CAPD: The Most Common ‘Hidden Hearing Loss’: Central auditory processing disorder—and not cochlear synaptopathy—is the most likely source of difficulty understanding speech in noise (despite normal audiograms).
Publication: The ASHA Leader
Volume 23, Number 3
Pages 6-9
Recently, there’s been growing use of the term hidden hearing loss (HHL) to describe difficulty understanding speech in noise despite normal audiograms.
For example, The ASHA Leader recently explored what might underlie the phenomenon. And in the journal Hearing Research in 2017, Charles Liberman and Sharon Kujawa wrote that HHL results from cochlear synaptopathy, or the loss of afferent fiber communication at the inner hair cell ribbon synapse.
It is our position, however, that central auditory processing disorder (CAPD) is the most likely source of hidden hearing loss. CAPD results from deficits in perceptual processing of auditory stimuli in the central nervous system. It is characterized by difficulty recognizing speech in noise despite normal pure-tone thresholds.
We base our assertion on the frequency of adults with central auditory nervous system pathology and children with CAPD and learning problems who struggle with understanding speech in noise despite normal pure-tone audiograms (for example, this article from the International Journal of Audiology, and other studies). There are also other disorders involving auditory dysfunction not accurately revealed by the pure-tone audiogram. These include pure word (central) deafness and some eighth-nerve disorders.
Here we provide an overview of the limits of the pure-tone audiogram, the origins of HHL, and possible clinical correlates of cochlear synaptopathy. We also consider using the central auditory test battery to identify the source of speech-recognition-in-noise difficulties not revealed by the pure-tone audiogram.
Audiogram limits
There is little debate that the audiogram is the hallmark measure used to assess hearing loss. However, it is severely limited in its ability to provide information with respect to auditory function beyond sensitivity. As documented by Ettore Bocca and colleagues in the 1950s (see sources below), patients with significant central auditory dysfunction can present with normal audiograms.
People can even render normal audiometric thresholds when there’s clear damage to the cochlea and auditory nerve fibers. As explained by Sharon Kujawa and M. Charles Liberman in 2009 (see sources), these cases may be due to compromise of inner hair cells that respond to supra-threshold stimuli, but do not contribute to threshold detection. Thus, their loss does not elevate thresholds.
This finding has led to use of the term HHL. However, the evidence for this condition in humans is controversial (see sources). What is not controversial, however, is that:
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Hearing thresholds do not necessarily indicate normal hearing, as many patients are often incorrectly counseled.
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If the term HHL is used clinically, the best example (too often overlooked) is CAPD. And, as identified with appropriate and efficient tools, CAPD may not be truly hidden.
Animal versus human studies
Animal studies indicate a link between noise exposure and isolated cochlear nerve degeneration. As Sharon Kujawa and M. Charles Liberman reported in 2006 (see sources), at 24 hours post-noise exposure, adult mice showed elevated thresholds of (high-frequency) neural responses and of distortion product otoacoustic emissions (DPOAEs). They also had preserved outer and inner hair cells, despite degeneration of inner hair cell synapses at high-frequency cochlear areas.
Eight weeks later, DPOAEs had fully recovered, while the amplitudes of the auditory brain stem response (ABR) and the compound action potential remained depressed, with a persistent loss of high-frequency cochlear neuron terminals that dramatically deteriorated a year later. The researchers suggested that glutamate excitotoxicity is responsible for this noise-induced cochlear synaptopathy that affects high-threshold, low-spontaneous rate fibers.
Evidence of cochlear synaptopathy in humans after noise exposure or with aging remains inconclusive. Roland Schaette and David McAlpine proposed in 2011 that cochlear synaptopathy and deafferentation lead to increased central gain in the brainstem and the tinnitus percept. However, their findings of reduced ABR wave I with preserved wave V amplitude in normal-hearing females with tinnitus have not been consistently replicated.
For example, Garreth Prendergast and colleagues’ 2017 detailed study of 138 normal-hearing adults with moderate noise exposure history did not reveal any strong correlation between noise exposure or electrophysiological indexes of synaptopathy and psychoacoustic tasks. One of the authors, Doris-Eva Bamiou, audited 25 consecutive people with speech-in-noise deficits and found no alteration of ABR wave I. Although cochlear synaptopathy has been reported in human temporal bones of older adults, evidence from psychoacoustic studies is only emerging (see sources).
These data and other human clinical data indicate that HHL due to cochlear synaptopathy does not seem to have a strong clinical correlate. Moreover, the data are consistent with Andrew J. Oxenham’s 2016 signal detection model that predicts psychoacoustic performance will be affected only in the presence of a severe degree of synaptopathy.
It is imperative that audiologists go beyond the basic audiological evaluation to determine the true source of “hidden” hearing loss.
Central auditory processing test battery
There are no commonly used clinical tools to identify HHL. By contrast, central auditory deficits and associated symptoms hidden by normal pure-tone thresholds can be revealed by a number of sensitized behavioral (and electrophysiological) tests (see graphic at left). Results of these measures often correspond to the patient’s symptoms and provide a basis for differential diagnosis and treatment. They also provide a vehicle to move audiology beyond the limitations of the pure-tone audiogram to accurately reflect the integrity of the entire peripheral and central auditory system.
