Introduction: Motor Speech Disorders in Idiopathic Speech Delay and in Complex Neurodevelopmental Disorders: Introduction.
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ABSTRACT:
SUBMITTER: Shriberg LD
PROVIDER: S-EPMC6594421 | biostudies-literature | 2019
REPOSITORIES: biostudies-literature
Publications
Introduction: Motor Speech Disorders in Idiopathic Speech Delay and in Complex Neurodevelopmental Disorders: Introduction.
Clinical linguistics & phonetics 20190101 8
This introduction to a special issue of <i>Clinical Linguistics & Phonetics</i> includes an overview of the contents of each of the six articles. Each of the articles use the finalized version of the Speech Disorders Classification System (SDCS). ...[more]
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Project description:The goal of this research was to obtain initial estimates of the prevalence of each of four types of motor speech disorders in children with idiopathic Speech Delay (SD) and to use findings to estimate the population-based prevalence of each disorder. Analyses were completed on audio-recorded conversational speech samples from 415 children recruited for research in idiopathic SD in six USA cities during the past three decades. The speech and motor speech status of each participant was cross-classified using standardized measures in the finalized version of the Speech Disorders Classification System described in the Supplement. Population-based prevalence estimates for the four motor speech disorders were calculated from epidemiological studies of SD conducted in Australia, England, and the USA. A total of 82.2% of the 415 participants with SD met criteria for No Motor Speech Disorder at assessment, 12% met criteria for Speech Motor Delay, 3.4% met criteria for Childhood Dysarthria, 2.4% met criteria for Childhood Apraxia of Speech, and 0% met criteria for concurrent Childhood Dysarthria and Childhood Apraxia of Speech. The estimated population-based prevalence of each of the first three motor speech disorders at 4 to 8 years of age were Speech Motor Delay: 4 children per 1,000; Childhood Dysarthria: 1 child per 1,000; and Childhood Apraxia of Speech: 1 child per 1,000. The latter finding cross-validates a prior prevalence estimate for Childhood Apraxia of Speech of 1-2 children per 1,000. Findings are interpreted to indicate a substantial prevalence of motor speech disorders in children with idiopathic SD. Abbreviations: CAS, childhood apraxia of speech; CD, childhood dysarthria; CND, complex neurodevelopmental disorders; DI, dysarthria index; DSI, dysarthria subtype indices; MSD, motor speech disorder; No MSD, no motor speech disorder; NSA, normal(ized) speech acquisition; PEPPER, programs to examine phonetic and phonologic evaluation records; PM, pause marker; PMI, pause marker index; PSD, persistent speech delay; PSE, persistent speech errors; SD, speech delay; SDCS, speech disorders classification system; SDCSS, speech disorders classification system summary; SE, speech errors; SMD, speech motor delay.
| S-EPMC6633906 | biostudies-literature
Project description:Estimates of the prevalence of speech and motor speech disorders in persons with complex neurodevelopmental disorders (CND) can inform research in the biobehavioural origins and treatment of CND. The goal of this research was to use measures and analytics in a diagnostic classification system to estimate the prevalence of speech and motor speech disorders in convenience samples of speakers with one of eight types of CND. Audio-recorded conversational speech samples from 346 participants with one of eight types of CND were obtained from a database of participants recruited for genetic and behavioural studies of speech sound disorders (i.e., excluding dysfluency) during the past three decades. Data reduction methods for the speech samples included narrow phonetic transcription, prosody-voice coding, and acoustic analyses. Standardized measures were used to cross-classify participants' speech and motor speech status. Compared to the 17.8% prevalence of four types of motor speech disorders reported in a study of 415 participants with idiopathic Speech Delay (SD), 47.7% of the present participants with CND met criteria for one of four motor speech disorders, including Speech Motor Delay (25.1%), Childhood Dysarthria (13.3%), Childhood Apraxia of Speech (4.3%), and concurrent Childhood Dysarthria and Childhood Apraxia of Speech (4.9%). Findings are interpreted to indicate a substantial prevalence of speech disorders, and notably, a substantial prevalence of motor speech disorders in persons with some types of CND. We suggest that diagnostic classification information from standardized motor speech assessment protocols can contribute to research in the pathobiologies of CND. Abbreviations: 16p: 16p11.2 deletion and duplication syndrome; 22q: 22q11.2 deletion syndrome; ASD: Autism Spectrum Disorder; CAS: Childhood Apraxia of Speech; CD: Childhood Dysarthria; CND: Complex Neurodevelopmental Disorder; DS: Down syndrome; FXS: Fragile X syndrome; GAL: Galactosemia; IID: Idiopathic Intellectual Disability; MSD: Motor Speech Disorder; No MSD: No Motor Speech Disorder; NSA: Normal(ized) Speech Acquisition; PEPPER: Programs to Examine Phonetic and Phonologic Evaluation Records; PSD: Persistent Speech Delay; PSE: Persistent Speech Errors; SD: Speech Delay; SDCS: Speech Disorders Classification System; SDCSS: Speech Disorders Classification System Summary; SE: Speech Errors; SMD: Speech Motor Delay; SSD: Speech Sound Disorders; TBI: Traumatic Brain Injury.
