finally, we attempt to distinguish between otitis media with effusion and acute otitis media, a clinical subclassification important for the choice of treatment. RESULTS: The approach shows high performance on the overall otitis media detection with an accuracy of 92.6%. However, the approach is not able to distinguish between specific types of otitis media. CONCLUSION: Out approach can detect otitis media with high accuracy and the wideband tympanogram holds more diagnostic information than the commonly used techniques wideband absorbance measurements and simple tympanograms. SIGNIFICANCE: This study shows how advanced deep learning methods enable automatic diagnosis of otitis media based on wideband tympanometry measurements, which could become a valuable diagnostic tool.

Inter-rater reliability of the diagnosis of otitis media based on otoscopic images and wideband tympanometry measurements.

OBJECTIVES: This study aims to investigate the inter-rater reliability and agreement of the diagnosis of otitis media with effusion, acute otitis media, and no effusion cases based on an otoscopy image and in some cases an additional wideband tympanometry measurement of the patient. METHODS: 1409 cases were examined and diagnosed by an otolaryngologist in the clinic, and otoscopy examination and wideband tympanometry (WBT) measurement were conducted. Afterwards, four otolaryngologists (Ear, Nose, and Throat doctors, ENTs), who did not perform the acute examination of the patients, evaluated the otoscopy images and WBT measurements results for diagnosis (acute otitis media, otitis media with effusion, or no effusion). They also specified their diagnostic certainty for each case, and reported whether they used the image, wideband tympanometry, or both, for diagnosis. RESULTS: All four ENTs agreed on the diagnosis in 57% of the cases, with a pairwise agreement of 74%, and a Light's Kappa of 0.58. There are, however, large differences in agreement and certainty between the three diagnoses. Acute otitis media yields the highest agreement (77% between all four ENTs) and certainty (0.90), while no effusion shows much lower agreement and certainty (34% and 0.58, respectively). There is a positive correlation between certainty and agreement between the ENTs across all cases, and both certainty and agreement increase for cases where a WBT measurement is shown in addition to the otoscopy image. CONCLUSIONS: The inter-rater reliability between four ENTs was high when diagnosing acute otitis media and lower when diagnosing otitis media with effusion. However, WBT can add valuable information to get closer to the ground-truth diagnosis without myringotomy. Furthermore, the diagnostic certainty increases when the WBT is examined together with the otoscopy image.

Deep metric learning for otitis media classification.

In this study, we propose an automatic diagnostic algorithm for detecting otitis media based on otoscopy images of the tympanic membrane. A total of 1336 images were assessed by a medical specialist into three diagnostic groups: acute otitis media, otitis media with effusion, and no effusion. To provide proper treatment and care and limit the use of unnecessary antibiotics, it is crucial to correctly detect tympanic membrane abnormalities, and to distinguish between acute otitis media and otitis media with effusion. The proposed approach for this classification task is based on deep metric learning, and this study compares the performance of different distance-based metric loss functions. Contrastive loss, triplet loss and multi-class N-pair loss are employed, and compared with the performance of standard cross-entropy and class-weighted cross-entropy classification networks. Triplet loss achieves high precision on a highly imbalanced data set, and the deep metric methods provide useful insight into the decision making of a neural network. The results are comparable to the best clinical experts and paves the way for more accurate and operator-independent diagnosis of otitis media.

Morphological correlates of hearing loss after cochlear implantation and electro-acoustic stimulation in a hearing-impaired Guinea pig model.

