Differential Diagnosis of Childhood Apraxia of Speech Compared to Other Speech Sound Disorders: A Systematic Review

Purpose: The aim of this study was to determine the discriminative features that might contribute to differentiation of childhood apraxia of speech (CAS) from other speech sound disorders (SSDs). Method: A comprehensive literature search was conducted for articles or doctoral dissertations that included \u3e 1 child with CAS and \u3e 1 child with SSD. Of 2,071 publications screened, 53 met the criteria. Articles were assessed for (a) study design and risk of bias; (b) participant characteristics and confidence in diagnosis; and (c) discriminative perceptual, acoustic, or kinematic measures. A criterion was used to identify promising studies: American Academy of Neurology study design (Class III+), replicable participant descriptions and adequate confidence in diagnosis (\u3e 3), and \u3e 1 discriminative and reliable measure. Results: Over 75% of studies were retrospective, case-control designs and/or assessed English-speaking children. Many studies did not fully describe study design and quality. No studies met the Class I (highest) quality rating according to American Academy of Neurology guidelines. CAS was mostly compared to speech delay/phonological disorder. Only six studies had diagnostic confidence ratings of 1 (best). Twenty-six studies reported discriminative perceptual measures, 14 reported discriminative acoustic markers, and four reported discriminative kinematic markers. Measures were diverse, and only two studies directly replicated previous findings. Overall, seven studies met the quality criteria, and another eight nearly met the study criteria to warrant further investigation. Conclusions: There are no studies of the highest diagnostic quality. There are 15 studies that can contribute to further diagnostic efforts discriminating CAS from other SSDs. Future research should utilize careful diagnostic design, support replication, and adhere to standard reporting guidelines

Reliance on auditory feedback in children with childhood apraxia of speech

AbstractChildren with childhood apraxia of speech (CAS) have been hypothesized to continuously monitor their speech through auditory feedback to minimize speech errors. We used an auditory masking paradigm to determine the effect of attenuating auditory feedback on speech in 30 children: 9 with CAS, 10 with speech delay, and 11 with typical development. The masking only affected the speech of children with CAS as measured by voice onset time and vowel space area. These findings provide preliminary support for greater reliance on auditory feedback among children with CAS.Learning outcomes: Readers of this article should be able to (i) describe the motivation for investigating the role of auditory feedback in children with CAS; (ii) report the effects of feedback attenuation on speech production in children with CAS, speech delay, and typical development, and (iii) understand how the current findings may support a feedforward program deficit in children with CAS

The Role of Candidate-Gene \u3cem\u3eCNTNAP2\u3c/em\u3e in Childhood Apraxia of Speech and Specific Language Impairment

Childhood apraxia of speech (CAS) is a debilitating pediatric speech disorder characterized by varying symptom profiles, comorbid deficits, and limited response to intervention. Specific Language Impairment (SLI) is an inherited pediatric language disorder characterized by delayed and/or disordered oral language skills including impaired semantics, syntax, and discourse. To date, the genes associated with CAS and SLI are not fully characterized. In the current study, we evaluated behavioral and genetic profiles of seven children with CAS and eight children with SLI, while ensuring all children were free of comorbid impairments. Deletions within CNTNAP2 were found in two children with CAS but not in any of the children with SLI. These children exhibited average to high performance on language and word reading assessments in spite of poor articulation scores. These findings suggest that genetic variation within CNTNAP2 may be related to speech production deficits