| S-EPMC6633911 | biostudies-literature
Project description:Recent studies report prevalence, phenotype, and persistence findings for a paediatric motor speech disorder in addition to childhood dysarthria and childhood apraxia of speech termed Speech Motor Delay (SMD). The aim of the present study was to determine if there is a frequent acoustic sign of SMD, with implications for theory, assessment, and treatment. We examined the frequency of 19 acoustic signs of SMD in audio recordings of continuous speech and word-imitation tasks in three groups of speakers with SMD: 50 children (mean age 5.1 years) with idiopathic Speech Delay (SD) from 6 USA cities; 87 children, adolescents, and adults with eight types of complex neurodevelopmental disorders; and 9 children (mean age 8.8 years) with persistent idiopathic SD from a population-based study of children in the South West of England. The 19 acoustic signs of imprecise or unstable speech, prosody, and voice were standardized on typical speakers of the appropriate dialect. The criterion for a frequent acoustic sign was that it occurred in at least 50% of participants with SMD in each of the three groups. Findings indicated that lengthened mid-vowels and diphthongs was the one sign that met criteria, occurring in 64.4% of the 146 participants with SMD, including 71% of the 87 participants with complex neurodevelopmental disorders. Findings are interpreted to support the potential of this acoustic sign, and possibly several others associated with temporal dimensions of speech sound development, to inform explication of the neuromotor substrates of SMD.
| S-EPMC6594422 | biostudies-literature
Project description:Purpose To test the hypothesis that children with classic galactosemia and speech disorders are at risk for co-occurring strength and coordination disorders. Method This is a case-control study of 32 children (66% male) with galactosemia and neurologic speech disorders and 130 controls (50% male) ages 4-16 years. Speech was assessed using the Percentage of Consonants Correct (PCC) metric from responses to the Goldman-Fristoe Test of Articulation-2 and from a 5-min recorded speech sample, hand and tongue strength using the Iowa Oral Performance Instrument, and coordination using the Movement Assessment Battery for Children. The number of days on milk during the neonatal period was obtained by parent report. Analyses of covariance, distributions, and correlations were used to evaluate relationships among speech, strength, coordination, age, gender, and days on milk. Results Children with galactosemia had weaker hand and tongue strength and most (66%) had significant coordination disorders, primarily affecting balance and manual dexterity. Among children with galactosemia, children with more speech errors and classified as childhood apraxia of speech (n = 7) and ataxic dysarthria (n = 1), had poorer balance and manual dexterity, but not weaker hand or tongue strength, compared to the children with fewer speech errors. The number of days on milk during the neonatal period was associated with more speech errors in males but not in females. Conclusion Children with galactosemia have a high prevalence of co-occurring speech, coordination, and strength disorders, which may be evidence of a common underlying etiology, likely associated with diffuse cerebellar damage, rather than distinct disorders.