Hybrid or electro-acoustic stimulation (EAS) cochlear implants (CIs) are designed to provide high-frequency electric hearing together with residual low-frequency acoustic hearing. However, 30-50% of EAS CI recipients lose residual hearing after implantation. The objective of this study was to determine the mechanisms of EAS-induced hearing loss in an animal model with high-frequency hearing loss. Guinea pigs were exposed to 24 h of noise (12-24 kHz at 116 dB) to induce a high-frequency hearing loss. After recovery, two groups of animals were implanted (n = 6 per group), with one group receiving chronic acoustic and electric stimulation for 10 weeks, and the other group receiving no stimulation during this time frame. A third group (n = 6) was not implanted, but received chronic acoustic stimulation. Auditory brainstem responses were recorded biweekly to monitor changes in hearing. The organ of Corti was immunolabeled with phalloidin, anti-CtBP2, and anti-GluR2 to quantify hair cells, ribbons and post-synaptic receptors. The lateral wall was immunolabeled with phalloidin and lectin to quantify stria vascularis capillary diameters. Bimodal or trimodal diameter distributions were observed; the number and location of peaks were objectively determined using the Aikake Information Criterion and Expectation Maximization algorithm. Noise exposure led to immediate hearing loss at 16-32 kHz for all groups. Cochlear implantation led to additional hearing loss at 4-8 kHz; this hearing loss was negatively and positively correlated with minimum and maximum peaks of the bimodal or trimodal distributions of stria vascularis capillary diameters, respectively. After chronic stimulation, no significant group changes in thresholds were seen; however, elevated thresholds at 1 kHz in implanted, stimulated animals were significantly correlated with decreased presynaptic ribbon and postsynaptic receptor counts. Inner and outer hair cell counts did not differ between groups and were not correlated with threshold shifts at any frequency. As in the previous study in a normal-hearing model, stria vascularis capillary changes were associated with immediate hearing loss after implantation, while little to no hair cell loss was observed even in cochlear regions with threshold shifts as large as 40-50 dB. These findings again support a role of lateral wall blood flow changes, rather than hair cell loss, in hearing loss after surgical trauma, and implicate the endocochlear potential as a factor in implantation-induced hearing loss. Further, the analysis of the hair cell ribbons and post-synaptic receptors suggest that delayed hearing loss may be linked to synapse or peripheral nerve loss due to stimulation excitotoxicity or inflammation. Further research is needed to separate these potential mechanisms of delayed hearing loss.

Factors associated with hearing loss in a normal-hearing guinea pig model of Hybrid cochlear implants.

The Hybrid cochlear implant (CI), also known as Electro-Acoustic Stimulation (EAS), is a new type of CI that preserves residual acoustic hearing and enables combined cochlear implant and hearing aid use in the same ear. However, 30-55% of patients experience acoustic hearing loss within days to months after activation, suggesting that both surgical trauma and electrical stimulation may cause hearing loss. The goals of this study were to: 1) determine the contributions of both implantation surgery and EAS to hearing loss in a normal-hearing guinea pig model; 2) determine which cochlear structural changes are associated with hearing loss after surgery and EAS. Two groups of animals were implanted (n = 6 per group), with one group receiving chronic acoustic and electric stimulation for 10 weeks, and the other group receiving no direct acoustic or electric stimulation during this time frame. A third group (n = 6) was not implanted, but received chronic acoustic stimulation. Auditory brainstem response thresholds were followed over time at 1, 2, 6, and 16 kHz. At the end of the study, the following cochlear measures were quantified: hair cells, spiral ganglion neuron density, fibrous tissue density, and stria vascularis blood vessel density; the presence or absence of ossification around the electrode entry was also noted. After surgery, implanted animals experienced a range of 0-55 dB of threshold shifts in the vicinity of the electrode at 6 and 16 kHz. The degree of hearing loss was significantly correlated with reduced stria vascularis vessel density and with the presence of ossification, but not with hair cell counts, spiral ganglion neuron density, or fibrosis area. After 10 weeks of stimulation, 67% of implanted, stimulated animals had more than 10 dB of additional threshold shift at 1 kHz, compared to 17% of implanted, non-stimulated animals and 0% of non-implanted animals. This 1-kHz hearing loss was not associated with changes in any of the cochlear measures quantified in this study. The variation in hearing loss after surgery and electrical stimulation in this animal model is consistent with the variation in human patients. Further, these findings illustrate an advantage of a normal-hearing animal model for quantification of hearing loss and damage to cochlear structures without the confounding effects of chemical- or noise-induced hearing loss. Finally, this study is the first to suggest a role of the stria vascularis and damage to the lateral wall in implantation-induced hearing loss. Further work is needed to determine the mechanisms of implantation- and electrical-stimulation-induced hearing loss.

An Src-protein tyrosine kinase inhibitor to reduce cisplatin ototoxicity while preserving its antitumor effect.

