Cochlear Loss Research Articles

A Modelling Study on the Comparison of Predicted Auditory Nerve Firing Rates for the Personalized Indication of Cochlear Implantation

The decision of whether to perform cochlear implantation is crucial because implantation cannot be reversed without harm. The aim of the study was to compare model-predicted time–place representations of auditory nerve (AN) firing rates for normal hearing and impaired hearing with a view towards personalized indication of cochlear implantation. AN firing rates of 1024 virtual subjects with a wide variety of different types and degrees of hearing impairment were predicted. A normal hearing reference was compared to four hearing prosthesis options, which were unaided hearing, sole acoustic amplification, sole electrical stimulation, and a combination of the latter two. The comparisons and the fitting of the prostheses were based on a ‘loss of action potentials’ (LAP) score. Single-parameter threshold analysis suggested that cochlear implantation is indicated when more than approximately two-thirds of the inner hair cells (IHCs) are damaged. Second, cochlear implantation is also indicated when more than an average of approximately 12 synapses per IHC are damaged due to cochlear synaptopathy (CS). Cochlear gain loss (CGL) appeared to shift these thresholds only slightly. Finally, a support vector machine predicted the indication of a cochlear implantation from hearing loss parameters with a 10-fold cross-validated accuracy of 99.2%.

Emissões otoacústicas evocadas na doença de Ménière

ABSTRACT Purpose To verify the responses of Evoked Otoacoustic Emissions by transient stimulus and distortion product in individuals with Ménière’s Disease. Methods Cross-sectional study with a sample composed of 60 individuals, aged 19 to 75 years, divided into two groups: study group, with 32 individuals with a medical diagnosis of Ménière’s disease, without other risks and a control group formed by 28 individuals with cochlear loss without Meniere’s disease, age and sex matched to the study group. Eligibility criteria: type A curve, without conductive or mixed loss or suspected retrocochlear alteration. The audiological evaluation consisted of anamnesis, inspection of the external acoustic meatus, pure tone audiometry, logoaudiometry, measures of acoustic immittance and transient evoked otoacoustic emissions and distortion product. Results Individuals with Ménière’s disease had a higher occurrence of unilateral hearing loss, low pitch tinnitus, vertigo and ear fullness in relation to the control. In these individuals, there was greater incompatibility between the results of OAE and pure tone audiometry: in unilateral hearing loss, alterations in OAE were observed in ears with normal hearing thresholds on the contralateral side, characterizing cochlear dysfunctions. In the ears with cochlear loss, there was the presence of TEOAE and absence of DPOAE, in contrast to the control group, which showed the absence of TEOAE and DPOAE, as expected in cochlear losses of other etiologies. Conclusion The investigation of emissions in Ménière’s disease identified cochlear dysfunction in the contralateral ear in unilateral cases and the presence of TOAE with absence of DPOAE in ears with hearing loss, differentiating from cochlear losses of other etiologies.

Conductive hearing loss during development does not appreciably alter the sharpness of cochlear tuning

An increasing number of studies show that listeners often have difficulty hearing in situations with background noise, despite normal tuning curves in quiet. One potential source of this difficulty could be sensorineural changes in the auditory periphery (the ear). Signal in noise detection deficits also arise in animals raised with developmental conductive hearing loss (CHL), a manipulation that induces acoustic attenuation to model how sound deprivation changes the central auditory system. This model attributes perceptual deficits to central changes by assuming that CHL does not affect sensorineural elements in the periphery that could raise masked thresholds. However, because of efferent feedback, altering the auditory system could affect cochlear elements. Indeed, recent studies show that adult-onset CHL can cause cochlear synapse loss, potentially calling into question the assumption of an intact periphery in early-onset CHL. To resolve this issue, we tested the long-term peripheral effects of CHL via developmental bilateral malleus displacement. Using forward masking tuning curves, we compared peripheral tuning in animals raised with CHL vs age-matched controls. Using compound action potential measurements from the round window, we assessed inner hair cell synapse integrity. Results indicate that developmental CHL can cause minor synaptopathy. However, developmental CHL does not appreciably alter peripheral frequency tuning.