| S-EPMC3755563 | biostudies-literature
Project description:The goal of this research was to assess the support for motor speech disorders as explanatory constructs to guide research and treatment of reduced intelligibility in persons with Down syndrome (DS). Participants were the 45 adolescents with DS in the prior paper who were classified into five mutually-exclusive motor speech classifications using the Speech Disorders Classification System. An ordinal index classified participants' percentage of intelligible words in conversation as High (≥ 85%), Moderate (80% - 84.9%), or Low (< 80%). Statistical analyses tested for significant differences in intelligibility status associated with demographic, intelligence, and language variables, and intelligibility status associated with motor speech classifications and speech, prosody, and voice variables. For the 10 participants who met criteria for concurrent Childhood Dysarthria and Childhood Apraxia of Speech at assessment, 80% had reduced (Moderate or Low) intelligibility and 20% had High intelligibility (significant effect size: 0.644). Proportionally more of the 32 participants who met criteria for either dysarthria or apraxia had reduced intelligibility (significant effect size: 0.318). Low intelligibility was significantly associated with across-the-board reductions in phonemic and phonetic accuracy and with inappropriate prosody and voice. Findings are interpreted as support for motor speech disorders in adolescents with DS as explanatory constructs for their reduced intelligibility. Pending cross-validation of findings in diverse samples of persons with DS, studies are needed to assess the efficacy of motor speech classification status to guide selection of treatment methods and intelligibility targets. Abbreviations: CAS: Childhood Apraxia of Speech; CD: Childhood Dysarthria; DS: Down syndrome; II: Intelligibility Index; No MSD: No Motor Speech Disorder; OII: Ordinal Intelligibility Index; PSD: Persistent Speech Delay; SDCS: Speech Disorders Classification System; SMD: Speech Motor Delay.
| S-EPMC6604063 | biostudies-literature
Project description:Movement atypicalities in speed, coordination, posture, and gait have been observed across the autism spectrum (AS) and atypicalities in coordination are more commonly observed in AS individuals without delayed speech (DSM-IV Asperger) than in those with atypical or delayed speech onset. However, few studies have provided quantitative data to support these mostly clinical observations. Here, we compared perceptual and motor performance between 30 typically developing and AS individuals (21 with speech delay and 18 without speech delay) to examine the associations between limb movement control and atypical speech development. Groups were matched for age, intelligence, and sex. The experimental design included: an inspection time task, which measures visual processing speed; the Purdue Pegboard, which measures finger dexterity, bimanual performance, and hand-eye coordination; the Annett Peg Moving Task, which measures unimanual goal-directed arm movement; and a simple reaction time task. We used analysis of covariance to investigate group differences in task performance and linear regression models to explore potential associations between intelligence, language skills, simple reaction time, and visually guided movement performance. AS participants without speech delay performed slower than typical participants in the Purdue Pegboard subtests. AS participants without speech delay showed poorer bimanual coordination than those with speech delay. Visual processing speed was slightly faster in both AS groups than in the typical group. Altogether, these results suggest that AS individuals with and without speech delay differ in visually guided and visually triggered behavior and show that early language skills are associated with slower movement in simple and complex motor tasks.
| S-EPMC5008150 | biostudies-literature
Project description:Speech Motor Delay (SMD) is a recently proposed childhood motor speech disorder characterized by imprecise and unstable speech, prosody, and voice that does not meet criteria for either Childhood Dysarthria or Childhood Apraxia of Speech. The goals of the present research were to obtain information on the phenotype of SMD and initial information on the persistence of SMD in children receiving treatment for idiopathic Speech Delay (SD). Five questions about the phenotype and persistence of SMD were posed using a database of audio-recordings and participant records and longitudinal data from audio-recordings of children with early SMD treated for SD. Three phenotype questions examined associations between participant risk factors and prevalence of SMD, and described the most frequent speech, prosody, and voice signs of early SMD. To provide initial estimates of the persistence of SMD, two questions examined associations between the persistence of SMD and participant risk factors using the audio-recordings of 14 participants with SMD treated for idiopathic SD. Phenotype findings indicated that SMD is characterized by across-the-board delays in the spatiotemporal precision and stability of speech, prosody, and voice production. Persistence findings indicated that although most participants normalized early SMD by 6 years of age, SMD persisted until at least late adolescence in 21.4% of participants. Findings are interpreted to support the construct validity of SMD and the potential for research using additional assessment modalities to explicate its genomic and neuromotor causal pathways. Abbreviations: CAS: Childhood Apraxia of Speech; CD: Childhood Dysarthria; MSD: Motor Speech Disorder; No MSD: No Motor Speech Disorder; PSI: Precision-Stability Index; SD: Speech Delay; SMD: Speech Motor Delay; SSD: Speech Sound Disorders.
