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International Journal of Audiology 2013; 52: 3–13 Discussion Paper Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. Evolving concepts of developmental auditory processing disorder (APD): A British Society of Audiology APD Special Interest Group ‘white paper’ David R. Moore*, Stuart Rosen†, Doris-Eva Bamiou‡, Nicole G. Campbell§ & Tony Sirimanna# *MRC Institute of Hearing Research, Nottingham, UK, †UCL Speech, Hearing & Phonetic Sciences, London, UK, ‡UCL Ear Institute and Neuro-otology Department, National Hospital for Neurology and Neurosurgery, London, UK, §Institute of Sound and Vibration Research, University of Southampton, Southampton, UK, #Department of Audiology & Audiological Medicine, Great Ormond Street Hospital, London, UK Abstract Children with listening difficulties, but normal audiometry, may be diagnosed with APD. The diagnosis is typically based on poor performance on tests of perception of both non-speech and speech stimuli. However, non-speech test results correlate only weakly with evaluations of speech-in-noise processing, cognitive skills, and caregiver evaluations of listening ability. The interpretation of speech test results is confounded by the involvement of language processing mechanisms. Overall, listening ability is associated more with higher-level, cognitive and analytic processing than with lower-level sensory processing. Current diagnosis of a child with APD, rather than another problem (e.g. language impairment, LI), is determined more by the referral route than by the symptoms. Co-occurrence with other learning problems suggests that APD may be a symptom of a more varied neurodevelopmental disorder. Alternately, APD has been proposed as a cause of language-based disorders, but there is no one-to-one mapping between listening and language among individuals. Screening for APD may be most appropriately based on a well-validated, caregiver questionnaire that captures the fundamental problem of listening difficulties and identifies areas for further assessment and management. This approach has proved successful for LI, and may in future serve as a metric to help assess other, objective testing methods. Foreword Auditory processing disorder (APD) has a long (⬎ 30 years) and controversial history. The controversies concern absolutely fundamental issues: the definition of APD, its neural basis, test validity and standardization, differentiation from other disorders, and even whether it exists as an independent disorder (Jerger, 2009). To evaluate and interpret the scientific evidence on APD, and to advise the audiology profession, the British Society of Audiology (BSA) established a Special Interest Group (BSA SIG) on APD in 2003. That group has recently published two key documents, a ‘Position Statement’ and a ‘Management Overview’ (BSA, 2011, a,b. See www.thebsa.org.uk ‘Procedures and Publications’). In formulating the new position statement, it became clear to the group that several significant differences were developing between their interpretation of the evidence concerning APD and that of the American Academy of Audiology (AAA), as stated in their recently published ‘Guidelines for the diagnosis, treatment and management of children and adults with central auditory processing disorder’ (AAA, 2010). To address these differences, and borrowing from British Parliamentary procedure, the BSA SIG decided to develop a ‘white paper’, a discussion document that could then receive an international set of commentaries from other research groups working on APD. An approach was made to the editor of the International Journal of Audiology who agreed to this suggestion. This paper, and the associated commentaries that follow, are the result. Key Words: Behavioral measures; paediatric; speech perception; psychoacoustics/hearing science Introduction Some people who report listening difficulties in everyday situations are found to have normal pure-tone thresholds (Hind et al, 2011). Often, these people are simply told that nothing is amiss and sent on their way. However, in many audiology services around the world, they are invited to complete additional tests to investigate the possibility of an ‘auditory processing disorder’ (APD). Based on the results of these tests, APD may be diagnosed and a management regimen recommended (AAA, 2010). There is no doubt that auditory processing disorders can arise from frank lesions in the central auditory system or may co-exist with, and/or be linked to peripheral hearing loss (BSA, 2011a). Our focus here, however, is on the type of APD that appears to be a developmental disorder, and is of most concern in children, not least because of the impact it may have on social development and on academic performance. APD diagnosis is typically based, in North America, Europe and Australasia, on poor performance on at least one core test of ‘auditory processing’ (AP). Core AP tests include both speech- and non-speech-based tasks, the most commonly used of which are duration and frequency patterns, dichotic words or sentences, and Correspondence: David R. Moore, MRC Institute of Hearing Research, Nottingham, UK. E-mail: [email protected] (Received 14 March 2012; accepted 15 August 2012) ISSN 1499-2027 print/ISSN 1708-8186 online © 2013 British Society of Audiology, International Society of Audiology, and Nordic Audiological Society DOI: 10.3109/14992027.2012.723143 4 D. R. Moore et al. Abbreviations Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. AAA APD ASHA BSA CANS SLI American Academy of Audiology Auditory processing disorder American Speech-Language-Hearing Association British Society of Audiology Central auditory nervous system Specific language impairment speech which has either been degraded by low-pass filtering, or put in a background of noise (AAA, 2010; Emanuel et al, 2011). Management strategies tend to focus on improving listening skills, on the acoustic environment, on electronic delivery of enhanced signal-to-noise ratios, and on auditory training (BSA, 2011b). the cerebral cortex should be considered part of an extended CANS (Moore, 2012). These cortical regions show evoked responses to acoustic stimulation (Poremba et al, 2003), damage to them produces auditory perceptual difficulties (Griffiths et al, 2010), and they subserve the transition between coding simple and more complex auditory attributes of sounds including speech (Scott & Johnsrude, 2003; Scott, 2012). These and other regions (e.g. the cerebellum; Callan et al, 2006) also mediate the cortical processing of, and integration with, the higher-order cognitive components of sound perception. They have strong reciprocal connections with classical auditory cortical areas and, through the auditory cortex, descending connections down to the entire sub-cortical auditory system. They are thus able to influence the neural processing of sound on its way up from the ear (Moore, 2012). Attention and memory Difficulties defining APD No one has developed a satisfactory definition of APD, but we now know more about what it is not (Burkard, 2009). Successive position statements from ASHA, AAA, and BSA have suggested that APD arises from deficiencies in the central auditory nervous system (CANS; the brain pathway from cochlear nerve to auditory cortex) leading to impaired performance on basic psychoacoustic tasks (e.g. temporal processing and binaural interaction). Complex hearing tasks (sound localization, pattern recognition, performance with degraded signals or competing sounds) are also listed (ASHA, 1996). However, a number of studies (Watson & Kidd, 2009; Moore et al, 2010) have failed to find any close or consistent correlation between performance on non-speech psychoacoustic tasks and indicators of listening and learning problems, including academic ability, cognitive skills, speech-in-noise perception, and caregiver ratings of communication and listening skills. These findings suggest that psychoacoustic performance is not a good indicator of the reasons that people get referred for APD (the ‘clinical presentation’). Insofar as electrophysiologic responses like the complex (speech) auditory brainstem response (cABR) also reflect the fidelity of lowlevel sensory encoding, even if tuned by top-down influences over the long term (Krishnan et al, 2005; Kraus & Chandrasekaran, 2010), it seems unlikely that such measures will prove any more useful than direct behavioural measures of low-level sensory processes. Some speech-based hearing tasks may be better predictors (e.g. LiSN-S; Cameron & Dillon, 2008), but these involve substantial processing beyond the CANS, specifically in systems that are specialized for language. More generally, all auditory tests, whether language-based