Neuroplastic changes in auditory cortex induced by long-duration “non-traumatic” noise exposures are triggered by deficits in the neural output of the cochlea

Long-term exposure to moderate intensity noise that does not cause measureable hearing loss can cause striking changes in sound-evoked neural activity in auditory cortex. It is unclear if these changes originate in the cortex or result from functional deficits in the neural output of the cochlea. To explore this issue, rats were exposed for 6-weeks to 18–24 kHz noise at 45, 65 or 85 dB SPL and then compared the noise-induced changes in the cochlear compound action potential (CAP) with the neurophysiological alterations in the anterior auditory field (AAF) of auditory cortex. The 45-dB exposure, which had no effect on the cochlear CAP also had no effect on the AAF. In contrast, the 85-dB exposure greatly reduced CAP amplitudes at high frequencies, but had little or no effect on low frequencies. Despite the large reduction in high-frequency CAP neural responses, high frequency AAF neural responses (spike rate and local field potential amplitude) remained largely within normal limits, evidence of central gain compensation. AAF responses were also enhanced at the low frequencies even though CAP responses were normal; this AAF hyperactivity only occurred at low-moderate intensities (level-dependent enhanced central gain). The 65-dB exposure also caused a moderate reduction in high-frequency CAP amplitudes. Notwithstanding this cochlear loss, AAF responses were boosted into the normal range, evidence of homeostatic gain compensation. Our results suggest that the noise-induced neuroplastic changes in the auditory cortex from so-called “non-traumatic” exposures are triggered from functional deficits in the neural output of the cochlea.

Recent Advances in Understanding Audiovestibular Loss of a Vascular Cause.

Acute audiovestibular loss is characterized by abrupt onset of prolonged (lasting days) vertigo and hearing loss. Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) is known to be the leading cause of acute audiovestibular loss. So far, eight subgroups of AICA territory infarction have been identified according to the patterns of audiovestibular dysfunctions, among which the most common pattern is the combined loss of auditory and vestibular functions. Unlike inner ear dysfunction of a viral cause, which can commonly present as an isolated vestibular (i.e., vestibular neuritis) or cochlear loss (i.e., sudden deafness), labyrinthine dysfunction of a vascular cause rarely results in isolated loss of vestibular or auditory function. As audiovestibular loss may precede the central symptoms or signs of an ischemic stroke in the posterior circulation, early diagnosis and proper management of audiovestiubular loss may provide a window to prevent the progression of infarction to larger areas of the posterior circulation. A clinician should consider the possibility that acute audiovestibular loss may herald impending AICA territory infarction, especially when patients have basilar artery occlusive disease close to the origin of the AICA on brain MRA. This review aims to highlight the recent advances in understanding audiovestibular loss of a vascular cause and to address its clinical significance.

On the Interplay Between Cochlear Gain Loss and Temporal Envelope Coding Deficits.

Hearing impairment is characterized by two potentially coexisting sensorineural components: (i) cochlear gain loss that yields wider auditory filters, elevated hearing thresholds and compression loss, and (ii) cochlear neuropathy, a noise-induced component of hearing loss that may impact temporal coding fidelity of supra-threshold sound. This study uses a psychoacoustic amplitude modulation (AM) detection task in quiet and multiple noise backgrounds to test whether these aspects of hearing loss can be isolated in listeners with normal to mildly impaired hearing ability. Psychoacoustic results were compared to distortion-product otoacoustic emission (DPOAE) thresholds and envelope-following response (EFR) measures. AM thresholds to pure-tone carriers (4 kHz) in normal-hearing listeners depended on temporal coding fidelity. AM thresholds in hearing-impaired listeners were normal, indicating that reduced cochlear gain may counteract how reduced temporal coding fidelity degrades AM thresholds. The amount with which a 1-octave wide masking noise worsened AM detection was inversely correlated to DPOAE thresholds. The narrowband noise masker was shown to impact the hearing-impaired listeners more so than the normal hearing listeners, suggesting that this masker may be targeting a temporal coding deficit. This study offers a window into how psychoacoustic difference measures can be adopted in the differential diagnostics of hearing deficits in listeners with mixed forms of sensorineural hearing loss.

Gene and drug delivery system and potential treatment into inner ear for protection and regeneration.

The most common type of hearing loss results from damage to the cochlea including lost hair cells (HCs) and spiral ganglion neurons (SGNs). In mammals, cochlear HC loss causes irreversible hearing impairment because this type of sensory cell cannot regenerate. The protection from SGN from degeneration has implications for cochlear implant to patients with severe deafness. This review summarizes the several treatments for HC regeneration based on experiments. We discuss how transgene expression of the neurotrophic factor can protect SGN from degeneration and describe potential new therapeutic interventions to reduce hearing loss. We also summarized viral vectors and introduced the gene and drug delivery system for regeneration and protection of cochlear HCs. Finally, we introduce the novel endoscopy we developed for local injection into cochlea.