| S-EPMC6604054 | biostudies-literature
Project description:Purpose Operationalized treatments for school-age children with speech sound disorders may result in more replicable and evidence-based interventions. This tutorial describes Speech Motor Chaining (SMC) procedures, which are designed to build complex speech around core movements by incorporating several principles of motor learning. The procedures systematically manipulate factors such as feedback type and frequency, practice variability, and stimulus complexity based on the child's performance. Method The rationale and procedures for SMC are described. Examples are presented of how to design stimuli, deliver feedback, and adapt the approach. Free resources are provided to guide clinicians through implementation of the procedure. Data on fidelity of implementation and dose per session are presented. Clinical and research evidence is provided to illustrate likely outcomes with the procedure. Results SMC is a method that can result in successful acquisition of target speech patterns and generalization to untrained words. Most clinicians can implement the procedure with over 90% fidelity, and most children can achieve over 200 trials per session. Conclusion Clinicians and researchers can use or adapt the operationally defined SMC procedures to incorporate several principles of motor learning into treatment for school-age children with speech sound disorders. Supplemental Material https://osf.io/5jmf9/.
| S-EPMC6802861 | biostudies-literature
Project description:Delineating candidate genes at the chromosomal breakpoint regions in the apparently balanced chromosome rearrangements (ABCR) has been shown to be more effective with the emergence of next-generation sequencing (NGS) technologies. We employed a large-insert (7-11 kb) paired-end tag sequencing technology (DNA-PET) to systematically analyze genome of four patients harbouring cytogenetically defined ABCR with neurodevelopmental symptoms, including developmental delay (DD) and speech disorders. We characterized structural variants (SVs) specific to each individual, including those matching the chromosomal breakpoints. Refinement of these regions by Sanger sequencing resulted in the identification of five disrupted genes in three individuals: guanine nucleotide binding protein, q polypeptide (GNAQ), RNA-binding protein, fox-1 homolog (RBFOX3), unc-5 homolog D (C.elegans) (UNC5D), transmembrane protein 47 (TMEM47), and X-linked inhibitor of apoptosis (XIAP). Among them, XIAP is the causative gene for the immunodeficiency phenotype seen in the patient. The remaining genes displayed specific expression in the fetal brain and have known biologically relevant functions in brain development, suggesting putative candidate genes for neurodevelopmental phenotypes. This study demonstrates the application of NGS technologies in mapping individual gene disruptions in ABCR as a resource for deciphering candidate genes in human neurodevelopmental disorders (NDDs).
| S-EPMC3946304 | biostudies-literature
Project description:Rnd proteins are a subfamily of Rho GTPases involved in the control of actin cytoskeleton dynamics and other cell functions such as motility, proliferation and survival. Unlike other members of the Rho family, Rnd proteins lack GTPase activity and therefore remain constitutively active. We have recently described that RhoE/Rnd3 is expressed in the Central Nervous System and that it has a role in promoting neurite formation. Despite their possible relevance during development, the role of Rnd proteins in vivo is not known. To get insight into the in vivo function of RhoE we have generated mice lacking RhoE expression by an exon trapping cassette. RhoE null mice (RhoE gt/gt) are smaller at birth, display growth retardation and early postnatal death since only half of RhoE gt/gt mice survive beyond postnatal day (PD) 15 and 100% are dead by PD 29. RhoE gt/gt mice show an abnormal body position with profound motor impairment and impaired performance in most neurobehavioral tests. Null mutant mice are hypoactive, show an immature locomotor pattern and display a significant delay in the appearance of the hindlimb mature responses. Moreover, they perform worse than the control littermates in the wire suspension, vertical climbing and clinging, righting reflex and negative geotaxis tests. Also, RhoE ablation results in a delay of neuromuscular maturation and in a reduction in the number of spinal motor neurons. Finally, RhoE gt/gt mice lack the common peroneal nerve and, consequently, show a complete atrophy of the target muscles. This is the first model to study the in vivo functions of a member of the Rnd subfamily of proteins, revealing the important role of Rnd3/RhoE in the normal development and suggesting the possible involvement of this protein in neurological disorders.
| S-EPMC3084285 | biostudies-literature