Consonant production patterns of young severely language-delayed children with autism

McCleery, Joseph P.; Tully, Lisa; Slevc, L. Robert; Schreibman, Laura

doi:10.1016/j.jcomdis.2005.12.002

Cited by 58 publications

(32 citation statements)

References 28 publications

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“…Thus, for most persons with verbal ASD, the speech processes in typical acquisition and performance—encoding phonological representations, retrieving the representations, transcoding representations to gestures underlying speech production (i.e., planning/programming), and executing the neuromotor commands for speech—are largely intact (e.g., McCleery, Tully, Slevc, & Schreibman, 2006). As concluded over a decade ago by Kjelgaard and Tager-Flusberg (2001) and as shown by the estimates in Table 2, articulation seems to be “spared” in most children with ASD.…”

Section: Discussionmentioning

confidence: 99%

The Hypothesis of Apraxia of Speech in Children with Autism Spectrum Disorder

Shriberg

Paul

Black

et al. 2010

J Autism Dev Disord

152

136

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In a sample of 46 children aged 4 to 7 years with Autism Spectrum Disorder (ASD) and intelligible speech, there was no statistical support for the hypothesis of concomitant Childhood Apraxia of Speech (CAS). Perceptual and acoustic measures of participants' speech, prosody, and voice were compared with data from 40 typically-developing children, 13 preschool children with Speech Delay, and 15 participants aged 5 to 49 years with CAS in neurogenetic disorders. Speech Delay and Speech Errors, respectively, were modestly and substantially more prevalent in participants with ASD than reported population estimates. Double dissociations in speech, prosody, and voice impairments in ASD were interpreted as consistent with a speech attunement framework, rather than with the motor speech impairments that define CAS. Key Words: apraxia, dyspraxia, motor speech disorder, speech sound disorder A continuing question about persons with Autism Spectrum Disorder (ASD) is whether reported diminished abilities in gross, fine, and oral motor control are causally associated with reported deficits in speech acquisition and performance. The classification term for the speech deficit in question, recently adapted by the American Speech-Language-Hearing Association (ASHA;2007a, 2007b, is Childhood Apraxia of Speech (CAS). Medical literatures and speech literatures in other countries continue to prefer several other classificatory terms for this disorder, including dyspraxia and developmental verbal dyspraxia. "Childhood" apraxia of speech differentiates congenital and early acquired forms of apraxia of speech from adult acquired forms, but creates a nosological problem because childhood apraxia of speech generally persists into adulthood. We will use the ASHA (2007a) recommended term-CAS.The strong form of the hypothesis in the title of this paper, hereafter, the 'CAS-ASD' hypothesis, is that CAS is a sufficient cause of lack of speech development in at least some children classified as nonverbal ASD. The weak form of the CAS-ASD hypothesis is that CAS contributes to the inappropriate speech, prosody, and/or voice features reported in some children and adults with verbal ASD. Although the present report addresses only the weak form of the hypotheses, the conceptual framework and implications for treatment NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript apply to both forms of the hypothesis. Forthcoming research addresses the strong form of the hypothesis. The following sections provide (a) rationales for the CAS-ASD hypothesis, (b) an overview of idiopathic speech sound disorders, and (c) a summary of speech, prosody, and voice findings in verbal ASD. Rationales for the CAS-ASD HypothesisThe American Speech-Language-Hearing Association Position Statement recommends the following definition of CAS:Childhood apraxia of speech (CAS) is a neurological childhood (pediatric) speech sound disorder in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscula...

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Section: Discussionmentioning

confidence: 99%

The Hypothesis of Apraxia of Speech in Children with Autism Spectrum Disorder

Shriberg

Paul

Black

et al. 2010

J Autism Dev Disord

152

136

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“…Gernsbacher and colleagues (2008) observed that blowing raspberries and grabbing dangling toys correlated with later verbal fluency. Oromotor difficulties may explain the limited phonological development of minimally-fluent children with AD early in their development who, because of the relative ease with which they produce necessary articulatory movements, are more likely to produce vowels than consonants (Wetherby et al 1989) and voiced rather than voiceless consonants (e.g.,/d/vs./t/) (McCleery et al 2006). These problems can affect phonological development which may subsequently interact with lexical and grammatical development at early stages of language acquisition.…”