Ototoxicity remains a major dose-limiting side effect of cisplatin. The current studies were carried out to evaluate the effectiveness of a novel Src-protein tyrosine kinase inhibitor in protecting the ear from cisplatin ototoxicity without compromising cisplatin's antitumor effects. The Src inhibitor has been shown to be effective in protecting the ear from noise-induced hearing loss. Three studies were carried out to determine whether this compound has otoprotective activity in rats treated with cisplatin. The first two studies used the Src inhibitor as a cotreatment with single doses of cisplatin in Fischer 344/NHsd rats and nude rats, respectively. Cochlear damage was assessed by auditory brainstem response threshold shifts and outer hair cell loss. The third study was carried out in nude rats with implanted HT-29 tumors, and the Src inhibitor was administered as a cotreatment with a lower dose of cisplatin. Cochlear damage and changes in tumor volume were assessed in the third study. In the first two studies, cotreatment with the Src inhibitor reduced cisplatin-induced hearing loss significantly. In the third study, little hearing loss was induced because of the use of a lower dose of cisplatin. However, cotreatment with the Src inhibitor did not exert a negative effect on cisplatin's slowing of tumor growth in the treated rats. The findings suggest that the Src inhibitor may provide an effective cotreatment with cisplatin to reduce cisplatin's ototoxicity, without compromising its antitumor capability.

Expression pattern of oxidative stress and antioxidant defense-related genes in the aging Fischer 344/NHsd rat cochlea.

The biological mechanisms that give rise to age-related hearing loss (ARHL) are still poorly understood. However, there is growing recognition that oxidative stress may be an important factor. To address this issue, we measured the changes in the expression of cochlear oxidative stress and antioxidant defense-related genes in young (2 months old), middle-aged (12 months old), and old (21-25 months old) Fischer 344/NHsd (F344/NHsd) rats and compared gene expression changes with ARHL. A quantitative real-time reverse transcription polymerase chain reaction array revealed a significant age-related downregulation of only 1 gene, stearoyl-coenzyme A desaturase 1, and upregulation of 12 genes: 24-dehydrocholesterol reductase; aminoadipate-semialdehyde synthase; cytoglobin; dual oxidase 2; glutathione peroxidase 3; glutathione peroxidase 6; glutathione S-transferase, kappa 1; glutathione reductase; nicotinamide adenine dinucleotide phosphate (NAD(P)H) dehydrogenase, quinone 1; solute carrier Family 38, Member 5; thioredoxin interacting protein; and vimentin. Statistical analyses revealed significant correlations between gene expression and auditory function in 8 genes. Our results identified specific subsets of oxidative stress genes that appear to play an important role in ARHL in the Fischer 344/NHsd rat.

Interaural stacked auditory brainstem response measures for detecting small unilateral acoustic tumors.

The Stacked auditory brainstem response (SABR) was developed and investigated as a screening tool for small (≤1 cm) unilateral acoustic tumors (vestibular schwannomas) that were missed by standard clinical auditory brainstem response (ABR) measures [Don et al.: Am J Otol 1997;18:608-621; Audiol Neurotol 2005;10:274-290]. While the SABR measure provided much greater sensitivity than the standard ABR measures for small tumor detection, we believed that the large intersubject variability of the SABR measure compromised both the sensitivity and specificity of the measure. However, as we demonstrate in this paper, the variability between ears of a given individual is small. Thus, we introduced an interaural SABR (ISABR) amplitude difference measure to improve the sensitivity and specificity of the SABR amplitude measure to detect small unilateral acoustic tumors. Its main advantages are two-fold. First, it is somewhat immune to variables that affect the absolute SABR amplitudes because it is a relative measure. Second, it is better at assessing tumor patients with very large and non-tumor patients with very small absolute SABR amplitudes. We believe that the ISABR is a useful addition to ABR measures aimed at detecting the presence of unilateral acoustic tumors.

Too much of a good thing: long-term treatment with salicylate strengthens outer hair cell function but impairs auditory neural activity.

Aspirin has been extensively used in clinical settings. Its side effects on auditory function, including hearing loss and tinnitus, are considered as temporary. A recent promising finding is that chronic treatment with high-dose salicylate (the active ingredient of aspirin) for several weeks enhances expression of the outer hair cell (OHC) motor protein (prestin), resulting in strengthened OHC electromotility and enhanced distortion product otoacoustic emissions (DPOAE). To follow up on these observations, we carried out two studies, one planned study of age-related hearing loss restoration and a second unrelated study of salicylate-induced tinnitus. Rats of different strains and ages were injected with salicylate at a dose of 200 mg/kg/day for 5 days per week for 3 weeks or at higher dose levels (250-350 mg/kg/day) for 4 days per week for 2 weeks. Unexpectedly, while an enhanced or sustained DPOAE was seen, permanent reductions in the amplitude of the cochlear compound action potential (CAP) and the auditory brainstem response (ABR) were often observed after the chronic salicylate treatment. The mechanisms underlying these unexpected, permanent salicylate-induced reductions in neural activity are discussed.