or not, involve varying levels of cognitive engagement, so impaired attention or memory can and does contribute to impaired auditory perception (see below). In an attempt to retain the specificity of APD distinct from other developmental disorders, definitions have included clauses that exclude broad cognitive deficits, particularly problems in attention. However, attention, as reflected in variable performance on tests of AP, correlates far more with clinical presentation measures of APD than does test threshold, the usual index of performance (Moore et al, 2010). Lessons from auditory neuroscience Impaired auditory perception has traditionally been thought to be caused by innate or acquired malfunction of the ear, nerve or the CANS, excluding other brain regions. Only recently has it become clear that the anterior lateral, frontal, and parietal lobes of It is a matter of everyday experience that we must attend to sounds to hear them properly (i.e. to listen). In addition, because sound stimuli evolve across time, we need to remember what has gone before, and integrate sound information across time. Finally, we need to act on the sound we hear, for example by rehearsing the acoustic image, moving it into longer term memory (Ronnberg et al, 2011), or by making some other response such as (more prosaically) pushing a button to show that we have heard the sound. The act of processing what is heard is thus complex and involves the intertwining of auditory, cognitive (including attention and memory), and language mechanisms (Medwetsky, 2011). Attention and memory are inextricably linked with all forms of sensory perception. It thus makes little sense to exclude the possibility that they contribute to APD. Psychologists have an elaborate set of terms to describe various aspects of attention and memory, but the important things for listening are that we can detect, discriminate, remember, understand, and act on a given pattern of auditory stimulation. For this reason, the most informative measures of auditory cognition related to attention and memory are likely to be those that are closely related to, and integrated with the auditory task being performed. For instance, while detection and discrimination thresholds are the standard measures of auditory performance, the variability of threshold across time appears to be a useful indicator of auditory attention, on the reasonable assumption that the sensory coding of a sound is relatively invariant over the course of a testing session. In fact, auditory threshold variability in children has been shown to be related to parental evaluations of everyday listening skills. It therefore follows that impaired everyday listening will be associated with more variable performance arising from inattention (Moore et al, 2008, 2010). Speech perception and APD Although general auditory problems may be an important aspect of APD, the vast majority of concerns centre around aspects of language, particularly speech perception. For example, of 13 behavioural manifestations said to be common among people referred for APD in the AAA Clinical Practice Guidelines, nine directly involve speech perception and one other the development of literacy (AAA, 2010). Speech is a highly redundant stimulus, meaning that it is only under challenging listening conditions (but ones that occur often in everyday life) that a speech processing difficulty may become apparent. This leads to a fundamental question about the nature of APD. Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. Developmental auditory processing disorder Is it a problem with the processing of all auditory signals, or is it specific to speech signals? We do not currently know the answer to this question, since it is possible that performance of other complex, but non-speech tasks, either auditory or non-auditory, is also deficient in those having the clinical presentation of APD. Although it is possible to construct nonspeech auditory discrimination tasks which incorporate the kind of spectro-temporal complexity found in speech and are essential for its perception, such stimuli have not been used in investigations of APD. If the problem is specific to speech, it may involve a very low, perhaps phonetic, level of linguistic processing, since performance of low redundancy speech tasks (e.g. identification of VCV nonsense syllables against a nonsense speech masker) by children is also related to parental reports of poor listening and communication (Moore et al, 2010). This is not to say that higher levels of linguistic processing could not also be compromised. Almost all test batteries for APD incorporate speech-based test material. Poor performance on these tests could mean a problem with the processing of basic sounds by the CANS, or problems in memory and/or attention, or it could mean a problem decoding the more abstract aspects of speech—phonetics, syntax, semantics, and vocabulary. For example, the commonly used SCAN-C (Keith, 2000) and more recent SCAN-3 (Keith, 2009) have a variety of difficulties when it comes to interpreting poor performance. Two of the subtests use a dichotic presentation of competing words or sentences. Such paradigms have long been used in experimental psychology (Broadbent, 1958), and are more-often considered assessments of attention and memory than auditory processing. An added complication is that the competing sentences subtest requires the participant to repeat back a sentence played to one ear while ignoring a different sentence in the other. However, performance on a sentence repetition task in quiet was found to be the best predictor (of four) of language impairment (Conti-Ramsden et al, 2001). Children with language impairment may thus do poorly on this test for reasons unrelated to an auditory processing problem. Consider finally the filtered words subtest, in which low-pass filtered monosyllabic words are presented for identification. What kind of auditory processing deficit could possibly impair performance for stimuli like this, when there is less information to process? How can this test be anything more than a test of linguistic competence, in guessing a whole from limited information? (Loo et al, 2012). Testing and diagnosing APD How then should we screen for and diagnose APD? For screening, it seems to make sense to return to the clinical presentation. The most common reason for APD referrals is listening problems, associated with a wide variety of scenarios including difficulty in noisy environments, inability to follow conversations and, for children, concerns about speech production, hearing in class, inattention (Hind et al, 2011) and poor academic performance. Clinicians presented with these problems almost always take a clinical history. This may be a checklist of commonly reported problems (a ‘structured history’) or a more eclectic and individualized assessment. Such assessments, however, are subject to the particular views and knowledge of the interviewer. Importantly, it is difficult to recommend clear, mutually agreed guidelines to practitioners, especially those unfamiliar with all the various forms of presentation. We suggest that a better way to capture and characterize the nature of the children’s problems is to give them, or their caregiver, a well-validated questionnaire. For screening and diagnosis of language and attention difficulties such questionnaires are already 5 available: the Children’s Communication Checklist (CCC-2; Bishop, 2003) and the Conners Rating Scales (Conners, 1996), respectively. Currently available questionnaires of listening difficulties, such as the Children’s Auditory Processing Performance Scale (the CHAPPS; Smoski et al, 1992) lack such validation. A secondary reason for developing such a questionnaire is as an index of the clinical presentation against which research evaluations of other methods of testing may be compared. The need for this cannot be overstated; a recent study identified nine different sets of diagnostic criteria for APD (including BSA, AAA, and ASHA guidelines) and the resulting rates of diagnosis of APD ranged from 7.3% to 96% (Wilson et al, 2012). Unsurprisingly, in light of this evidence, the validity and reliability of APD diagnosis continues to be questioned, with serious implications for access to appropriate educational support and management of those affected. Co-occurrence of APD with other learning difficulties Children with listening difficulties often have other problems consistent with alternative and more recognized diagnoses. The clinical presentation of APD has much in common with the most common developmental language disorders—specific language impairment (SLI) and dyslexia. Children diagnosed with any one of these conditions score similarly on a