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A Tutorial on Auditory Neuropathy/ Dyssynchrony for the Speech-Language Pathologist and Audiologist

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A Tutorial on Auditory Neuropathy/ Dyssynchrony for the Speech-Language Pathologist and Audiologist A Tutorial on Auditory Neuropathy/ Dyssynchrony for the Speech-Language Pathologist and Audiologist Kristin Uhler, Ph.D., CCC-A, FAAA,1 Amanda Heringer, B.A. (Au.D. candidate),2 Nanette Thompson, M.A., CCC-SLP,3 and Christine Yoshinaga-Itano, Ph.D.2 ABSTRACT This article presents information about developmental out- comes of children with auditory neuropathy/auditory dyssynchrony (AN). Colorado data on the number of children screened and the number of children identified with unilateral and bilateral AN will be described. Descriptive information about the percent of children with AN with cognitive disability and disabilities other than hearing loss will be presented. Language outcomes of children with normal cognitive development will be presented. This article will also provide informa- tion about etiologies and audiological information of children with AN. It includes assessment tools that have been useful in decision making for children with AN. KEYWORDS: Auditory neuropathy, auditory dyssynchrony, auditory neural hearing loss, auditory neuropathy spectrum Downloaded by: SASLHA. Copyrighted material. disorder, language development Learning Outcomes: As a result of this activity, the reader will be able to (1) describe the anticipated number of children with auditory neuropathy/auditory dyssynchrony (AN) with cognitive disability and the percentage of children anticipated with any disability other than hearing loss, (2) describe the etiologies associated with AN, (3) describe the considerations for cochlear implant candidacy of children with AN, (4) describe an assessment procedure that can be used in the first year of life to examine the child’s vocal development and the contribution of auditory skill to that development, (5) discuss issues related to choices of communication approaches and AN. 1University of Colorado, Denver—Medical Campus, Maximizing Intervention for Children Who Are Deaf and Denver, Colorado; 2University of Colorado, Boulder, Boul- Hard of Hearing; Guest Editors, Cheryl DeConde John- der, Colorado; 3University Hospital, Aurora, Colorado. son, Ed.D. and Christine Yoshinaga-Itano, Ph.D. Address for correspondence and reprint requests: Chris- Semin Speech Lang 2012;33:354–366. Copyright tine Yoshinaga-Itano, Ph.D., Department of Speech, Lan- # 2012 by Thieme Medical Publishers, Inc., 333 Seventh guage, and Hearing Sciences, University of Colorado, CB Avenue, New York, NY 10001, USA. Tel: +1(212) 584- 409, Boulder, CO 80309-0409 (e-mail: Christie.yoshi@ 4662. colorado.edu). DOI: http://dx.doi.org/10.1055/s-0032-1326917. ISSN 0734-0478. 354 A TUTORIAL ON AUDITORY NEUROPATHY/DYSSYNCHRONY/UHLER ET AL 355 Auditory neuropathy (AN) is a disorder care professionals, and families with an abun- that was first identified in 1996; however, it is dance of unanswered questions.10 not as rare as once thought.1,2 Hinchcliffe and AN is characterized by abnormal temporal colleagues3 were the first to report the charac- encoding and neural asynchrony. It leads to teristics of AN in a Nigerian sample. In 1996, delayed speech acquisition, verbal learning dis- Starr et al4 assessed individuals with similar ability, and HL. The consequences of these characteristics and developed the term auditory factors can negatively affect a child’s social, neuropathy. Researchers have long disagreed emotional, physical, and educational over the term auditory neuropathy. Opponents development.11–13 argued that AN implied a known pathology of Audiological Characteristics of AN. Audio- the eighth nerve limited to the spiral ganglion logically, AN is characterized by present tran- cells and their axons; and, as research has sient otoacoustic emissions (OAEs); the expanded our knowledge regarding AN, we presence of the cochlear microphonic (CM); know that AN is much more complex. There the absence or abnormality (prolonged latency may be many etiologies and multiple locations or poor morphology) of an automated brain affected such as the inner hair cells, the spiral stem response (ABR); elevated or absent middle ganglion fibers, the myelinated fibers of the ear muscle reflexes (MEMR), also known as eighth cranial nerve, and the brain stem. There- acoustic reflexes; normal tympanometry; and no fore, in 2008, experts at the International evidence of a space occupying lesion upon Newborn Hearing Screening Conference neurological examination. Individuals with coined the term auditory neuropathy spectrum AN display normal to profound HL that may disorder (ANSD) because the issues regarding fluctuate, be characterized with poor speech the disorder lie on a continuum. They stated perception ability (particularly in the presence that AN should be restricted to cases where the of noise) that may not correlate to the audio- locus of the pathology is identified as the spiral gram, and a flat or reverse slope audiogram ganglion cells or the eighth cranial nerve.5–8 configuration is common. These individuals The interested reader