20Q: CAPD - Fundamentals

From the Desk of Gus Mueller

The ’60s and ‘70s were exciting times for clinical audiologists conducting behavioral testing. Differentiating conductive from sensorineural pathologies had become rather mundane, but now, armed with tests such as the ABLB, Békésy audiometry, tone decay and PI/PB rollover, we became “tumor hunters extraordinaire.” And, our inquisitive journey beyond the cochlea did not stop at nerve VIII. It was also during this time that we learned of new audiologic tests of central auditory function—tests sensitive enough to maybe even separate brainstem from cortical disorders. Pretty amazing stuff.

In was in the 1960s that central auditory processing tests like the still-popular Dichotic Digits, SSI and SSW were introduced. Regular 20Q readers might recall that we addressed this topic five years ago, with a special 50^th year anniversary article by Doreen Kimura, the pioneer of dichotic speech testing, which included comments by James Jerger, Jack Katz and Frank Musiek. This month at 20Q we’re going to go a little deeper into the area of central auditory processing disorder (CAPD), by reviewing some of the underlying principles and fundamentals. And, we have found an author equal to our other experts, who has devoted her career to this intriguing topic.

Gail D. Chermak, PhD is professor of audiology and chair of the Department of Speech and Hearing Sciences, Elson S. Floyd College of Medicine, at Washington State University Health Sciences Spokane, Washington. She is an internationally recognized authority on CAPD and has authored or edited six books on the topic. Most of you are familiar with her two-volume Handbook of Central Auditory Processing Disorder, edited with Frank Musiek, now in its 2^nd edition, which is considered the definitive text on CAPD.  Dr. Chermak has received numerous honors and awards, including the American Academy of Audiology’s Distinguished Achievement Award and Honors of the American Speech-Language-Hearing Association. 

For both the AAA and the ASHA, if the topic was CAPD, there is a good chance that Dr. Chermak has been involved. She has chaired numerous committees and task forces, authored technical reports, position statements and clinical practice guidelines, and served as program chair for the first and second global conferences on CAPD held in conjunction with the 2012 and 2014 AAA conventions. 

Not all audiologists specifically test for CAPD, but it certainly is an area that we all must be familiar with. In this 20Q, Gail nicely reviews important background information, and relates these concepts and research findings to our typical clinical practice. In fact, she has so many excellent things to say, I’m not sure that we will be able to finish everything within the boundaries of 20 Questions. Stay tuned.  

 

Gus Mueller, PhD
Contributing Editor
July 2016

 

To browse the complete collection of 20Q with Gus Mueller CEU articles, please visit www.audiologyonline.com/20Q

20Q: CAPD - Fundamentals
 

      Gail Chermak

1.  Let’s start with the basics.  What is your definition of a central auditory processing disorder (CAPD)?

This isn’t just my definition, but one that has been agreed upon by several experts.  CAPD is a disorder of the central auditory nervous system (CANS) (ASHA, 2005; AAA, 2010; Musiek & Chermak, 2014). CAPD manifests as deficits in the perceptual processing of auditory stimuli in the central nervous system, and in the underlying neurobiological activity that gives rise to the electrophysiological auditory potentials, and affects individuals across the lifespan. CAPD frequently is seen with a number of co-morbid disorders (e.g., attention deficit hyperactivity disorder [ADHD], learning disabilities, certain types of dementia, psychiatric disorders, age-related CNS changes or central presbycusis); however, CAPD manifests primarily in the auditory modality and is diagnosed using a battery of sensitized auditory tests and procedures. 

2. What are the perceptual processing deficits that you mention? 

CAPD affects perceptual and neural processes underlying: sound localization and lateralization; auditory discrimination; auditory pattern recognition; temporal processing; auditory performance with competing or degraded acoustic signals; and other deficits (e.g., spatial processing or spatial release from masking) (ASHA, 2005; Musiek & Chermak, 2014).

3. I thought that we changed the name to “APD” several years back, but I see you are using “CAPD”?  

True, some have expressed a preference for the term auditory processing disorder (APD), a term that acknowledges the interaction between the periphery and the central auditory system.  You are probably referring to the Jerger & Musiek (2000) paper.  However, CAPD is a more ecologically valid, operational term and definition, which is representative of how processing actually occurs, and suggests how to measure the perceptual processes and underlying neurobiologic activity.  The perceptual processes that constitute central auditory processing are performed in the brain (i.e., centrally). Sensitized tests that challenge our intrinsically redundant CANS (e.g., dichotic tests, frequency and duration pattern tests, gap detection tests) must be employed to reveal central auditory processing deficits. 