wide range of auditory, cognitive, and communication evaluations, at least on the group level (Dawes et al, 2009; Dawes & Bishop, 2010; Miller & Wagstaff, 2011; Sharma et al, 2009; Ferguson et al, 2011). There is also some evidence of a higher incidence of symptoms related to autism spectrum disorders in children diagnosed with APD but not, importantly, in children diagnosed with dyslexia (Dawes & Bishop, 2010). These overlaps could arise for a number of reasons. First is the possibility that not all of these disorders are, in fact, distinct from one another. Given that the methods currently used to diagnose APD largely lack an evidence base, and are often based on tests like the SCAN which would be expected to be difficult for children with language impairment, it is hardly surprising that there is a lot of comorbidity between APD and SLI. In this view, the diagnosis of any particular child with APD is determined more by the referral route than by the symptoms. Second is the rather more interesting theoretical position that language disorders like SLI and dyslexia are in fact caused by an APD. This idea has been promulgated most extensively by Tallal and her colleagues, identifying a deficit in rapid auditory temporal processing as key (Tallal, 2004). Although there is still much controversy about this hypothesis (see Rosen, 2003 for a review), only some children with language and reading difficulties have impaired auditory processing and, even in those cases, the impairment is not restricted to temporal processing. Furthermore, many children identified with an APD do not develop a language disorder, although this may be because they compensate for their APD. In short, there is no oneto-one mapping between listening and language difficulties. Third is the possibility that all these features are symptomatic of a more general neurodevelopmental delay. This hypothesis is attractive because it allows both for the co-occurrence of symptoms across disorders and for the considerable differences observed between children receiving a single diagnosis. There are, however, two major objections to this idea, one theoretical, and one practical. Theoretically, it is crucial to note that the close similarities between children with dyslexia or SLI and APD are only true on the group level. There are many children with APD who are not language impaired and vice versa. The evidence on Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. 6 D. R. Moore et al. this issue is very clear, even for the closely related disorders of dyslexia and SLI. For these it is known that there is quite a high degree of comorbidity, but they are still known to be distinct disorders, with good evidence for different genetic bases to the two (Pennington & Bishop, 2009). Practically, it would be a major challenge for care services to be able to manage a single, more broadly-ranging diagnosis. While parallel, multi-disciplinary intervention may be the best solution, efficiency suggests that a more hierarchical referral and management process, in which audiologists and other relevant single-specialist professionals (e.g. speech-language therapists/pathologists) could be trained and involved, would be more realistic. More complex models of comorbidity, involving multiple overlapping risk factors (Pennington & Bishop, 2009), might be more suitable, insofar as the focus is on the identification of the crucial risk factors and how they interact to produce any particular developmental disorder. Conclusions • Developmental APD is considered as a diagnosis when people referred to audiology services with concerns about ‘listening’ are found not to have a peripheral hearing problem or a neurological lesion. • There is currently no clear evidence that auditory sensory processing is the core problem underlying developmental APD. • Impaired listening is associated with poor attention and working memory. • APD often co-occurs with other learning and language disorders, so may indicate a broader and more varied neurodevelopmental disorder. • A high-quality and validated questionnaire aimed at screening for APD could pave the way for the development of more sensitive diagnostic measures. Acknowledgements Written on behalf of the BSA APD Special Interest Group. David R. Moore and Stuart Rosen contributed equally to writing the paper. Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. References American Academy of Audiology (AAA). 2010. Diagnosis, treatment and management of children and adults with central auditory processing disorder. pp. 1–53. http://www.audiology.org/resources/documentlibrary/ Documents/CAPD%20Guidelines%208-2010.pdf American Speech-Language-Hearing Association (ASHA). 1996. Central auditory processing: Current status of research and implications for clinical practice. Am J Audiol, 5, 41–54. Bishop D.V.M. 2003. The Children’s Communication Checklist. 2: Second Edition. London: The Psychological Corporation. British Society of Audiology (BSA). 2011a. Position statement: Auditory processing disorder (APD). pp. 1–9. http://www.thebsa.org.uk/images/ stories/docs/BSA_APD_PositionPaper_31March11_FINAL.pdf British Society of Audiology (BSA). 2011b. Practice guidance: An overview of current management of auditory processing disorder (APD). pp. 1–60. http://www.thebsa.org.uk/images/stories/docs/BSA_APD_ Management_1Aug11_FINAL_amended17Oct11.pdf Broadbent D. 1958. Perception and Communication. London: Pergamon Press. Burkard R. 2009. Foreword. In: A. Cacace, D. McFarland (eds.) Controversies in Central Auditory Processing Disorders. San Diego, USA: Plural Publishing, pp. vii–viii. Callan D.E., Tsytsarev V., Hanakawa T., Callan A.M., Katsuhara M. et al. 2006. Song and speech: Brain regions involved with perception and covert production. Neuroimage, 31, 1327–42. Cameron S. & Dillon H. 2008. The listening in spatialized noise-sentences test (LISN-S): Comparison to the prototype LISN and results from children with either a suspected (central) auditory processing disorder or a confirmed language disorder. J Am Acad Audiol, 19, 377–91. Chandrasekaran B. & Kraus N. 2010. The scalp-recorded brainstem response to speech: Neural origins. 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Communication, listening, speech, and cognition in children diagnosed with auditory processing disorder (APD) or specific language impairment (SLI). J Speech Lang Hear Res, 54, 211–227. Griffiths T.D., Bamiou D-E. & Warren J.D. 2010. Disorders of the auditory brain. In: Rees, Palmer (eds.) Oxford Handbook of Auditory Science: The Auditory Brain. Oxford: Oxford University Press, pp. 509–542. Hind S.E., Haines-Bazrafshan R., Benton C.L., Brassington W., Towle B. et al. 2011.Prevalence of clinical referrals with normal audiometry. Int J Audiol, 50, 708–16. Jerger J. 2009. The concept of auditory processing disorder: A brief history. In: Cacace and McFarland (eds.) Controversies in Central Auditory Processing Disorder. San Diego, USA: Plural, pp. 1–14. Keith R.W. 2000. Development and standardization of SCAN-C Test for auditory processing disorders in children. J Am Acad Audiol, 11, 438–45. Keith R.W. 2009. SCAN-3:C: Tests for Auditory Processing Disorders in Children. San Antonio, USA: The Psychological Corporation. Kraus N. & Chandrasekaran B. 2010. Music training for the development of auditory skills. Nat Rev Neurosci, 11, 599–605. Krishnan A., Xu Y.S., Gandour J. & Cariani P. 2005. Encoding of pitch in the human brainstem is sensitive to language experience. Cogn Brain Res, 25, 161–168. Loo J.H.Y., Bamiou D.E. & Rosen S. 2012. The impacts of language background and language-related disorders in auditory processing assessment. J Speech Lang Hear Res, in press. Medwetsky L. 2011. Spoken language processing model: Bridging auditory and language processing to guide assessment and intervention. Lang Speech Hear Serv Sch, 42, 286–96. Miller C.A. & Wagstaff D.A. 2011. Behavioral profiles associated with auditory processing disorder and specific language impairment. J Commun Disord, 44, 745–63. Moore, D.R. 2012. Listening difficulties in children: Bottom-up and top-down contributions. J Commun Disord, (Epub ahead of print. PMID: 22766459). Moore D.R., Ferguson M.A., Edmondson-Jones A.M., Ratib S. & Riley A. 2010. The nature of auditory processing disorder in children. Pediatrics, 126, e382–e390. Moore D.R., Ferguson M.A., Halliday L.F. & Riley A. 2008. Frequency discrimination in children: Perception, learning, and attention. Hear Res, 238, 147–154. Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. Developmental auditory processing disorder Pennington B.F. & Bishop D.V.M. 2009. Relations among speech, language, and reading. Ann Rev Psychol, 60, 283–306. Poremba A., Saunders R.C., Crane A.M., Cook M., Sokoloff L. et al. 2003. Functional mapping of the primate auditory system. Science, 299, 568–572. Rönnberg J., Danielsson H., Rudner M., Arlinger S., Sternäng O. et al. 2011. Hearing loss is negatively related to episodic and semantic long-term memory but not to short-term memory. J Speech Lang Hear Res, 54, 705–26. Rosen S. 2003. 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In: Cacace and McFarland (eds.), Current Controversies in Central Auditory Processing Disorder (CAPD). San Diego, USA: Plural Publishing Inc. Wilson W.J. & Arnott W. 2012 Using different criteria to diagnose (C)APD: How big a difference does it make? J Speech Lang Hear Res, (Epub ahead of print PMID: 22761321). The following groups agreed to provide comments on the preceding paper Teri James Bellis, The University of South Dakota Gail Chermak, Washington State University Jeff Weihing, University of Louisville Frank Musiek, University of Connecticut As Moore et al note, there are significant differences in the evaluation and interpretation of evidence on APD (or central auditory processing disorder (CAPD) as the disorder is referred to in the United States to emphasize its origins in the central nervous system), as reflected in recent position statements and guidelines (AAA, 2010; ASHA, 2005a, b; BSA, 2011a, b). We address our primary concerns with their interpretation of the evidence here. Moore et al state “There is no doubt that auditory processing disorders can arise from frank lesions in the central auditory system… Our focus here, however, is on the type of APD that appears to be a developmental disorder, and is of most concern in children...” The implication of the distinction they construct is that CAPD in children is not neurobiological. In fact, whether the source of central auditory nervous system (CANS) dysfunction is benign (maturational or neuroanatomical) or the result of frank neurological lesion or compromise, the underlying source of the resulting central auditory deficits and CAPD originate in the central nervous system (Chermak & Musiek, 2011). We also strongly disagree with their statement “That the methods currently used to diagnose APD largely lack an evidence base…”, and their conclusion that “There is currently no clear evidence that auditory sensory processing is the core problem underlying APD.” There are, in fact, multiple lines of evidence confirming a core sensory processing deficit in CAPD, including literature documenting CAPD in adults with confirmed CANS lesions (see Musiek et al, 1994, for a representative example), 7 reports demonstrating the neuroanatomic source of CAPD in some children (Boscariol and colleagues, 2009, 2010, 2011), similar central auditory test performance across children diagnosed with CAPD with and without confirmed neurologic lesions of the CANS (Jerger et al, 1988), and, as importantly, similar central auditory test performance patterns across children and adults with CAPD (e.g. as in dichotic deficits (Musiek & Weihing, 2011)). Moreover, there are plausible mechanisms explaining what would cause this similarity to arise between neurologic patients and pediatric populations. For instance, when one considers the course of neuromaturation in the brain, it becomes clear that areas critical to auditory processing (e.g. corpus callosum) are often affected by delayed neuromaturation. Therefore, these areas are often found to be deficient in cases of CAPD (Musiek et al, 1984; Bellis & Wilber, 2001, Musiek & Weihing, 2011). Moore et al question the utility of using both speech and nonspeech test stimuli for diagnosis stating that “...non-speech test results correlate only weakly with ... speech-in-noise processing, cognitive skills and caregiver evaluations of listening ability”, and that “Speech test interpretation is confounded by the involvement of brain language processing mechanisms.” While we agree that there is potential for language and cognitive (e.g. memory, attention) confounds, this is true of any task that requires cooperation and behavioral response on the part of the child being tested. As with any psychophysical measure (including pure-tone threshold testing), experienced clinicians must be on the lookout for test-related indicators of attention and related confounds. In CAPD testing, these confounds can be minimized by using simple speech stimuli (e.g. digits), minimizing memory loading, utilizing intra-test measures which control, in part, for non-auditory factors (e.g. left vs. right ear performance; see Bellis et al, 2011), and by employing a multidisciplinary team approach through which information regarding attention, memory, language, and other functions is available. Additional controls in cases in which the possible presence of a linguistic or memory confound exists may include assessing performance in the non-manipulated condition (e.g. monaural versus dichotic, nonfiltered versus filtered, etc.) to ensure that performance deficits seen on CAPD tests are due to the acoustic manipulations rather than to lack of familiarity with the language and/or significantly reduced memory skills. Inclusion of speech stimuli allows the audiologist to obtain information regarding speech processing mechanisms in the CANS which are not necessarily revealed through non-speech stimuli (Grossman et al, 2010). Further, these stimuli have ecological value, and because the degree of temporal processing required for accurate perception of spoken language is significantly greater than required for perception of non-speech sounds, processing of speech signals may be more vulnerable to disruption by CANS dysfunction (e.g. Fitch et al, 1997; Griffiths et al, 1999; Shannon et al, 1995; Zatorre & Belin, 2001); therefore, in some cases central auditory processing deficits may only be revealed using speech tasks (e.g. Benavidez et al, 1999; Johnson et al, 2005; Russo et al, 2005). Moore et al’s concern that non-speech test results correlate weakly with speech-in-noise processing, deficiencies of which are a hallmark of central auditory processing disorder, argues for the inclusion of speech tests in the test battery used to identify CAPD. Regarding Moore et al’s concern about poor correlations between non-speech test results and cognitive skills, academic and learning abilities, caregiver evaluations of listening ability, and even some (language-loaded) speech-in-noise tasks, we would note that there is no reason to expect or demand strong correlations between measures of CANS function and these indicators of higher-order functions. Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. 8 D. R. Moore et al. While auditory perceptual difficulties are sometimes seen in children with other primary diagnoses, including language impairment, attention deficits, and autism (Chermak et al, 1998; Rinker et al, 2007; O’Connor, 2012), neither speech nor non-speech behavioral central auditory perceptual tests are designed to be sensitive to these higher-order deficits (Musiek et al, 2005). Further, we would note that there is generally little agreement between caregiver/informant subjective reports of listening skills and children’s actual performance on central auditory measures (Drake et al, 2006; Lam & Sanchez, 2007; Wilson et al, 2011). Hence, the weak correlation between nonspeech diagnostic measures and subjective questionnaires does not throw into question the utility of non-speech tests, but rather leads to questions regarding the appropriate use of caregiver rating scales. Moore et al dismiss electrophysiological measures that use speech stimuli stating “... it seems unlikely that such measures will prove any more useful than direct behavioural measures of low-level sensory processes.” There is accumulating evidence that a wide range of electrophysiological measures provide an objective look at the CANS and that some of these measures correlate with many of the skills and abilities which Moore et al find lacking for non-speech tests. Thus, not only do we find this evidence in the ABR to complex stimuli (cABR)(e.g. Banai et al, 2009, 2005; Billiet & Bellis, 2011; Kraus et al, 1996), but in the auditory middle latency response (e.g. Purdy et al, 2002; Schochat et al, 2010), the auditory late response (e.g. McArthur et al, 2009), and event related potentials, such as the P300 & mismatch-negativity (e.g. Sharma et al, 2006; Jirsa & Clontz, 1990) as well. Moore et al correctly note that impaired listening can be associated with poor attention and working memory; however, their assertion that “Overall, listening ability is associated more with higher-level, cognitive and analytic processing than with lower-level sensory processing” does not logically follow. There is no question that working memory supports listening skills such as localization ability (Martinkauppi