is referred to Rapin and may vary significantly from one another in their Gravel9 for an in-depth discussion regarding ability to use temporal cues because AN results the anatomical structures of the auditory system in degraded processing of temporal cues in and what sites of pathology constitute the speech.2,6,7,9,11,12,14–17 Sininger and Starr18 definition of a neuropathy. Rapin and Gravel state that AN is typically bilateral and shows argue that the site of pathology is rarely attrib- no gender preference. Prevalence of AN has Downloaded by: SASLHA. Copyrighted material. uted to the spiral ganglion cells, but rather to been found to be 10% of the children identi- the central auditory pathway, leading them to fied with HL from the universal newborn conclude that the term AN is a misnomer. hearing screening (UNHS) programs.11,17,19 Although it is true that there is a complex Sites of Lesion and AN. The specific sites and spectrum of children with auditory neural hear- mechanisms of AN are not yet known and the ing loss (HL), the use of the term that includes variable behavior of the disorder means that the “spectrum disorder” has been very confusing for disorder can improve, remain stable, or worsen parents who have greater familiarity with “au- over time. The inconsistency in the clinical course tism spectrum disorder” and we are therefore, in and the prognosis often makes management of this article, referring to the disorder as AN, the disorder difficult. Individuals with AN are though we acknowledge that there is a signifi- often misdiagnosed as having central auditory cant number of children with auditory dyssyn- processing disorder or attention deficit disorder chrony and that there is great variety or a due to their inability to attend to a signal in “spectrum” of characteristics. The use of AN noise.2,6,10 Research has shown evidence that AN in this article is meant to encompass the het- is a hearing disorder where sound enters the ear erogeneity of the disorder. Terminology aside, normally but the transmission of signals from the the transient behavior of the disorder and the inner ear to the brain is impaired. multiple theories surrounding its epidemiology, Research by Akman et al2 and Foerst et al7 etiology, and prognosis leave researchers, health concludes that possible sites of lesion include 356 SEMINARS IN SPEECH AND LANGUAGE/VOLUME 33, NUMBER 4 2012 the inner hair cells, the tectorial membrane, the fants. Recently, emerging bodies of evidence synaptic junctions between the inner hair cells, have surfaced suggesting that the auditory the auditory neurons in the spiral ganglion, the nervous system is the most sensitive nervous eighth nerve fibers, or a combination of the system to the effects of bilirubin toxicity, lead- above. In addition, they state that neural prob- ing to the conclusion that severe hyperbilirubi- lems may be axonal or demyelinating, may nemia often results in a sensorineural hearing affect the afferent and efferent pathways, and loss (SNHL). Akman et al2 sought to evaluate if may possibly relate to the biochemical abnor- a correlation existed between increased serum malities that involve the release of bilirubin and neuron-specific enolase (NSE) neurotransmitters. assays and AN. They examined 19 infants AN and Comorbidities. Previous research who were treated for hyperbilirubinemia. has shown that AN may coexist or be associated None of these infants had a 5-minute Apgar with a multitude of other disorders, but may be score of less than 7, and infants with bilirubin diagnosed in individuals with no risk factors or levels above 20 mg/dL were given a full assess- associated disorders. Some of the associated ment, screened for glucose-6-phosphate dehy- disorders include Friedreich’s ataxia, hydro- drogenase deficiency, and treated with cephalus, ischemic-hypoxic neuropathy, spino- phototherapy and/or exchange transfusion. cerebellar degeneration, Charcot-Marie-Tooth All infants returned to normal after therapy, neuropathy syndrome, hereditary sensory mo- which eliminated the possibility of Crigler- tor neuropathies, perinatal intracranial hemor- Najjar syndrome. The 19 infants were split rhage, low birth weight, poor Apgar scores, into two groups: group A had total bilirubin hyperbilirubinemia, prematurity, ototoxic drug equal 20 to 25 mg/dL and group B had total exposure, mechanical ventilation, cerebral pal- bilirubin over 25 mg/dL. These infants were sy, anoxia, other peripheral neuropathies, or an compared with a control group; seven of these underlying genetic cause.11,15,17 infants were diagnosed with AN by utilization Risk Factors and AN. Dowley et al14 con- of ABR, transient evoked OAE, and presence ducted a study in the United Kingdom that of a CM, six being within group B and one examined the audiological data from the local infant within group A. Repeatable ABRs at 3 to newborn hearing screening program. Out of the 4 months and again at age 1 year showed no 45,050 infants screened, 30 were diagnosed improvement for five of the seven infants. One with hearing impairment, and 12 of those 30 infant was lost to follow-up and one infant was babies were also diagnosed with AN, making deceased at 2 months of age.
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