Alterações auditivas associadas a complicações e comorbidades no diabetes mellitus tipo 2

OBJETIVO: Investigar a presença de alterações auditivas, representadas por diminuição do limiar audiométrico e/ou ausência de emissões otoacústicas, associadas às características gerais, complicações crônicas e comorbidades em pacientes com diabetes tipo 2. MÉTODOS: Estudo realizado em unidade de atenção secundária, em Fortaleza, de abril a julho de 2010. Amostra de 152 pacientes de 36 a 60 anos de idade, portadores de diabetes tipo 2. Analisou-se dados clínicos relacionados ao diabetes e à avaliação audiológica, composta por audiometria tonal liminar, emissões otoacústicas evocadas por estímulo transiente e emissões otoacústicas evocadas produto de distorção. RESULTADOS: O gênero feminino predominou, com 95 (62,5%) pacientes. A média de idade foi 53,4 anos. Verificou-se perda auditiva sensorioneural em 96 (63,2%) pacientes, sendo a maioria perda coclear (83,3%). Cento e catorze pacientes (75%) apresentaram ausência de emissões transientes e 120 (78,9%), ausência de emissões produto de distorção. Os homens diabéticos demonstraram 4,4 vezes mais chance de perda auditiva que as mulheres. Quanto maior o tempo da doença, maior a probabilidade de perda auditiva. Os pacientes diabéticos acima de 50 anos também apresentaram maior chance para perda auditiva. CONCLUSÃO: Das comorbidades e complicações associadas ao diabetes, o sobrepeso/obesidade constitui fator de risco para alteração auditiva, estando associado à perda auditiva e ausência de emissões transientes. Os pacientes diabéticos com sobrepeso/obesidade apresentaram três vezes mais chances de alterações na audiometria e emissões otoacústicas.

Vowel Identification by Amplitude and Phase Contrast

Vowel identification is largely dependent on listeners' access to the frequency of two or three peaks in the amplitude spectrum. Earlier work has demonstrated that, whereas normal-hearing listeners can identify harmonic complexes with vowel-like spectral shapes even with very little amplitude contrast between "formant" components and remaining harmonic components, listeners with hearing loss require greater amplitude differences. This is likely the result of the poor frequency resolution that often accompanies hearing loss. Here, we describe an additional acoustic dimension for emphasizing formant versus non-formant harmonics that may supplement amplitude contrast information. The purpose of this study was to determine whether listeners were able to identify "vowel-like" sounds using temporal (component phase) contrast, which may be less affected by cochlear loss than spectral cues, and whether overall identification improves when congruent temporal and spectral information are provided together. Five normal-hearing and five hearing-impaired listeners identified three vowels over many presentations. Harmonics representing formant peaks were varied in amplitude, phase, or a combination of both. In addition to requiring less amplitude contrast, normal-hearing listeners could accurately identify the sounds with less phase contrast than required by people with hearing loss. However, both normal-hearing and hearing-impaired groups demonstrated the ability to identify vowel-like sounds based solely on component phase shifts, with no amplitude contrast information, and they also showed improved performance when congruent phase and amplitude cues were combined. For nearly all listeners, the combination of spectral and temporal information improved identification in comparison to either dimension alone.

Evidence for basal distortion-product otoacoustic emission components

Distortion-product otoacoustic emissions (DPOAEs) were measured with traditional DP-grams and level/phase (L/P) maps in rabbits with either normal cochlear function or unique sound-induced cochlear losses that were characterized as either low-frequency or notched configurations. To demonstrate that emission generators distributed basal to the f(2) primary-tone contribute, in general, to DPOAE levels and phases, a high-frequency interference tone (IT) was presented at 1/3 of an octave (oct) above the f(2) primary-tone, and DPOAEs were re-measured as "augmented" DP-grams (ADP-grams) and L/P maps. The vector difference between the control and augmented functions was then computed to derive residual DP-grams (RDP-grams) and L/P maps. The resulting RDP-grams and L/P maps, which described the DPOAEs removed by the IT, supported the notion that basal DPOAE components routinely contribute to the generation of standard measures of DPOAEs. Separate experiments demonstrated that these components could not be attributed to the effects of the 1/3-oct IT on f(2), or DPOAEs generated by the addition of a third interfering tone. These basal components can "fill in" the lesion estimated by the commonly employed DP-gram. Thus, ADP-grams more accurately reveal the pattern of cochlear damage and may eventually lead to an improved DP-gram procedure.