et al, 2000) and speech recognition in noise (Akeroyd, 2008; Wong et al, 2009). However, lower-level sensory processes also have a profound impact on these skills, as even moderate declines in peripheral auditory acuity lead to a systematic down regulation of neural activity during the processing of higher-level aspects of speech (e.g. sentence comprehension) (Peele et al, 2011). These interactions arise from brain organization and the nature of information processing and they do not, therefore, negate what we learn about lower-level sensory processing from sensitized (i.e. efficient) behavioral and electrophysiological measures of CANS dysfunction. Moore et al state that the “The current diagnosis of a child with CAPD, rather than another learning problem is often determined more by the referral route than by the symptoms.” First, we must emphasize that CAPD is not a learning problem. Second, the use of teacher/parent report, as recommended by Moore et al, can lead to inaccurate diagnosis. As shown by Wilson (2012), many children perform well on performance-based measures of central auditory processing despite caregiver-reports of these children encountering listening difficulties. It is likely that using caregiver-report to diagnosis CAPD, as in Ferguson et al (2011), has contributed to the observed overlap between CAPD and SLI noted by Moore et al. Nonetheless, we are sensitive to Moore et al’s concern that diagnoses given to children often are influenced by the professional seeing the child perhaps more so than guided by the symptoms. We would argue that multidisciplinary teams working in cooperation rather than competition, using measures with documented sensitivity and validity for CAPD (as well as language, learning, listening, reading, etc.) would address their concern. Contrary to Moore et al’s position that the co-occurrence of CAPD with other learning problems “... suggests that APD may be considered a symptom of a more varied neurodevelopmental disorder,” we would argue that co-morbidity does not invalidate a sensory-perceptual diagnosis, if such diagnosis is based on an efficient test battery. Finally, we are concerned about the potential adverse impact for treatment and management of children with CAPD were Moore et al’s recommendation adopted that “Assessment of APD may be most appropriately based on a well-validated, caregiver questionnaire that captures the fundamental presenting problem of listening difficulties.” There is no question that questionnaires have value; however, employing a questionnaire to assess CAPD would suggest to professionals and insurers that evaluating children who demonstrate behaviors consistent with ‘listening’ or auditory problems need not include a controlled battery of central auditory (and peripheral auditory) tests. Given the limitations of questionnaires, as noted above, their exclusive use for diagnosis of CAPD would lead to uncertain diagnoses, less precise information to guide intervention, and certainly less well targeted and therefore less effective and efficient intervention. In closing, we commend our colleagues for their work in this area and for providing an opportunity for discussion of a range of issues which must be resolved to ensure delivery of the best clinical services to children with CAPD. References American Academy of Audiology, 2010. Guidelines for the diagnosis, treatment, and management of children and adults with central auditory processing disorder. Available at: http://www.audiology.org/resources/ documentlibrary/Documents/CAPD%20Guidelines%208-2010.pdf American Speech-Language-Hearing Association, 2005a. (Central) Auditory processing disorders. Available at: http://www.asha.org/members/ deskref-journals/deskref/default. American Speech-Language-Hearing Association, 2005b. (Central) Auditory processing disorders: The role of the audiologist (position statement). Available at: Available at http://www.asha.org/members/deskref-journals/deskref/default. Banai K., Hornickel J., Skoe E., Nicol T., Zecker S. et al. 2009. 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Position statement: Auditory processing disorder (APD). Available at: http://www.thebsa.org.uk/ images/stories/docs/BSA_APD_PositionPaper_31March 11_FINAL.pdf British Society of Audiology (BSA), 2011b. Practice guidance: An overview of current management of auditory processing disorder (APD). Available at: http://www.thebsa.org.uk/images/stories/docs/BSA_APD_ Management_1Aug11_ FINAL_amended17Oct11.pdf Chermak C. & Musiek F., 2011. Neurological substrate of central auditory processing deficits in children. Current Pediatric Reviews, 7(3), 541–251. Chermak G.D., Hall J.W. 3rd, Musiek F.E. 1999. Differential diagnosis and management of central auditory processing disorder and attention deficit hyperactivity disorder. J Am Acad Audiol, 10(6), 289–303. Drake M., Brager M., Leyendecker J., Preston M., Shorten E. et al, 2006. Comparison of the CHAPPS screening tool and APD diagnosis. Poster presented at the annual convention of the American Speech-LanguageHearing Association, Miami Beach, USA. Ferguson M.A., Hall R.L., Riley A. & Moore D.R. 2011. Communication, listening, cognitive and speech perception skills in children with auditory processing disorder (APD) or specific language impairment (SLI). J Speech Lang Hear Res, 54(1), 211–227. Fitch R.H., Miller S. & Tallal P. 1997. Neurobiology of speech perception. Ann Rev Neurosci, 20, 331–353. Griffiths T., Rees A. & Green G. 1999. Disorders of human complex sound processing. Neurocase, 365–378. Grossmann T., Oberecker R., Koch S.P. & Friederici A.D. 2010. The developmental origins of voice processing in the human brain. Neuron, 65(6), 852–858. Jerger S., Johnson K. & Loiselle L. 1988. Pediatric central auditory dysfunction: Comparison of children with a confirmed lesion versus suspected processing disorders. Am J Otology, 9, 63–71. Jirsa R.E. & Clontz K.B. 1990. Long latency auditory event-related potentials from children with auditory processing disorders. Ear Hear, 11(3), 222–232. Johnson K.L., Nicol T.G. & Kraus N. 2005. Brain stem response to speech: A biological marker of auditory processing. Ear Hear, 26(5), 424–434. Kraus N., McGee T.J., Carrell T.D., Zecker S.G., Nicol T.G. et al, 1996. Auditory neurophysiologic responses and discrimination deficits in children with learning problems. Science, 273(5277), 971–973. Lam E. & Sanchez L. 2007. Evaluation of screening instruments for auditory processing (APD) in a sample of referred children. Aust NZ J Audiol, 29, 26–39. McArthur G., Atkinson C. & Ellis D. 2009. Atypical brain responses to sounds in children with specific language and reading impairments. Dev Sci, 12(5), 768–783. Musiek F.E., Baran J.A. & Pinheiro M.L. 1994. Neuroaudiology: Case Studies 1st ed. Singular. Musiek F.E., Bellis T.J. & Chermak G.D. 2005. Nonmodularity of the central auditory nervous system: Implications for (central) auditory processing disorder. Am J Audiol, 14(2), 128–138; discussion 143–150. Musiek F.E., Gollegly K.M. & Baran J.A. 1984. Myelination of the corpus callosum and central auditory processing problems in children: Theoretical and clinical correlates. Semin Hearing, 5, 231–241. Musiek F. & Weihing J. 2011. Perspectives on dichotic listening and the corpus callosum. Brain Cogn, 76, 225–232. O”Connor K. 2012. Auditory processing in autism spectrum disorder: A review. Neurosci Biobehav Rev, 36(2), 836–54. Peelle J.E., Troiani V., Grossman M. & Wingfield A., 2011. Hearing loss in older adults affects neural systems supporting speech comprehension. J. Neurosci, 31(35), 12638–12643. Purdy S., Kelly A. & Davies M. 2002. Auditory brainstem response, middle latency response, and late cortical evoked potentials in children with learning disabilities. J Am Acad Audiol, 13, 367–382. Rinker T., Kohls G., Richter C., Maas V., Schulz E. et al. 2007. Abnormal frequency discrimination in children with SLI as indexed by mismatch negativity (MMN). Neurosci Lett, 413(2), 99–104. 