Age-related hearing loss: is it a preventable condition?

Numerous techniques have been tested to attempt to prevent the onset or progression of age-related hearing loss (ARHL): raising the animals in an augmented acoustic environment (used successfully in mouse and rat models), enhancing the antioxidant defenses with exogenous antioxidant treatments (used with mixed results in mouse and rat models), raising the animals with a calorie restricted diet (used successfully in mouse and rat models), restoring lost endocochlear potential voltage with exogenous electrical stimulation (used successfully in the Mongolian gerbil model), and hypothetical enhancement of outer hair cell electromotility with salicylate therapy. Studies of human ARHL have revealed a set of unique hearing loss configurations with unique underlying pathologies. Animal research has developed models for the different forms of age-related peripheral pathology. Using the animal models, different techniques for prevention of ARHL have been developed and tested. The current review discusses ARHL patterns in humans and animal models, followed by discussions of the different prevention techniques.

Ameliorative effects of an augmented acoustic environment on age-related hearing loss in middle-aged Fischer 344/NHsd rats.

OBJECTIVES/HYPOTHESIS: To investigate the effects of an augmented acoustic environment (AAE) on age-related hearing loss (ARHL) and outer hair cell (OHC) pathology in middle-aged Fischer 344/NHsd (F344/NHsd) rats. METHODS: Eleven F344/NHsd rats were divided into two groups: 1) the AAE group (n = 5), which was exposed to 4-20 kHz broadband noise at 80 dB SPL for 12 h/d, 5 d/wk for 13 weeks starting from 16 months of age; and 2) the control group (n = 6), which did not receive the AAE during the same time span. Auditory brainstem response thresholds were obtained at different time points, and OHC pathology was examined after 13 weeks of AAE using propidium iodide and antiprestin antibody staining. RESULTS: The AAE-treated rats showed smaller mean threshold shifts (-1 to -3 dB) at 20-40 kHz than the control group (7.5-16.7 dB) at 13 weeks. No significant group differences were observed in the percentage of missing OHCs or abnormal OHC nuclei. However, examination of prestin in a pair of AAE and control rats revealed more uniform prestin staining intensity among OHCs in the AAE-treated cochlea than in the control cochlea. CONCLUSIONS: Thirteen-week AAE treatment in the middle-aged F344/NHsd rats slowed progression of ARHL. The AAE did not show a significant effect on OHC degeneration, but it is speculated that the AAE may maintain the integrity of prestin to preserve OHC functionality. However, further study is warranted to understand the protective mechanism of AAE as an intervention against ARHL.

The effects of acoustic environment after traumatic noise exposure on hearing and outer hair cells.

Previous studies reported that exposure to non-traumatic level sounds after traumatic noise exposure reduced the degree of noise-induced hearing loss and hair cell stereocilia damage. The current study investigated the effects of a 3-day post-noise acoustic environment on the degree of noise-induced hearing loss and cochlear damage. Female chinchillas were exposed to traumatic continuous noise (4 kHz octave-band noise) at 107 dB SPL for 1h and then placed in either an augmented acoustic environment (AAE) or deprived acoustic environment (DAE) for 3 days. The AAE group was exposed to a broad-band noise (4-20 kHz) at 80 dB SPL and the DAE animals were fit with conventional earplugs to minimize the level of acoustic stimulation. Auditory brainstem responses (ABRs) were recorded before and 3 days after the traumatic noise exposure. The AAE group showed a significantly lower average threshold shift at the frequencies of 4 and 8 kHz (p<0.01). Correspondingly, significantly fewer missing and dying outer hair cells (OHCs) were observed in the AAE group than in the DAE group. Although the cochlear reduced and oxidized glutathione levels (GSH and GSSG, respectively) were essentially the same in two groups at day 3, significant correlations were found between GSSG levels and mean ABR threshold shift (1-16 kHz) in the AAE group; as well as GSSG and percentage of total OHC loss in the DAE group. The results suggest that post-noise acoustic environment influenced the degree of hearing loss and OHC deterioration after traumatic noise exposure.

Aging outer hair cells (OHCs) in the Fischer 344 rat cochlea: function and morphology.