Section: Prelinguistic Risk Of Language Impairmentmentioning

confidence: 99%

The Ontogenesis of Language Impairment in Autism: A Neuropsychological Perspective

Stefanatos

Baron

2011

Neuropsychol Rev

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Autistic Disorder (AD) is a phenotypically heterogeneous condition characterized by impairments in social interaction, communication, and the presence of repetitive behavior and restricted interests. It is a model syndrome to investigate neural interaction and integration at the nexus of language and social cognition. This paper considers the problems of language acquisition in AD from an evolutionary and ontogenetic context. Following a review of normal language development during the formative years of brain development, we examine what is known about infant linguistic and nonlinguistic precursors of language acquisition in AD and examine how anomalies of several processes relate to language abnormalities manifest by the early elementary school years. Population heterogeneity and practical limitations inherent to the study of children currently limit a comprehensive understanding of the significance of specific neurological abnormalities in relation to observed deficits. However, convergent evidence implicates anomalies of a widely distributed neural network, involving superior temporal sulcus, superior temporal gyrus, supramarginal gyrus, insula, inferior frontal gyrus, hippocampus, amygdala and cerebellum. These anomalies reflect the cumulative effects of genetic, epigenetic and environmental influences. Neuropsychological studies of language in AD provide an important means to define the phenotypic variation resulting from alterations in neural architecture. By mapping broad relationships between key symptoms, neuropsychological impairment and neural substrate, information derived from these studies enable a level of analysis that bridges the gap between the genome and the syndrome. Further study of children during the critical first 2 years of life using behavioral, electrophysiological, and functional neuroimaging methods is essential.

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“…Delays in expressive language development, poor social use of language, and unusual speech patterns such as echolalia and dysfluences have been well established in children with autism [67][68][69][70][71] and in children with FXS [72][73][74][75][76]. However, comparatively few studies have compared language performance across both groups in the same study.…”

Section: Fragile X Syndrome and Autism: Converging And Diverging Cognmentioning

confidence: 99%

Fragile X Syndrome and Autism: Common Developmental Pathways?

Cornish¹,

Turk²,

Levitas

2007

CPR

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Identifying atypical trajectories that distinguish children with differing developmental disorders from each other and from typically developing children is a potentially powerful tool for early ascertainment and treatment of syndrome specific proficiencies and deficiencies. The past decade has seen unparalleled advances in the fields of molecular genetics, pediatrics, developmental cognitive neuroscience and brain imaging. Collaboratively, these advances have facilitated our understanding of how genes can impact upon early development, through the identification of specific patterns of cognitive and behavior processing and the deficits in these domains that are typical to a specific developmental disorder. These advances have also made early diagnoses possible for many developmental disorders, including those for which genetic etiology has yet to be determined, such as is the case for most individuals with autism, or disorders such as fragile X syndrome that result from the silencing of a single gene. This early identification necessitates thorough investigation of the impact of a condition across the lifespan beginning in early childhood when interventions are most likely to have significant benefit. This is especially relevant for disorders that at first glance appear to share overlapping behavioral and clinical symptomology. In the case of autism and fragile X syndrome, commonalties in social and communication profiles are now well documented in early childhood. However, to what degree symptom overlap implies common developmental pathways or etiologies remains unclear. The focus of this review will be to critically evaluate whether so called 'commonalities' in phenotypic outcomes actually reflect very different developmental pathways that diverge over developmental time and across syndromes. More detailed knowledge of these profiles will facilitate early timing of tailored interventions that will promote optimal development resulting in significant educational, clinical, and adaptive benefits across a child's lifespan.

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Consonant production patterns of young severely language-delayed children with autism

Cited by 58 publications

References 28 publications

The Hypothesis of Apraxia of Speech in Children with Autism Spectrum Disorder

The Hypothesis of Apraxia of Speech in Children with Autism Spectrum Disorder

The Ontogenesis of Language Impairment in Autism: A Neuropsychological Perspective

Fragile X Syndrome and Autism: Common Developmental Pathways?

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