4. So today, CAPD is pretty much the accepted term? 

Importantly, CAPD is the terminology used in the most recent International Classification of Disease (ICD-10), which went into effect in the United States on October 1, 2015. ICD-10, the standard diagnostic tool for epidemiology, health management, and clinical purposes, assigns central auditory processing disorder diagnosis code H93.25.  This code specifies, “A disorder characterized by impairment of auditory processing, resulting in deficiencies in the recognition and interpretation of sounds by the brain. Causes include brain maturation delays and brain traumas or tumors. Excludes mixed receptive-expressive language disorder.” This definition of CAPD clearly reflects the categories of causation that Musiek, Gollegly, and Ross (1985) described over 30 years ago.

5. Okay, CAPD it is!  Let’s talk about children.  Do they have different types of CAPD?

Children with CAPD and learning problems (neurodevelopmental CAPD) in the absence of an identifiable underlying neuropathology comprise the large majority of pediatric CAPD. Neurodevelopmental CAPD presumably is the result of some underlying benign, diffuse neuroanatomic/neuromorphological abnormalities (e.g., ectopias [normal but misplaced cells] or polymicrogyria [abnormally small gyri]). 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. A second type of neurodevelopmental CAPD is the result of neuromaturational delay, presumed to result from the slower course (delayed) of myelination or resulting from auditory deprivation. Neuromaturational lag comprises approximately 20-30% of pediatric CAPD, while the largest proportion of CAPD in children (60-70%) is classified as neuromorphological. 

6. Can CAPD be acquired in children?

A small percentage of pediatric CAPD may be acquired due to neurological disorders (5-10%). Among the acquired neurologic causes of CAPD in children are: seizure disorders (e.g., Landau Kleffner), neoplasms, neurodegenerative processes, traumatic brain injury, and cerebrovascular accidents. Acquired causes of CAPD in children also include metabolic disorders and genetic disorders (Chermak & Musiek, 2011). The extraordinarily long time course of CANS maturation exemplifies the difficulties of separating a slowly maturing but normal system, from a significantly disordered one. Presently, the only way to differentiate neuromaturational delay form a neuromorphological anomaly is to follow the patient with periodic, follow-up testing. 

7. What are the causes of CAPD in adults?

CAPD in adults may result from a diagnosed or undiagnosed neurodevelopmental disorder in childhood, or might be acquired.  Acquired CAPD in adults may be due to neurological lesions or compromise of the CANS, including neoplasms, neurodegenerative processes (e.g., multiple sclerosis, Alzheimer’s), head trauma, or impaired cerebral circulation (e.g., strokes). Additional acquired causes include aging/central presbycusis, noise exposure, or exposure to neurotoxic chemicals or heavy metals (e.g., styrene, lead, mercury). Interestingly, from the 7th decade (60’s) and beyond, central auditory function (as measured by behavioral tests) declines more than pure tone sensitivity or outer hair cell function (as measured by DPOAEs) (Gates, Anderson, Feeney et al., 2008). 

8. You mention CAPD from noise exposure?  I’ve always thought of that as a cochlear pathology?

Morest (1982) demonstrated that noise-induced hearing loss in animals was accompanied by damage to the (central) auditory brainstem neurons, highlighting transynaptic degeneration from the periphery to central auditory system. Kujawa and Liberman (2009) demonstrated that a single, moderately intense noise exposure for as little as two hours was sufficient to cause temporary threshold shift in mice as documented by distortion product otoacoustic emissions (DPOAE), auditory brainstem response (ABR) and compound action potentials (CAP). While the DPOAEs returned to normal shortly thereafter, the ABRs and CAPs remained affected. Histological analyses revealed intact cochlear hair cells; however, even after the thresholds returned to normal, there remained an acute loss of afferent nerve terminals. More recent findings demonstrate that exposure to moderate intensity levels of noise that do not cause peripheral hearing loss, can, nonetheless, over a period of time, result in damage to the CANS.  In these cases, performance deficits can be seen on measures of temporal processing and speech recognition in noise (Kumar, Ameenudin, & Sangamanatha, 2012; Pienkowski & Eggermont, 2012; Zhou & Merzenich, 2012). The Zhou and Merzenich study suggests the possibility that the auditory symptoms reported by a patient with history of noise exposure but with a normal audiogram might be related to compromise of the CANS. This possibility should compel audiologists to at least consider central auditory involvement in those with noise-induced hearing loss, and perhaps even in those with a history of noise exposure and auditory symptoms.   