9 Russo N.M., Nicol T.G., Zecker S.G., Hayes E.A. & Kraus N. 2005. Auditory training improves neural timing in the human brainstem. Behav Brain Res, 156(1), 95–103. Schochat E., Musiek F.E., Alonso R. & Ogata J. 2010. Effect of auditory training on the middle latency response in children with (central) auditory processing disorder. Brazil J Med Bio Res, 43(8), 777–785. Shannon R.V., Zeng F.G., Kamath V., Wygonski J. & Ekelid M. 1995. Speech recognition with primarily temporal cues. Science, 270 (5234), 303–304. Sharma M., Purdy S.C., Newall P., Wheldall K., Beaman R. et al. 2006. Electrophysiological and behavioral evidence of auditory processing deficits in children with reading disorder. Clin Neurophysiol, 117(5), 1130–1144. Wilson W.J. & Arnott W. 2012. Effect of differential diagnostic criteria on the diagnosis of (C)APD. Presentation at the Global Perspectives on Auditory Processing Disorder Conference, Boston, USA. Wilson W.J., Jackson A., Pender A., Rose C., Wilson J. et al. 2011. The CHAPS, SIFTER, and TAPS-R as predictors of (C)AP skills and (C)APD. J Speech Lang Hear Res, 54(1), 278–291. Zatorre R.J. & Belin P., 2001. Spectral and temporal processing in human auditory cortex. Cereb Cortex, 11(10), 946–953. Comments from: Harvey Dillon, National Acoustic Laboratories, Sydney, Australia Sharon Cameron, National Acoustic Laboratories, Chatswood, Australia The White Paper raises some very relevant issues regarding concepts related to APD. It is helpful that the authors have specified the disorder under discussion as being developmental in nature which is indeed the most common form of APD to be encountered clinically. This is not to say that all forms of APD are developmental, or that developmental problems will self-resolve with time. However, in the first of their concluding statements the authors refer to developmental APD as being considered a ‘diagnosis’ when “… people referred to auditory services with concerns about ‘listening’ are found not to have a peripheral hearing problem or a neurological lesion”. This statement suggests that anyone with normal hearing thresholds and no identified brain lesion who has concerns regarding their ability to ‘listen’ has developmental APD. We assume that this definition of developmental APD is derived from the authors’ belief that there are no assessment tools— either behavioural or electrophysiological—that can accurately and unequivocally diagnose such a ‘disorder’. To this end, the authors conclude that performance on nonspeech tests is only weakly correlated with indicators of listening and learning problems (such as speech-in-noise perception and academic performance) which they term the ‘clinical presentation’. Whereas the authors acknowledge that some speech-based assessments tools—such as the Listening in Spatialized Noise– Sentences test (LiSN-S)—may be better predictors of clinical presentation, performance on such tests may be too strongly influenced by higher-order processes such as language ability, attention, and memory to be valid indicators of basic auditory processing abilities. Degree of variability across performance on a range of AP tests is suggested as correlating better with clinical presentation than the threshold achieved on any one test. Our interpretation of the White Paper is that, based on the abovementioned problems that the authors consider are inherent within the currently available APD test battery, the best AP diagnosis is achieved via parental report, preferably using a well validated questionnaire. 10 D. R. Moore et al. Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. Whereas we agree with many of the opinions expressed in this paper, we would like to take this opportunity to expand and challenge some of the conclusion drawn as follows: 1. The term APD, be it developmental or otherwise, is a largely useless descriptor for clinicians and parents alike, akin to a doctor providing a diagnosis of a “sore leg” when a patient has a fractured patella. In order for appropriate management to be effective—be it deficit-specific remediation or some form of compensation—the clinician must be aware of the exact nature of the deficit they are required to manage. It is unlikely that such a diagnosis can be achieved from examining a questionnaire. We suggest that specific sub-types of auditory processing disorders be defined that can be diagnosed using sensitive and specific, ecologically valid, behavioural, or electrophysiological tests (incorporating speech or non-speech stimuli) that have extensive, age-specific normative data and have been rigorously evaluated in the target population. 2. We agree that higher-order cognitive abilities can impact on the performance of many tests currently used to assess AP disorders. This fact was extremely influential in the development of the LiSN-S (Cameron & Dillon, 2007). The target stimuli were specifically developed for children from four years of age. The rule of measuring performance as the difference in dB between various test conditions was specifically adopted to minimize the effect of language and other cognitive functions on test performance (if the performance of the client was impacted by such issues the difference between two test conditions that differed only in one aspect—e.g. spatial location of the maskers—would be minimally impacted). Intermittent variations in attention can, however, occur with any test battery, be it auditory or cognitive, and must be managed by the professional administering the tests. 3. The statement that “attention, as reflected in variable performance on tests of AP, correlates far more with clinical presentation measures of APD than does test threshold” appears to arise from performance on a long and repetitive test battery reported by Moore et al 2010. It is not surprising that the children who most quickly gave up on trying their hardest at some or all tests (and hence had variable performance) tended to be those most likely to exhibit the type of problems that cause their teachers or parents to seek an APD assessment. Moore et al have labelled the underlying attribute as attention. It could equally be labelled as motivation, vigilance, or perseverance. Irrespective of the label applied, the impact of such an attribute on some test scores does not logically mean that the symptoms thought to be associated with APD cannot also be associated with the scores obtained on other tests where the attention/motivation/ vigilance/perseverance of the child has been maintained through suitably short tests or suitably interesting test design and administration. 4. We agree that short term and/or working memory deficits or attention problems can have a negative impact on AP test performance; however this issue should not deter the clinician from performing an AP assessment. The clinician can include in the battery a test of auditory memory, or perhaps even auditory continuous performance, and evaluate overall AP performance in light of these test results. 5. In respect to the authors’ conclusion that there is “...currently no clear evidence that auditory sensory processing is the core problem underlying APD”, we assume that the authors believe that attention, memory, and higher order language skills account for all instances of (developmental) APD published to date in the literature. One reason for this belief may be that many studies have specifically targeted children with conditions such as language impairment or dyslexia. These higher order conditions may have impacted on the AP test results. In our studies with the LiSN-S we took great care to separate groups based on presenting profile and to examine test results accordingly. As such, Cameron & Dillon (2008) found that nine children, recruited with a presenting profile of difficulty understanding speech in the classroom with IQ results within normal limits and no other diagnosed disorder, were all outside normal limits on the spatially-separated conditions of the LiSN-S, whereas eleven children with a cognitive deficit of some type all performed within normal limits on all LiSN-S conditions. These results provide evidence of a specific auditory sensory processing deficit (which we termed spatial processing disorder or SPD) as the core problem in these particular children who presented with listening deficits in the absence of any other condition. The fact that the children with SPD were all within normal limits on the conditions of the LiSN-S where the target and masker stimuli were collocated (i.e. where no spatial processing was required) further strengthens the argument for a specific form of auditory sensory processing being the core problem for these children. Studies have also shown (individual and group results) that SPD is totally reversible in children with SPD (Cameron & Dillon 2011), that the remediation occurs only with deficit-specific training, and that the improvement posttraining is reflected in patient, parent, and teacher questionnaires concerning real-life listening (Cameron et al, submitted). So while we do not doubt that a proportion of children have a deficit in auditory vigilance or attention, our own studies have shown that at least one auditory sensory deficit does indeed exist and can be remediated, thereby improving quality of life. We are not suggesting that SPD will be the only auditory deficit that can be identified, and for which the effects of remediation will generalize to real life. 6. In respect to the authors’ concluding point, we support the need for a high-quality and validated