This research program has developed a unique classification system for Speech Sound Disorders (SSD) termed the Speech Disorders Classification System (SDCS). Research goals are to understand the causal pathways that lead to each of eight subtypes of SSD so that clinicians can select the appropriate intervention approach for each child, and researchers can conduct studies that should lead to prevention of some subtypes of SSD. The final phase of this project will complete all goals by obtaining new information in three study series. Diagnostic Accuracy Studies. Using a unique risk factor classification system for SSD, including genomic and environmental variables, we will document speech error differences associated with how children encode speech signals, how they store and access linguistic representations of speech, and how they transcode representations into the movement gestures for speech production. Prevalence Studies. Our research indicates significant differences in the prevalence of subtypes of SSD and in the rates and types of normalization outcomes. The proposed research will estimate both clinical prevalence rates and population prevalence rates for six subtypes of SSD. Speech Processing Studies. Our studies have motivated questions about speech processing differences and similarities in speakers from different causal backgrounds. In addition to studies of speakers with speech delay and motor speech disorders of unknown origin, our questions will be informed by assessment data from speakers with Down syndrome, 22q11.2 deletion (Velocardiofacial) syndrome, Galactosemia, Joubert syndrome, and Rolandic Epilepsy. A number of hypotheses about speech processing differences between and within study groups will be addressed, including a focus on support for a speech sound disorder termed Childhood Apraxia of Speech and a placeholder motor speech disorder we term Motor Speech Disorder-Not Otherwise Specified. Relevance The high prevalence of SSD at 6 years of age (3.8%: Shriberg, Tomblin, and McSweeny, 1999), persisting to 8 years of age (3.6%: Wren et al., 2009), places SSD among the most frequently occurring childhood disorders warranting public health resources for research in prevention, assessment, and treatment. SSD puts a child at risk for literacy development, reduced peer acceptance, and limitations in vocational options. Findings from this research should have substantial impact on research and clinical practice for this significant childhood communicative disorder.
Approximately 4% of six-year-old children in the United States have speech sound disorders of unknown origin that place them at risk for reading disability, psychosocial handicap, and vocational limitations. This research seeks to identify the causes of children's speech sound disorders, with emphasis on the individual and multiple roles of heredity, middle ear disease, speech motor control, and psychosocial processes as risk factors. Our goal is to develop procedures to identify which one or more causal pathway is most likely for each child so clinicians can make accurate prognoses and provide targeted treatment, and researchers can develop ways to prevent speech sound disorders and/or reduce their negative effects on children's development.
|Snijders Blok, Lot; Rousseau, Justine; Twist, Joanna et al. (2018) CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language. Nat Commun 9:4619|
|Shriberg, Lawrence D; Strand, Edythe A; Fourakis, Marios et al. (2017) A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: Introduction. J Speech Lang Hear Res 60:S1094-S1095|
|Shriberg, Lawrence D; Strand, Edythe A; Fourakis, Marios et al. (2017) A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: IV. The Pause Marker Index. J Speech Lang Hear Res 60:S1153-S1169|
|Shriberg, Lawrence D; Strand, Edythe A; Fourakis, Marios et al. (2017) A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: III. Theoretical Coherence of the Pause Marker with Speech Processing Deficits in Childhood Apraxia of Speech. J Speech Lang Hear Res 60:S1135-S1152|
|Shriberg, Lawrence D; Strand, Edythe A; Fourakis, Marios et al. (2017) A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: II. Validity Studies of the Pause Marker. J Speech Lang Hear Res 60:S1118-S1134|
|Shriberg, Lawrence D; Strand, Edythe A; Fourakis, Marios et al. (2017) A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: I. Development and Description of the Pause Marker. J Speech Lang Hear Res 60:S1096-S1117|
|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|
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