As previously reported [Popelar, J., Groh, D., Pelanova, J., Canlon, B., Syka, J., 2006. Age-related changes in cochlear and brainstem auditory functions in Fischer 344 rats. Neurobiol. Aging 27, 490-500; Buckiova, D., Popelar, J., Syka, J., 2007. Aging cochleas in the F344 rat: morphological and functional changes. Exp. Gerontol. 42, 629-638; Bielefeld, E.C., Coling, D., Chen, G.D., Li, M.N., Tanaka, C., Hu, B.H., Henderson, D., 2008. Age-related hearing loss in the Fischer 344/NHsd rat substrain. Hear. Res. 241, 26-33], aged Fischer 344 (F344) rats with severe hearing loss retain many outer hair cells (OHCs) especially in the middle turn of the cochlea. The current study confirmed the previous findings showing that aged OHCs were present, but dysfunctional. Distortion product otoacoustic emissions (DPOAE), which are believed to reflect in vivo OHC motility, were absent in the aged rats while the majority of OHCs (>80%) were present and morphologically intact. There was no detectable injury of OHC stereocilia as assessed by actin-staining and examination under the light microscope. Cochlear microphonics (CM) at 12kHz, recorded from the middle turn, only showed a slight age-related reduction, indicating a normal mechanoelectrical transduction apparatus in the remaining OHCs in the cochlear regions with 10-20% OHC loss. Activities of succinate dehydrogenase (SDH), an enzyme shared by the citric acid cycle and the mitochondrial electron transport chain (METC), were also at normal levels in aged OHCs. Importantly, aged OHCs showed reduced levels of prestin immunolabeling compared to young controls. Together with our previous finding showing that the stria vascularis and endocochlear potential were essentially normal in aged F344 rats [Bielefeld, E.C., Coling, D., Chen, G.D., Li, M.N., Tanaka, C., Hu, B.H., Henderson, D., 2008. Age-related hearing loss in the Fischer 344/NHsd rat substrain. Hear. Res. 241, 26-33], the results suggest that disruption of prestin is the major cause of DPOAE loss and loss of cochlear sensitivity.

Relation between outer hair cell loss and hearing loss in rats exposed to styrene.

The relationship between outer hair cell (OHC) loss and cochlear sensitivity is still unclear, because in many animal models there exist surviving but dysfunctional OHCs and also injured/dead inner hair cells (IHC). Styrene is an ototoxic agent, which targets and destroys OHCs starting from the third row to the second and first rows depending on the exposure level. The remaining cells may be less affected. In this experiment, rats were exposed to styrene by gavage at different doses (200-800 mg/kg/day) for varying periods (5 days/week for 3-12 weeks). An interesting finding was that the cochlear sensitivity was not affected in a few rats with all OHCs in the third row being destroyed by styrene. A further loss of OHCs was usually accompanied with a linear input/output (I/O) function of cochlear compound action potentials (CAP), indicating the loss of cochlear amplification. However, normal CAP amplitudes at the highest stimulation level of 90 dB SPL were often observed when all OHCs were destroyed, indicating normal function of the remaining IHCs. The OHC-loss/hearing-loss relation appeared to be a sigmoid-type function. Initially, styrene-induced OHC losses (<33%) did not result in a significant threshold shift. Then CAP threshold shift increased dramatically with OHC loss from 33% to 66%. Then, CAP threshold changed less with OHC loss. The data suggest a tri-modal relationship between OHC loss and cochlear amplification. That is, under the condition that all surviving OHCs are ideally functioning, the cochlear amplifier is not affected until 33% of OHCs are absent, then the gain of the amplifier decreases proportionally with the OHC loss, and at last the amplifier may fail completely when more than 67% of OHCs are lost.

Age-related hearing loss in the Fischer 344/NHsd rat substrain.

Studies of the F344 rat have shown a variety of age-related auditory anatomy and physiology changes. The current study was undertaken to clarify the ARHL in the F344 rat, by examining the auditory pathway of the F344/NHsd substrain that is distributed by Harlan Laboratories for research in the United States. The F344/NHsd rat begins to lose its hearing at about 12 months, and by 24 months, there are 50-60 dB auditory brainstem response threshold shifts at 20 and 40 kHz and 20 dB losses at 5-10 kHz. Distortion product otoacoustic emissions (DPOAE) amplitudes at 1.8-12 kHz stimuli were depressed in the older (18-24 months) rats. Amplitude input-output functions of the compound action potential (CAP) were also depressed across frequency. The endocochlear potential (EP) was 90-100 mV in the 3 month old rats. All but one of the 24 month old rats' EPs were in the +75-85 mV range. Tympanometry revealed no differences in middle ear function between the young and older rats. Collectively, these findings suggest damage to the outer hair cells, but anatomical examination of the outer hair cells revealed a relative lack of cell loss compared to the magnitude of the hearing and DPOAE loss.