The Complexity of Auditory Aging

Age-related decline in hearing is the result of complex changes in audibility, suprathreshold processing, and cognition. Changes in cochlear structures, whether from biological aging of the structures themselves or secondary to intrinsic and extrinsic influences that occur with the passage of time, result in hearing sensitivity loss. The outward expression of the underlying disorder is fairly consistent. That is, loss of function of cochlear hair cells and other structures consistently manifest hearing sensitivity loss and the consequent deficits in audibility. Age-related changes in auditory nervous system structures may also play a role in overall hearing capability, although the outward expression of the disorder is likely to be subtler than cochlear loss in a given individual and considerably more variable among individuals. Regardless, the complex hearing disorder associated with the aging process can have a significant impact on overall wellness. This review article provides an overview of aging and age-related decline in audition, with an emphasis on speech perceptual deficits with aging.

Enhanced cochlear acoustic sensitivity and susceptibility to endotoxin are induced by adrenalectomy and reversed by corticosterone supplementation in rat

Glucocorticoid receptors are widely distributed in the cochlea but their role remains poorly known. Previous studies provided contradictory reports on a possible cochlear acoustic hypersensitivity induced by adrenal insufficiency, while several experiments agree on a significant action of glucocorticoid receptors in adverse conditions such as acoustic trauma and restraint stress. The present experiments confirmed a cochlear acoustic hypersensitivity induced by adrenalectomy and reversed by corticosterone supplementation. These observations point to a significant role of corticosteroids in basal cochlear functioning. The glucocorticoids are known to be essential for limiting and resolving inflammatory processes. The endotoxin Escherichia coli lipopolysaccharide is widely used to induce inflammatory reactions. However, in various organs several toxic processes of this endotoxin are not influenced by glucocorticoids. From previous experiments on the cochlea there is no evidence that glucocorticoids are an essential factor against endotoxin cochlear toxicity. In the present experiments it was found that adrenalectomy greatly increased the cochlear susceptibility to endotoxin; the effect was reversed by providing corticosterone supplementation. This shows the essential role of corticosterone in this cochlear inflammation model. In previous studies local administration (at the cochlear base) of endotoxin was used and losses of cochlear acoustic sensitivity were found predominantly at high frequencies; in contrast, the systemic injection used in this study produced a cochlear loss of acoustic sensitivity at all frequencies, indicating a uniform cochlear sensitivity to the toxic effects of endotoxin.

Effects of cochlear hearing loss on perceptual grouping cues in competing-vowel perception

This study compared how normal-hearing listeners (NH) and listeners with moderate to moderately severe cochlear hearing loss (HI) use and combine information within and across frequency regions in the perceptual separation of competing vowels with fundamental frequency differences (deltaF0) ranging from 0 to 9 semitones. Following the procedure of Culling and Darwin [J. Acoust. Soc. Am. 93, 3454-3467 (1993)], eight NH listeners and eight HI listeners identified competing vowels with either a consistent or inconsistent harmonic structure. Vowels were amplified to assure audibility for HI listeners. The contribution of frequency region depended on the value of deltaF0 between the competing vowels. When deltaF0 was small, both groups of listeners effectively utilized deltaF0 cues in the low-frequency region. In contrast, HI listeners derived significantly less benefit than NH listeners from deltaF0 cues conveyed by the high-frequency region at small deltaF0's. At larger deltaF0's, both groups combined deltaF0 cues from the low and high formant-frequency regions. Cochlear impairment appears to negatively impact the ability to use F0 cues for within-formant grouping in the high-frequency region. However, cochlear loss does not appear to disrupt the ability to use within-formant F0 cues in the low-frequency region or to group F0 cues across formant regions.

