This article is republished with permission of Hearing Review

 

Research | May 2017 Hearing Review

By Gail D. Chermak, PhD, Frank E. Musiek, PhD, and Jeffrey Weihing, PhD

 

There is general scientific agreement on the definition, diagnosis, and treatment of CAPD

Central auditory processing disorder (CAPD) is a complex and evolving subject, but remains a solid diagnostic entity. While there is some variance in diagnostic criteria across US and European professional association guidelines, this simply reflects the need for additional research with participants with confirmed CAPD. A considerable body of research exists demonstrating the efficiency of individual central auditory tests and central auditory test batteries based on performance of individuals with confirmed CANS lesions, including such lesions in children. This article provides information that will assist clinicians in making informed, evidence-based clinical decisions about CAPD.

The recommended practices for diagnosis and intervention for central auditory processing disorder (CAPD) are dynamic, undergoing review and refinement as new research emerges.1 These recommended practices have been developed by consensus groups within the American Academy of Audiology (AAA)2 and the American Speech-Language-Hearing Association (ASHA),3 with careful consideration of the merits of various positions surrounding points of disagreement. Nonetheless, a number of controversial issues continue to appear in the literature. In this article, we present our perspective on a number of these issues, with a focus on the current state of the evidence supporting our viewpoint. Our goal is to provide information that will assist clinicians in making informed, evidence-based clinical decisions.

Research Participants: “Diagnosed with” vs “Suspected of” CAPD

In our view, a number of controversial positions are the result of poorly designed research studies. Several recently published reviews of the literature pertaining to diagnosis and intervention for CAPD in children have reached conclusions critical of the very concept of CAPD, as well as the tools used to diagnose CAPD, and the benefits of auditory training.4-7 We would argue that many of the conclusions reached in these reviews were based on reports that included participants “suspected of CAPD” and/or relied on parent or teacher reports as substitutes for diagnosis based on evidence.8-10 Drawing conclusions based on performance of poorly defined participants poses significant threats to the validity of the research. The results of any study that uses the metric of  “suspected of CAPD” or “listening difficulties” cannot be relied upon, because one cannot be sure whether the participants in the study presented any type of true auditory deficit. Moreover, the participants may have had a wide range of unidentified issues. Efficient (ie, sensitive and specific) clinical tests of auditory processing should be used to clearly define participants and identify and describe known comorbidities so that analyses can be conducted and results interpreted accordingly.11

 

CAPD: An ICD-10 Diagnostic Entity  

A recent opinion article challenged the veracity of CAPD as a diagnostic entity, characterizing it as “ill-defined” and “poorly understood.”4 While there is some disagreement between professional associations in the United States and European associations like the British Society of Audiology (BSA),12 the two major sets of guidelines published by AAA and ASHA present consistent positions and recommendations.2,3 Moreover, CAPD is listed in the ICD-10 under ear diseases (code H93.25) for both acquired and congenital CAPD, which confirms the physiological nature of this disorder and supports the medical necessity for care. Given the inclusion of CAPD in the ICD-10, coupled with a recent US Ninth District Circuit Court precedent-setting ruling13 that children with CAPD are entitled to receive services in schools under the category of “other health impaired” (OHI), and that audiologists are the professionals qualified to diagnose CAPD, the legitimacy of CAPD diagnosis for children is extremely well -supported and established for a population who has long been underserved in our schools, as well as for adults seeking help for CAPD.

 

Behavioral Characteristics of CAPD

Clinicians must be critical of incorrect assertions that CAPD is characterized by inattention, daydreaming, and generalized listening difficulties, and then use those characterizations to argue that these behaviors are more characteristic of other disorders (eg, attention deficit hyperactivity disorder [ADHD]) and not CAPD. In fact, these are not the most common behavioral characteristics of CAPD. Most authors and professional association guidelines place greater emphasis on more specific auditory disorders (in contrast to cognitive issues of inattention and daydreaming) and generalized “listening difficulties.” The most common behavioral characteristics of CAPD are difficulty understanding spoken language in competing message or noise backgrounds, in reverberant acoustic environments, or when rapidly presented; difficulty with similar sounding words; and difficulty following complex auditory directions/commands, among others.2,3,14-16