9. What exactly is happening in the brain with CAPD?

Much of what is happening, or isn’t happening, is related to the role of myelin and neuroplasticity.  The CANS requires considerable time to mature, especially the corpus callosum, as well as intra-hemispheric connections (e.g., arcuate fasciculus). Myelination is key to neuromaturation, which may require 12-14 years before it approximates adult levels. The extended time course of the normal neuromaturational process is seen, for example, in children’s dichotic listening performance, which does not reach adult levels until approximately 10 years of age. The normal neuromaturational time course also explains interaural asymmetries on dichotic listening during the developmental process. Concerns are raised when this asymmetry exceeds norms or when the asymmetry fails to resolve to adult levels (Musiek, Gollegly, & Baran, 1984). Some children’s CANS maturation may lag causing their central auditory processing abilities to lag. They may not be able to handle complex listening situations as well as children whose CANS are developing on track. 

10. Do these children ever catch up, or do they just become adults with CAPD?

In many cases, these children do “catch up,” often by the time they are teenagers. The neurodevelopmental time course is the reason we need age specific norms to interpret central auditory test performance, as well as interpret auditory evoked potentials.  Neuroplasticity results from the activation of previously inactive neuronal tissue and/or improved neural synchrony, as well as the development of more efficient synaptic connections within the brain secondary to stimulation (Edelman & Gally, 2001; Schnupp et al., 2011). Neuroplasticity leads to the reorganization or remapping of the cortex (and the brainstem) by experience. Stimulation and training induce plasticity and the remapping of the cortex is reflected in behavioral change (i.e., learning). Although plasticity decreases from early to late adulthood (Wengner et al., 2012), mature sensory systems retain the potential for extensive plasticity triggered by changes in prevailing stimulation and/or by learning driven by behavioral demands (Lovden et al., 2013, Pienkowski & Eggermont, 2011; see Feldman & Brecht, 2005 & Ohl & Scheich, 2005 for reviews). Clearly, neuroplasticity is pivotal to rehabilitation and is best exploited through early identification and intervention.

11. Which areas of the brain are involved in CAPD?

Most activity underlying auditory processing occurs in the primary auditory cortex and brainstem. The auditory system is extensive, involving temporal, frontal, parietal, limbic and insular cortices, the corpus callosum, and subcortical regions, including the basal ganglia (striatum and amygdala), the thalamus (e.g., medial geniculate body), and the reticular activating system of the brainstem. The cerebellum also is involved in sensory perception (see Baumann et al., 2014 for review) during auditory stimulation.  

12. The cerebellum?  Interesting!

Yes, research has shown that patients with cerebellar degeneration demonstrate deficits in temporal and pitch discrimination despite normal pure tone thresholds (Parsons et al., 2009; Pastor et al., 2004). The auditory system also overlaps with other systems, including other sensory systems, language processing, cognition and executive control, and motor control (Bayazit et al., 2009; Poldrack et al., 2001; Poremba et al., 2003; Wong et al., 2009). Given the extensive representation of the auditory system, its overlapping neural substrate, and the range of potentially abnormal neurophysiologic representations of auditory stimuli, it is not surprising to find CAPD in many populations across the spectrum.

13.  Do we have evidence to infer or observe CANS involvement in children with CAPD?

We have known for some time that children with neurodevelopmental (neuromorphological) CAPD perform similarly as children with confirmed CANS lesions on central auditory tests (Jerger et al., 1988). Recent reports using electrophysiological procedures, behavioral central auditory tests, and brain imaging studies have confirmed cortical developmental anomalies (i.e., microgyria, ectopia) underlying at least some CAPD in children (Boscariol et al., 2009, 2010a, 2010b, 2011, 2015). Grindle et al. (2010) also documented a left temporal lobe lesion consistent with an arachnoid cyst in an 8-year-old with central auditory processing (tests and symptoms) deficits.                                      

14.  What are characteristic symptoms and complaints of individuals ultimately diagnosed with CAPD?

Individuals with CAPD present a range of functional deficits consistent with their underlying auditory problem. However, these symptoms and complaints are not unique to CAPD and could signal the presence of any number of other disorders (e.g., language processing, peripheral hearing loss, cognitive deficits, etc.). Among the most frequently seen symptoms or complaints are difficulty: understanding spoken language in competing message or noise backgrounds, in reverberant acoustic environments, or when rapidly presented; localizing the source of an auditory signal; with subtle intonation and prosodic cues, with similar sounding words, following complex auditory directions/commands, and “hearing” on the phone. (See Wilson (2014) for review of screening questionnaires). 