A pilot case control follow-up study on hearing in children treated with tobramycin in the newborn period

Objective: To assess the occurrence of hearing loss in children due to neonatal exposure to long courses of tobramycin and/or high tobramycin serum concentrations. Methods: This was a pilot case–control study in 3–4-year old children. Data on tobramycin administration were abstracted from the patient files of an earlier study. Patients exposed in the neonatal period to either long courses (>7 days) or high serum concentrations of tobramycin constituted the study group. The control group consisted of patients without tobramycin exposure. Patients were matched for other risk factor according to criteria of the joint committee on infant hearing. All patients underwent the following investigations: otoscopy and pneumatic otoscopy, followed by impedance audiometry, to exclude middle ear effusion. Click-evoked oto-acoustic emissions (ce-OAE) as well as distortion product oto-acoustic emissions (dp-OAE), tested at f2 frequencies ranging from 1 to 10 kHz, were measured to assess hearing. All patients with abnormal ce-OAE results underwent brainstem electric response audiometry (BERA) as well. Since aminoglycoside ototoxicity is usually bilateral, results were compared per patient and not per ear. Results: A total of 29 patients were tested. Eleven patients were excluded due to middle ear effusion. Data for 18 patients were analyzed. In the tobramycin treated group ( n=9) both ce-OAE and dp-OAE (at all tested frequencies) were not detectable in six ears of three patients. All other patients had normal ce-OAE's as well as normal dp-OAE's in this frequency range. Difference between the tobramycin treated and control group for OAE as well as dp-OAE showed a trend ( P=0.08). In all three patients with undetectable emissions BERA confirmed a cochlear loss of 60–70 dB at 3 kHz in both ears. These three patients had the longest total exposure to tobramycin: 20–24 days and 84–92 mg/kg, respectively. No relation to either peak or trough serum concentrations could be detected. Conclusion: There was no statistical relation between hearing loss and tobramycin exposure, probably due to sample size. Our results do indicate a need for a case–control follow-up study of hearing in neonates exposed to long courses of aminoglycosides.

It’s not your father’s recruitment: A new view of loudness growth in cochlear hearing loss

For over 60 years, one of the most commonly held beliefs in audiology has been that loudness grows more rapidly than normal near the elevated thresholds of listeners with cochlear hearing losses. This belief was based on the untested assumption that loudness at threshold is the same—often incorrectly assumed to be zero—in normal listeners and listeners with cochlear hearing losses. Recent tests of this assumption indicate that loudness at threshold is not zero in either group of listeners. These data also indicate that loudness near threshold grows at a normal rate in listeners with cochlear hearing losses. In other words, recruitment in the sense of a rapid growth of loudness near an elevated threshold does not occur. How, then, can intense sounds have approximately normal loudness in listeners with cochlear hearing losses? The explanation is that loudness at threshold is greater when the threshold is elevated by a cochlear loss than when it is normal. We call this softness imperception. Therefore, listeners with cochlear hearing losses not only have reduced dynamic range of audibility; they also have reduced dynamic range of loudness. Implications for the design of hearing aids will be discussed. [Work supported by NIH/NIDCD grant R01DC02241.]

Gap duration discrimination in listeners with cochlear hearing loss: effects of gap and marker duration, frequency separation, and mode of presentation.

This study examined the effects of cochlear hearing loss on gap duration discrimination (GDD), with particular interest in whether cochlear hearing loss results in increased difficulty for across-channel temporal judgments. The hypothesis being tested was that listeners with cochlear loss would perform as well as normal-hearing listeners for all within-channel conditions but would exhibit relatively greater performance deficits in the across-channel conditions. A subsidiary aim was to determine whether, in normal-hearing listeners, the across-channel effects previously observed for minimal-duration standard gaps also existed for relatively long standard gaps. Two experiments were undertaken, one dealing with monaural conditions and one dealing with dichotic conditions. The monaural results indicated that across-frequency GDD was poorer than isofrequency GDD, even for the longer gap durations of 35 and 250 ms examined here. However, the results showed no effect of hearing loss on GDD. Rather, GDD appeared to be sensitive to listener age, with younger listeners showing better performance in both within-channel and across-channel conditions. In addition, both within-channel and across-channel performance was sensitive to the duration of the leading gap marker. Finally, the pattern of dichotic "across-ear" performance was similar, but not equivalent, to that of monaural across-frequency performance.

Long-term follow-up of transtympanic gentamicin for Ménière's syndrome.