questionnaire and agree with the importance that the paper places on establishing the degree of difficulties experienced in real life. Such a measure could provide the gold standard used to assess whether a particular type of remediation has actually helped a child, rather than simply made the child more skilful in some test, the results of which caused the child to be diagnosed as “having APD”. Thank you for the opportunity to comment on this important and challenging topic. It will only be when we as a field have identified a set of auditory skills, each of which can be improved by an appropriate remediation, and when that remediation results in improved listening in daily life, demonstrated through suitable questionnaires, that we will have a meaningful idea of the scope of auditory processing abilities and disorders. Such a focus is more likely to be productive than a search for a single method of diagnosing a disorder that that we already know has different underlying deficits in different children. Comments from: James Jerger and Jeffrey Martin, The University of Texas at Dallas/Callier Center for Communication Disorders, Dallas, USA Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. Developmental auditory processing disorder We congratulate the Special Interest Group (SIG) of the British Society of Audiology (BSA), and the authors of this important “white paper”, for their willingness to attempt to make some sense of a substantial collection of very murky concepts, historical missteps, and contradictory data. In particular, they have highlighted the importance of cognitive and linguistic factors in understanding the nature of developmental listening problems. There can be no doubt that attention, memory, and language disorder are the elephants in the room. One can view them either as confounds in traditional behavioral tests of an assumed sensory disorder or, indeed, as key factors underlying the very nature of a “more general neurodevelopmental delay”. The important point made by the authors is that the situation is far more complicated than many clinicians and researchers, in a variety of disciplines, would have us believe. It would be a mistake to minimize efforts to document how (and when) genuine dysfunction in auditory processing leads to selective impairments in auditory perception, including the development of techniques for purposes of validation. Not incorporating evidence from neuropsychology and auditory neuroscience, highlighting the importance of cognition in APD research and clinical practice, would constitute a larger mistake. In fact, it is difficult to dismiss that such (cognitive) mechanisms could be equally responsible for some of our own past APD findings. Such is the path of science. We find ourselves in essential agreement with all of the authors’ conclusions, with the possible exception of reliance on questionnaires for diagnosis: surely we can do better than that. Can we not benefit, as so many other fields have, from decades of advances in neuropsychological evaluation, electroencephalographic averaging, and brain-imaging techniques to guide us? It is perhaps not premature to suggest that this paper serve as an impetus for the implementation of an international consensus conference on APD under the auspices of BSA-SIG. Response to the Reviewers' Comments from Moore, et al: We, the members of the BSA Special Interest Group on APD, would like to thank the three groups of reviewers for taking the trouble to comment on this ‘white paper’, and also the editor-in-chief of TIJA, Dr Ross Roeser, for organizing its appearance. We believe that all members of the international community want to achieve a shared understanding of APD, based on the highest level of scientific evidence and reasoning. As suggested by Drs. Jerger and Martin, an important goal is an international consensus, and we are delighted that the American Academy of Audiology now plans to make an APD symposium a regular (two-yearly) part of their annual meeting (Audiology Now!), following the successful symposium “Global Perspectives on (C)APD” which was held in Boston in March 2012. Because of some overlap in the points made by each group of reviewers, we have elected to organize our response in terms of the general issues raised by them, rather than dealing with each set of comments in turn. 11 no other known etiology and presumably present from birth), acquired (associated with a known peri- or post-natal event such as neurological trauma or infection), and secondary (occurring in association with a known genetic cause1 or peripheral hearing impairment). In the white paper, we deal only with the most common category, developmental APD. There is currently no evidence that developmental APD is caused by or associated with a specific neurological disorder. The evidence that some behaviours associated with developmental APD (e.g. atypical ear advantage) resemble those of patients with acquired APD does not mean that developmental APD is due to a recognized neurological disorder. Current understanding of other developmental disorders is also instructive in this respect. For example, the study of acquired dyslexia in adults, usually as the result of stroke, has provided few or no useful lessons for understanding developmental dyslexia in children. Studies of the sequelae of damage to a fully developed adult brain encourage the notion of either impaired or spared systems. By contrast, in a child without neurological damage, the development of various cognitive skills is highly interdependent, so separate skills cannot be considered in isolation (see Karmiloff-Smith, 1997; Karmiloff-Smith et al, in press). Sensory, perceptual, and cognitive aspects of hearing It is practically impossible fully to dissociate these different aspects of auditory processing because of the highly interconnected and recurrent nature of auditory system functional connectivity. Nevertheless, the ‘sensory’ part of hearing we take to be processing along the classic, ascending auditory system from the ear to primary auditory cortex. This is, of course, the main highway for delivery of auditory information. It is essentially the same in humans and other mammals, and functions fairly similarly during wakefulness, sleep, and under general anaesthesia. In contrast, ‘perception’ is the conscious interpretation of sensory signals, based on innate biology, experience and ‘cognition’ which includes attention, memory, language, and understanding. The growing recognition that cortical areas beyond the auditory cortex (anterior temporal, frontal, inferior parietal) are necessarily involved in perception, and should be regarded as part of the ‘central auditory nervous system’ (CANS), also makes categorical distinctions difficult. Similarly, descending pathways having their origins in the cortex and, relaying back down through the midbrain and the brainstem to the cochlea and middle ear, can transmit cognitively and perceptually relevant information to the very earliest stages of sensation, modulating and gating the input to the brain. That seems a good reason to drop the ‘C’ from (C)APD, the indisputable neuroscience showing that the ear, the recognized CANS, and much of the cerebral cortex are all necessary for normal hearing. It is universally recognized that the pure-tone audiogram does not provide a comprehensive assessment of auditory perception. But a finding of normal audiometry remains a strong indicator of normal peripheral function. In this sense, we can therefore agree that ‘auditory processing’ begins at the cochlear nerve. The neurobiological origin of APD and our focus on development It is an axiom of psychology and neuroscience that all behavior, whether normal or disordered, is biological in origin, although clearly formed by interaction with the environment. We have proposed elsewhere (BSA, 2011a) that APD should be divided into three categories: developmental (normal audiometry with Tests of auditory perception Two issues identified by the reviewers were the use of speech vs. non-speech tests, and the impact of cognition, specifically language difficulties, on speech-based test performance. These are, of course, related issues. We (BSA, 2011a) had proposed that, to Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. 