15.  Getting back to children—how does CAPD affect classroom behavior and academic performance?

The difficulties I mentioned earlier often manifest in the classroom as: delayed response to verbal instructions; inability to sort out the relevant and discard the irrelevant; misunderstanding  spoken language; greater difficulty for novel language; difficulty holding information in short term memory and manipulating information (i.e., working memory), which affects literacy, math, writing, listening and following directions (e.g., may recall last part of message, but forget the first part); difficulty note-taking; and significant difficulties acquiring phonics skills fundamental to reading (and spelling) due to poor representation of basic speech sounds.

16.  What is the prevalence of CAPD?

CAPD in children and adolescents is estimated as 5% (1 in 20), with a male: female ratio of 2:1 (Palfery & Duff, 2007). The prevalence of CAPD in older adults has been estimated as 24%-76% in community-based samples of adults 55 to 75 years and older (Golding et al., 2004) and 70% in a clinical sample of patients over age 60 (Stach et al.,1990).  When I say clinical samples, I am referring to research that describes participants who were seen in, or referred to, the clinic due to some reported auditory issue. In community-based or population-based sampling, the participants come from the community in general and are used to estimate the number of people in larger populations who have a specific disease or disorder. Golding and colleague's prevalence estimates were based on performance on Australian versions of the original Synthetic Sentence Identification (SSI) test and the Dichotic Sentence Identification (DSI) test, known as the Macquarie Synthetic Sentence Identification (MSSI) test and the Macquarie Dichotic Sentence Identification (MDSI) test. Stach et al. computed prevalence estimates on the basis of patterns of results on the Synthetic Sentence Identification (SSI) test (Jerger et al., 1986) and phonetically-balanced (PB) words.

17.   Are there specific risk factors for CAPD?

There are many.  Risk factors for CAPD include: neonatal factors associated w/neurological dysfunction, such as prematurity, low birth weight, hyperbilirubinemia, asphyxia, cytomegalovirus, etc.; extrinsic brain damage, including meningitis, encephalitis, Lyme disease, head trauma, exposure to heavy metals or organic solvents; prenatal drug exposure; postnatal anoxia; cerebrovascular disorders (e.g., stroke); metabolic disorders (e.g., diabetes); seizure disorders; family history of CAPD or related developmental disorder (including ADHD, dyslexia, language impairment, specific learning disability, delayed maturation of the CANS; history recurrent otitis media; and deafness (due to auditory deprivation). I should emphasize that hyperbilirubinemia affects the brainstem, and as such is a cause of CAPD, but not auditory neuropathy.  Auditory neuropathy typically results from the involvement of the inner hair cells, the synapse between the inner hair cells and the eighth nerve, or the eighth nerve itself (Starr et al., 1996).

18.   I assume that children with CAPD are provided services in the schools?

Not always.  Securing treatment such as individualized education plan (IEP) services for children with CAPD in schools has been challenging because CAPD has not been one of the 14 IDEA disability categories. Securing services under IDEA required that the child be diagnosed with one of the other qualifying disabilities (e.g., Language Impaired or ADHD which falls under ‘Other Health Impaired’ [OHI]). Recently, however, a U.S. Ninth Circuit Court of Appeals' decision designated CAPD as an OHI under IDEA and audiologists were named as the qualified provider to diagnose CAPD (see September 2014 ASHA Leader article). While the Ninth Circuit applies only to Guam and the nine states in its circuit (i.e., AK, AZ, CA, HI, ID, MT, NV, OR, WA), other districts may adopt the Ninth Circuit decision based on a 'persuasive law' precedent. This ruling means that, at least in the Ninth Circuit, children diagnosed with CAPD can be qualified for school services (an IEP) under the OHI disability category, even in the absence of a comorbid speech or language impairment or specific learning disability. Moreover, CAPD’s new ICD-10 classification (H93.25) as a medical diagnosis strengthens the case that CAPD is an organic condition, whether acquired or congenital.  It also increases the likelihood that CAPD services might now be available in schools through the 1973 Rehabilitation Act (section 504 plan of accommodations), which is funded under general education. In addition, children with behaviors suggestive of CAPD can access early intervention services through response to intervention (RTI) services, even before diagnosis is possible. and without an evaluation for special education.

19.  Does the OHI classification more or less guarantee services?

To provide IEP services requires a multidisciplinary special education evaluation documenting that the child does have CAPD, that there is an academic impact, and that the child requires specially designed instruction. In the absence of documentation satisfying all these requirements, the child with CAPD might still have to be provided services through 504 accommodations rather than specially designed instruction under an IEP.

20.  I want to talk about the identification and diagnosis of CAPD, but I just reached my limit of questions.  Can we continue this topic next month?

Sounds good—that’s an important area to discuss.  See you then.

Editor's note: Readers can access the follow up article here: 20Q: CAPD - Diagnosis and Intervention.

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