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 the performance of poorly defined participants pose 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 for 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 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 the 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