12 D. R. Moore et al. eliminate the influence of specifically language skills, it is necessary to use non-speech stimuli to demonstrate specifically auditory processing problems. We have never suggested that speech perception is unimportant, only that tests using speech necessarily engage language mechanisms that are not traditionally considered part of hearing. In fact, we argue strongly for the central role of speech perception in thinking about APD. The ‘clinical presentation’, the reason children are referred for APD assessment, is always related to listening and related communication difficulties, but never based on ‘auditory processing’ in the sense of basic psychoacoustic skills. In the white paper we noted that speech-based hearing tasks may be better predictors of the clinical presentation, but that these involve substantial processing beyond the CANS. Reviewers point to attempts made to limit involvement of higher level processing by, for example, comparing performance in two different conditions (e.g. monaural vs. dichotic, unfiltered vs. filtered, front vs. side sound delivery). These attempts limit cognitive involvement to different degrees: monaural vs. dichotic hardly at all, since different signals to each ear clearly pose a different cognitive challenge than the same signals to one ear. However, comparing target signals presented from different directions relative to a masking signal (spatial release from masking, SRM), as used in the LiSN-S (Cameron & Dillon, 2008), is a more subtle issue. A speech target in a speech masker is a highly complex acoustic signal involving both energetic and informational masking (Shinn-Cunningham, 2008). This means that while some of the SRM is due to binaural processing, presumably in the brainstem, some is due to language-based analysis of the signals, the informational content of which would differ in the two spatial conditions. So this example, which is cited by the reviewers as one in which care was taken to minimize cognitive processing, is one in which cognitive processing could account for a significant portion of the measured effect. Further research could help determine the size of that portion but, in simple terms, this means that spatial processing disorder (SPD), considered to be a ‘specific auditory sensory processing deficit’, may be at least somewhat dependent on language processing. This does not mean that the LiSN-S is a poor test of APD, or of SPD, only that it is extremely difficult to separate sensory and cognitive contributions to perception, especially when using speech-based tests. If APD is primarily a core sensory processing deficit, as argued by reviewers, then nonspeech tests should be sufficient to detect those deficits. Take, for example, sensitivity to amplitude modulation (AM), a key component of temporal processing ability on the scale of a few ms to hundreds of ms. Obtaining low AM thresholds, from say 2 to 1000 Hz in a temporal modulation transfer function (Viemeister, 1979), requires a much better ability to detect AM than understanding noise-vocoded speech (Shannon et al, 1995) which requires sensitivity only to modulation rates below about 20–50 Hz, and AM that is well above threshold. In short, the degree of temporal processing required for the accurate perception of spoken language is not significantly greater than that required for good performance in non-speech tasks, and is typically less. Questionnaires All three reviews expressed some reservations as well as some support for the use of questionnaires. We reinforce here the argument presented in the white paper that a well-validated questionnaire can serve two important purposes. First, it could serve as a standardised screening tool now and, probably, into the foreseeable future. We recognize that a questionnaire is not an end in itself, and is only one element of a potential diagnostic battery. However, it could replace or supplement clinical histories that vary in construct and interpretation with the skills and knowledge of the attending clinician2. Second, we urgently need a benchmark against which other potentially useful developments of sensitive and appropriate tests of auditory processing, including behavioural, electrophysiological, and molecular metrics, may be assessed. Our message is clear: unless a test is sensitive to the symptom (in this case, a listening problem) it is not diagnostic. Electrophysiology A claim often made about human electrophysiology is that it is somehow more objective than behavioural measures. We are tempted to make the opposite claim. Unless supported by behavioural evidence, electrophysiology is uninterpretable. Also, because electrophysiology, like behaviour, is an index of neural function, it will be generated by the same mechanisms and subject to the same influences as behaviour. Consider the complex auditory brainstem response (cABR). Recent work cited in the reviews has shown that various aspects of cABR waveform and timing are related to auditory performance (e.g. speech-in-noise perception) and influenced by experience (e.g. music and language training). But those findings provide potentially important research evidence on mechanisms of auditory function and dysfunction only because of their association with the relevant behaviour. How or where neural generators shape the cABR remains an almost completely open question. Recent studies (e.g. de Boer & Thornton, 2008; Bajo et al, 2010; Irving et al, 2011) suggest that descending pathways from the cortex modulate subtle aspects of auditory learning. In each case, however, those relationships are drawn on the basis of behaviour. It is clear that electrophysiology is clinically useful when behavioural measures are difficult or impossible to obtain (e.g. in infants) and where there is a relatively well understood relationship between a particular function and the site of generation of the electrical response (e.g. electrocochleography). The finding that central electrophysiological measures among individuals correlate better with higher level skills such as speech-in-noise perception than do simple non-speech behavioural measures only serves to reinforce our underlying hypothesis: Perceptual variation between individuals with normal peripheral hearing is more a topdown than a bottom-up phenomenon. A final practical and fundamental problem is that there are currently no available electrophysiological measures of sufficient utility and reliability to be useful in the clinical assessment of APD (McFarland & Cacace, 2012; Hornickel et al, 2012). A plethora of measures and stimuli is used inconsistently from study to study, with no clear evidence of replicability across studies. Epilogue Our hope is that the debate captured in our white paper and the following discussion will stimulate further, hypothesis-led research, culminating in evidence-based diagnosis and intervention. For clinicians, the question of what to do now about APD is probably best summarized in the recent paper of Dillon and colleagues (2012): “Patients will be best served by focusing on whether they have difficulty understanding speech, identifying the specific characteristics of this difficulty, and specifically remediating and/or managing those characteristics” (p. 97). Developmental auditory processing disorder Notes Int J Audiol Downloaded from informahealthcare.com by Hadassah college - Library on 04/23/13 For personal use only. 1. A ‘known genetic cause’ was not part of the proposal in BSA (2011a), but represents a potentially important omission that we would wish to add here. An example might be an association with Downs Syndrome. 2. It is worth making a general point here. Many clinicians are undoubtedly highly skilled at guiding a consultation towards the particular needs of a client, and that role will continue. However, evidence-based medicine also requires, where possible, the utilization of appropriate and well conducted research findings. Part of that process means that objectively derived test measures are usually preferable to measures that depend heavily on individual clinical skills. References Bajo V.M., Nodal F.R., Moore D.R. & King A.J. 2010. The descending corticocollicular pathway mediates learning-induced auditory plasticity. Nat Neurosci, 13, 253–60. British Society of Audiology (BSA). 2011a. Position Statement: Auditory processing disorder (APD). pp. 1–9 http://www.thebsa.org.uk/images/ stories/docs/BSA_APD_PositionPaper_31March11_FINAL.pdf Cameron S. & Dillon H. 2008. The listening in spatialized noise-sentences test (LISN-S): comparison to the prototype LISN, and results from children with either a suspected (central) auditory processing disorder or a confirmed language disorder. J Am Acad Audiol, 19, 377–391. 13 de Boer J. & Thornton A.R. 2008. Neural correlates of perceptual learning in the auditory brainstem: Efferent activity predicts and reflects improvement at a speech-in-noise discrimination task. J Neurosci, 28, 4929–37. Dillon H., Cameron S., Glyde H., Wilson W. & Tomlin D. 2012. An opinion on the assessment of people who may have an auditory processing disorder. J Am Acad Audiol, 23, 97–105. Hornickel J., Knowles E. & Kraus N. 2012. 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