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Hearing Journal:
doi: 10.1097/01.HJ.0000413511.54802.b3
Pathways

Pathways: “Comprehensive Auditory Function Testing Vital for Children with CAPD”

Chermak, Gail D. PhD

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Dr. Chermak is a professor and the chair of the Department of Speech and Hearing Sciences at Washington State University in Spokane. Dr. Musiek is a professor and the director of auditory research in the Department of Communication Sciences at the University of Connecticut in Storrs. Dr. Musiek is the clinical editor of Pathways.

Central auditory processing disorder or deficit has been linked to many etiologies, including neurologic lesions or compromise of the central auditory nervous system. We proposed many years ago three bases for CAPD in children who also presented with learning problems. (J Child Comm Dis 1985;9:43.)

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Although the incidence of children with central auditory processing disorder or deficit (CAPD) resulting from neurologic defects is considerably lower than that in children with CAPD, learning problems, and no identifiable neuropathology, some of the latter group also present with neurologic issues. Neurologic causes of CAPD may include seizure disorder (e.g., Laudau-Kleffner syndrome), traumatic brain injury, neoplasms, neurodegenerative disorders, neurotoxicity, cerebrovascular accidents, metabolic disorders, and genetic disorders that affect lesion sites of the central auditory nervous system (CANS). (Arch Dis Child 2001;85[5]:361; ASHA Lead 2009;14[15]:16.)

Figure. Gail D. Cher...
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Figure. Frank Musiek...
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CAUSES OF CAPD

Neuromaturational lag and neuroanatomical abnormalities form the foundation of CAPD in children. Those diagnosed with CAPD with a presumed underlying neuromaturational source present central auditory systems that appear to mature more slowly than seen in normal children, often secondary to auditory deprivation and delayed myelin maturation in the subcortex, cortex, and corpus callosum. (Arch Dis Child 2001;85[5]:361; Contemporary Perspectives in Hearing Assessment, Boston: Allyn & Bacon, 1999; Neuroaudiology Case Studies, San Diego: Singular, 1994; Semin Hear 1984:5[3]:231.)

These delays theoretically can result in decreased performance on central auditory tests and in hearing difficulties, and are likely related to the long maturational course of the CANS. (Semin Hear 1984;5[3]:231; Regional Development of the Brain in Early Life, Oxford: Blackwell Press, 1967; Dev Brain Res 1996;91[2]:274.)

Neuroanatomical abnormalities also cause CAPD in children, and result from irregular development of the higher auditory areas and yield abnormal anatomy. (Ann Neurol 1985;18[2]:222; Arch Neurol 1990;47[8]:919; Arq Neuropsiquiatr 2009;67[2B]:499; Brain Dev 2010;32[4]:299.) Neuroanatomical abnormalities are congenital and are not true neurologic disorders, in contrast to CAPD from neurologic disorders (congenital or acquired).

These neuroanatomical abnormalities include ectopic areas (misplaced, small nests of normal cells) and polymicrogyria (underdeveloped gyri in greater number than in normal brains) of the cortex, and other anatomical variances. The ectopic areas and polymicrogyria have been noted in children with learning problems (mostly in the left hemisphere and in the auditory cortex) by close examination of the brain postmortem. (Ann Neurol 1985;18[2]:222; Arch Neurol 1990;47[8]:919; Arq Neuropsiquiatr 2009;67[2B]:499; Brain Dev 2010;32[4]:299; Trans Am Neurol Assoc 1978;103:262.)

The planum temporal, which is typically larger on the left side of the brain in normal children, was shown to be symmetrical or larger on the right side in children with dyslexia. (Ann Neurol 1985;18[2]:222; Arch Neurol 1990;47[8]:919.) Other anatomical regions of the brain in children with learning problems appeared smaller, suggesting these areas are underdeveloped, when compared with normal controls. The abnormally small areas, interestingly, are the isthmus of the corpus callosum and the insula, which are auditory responsive areas. (The Auditory System: Anatomy, Physiology, and Clinical Correlates, Boston: Allyn & Bacon, 2007.)

The other area that has been shown to be reduced is the genu of the corpus callosum, which primarily contains fibers of the frontal lobe. (Arch Neurol 1990;47[8]:919.) Boscariol et al may offer the strongest evidence to date that structural changes in brain areas associated with auditory and language processing can lead to changes in auditory processing and therefore in language and learning. (Arq Neuropsiquiatr 2009;67[2B]:499; Brain Dev 2010;32[4]:299.)

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TESTING AND EVALUATING CAPD

Central auditory behavioral tests and electrophysiological procedures are used to evaluate pediatric patients with known or suspected neurologic involvement. All regions of the CANS can be assessed using auditory suggestions, electroacoustic procedures, and central auditory behavioral tests after careful assessment of the peripheral auditory system. Multidisciplinary evaluation is crucial to diagnosis and intervention given the potential for multiple system involvement, complex clinical profiles, and frequent comorbidities in children with neurologic problems.

Studies have confirmed that involvement of auditory regions (e.g., perisylvian polymicrogyria, cystic lesions in the left sylvian fissure) in children leads to performance deficits and patterns on central auditory tests compared with patients with documented CANS lesions. Autopsies show individuals with CAPD exhibit neuroanatomical abnormalities in auditory areas of the central nervous system. (Arq Neuropsiquiatr 2009;67[2-B]:499; Brain Dev 2010;32[4]:299; ASHA [2005] Central Auditory Processing Disorders. [See FastLinks.])

Deficit patterns from a central auditory test battery in children with hearing-related complaints but no identifiable lesions of the CANS mirror those patterns seen in children and adults with defined disorders of the CANS. These deficit patterns correlate with neuroimaging results. Common patterns indicate that lesion studies of adult and pediatric patients may serve as a gold standard for CAPD in children with no identifiable CANS lesion. (ASHA 2010. Guidelines for the diagnosis, treatment, and management of children and adults with central auditory processing disorder. [See FastLinks.])

Whether the source of CANS dysfunction is benign or the result of neurologic lesion or compromise, the source of CAPD is neurobiological, originating in the central nervous system. Frank Musiek, PhD, and I reviewed the neurologic issues underlying auditory processing deficits in children. (Current Ped Rev 2011;7[3]:241.)

The types of central auditory deficits in children with neurologic or neuroanatomical abnormalities (e.g., speech recognition difficulties in everyday listening environments) place them at risk for academic difficulties. Multidisciplinary evaluation is crucial given the complex clinical profiles and frequent comorbidities across this population. Comprehensive testing of auditory functions using behavioral and electrophysiological methods is important to identify children who can benefit from interventions, including assistive listening devices and environmental changes to improve signal-to-noise levels in the classroom. The range of therapeutic methods, including bottom-up auditory training and top-down language-based and cognitive-based therapies may prove useful. (Handbook of Central Auditory Processing Disorder, Comprehensive Intervention, [Vol. 2], San Diego: Plural Publishing, 2007.)

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FastLinks

* Read more about CAPD at http://bit.ly/ASHA-CAPD.

* AASHA's clinical guidelines for CAPD are available at: http://bit.ly/ASHA-guidelines.

* Click and Connect! Access the links in The Hearing Journal by reading this issue on thehearingjournal.com.

* Comments about this article? Write to HJ at HJ@wolterskluwer.com.

* Follow us on Twitter at twitter.com/hearingjournal.

© 2012 Lippincott Williams & Wilkins, Inc.

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