Three central test procedures—gap detection, pattern perception and dichotic listening—show documented value in defining deficits of the central auditory nervous system (CANS) despite the presence of normal pure-tone thresholds. These test procedures uncover HHL linked to neurological compromise of the CANS—an important but often overlooked clinical population. Here’s a closer look at these tests:
Gap detection tests. Studies show that this measure of temporal resolution is a strong indicator of central auditory dysfunction related to neurological disorders (see sources). A study by Frank Musiek and colleagues in 2005 revealed significant gap detection performance differences between control participants and people with strokes and temporal lobe epilepsy involving auditory central auditory regions.
Frequency and duration pattern tests. These temporal processing tests also separate control participants from those with neurologically based auditory disorders, according to research Musiek conducted with colleagues in 1990 (see sources).
Dichotic listening tests. In a 1997 paper, Musiek and Raymond M. Hurley demonstrated that dichotic listening procedures also are sensitive to central auditory dysfunction secondary to neurological insult. Participants in these studies and others have presented with essentially normal pure-tone thresholds, despite rather marked auditory deficits, consistent with symptoms presented by patients diagnosed with CAPD.
Further research is needed to determine the role of cochlear synaptopathy in human hearing loss. Audiologists will continue to see patients with complaints of difficulty understanding speech in background noise despite essentially normal pure-tone audiograms. It is imperative that audiologists go beyond the basic audiological evaluation to determine the true source of this “hidden” hearing loss. This requires using sensitive central auditory tests to determine the integrity of the central auditory system and apply appropriate treatment.
Additional CAPD Resources
ASHA CAPD Practice Portal Page
This newly launched online page provides one-stop access to information, evidence and resources on CAPD, and also offers tools, templates and patient/client handouts.
Audiology 2018: Central Auditory Processing Disorders
In this online conference, presenters examine the complexities of CAPD: selecting evidence-based measures for evaluation, interpreting results accurately, and developing useful and specific recommendations for intervention to achieve functional outcomes. Registration opens in July for this Oct. 10–22 event.
ASHA CAPD Evidence Map
This online tool is designed to help clinicians make evidence-based decisions. It includes external scientific evidence, clinical expertise and client perspectives, and provides current information related to assessment, treatment and service delivery.
Sources
American Academy of Audiology (AAA). Guidelines for the Diagnosis, Treatment, and Management of Children and Adults with Central Auditory Processing Disorder. Available at: https://www.audiology.org/publications-resources/document-library/central-auditory-processing-disorder
American Speech-Language-Hearing Association. (Central) Auditory Processing Disorders [Technical Report]. 2005. Available at http://www.asha.org/policy/TR2005-00043/
Bamiou, D. E., Iliadou, V. V, Zanchetta, S., & Spyridakou, C. (2015) What can we learn about auditory processing from adult hearing questionnaires? Journal of the American Academy of Audiology, 26(10), 824–837.
Bamiou, D. E., Werring, D., Cox, K., Stevens J., Musiek F. E., Brown M. M., & Luxon, L. M. (2012). Patient-reported auditory functions after stroke of the central auditory pathway. Stroke, 43(5), 1285–1289.
Bocca, E., Calearo, C., & Cassinari, V. (1954) A new method for testing hearing in temporal lobe tumours; Preliminary report. Acta Oto-Laryngologica, 44(3), 219.
Bocca, E., Calearo, C., Cassinari, V., & Migliavacca, F. (1955) Testing” cortical” hearing in temporal lobe tumours. Acta Oto-Laryngologica, 45(4), 289.
Hind, S. E., Haines-Bazrafshan, R., Benton, C. L., Brassington, W., Towle, B., & Moore, D. R. (2011) Prevalence of clinical referrals having hearing thresholds within normal limits. International Journal of Audiology, 50(10), 708–716.
Hurley, R., & Musiek, F. (1997). Effectiveness of three central auditory processing (CAP) tests in identifying cerebral lesions. Journal of the American Academy of Audiology, 8, 257–262.
Kujawa, S. G., & Liberman, M. C. (2006). Acceleration of age-related hearing loss by early noise exposure: Evidence of a misspent youth. Journal of Neuroscience, 26(7), 2115–2123.
Kujawa, S. G., & Liberman, M. C. (2009). Adding insult to injury: Cochlear nerve degeneration after “temporary” noise-induced hearing loss Journal of Neuroscience, 29(45), 14077–14085
Liberman, M. C., 7 Kujawa, S. G. (2017). Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms. Hearing Research, 349,138–147.
Musiek, F., Baran, J., & Pinheiro, M. (1990). Duration pattern recognition in normal subjects and patients with cerebral and cochlear lesions. Audiology, 29, 304–313.
Musiek, F., Shinn, J., Jirsa, R., Bamiou, D., Baran, J., & Zaidan, E. (2005) The GIN (Gaps in Noise) test performance in subjects with and without confirmed central auditory nervous system involvement, Ear & Hearing, 26, 608–618.
Oxenham, A. J. (2106). Predicting the perceptual consequences of hidden hearing loss. Trends in Hearing, 20:2331216516686768.
Prendergast, G., Guest, H., Munro, K. J., Kluk, K., Léger, A., Hall, D. A., … Plack, C. (2017). Effects of noise exposure on young adults with normal audiograms I: Electrophysiology. Hearing Research, 344, 68–81.
Prendergast, G., Millman, R. E., Guest H., Munro K. J., Kluk K., Dewey R. S., … Plack C. (2017). Effects of noise exposure on young adults with normal audiograms II: Behavioral measures. Hearing Research, 356, 74–86.
Schaette, R., & McAlpine, D. (2011). Tinnitus with a normal audiogram: physiological evidence for hidden hearing loss and computational model. The Journal of Neuroscience, 31(38), 13452–13457.
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