Clearly, these behaviors are not exclusive to CAPD. This is why one cannot diagnose CAPD on the basis of symptoms reported on questionnaires, and why audiologists must rely on efficient test batteries that are sensitive to the integrity of the central auditory nervous system (CANS), as delineated in the AAA and ASHA guidelines,2,3 and in Musiek and Chermak.17 Moreover, many children referred for CAPD evaluations because of “listening difficulties” actually perform quite well on central auditory processing measures,18,19 such that the use of reports of listening difficulties as a diagnostic marker for CAPD may lead to over-identification and overuse of the diagnostic label. Since central auditory measures show a significant degree of construct validity in neurological models of CAPD, this lack of agreement between observer-report and performance-based measures indicates that subjective report of listening difficulties is not predictive of true CAPD.

 

Causes of CAPD

Analogies have been made comparing CAPD to a broken arm, noting that the broken arm might have been caused by multiple types of accidents, and therefore, one cannot link a particular cause with the particular injury.4 However, brain injury is just one of the etiologies underlying CAPD. CAPD results from a number of issues affecting the CANS: neurological lesions or compromise of the CANS, including neoplasms, neurodegenerative processes (eg, multiple sclerosis, Alzheimer’s),20-22 or impaired cerebral circulation (eg, strokes)23,24; aging/central presbycusis25; noise exposure26; and exposure to neurotoxic chemicals or heavy metals (eg, styrene, lead, mercury).27

In fact, the large majority of children diagnosed with CAPD present neurodevelopmental CAPD (the result of some underlying benign, diffuse neuroanatomic/neuromorphological abnormalities) in the absence of an identifiable underlying neuropathology.28 In these cases, typically there is no identifiable lesion of the CANS and no apparent prenatal or perinatal, disease, injury, or exposure-related explanation for the CAPD.

Injury is not the underlying etiology for a second type of neurodevelopmental CAPD that results from neuromaturational delay, presumed to result from the slower course (delayed) of myelination or from auditory deprivation.29 The broken arm analogy ignores the fact that CAPD arises from a number of etiologies that all impact the CANS.30 Moreover, regardless of the etiology, the broken arm still moves consistent with the same underlying physical principles of movement and function. AAA guidelines2 support the use of an interpretive approach (as commonly used across many disciplines concerned with brain-behavior relationships) when test patterns that have been demonstrated to have good sensitivity and specificity in adults with confirmed CANS lesions23,31-33 are seen in children or older adults presenting that same pattern of test results. While the AAA guidelines2 recognize that an absolute gold standard may never exist due to the heterogeneity of the disorders affecting the CANS, accumulating evidence—including the studies by Boscariol et al34-38 detailed below—provide strong evidence that “structural changes in an area of the brain associated with auditory and language processing can lead to changes in auditory processing, and, therefore, in language and learning, as well.[p 16]”2

 

Minimizing Confounds in Diagnosing CAPD

Any behavioral test, including the pure tone audiogram, imposes some cognitive load (eg, attention, working memory). Although the processing deficits seen in CAPD bidirectionally interact with cognitive (and language) deficits, the functional deficits observed in individuals with CAPD derive from bottom-up (ie, sensory, data-driven) processing deficits.2 This was underscored recently by Gyldenkaerne et al39 who reported that cognitive measures explain only a minority of the variance in auditory processing measures, concluding that poor auditory processing certainly is not the mere reflection of attention deficits. Similarly, Weihing et al40 concluded that central auditory tests are not likely governed by cognition given the results of their factor analysis in which central auditory tests loaded on separate factors, suggesting a unique variance associated with each test. Grant41 reported that the performance of veterans with blast injuries differed from controls on central auditory tests, but not on cognitive tests. To distinguish between two or more conditions presenting with similar symptoms or attributes requires multidisciplinary, comprehensive assessment.

Means to minimize linguistic and cognitive confounds in the diagnosis of CAPD have been described in the literature for almost two decades42 and appear in our textbooks and professional association guidelines.2,3,17 Chermak et al43 reviewed approaches to minimize confounds that include using tests employing nonverbal stimuli (eg, gap detection, frequency and duration patterns, masking level difference), simple speech stimuli (eg, digits), electrophysiological procedures, and multidisciplinary assessment through which information regarding attention, memory, language, etc, is available to help differentiate CAPD from language-based or supramodal cognitive deficits, motor control issues, or learning, and leads to a diagnosis with a high degree of reliability and validity.

