This research program has developed an etiological classification system, the Speech Disorders Classification System (SDCS), that addresses both the distal and proximal causes of Speech Delay (SD). The long term objective is to contribute to the knowledge based needed for eventual prevention of SD. The two specific aims for the next proposed period are to extend the diagnostic accuracy of the SDCS and to complete a translational project that will make it freely available for research and practice. Ten databases will be used to complete six study series, including data from over 3,910 participants. Arm I: SDCS Validation. Three studies in Arm I will cross-validate and extend the diagnostic accuracy of the SDCS. A Reference Study will provide lifespan reference data for all SDCS measures, a Retrospective Study will provide the first retrospective test of the diagnostic accuracy of the SDCS, and a Prospective Study will provide the first prospective study of its diagnostic accuracy. Arm II: Descriptive-Explanatory Studies. Three studies in Arm II will provide diagnostic profiles and contribute to explanatory accounts for three etiological subtypes of SD. Speech Delay-Genetics studies will cross-validate phenotype markers and validate two new endophenotype markers in molecular genetics studies with collaborators at several sites. Speech-Delay-Otitis Media with Effusion (OME) studies will provide the first test of alternative severity levels of early fluctuant hearing loss associated with OME as risk factors for clinical and subclinical SD. Speech Delay-Apraxia of Speech (AOS) studies will provide the first comparative speech-prosody-voice data using the same perceptual- and acoustic-based measures for adult acquired AOS, AOS as a sequela of neurological disorder, AOS as a sign in complex neurodevelopmental disorders, and idiopathic childhood AOS. Arm III: Translational Project. A three-phase translational project will complete the SDCS software and develop multimedia SDCS training materials, beta test the software and training materials with samples of speech-language pathologists and children with SD of unknown origin, and make the SDCS and training materials freely available to qualified speech-language researchers and clinicians. The studies in this research program directly address the proximal and distal causes of SD of currently unknown origin. SD is risk factor for children's literacy achievement, positive self concept, peer acceptance, and limitations in vocational choices The high prevalence of SD at 6 years of age (3.8%: Shriberg, Tomblin, &McSweeny, 1999) places it among the most frequently occurring childhood disorders warranting public health resources for research in prevention, assessment, and treatment.7. PROJECT NARRATIVE Speech delays of currently unknown origin are a highly prevalent public health concern (3.8% at six years of age) that place children at risk for reading disability, psychosocial handicap, and vocational limitations. This research seeks to identify the causes of children's speech delays, with emphasis on the roles of heredity, early recurrent middle ear disease, and speech motor control. A translational project will provide speech-language pathologists with an assessment tool to make early and accurate diagnostic decisions, with implications for individualized treatment based on the type of speech delay.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Project (R01)
Project #
5R01DC000496-24
Application #
8260416
Study Section
Language and Communication Study Section (LCOM)
Program Officer
Shekim, Lana O
Project Start
1988-07-01
Project End
2013-06-30
Budget Start
2012-05-01
Budget End
2013-06-30
Support Year
24
Fiscal Year
2012
Total Cost
$552,337
Indirect Cost
$163,391
Name
University of Wisconsin Madison
Department
Pediatrics
Type
Other Domestic Higher Education
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
Truong, D T; Shriberg, L D; Smith, S D et al. (2016) Multipoint genome-wide linkage scan for nonword repetition in a multigenerational family further supports chromosome 13q as a locus for verbal trait disorders. Hum Genet 135:1329-1341
Mueller, Kathryn L; Murray, Jeffrey C; Michaelson, Jacob J et al. (2016) Common Genetic Variants in FOXP2 Are Not Associated with Individual Differences in Language Development. PLoS One 11:e0152576
Evans, P D; Mueller, K L; Gamazon, E R et al. (2015) A genome-wide sib-pair scan for quantitative language traits reveals linkage to chromosomes 10 and 13. Genes Brain Behav 14:387-97
Strand, Edythe A; Duffy, Joseph R; Clark, Heather M et al. (2014) The Apraxia of Speech Rating Scale: a tool for diagnosis and description of apraxia of speech. J Commun Disord 51:43-50
Raca, Gordana; Baas, Becky S; Kirmani, Salman et al. (2013) Childhood Apraxia of Speech (CAS) in two patients with 16p11.2 microdeletion syndrome. Eur J Hum Genet 21:455-9
Potter, Nancy L; Nievergelt, Yves; Shriberg, Lawrence D (2013) Motor and speech disorders in classic galactosemia. JIMD Rep 11:31-41
Shriberg, Lawrence D; Lohmeier, Heather L; Strand, Edythe A et al. (2012) Encoding, memory, and transcoding deficits in Childhood Apraxia of Speech. Clin Linguist Phon 26:445-82
Rice, Gregory M; Raca, Gordana; Jakielski, Kathy J et al. (2012) Phenotype of FOXP2 haploinsufficiency in a mother and son. Am J Med Genet A 158A:174-81
Tomblin, J Bruce; Mueller, Kathyrn L (2012) How Can the Comorbidity with ADHD Aid Understanding of Language and Speech Disorders? Top Lang Disord 32:198-206
Laffin, Jennifer J S; Raca, Gordana; Jackson, Craig A et al. (2012) Novel candidate genes and regions for childhood apraxia of speech identified by array comparative genomic hybridization. Genet Med 14:928-36

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