Recent studies have shown that transtympanic gentamicin for Ménière's syndrome is effective. Current treatment protocols vary. One concept has been to perform a chemical ablation; the other has been to perform a chemical alteration. Ablation requires multiple injections and is effective in controlling the vertigo, but it is associated with a significant incidence of hearing loss. Chemical alteration uses a minimal dose to reduce vestibular function without affecting cochlear function. Prospective. Tertiary medical center. Patients had classic unilateral Ménière's syndrome that was unresponsive to medical therapy. A single injection of gentamicin is given, and the patient is seen 1 month after injection. If indicated, the patient receives another injection and is reevaluated 1 month later. Control of vertigo and maintenance of hearing using the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) guidelines (1995). Fifty-six patients have documented follow-up for 2 years or more, and 21 have 4 years or more of follow-up. This article presents the 4-year results as outlined by the AAO-HNS guidelines. Vertigo classes A and B were seen in 82% of patients. The patients followed 2 to 4 years had 86% vertigo class A and B results. Those followed 4 years or more show 76% with a vertigo class A or B result. In this study there has been minimal cochlear loss. There was vestibular change clinically, which was documented by electronystagmography. It appears that a single transtympanic gentamicin injection is effective in controlling the vertigo of Ménière's syndrome. Cochlear impact has been minimal. It is most useful for those patients who have failed medical management and are severely affected but not totally incapacitated by the disease.

A study of the effects of cochlear loss on the auditory brainstem response (ABR) specificity and false positive rate in retrocochlear assessment.

The auditory brainstem response (ABR) test is widely used as a screen for retrocochlear dysfunction in individuals suffering idiopathic auditory and vestibular disturbance. Although its sensitivity for lesions of the lower brainstem is well established, hearing loss is known to have significant effects upon the test's specificity and false positive rate. This study analysed the effects of aspects of cochlear hearing loss including level, slope and general audiogram shape on these properties of the ABR test in a large clinical group. The study comprised 306 patients (153 male, 153 female) referred for ABR screening to exclude retrocochlear dysfunction. Of 566 ears meeting the inclusion criteria, 85 (15 per cent) failed the test. On follow-up eight ears (3 per cent) were confirmed to have some form of retrocochlear abnormality, seven of which were pathological. All had abnormal ABR results. No cases of retrocochlear abnormality were found in the ABR pass group. In those patients diagnosed as free of retrocochlear problems, the importance of the I-V interval as a primary index of function was confirmed. It displayed a high specificity (>90 per cent) which was largely independent of the level or slope of high-frequency hearing loss. In contrast wave V specificity decreased with increasing loss and increasing slope. Its value as a functional index was limited with losses greater than 70 dB HL in whom specificity fell below 70 per cent. The study concluded that, despite reducing interval availability above 60 dB HL, wave V latency cannot be used as an alternative index because it displays weakening specificity over this range of loss. With the problems inherent in applying latency corrections, the author advocates the use of improved procedures for wave I identification in these cases.

Cochlear Neuronal Loss as Determined by Use of a Neurofilament Protein Antibody in Cases of Bilateral Profound Deafness

The temporal bones of two patients with profound bilateral deafness from infancy were studied immunohistochemically, using a neurofilament protein antibody to detect the cochlear neuronal elements. One patient exhibited Mondini dysplasia of the inner ear, with the organ of Corti almost completely deteriorated. The other patient is the first reported case involving complete aplasia of the organ of Corti in all turns. In both cases, the immunohistochemical staining clearly revealed a severe reduction in the number of afferent neurons, such as dendrites, spiral ganglion cells and cochlear axons. The number of efferent spiral bundles in the osseous spiral lamina and intraganglionic portion also decreased in parallel with the reduction in the number of cochlear afferent neurons. Our results are inconsistent with previously reported cases of presbycusis and acquired deafness induced by the measles virus, in which efferent neurons were preserved while afferent neurons degenerated. The loss of both the efferent and afferent neurons might be characteristics of congenital deafness.

Further effects of cochlear loss on ICP loudness adaptation, and loudness constancy

ICP loudness adaptation depends on an ipsilateral comparison paradigm with a short increasing or decreasing referent value to reveal loudness adaptation. Janson et al. [Br. J. Audiol. 29, 288–297 (1996)] found the intensity-based function for ICP loudness adaptation for those with a high-frequency loss differed significantly from normal listeners. Loss of loudness constancy in normal listeners was consistent, loss in those with a cochlear loss showed a negative progression as intensity increased, as if it were the inverse of recruitment. The purpose of the present study was to compare ICP adaptation to recruitment. ICP adaptation and recruitment were tested in ten high-frequency loss (probably noise induced) and ten age-matched normal hearing individuals. Although the evidence for recruitment was generally found in those with hearing loss, there was no simple relationship to ICP adaptation. Variation among measures of recruitment, implications of abnormal loudness constancy for speech perception, and the possible use of measures of otoacoustic emissions for future studies will be discussed.