An alternative diagnostic test for active Ménière's disease and cochlear hydrops using high-pass noise masked responses: the complex amplitude ratio.

We [Don et al.: Otol Neurotol 2005;26:711-722] previously demonstrated that patients diagnosed with an active case of Ménière's disease could be distinguished from non-Ménière's normal-hearing subjects by a special auditory brainstem response method involving clicks and ipsilateral high-pass masking pink noise. Specifically, auditory brainstem responses to clicks presented alone and clicks with masking noise high-pass filtered at 8, 4, 2, 1 and 0.5 kHz were recorded. It was shown that the level of masking noise sufficient to progressively mask the response to clicks in non-Ménière's normal-hearing subjects was insufficient to appropriately mask the responses in Ménière's disease subjects, resulting in an obvious undermasked component. A relative latency measure of wave V or the undermasked component in the response to clicks with 0.5 kHz high-pass masking noise and wave V in the response to clicks presented alone clearly distinguished these two groups on an individual level, thus making it a valuable clinical tool. However, determining the peak latency of wave V or the undermasked component can be difficult in some cases. In anticipation of this difficulty, we investigated and present in this paper several amplitude measures that may help in the evaluation of these cases. One amplitude measure, the 'complex amplitude ratio', appears to be a good alternative when the latency measure of the undermasked component is difficult to determine.

A diagnostic test for Ménière's Disease and Cochlear Hydrops: impaired high-pass noise masking of auditory brainstem responses.

HYPOTHESIS: Endolymphatic hydrops in patients diagnosed with Ménière's disease causes changes in the response properties of the basilar membrane that lead to impaired high-pass noise masking of auditory brainstem responses to clicks. BACKGROUND: Ménière's disease is defined as the idiopathic syndrome of endolymphatic (cochlear) hydrops, which is an abnormal increase in the volume of cochlear fluid (endolymph) in the inner ear. Accurate detection and diagnosis are important but difficult because of the lack of sufficiently sensitive tests. METHODS: Two populations were compared: (1) 38 non-Ménière's normal-hearing subjects; and (2) 23 patients who, at the time of testing, continued to have at least three of the four hallmark symptoms (i.e., tinnitus, vertigo, fluctuating hearing loss, and fullness) used in the diagnosis of Ménière's disease. Auditory brainstem responses to clicks presented ipsilaterally with masking noise that was high-pass filtered at various frequencies were recorded. RESULTS: In the Ménière's patients, the masking noise is insufficient such that an undermasked Wave V is still present at a latency similar to that of Wave V in the response to the clicks alone. In the control non-Ménière's normal-hearing subjects, this undermasked component was either absent or significantly delayed because of the masking noise. The difference in the delays between these populations is such that the distributions do not overlap, resulting in 100% sensitivity and 100% specificity. CONCLUSION: This test is able to distinguish objectively active Ménière's disease in individuals and may show promise for tracking changes in the severity of the disease caused by progression or treatment.

The stacked ABR: a sensitive and specific screening tool for detecting small acoustic tumors.

The failure of standard ABR measures to detect small (< or =1 cm) acoustic tumors has led to the use of enhanced magnetic resonance imaging (MRI) as the standard to screen for small tumors. This study investigates the suitability of the stacked ABR as a sensitive screening alternative to MRI for small acoustic tumors (SATs). The objective of the study was to determine the sensitivity and specificity of the stacked ABR technique for detecting SATs. A total of 54 patients with acoustic tumors identified by MRI that were either < or =1 cm in size or undetected by standard ABR methods, irrespective of size, were studied. A control population of 78 nontumor normal-hearing subjects was also tested. For comparison, two standard ABR measures (IT5 and I-V delay) were also analyzed. The stacked ABR demonstrated 95% sensitivity and 88% specificity; 100% sensitivity was obtained at 50% specificity. Standard ABR measures were much poorer in detecting these tumors. In conclusion, the stacked ABR can be used as a sensitive, widely-available, cost-effective, and comfortable tool for screening SATs.