Using intra-test comparisons—performance-intensity functions; interaural (laterality) effects; assessing performance in non-manipulated conditions (eg, monaural versus dichotic)—helps to ensure that performance deficits seen on central auditory tests are due to the acoustic manipulations rather than to lack of familiarity with the language and/or significantly reduced memory skills. Moreover, audiologists can minimize confounds by use of central auditory tests less affected by attention in their test batteries.

Attention has relatively little effect on gap detection, as indexed by N1 amplitude. In fact, gap detection can be observed during sleep, as indexed by a large P2 amplitude.44 Gyldenkaerne et al39 reported the absence of significant correlations between sustained attention and masking level differences or the Gaps-In-Noise (GIN) test.45 Similarly, Campbell and Macdonald44 reported weak correlations between sustained auditory attention, dichotic digits, and frequency patterns, accounting for only 8% of shared variance. Based on a factor analysis, Weihing et al40 confirmed that central auditory processing tests load on separate factors when tests are scored using typical clinical conventions (eg, ear specific scoring). Their findings suggest that unique variance is associated with each test, and that central auditory processing tests are not likely governed by one construct (ie, cognition).

Indeed, as established by Brenneman et al,11 the relationship between central auditory tests (or any behavioral measure) and cognitive measures can appear to be stronger than actually is the case when participants with low cognition are not excluded from the analysis. Similarly, inflated cognition effects also can be obtained when participants with unknown cognitive status are included in study samples.9

Moreover, it is clear that CAPD does not merely reflect attention deficits. Abnormal performance on central auditory processing tests often occurs despite sustained attention within normal limits.39 Maturation rates for different auditory tasks are not correlated, as would be expected if nonsensory factors (eg, attention) placed a uniform influence on performance.46 These findings suggest that the extent of cognitive influence on central auditory processing is limited and that cognition does not drive central auditory processing performance.

Other compelling evidence that auditory and cognitive systems are identifiable and can be uniquely assessed include classic disassociation studies showing preservation of P300 in patients with damage to areas of the brain supporting memory, but absence of P300 in patients with lesions of auditory areas of the brain. More evidence is suggested by the reduction of the Na-Pa complex over the involved hemisphere in patients with temporal lobe lesions, but not in patients with cortical lesions not involving the temporal lobes,47-49 as well as auditory training studies that demonstrate improved central auditory processing with no change in memory following head trauma involving the superior temporal gyrus and hippocampus.50

There are reasons, however, to include behavioral measures employing speech stimuli in the CAPD test battery. Speech signals provide access to different CANS processing mechanisms than do non-speech stimuli.51 The degree of temporal processing required for accurate perception of spoken language is significantly greater than required for perception of non-speech sounds; therefore, processing of speech signals may be more vulnerable to disruption by CANS dysfunction.52-55 Central auditory processing deficits may only be revealed with speech tasks.56-58 Moreover, younger subjects may attend less to non-speech tasks which are more abstract than speech tasks, such that non-speech tests might actually inject the confound of attention. The upshot is that the CANS is the channel used to process speech and other acoustic signals, which is why speech and speech-in-noise tests are used in audiological evaluations and hearing aid evaluations.

 

 

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CORRESPONDENCE can be addressed to HR or Dr. Chermak at: chermak@wsu.edu

 

About the Authors

Gail Chermak, PhD, is Professor of Audiology and Chair of the Department of Speech and Hearing Sciences, Elson S. Floyd College of Medicine, Washington State University Health Sciences Spokane; Frank E. Musiek, PhD, is a Professor in the Department of Speech, Language, Hearing Sciences at the University of Arizona; and Jeffrey Weihing, PhD, is an Assistant Professor in the School of Medicine at the University of Louisville.

Citation for this article. Chermak GD, Musiek FE, Weihing J. Beyond controversies: The science behind central auditory processing disorder. Hearing Review. 2017;24(5):20-24.

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