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Purpose: A Phase I pilot study was designed to collect preliminary evidence on the use of the Kaufman Speech to Language Protocol (K-SLP; Kaufman, 2014) to treat children with childhood apraxia of speech. We hypothesized that the K-SLP approach would result in more accurate speech production in targeted words, whereas untrained (control) words and speech sounds would remain unchanged. Method: A single-case multiple-baseline across behaviors experimental design was used to see if experimental feasibility could be demonstrated. Two children each received a total of 12 1-hr treatment sessions over 3 weeks. The children's response to treatment and experimental control was measured by administering baseline, treatment, and post-treatment probes. Results: Both children showed some response to treatment, as measured by percent phonemes correct; however, the response to treatment varied. In general, for the treated words that improved with therapy, accuracy was maintained above baseline level during the maintenance phase. Minimal generalization was observed for this study, with only 1 participant generalizing treatment gains to 2 sets of untrained (similar) words. Conclusion: This Phase I pilot study provides limited preliminary evidence for the effectiveness of the K-SLP approach in treating childhood apraxia of speech in some children under the conditions specified in this study. Replication of these results in well-controlled studies is needed before this structured and operationalized version of the K-SLP approach can be recommended for clinical use.

A Phase I study was conducted to examine the treatment effectiveness of the Kaufman Speech to Language Protocol using a research-operationalised protocol. It was hypothesised that articulatory accuracy would improve as a result of the treatment and that these improvements would be maintained after treatment was discontinued. A single case experimental design was used to evaluate the effectiveness of the Kaufman Speech to Language Protocol. Four children with a confirmed childhood apraxia of speech diagnosis were included in this study. Each child received 12 individual 1 hr treatment sessions that each consisted of an approximation setting phase and a practice phase. Probe data was collected during treatment and at post-treatment time points to measure treatment effectiveness and to measure changes in the untreated words. Untreated (control) sounds were included to test whether recorded improvements in articulatory accuracy could be attributed to the Kaufman Speech to Language Protocol. Two of the four children demonstrated a response to the intervention and maintenance of these changes, while the two remaining children demonstrated some generalisation in the absence of improved target (treatment) words. No specific child factors were clearly associated with positive treatment outcomes. This study replicated the findings of an earlier pilot study and found that the operationalised protocol for the Kaufman Speech to Language Protocol is effective in improving articulatory accuracy for some children with childhood apraxia of speech. Additional replication with a further refined treatment protocol and a larger sample size is needed to support a recommendation of clinical use of the Kaufman Speech to Language Protocol. [ABSTRACT FROM AUTHOR]

Purpose: Previous articles in this supplement described rationale for and development of the pause marker (PM), a diagnostic marker of childhood apraxia of speech (CAS), and studies supporting its validity and reliability. The present article assesses the theoretical coherence of the PM with speech processing deficits in CAS. Method: PM and other scores were obtained for 264 participants in 6 groups: CAS in idiopathic, neurogenetic, and complex neurodevelopmental disorders; adult-onset apraxia of speech (AAS) consequent to stroke and primary progressive apraxia of speech; and idiopathic speech delay. Results: Participants with CAS and AAS had significantly lower scores than typically speaking reference participants and speech delay controls on measures posited to assess representational and transcoding processes. Representational deficits differed between CAS and AAS groups, with support for both underspecified linguistic representations and memory/access deficits in CAS, but for only the latter in AAS. CAS-AAS similarities in the age-sex standardized percentages of occurrence of the most frequent type of inappropriate pauses ("abrupt") and significant differences in the standardized occurrence of appropriate pauses were consistent with speech processing findings. Conclusions: Results support the hypotheses of core representational and transcoding speech processing deficits in CAS and theoretical coherence of the PM's pause-speech elements with these deficits.

Purpose: The goal of this article (PM I) is to describe the rationale for and development of the Pause Marker (PM), a single-sign diagnostic marker proposed to discriminate early or persistent childhood apraxia of speech from speech delay. Method: The authors describe and prioritize 7 criteria with which to evaluate the research and clinical utility of a diagnostic marker for childhood apraxia of speech, including evaluation of the present proposal. An overview is given of the Speech Disorders Classification System, including extensions completed in the same approximately 3-year period in which the PM was developed. Results: The finalized Speech Disorders Classification System includes a nosology and cross-classification procedures for childhood and persistent speech disorders and motor speech disorders (Shriberg, Strand, & Mabie, 2017). A PM is developed that provides procedural and scoring information, and citations to papers and technical reports that include audio exemplars of the PM and reference data used to standardize PM scores are provided. Conclusions: The PM described here is an acoustic-aided perceptual sign that quantifies one aspect of speech precision in the linguistic domain of phrasing. This diagnostic marker can be used to discriminate early or persistent childhood apraxia of speech from speech delay.

Purpose: The purpose of this 2nd article in this supplement is to report validity support findings for the Pause Marker (PM), a proposed single-sign diagnostic marker of childhood apraxia of speech (CAS). Method: PM scores and additional perceptual and acoustic measures were obtained from 296 participants in cohorts with idiopathic and neurogenetic CAS, adult-onset apraxia of speech and primary progressive apraxia of speech, and idiopathic speech delay. Results: Adjusted for questionable specificity disagreements with a pediatric Mayo Clinic diagnostic standard, the estimated sensitivity and specificity, respectively, of the PM were 86.8% and 100% for the CAS cohort, yielding positive and negative likelihood ratios of 56.45 (95% confidence interval [CI]: [1.15, 2763.31]) and 0.13 (95% CI [0.06, 0.30]). Specificity of the PM for 4 cohorts totaling 205 participants with speech delay was 98.5%. Conclusion: These findings are interpreted as providing support for the PM as a near-conclusive diagnostic marker of CAS.

Purpose: Three previous articles provided rationale, methods, and several forms of validity support for a diagnostic marker of childhood apraxia of speech (CAS), termed the pause marker (PM). Goals of the present article were to assess the validity and stability of the PM Index (PMI) to scale CAS severity. Method: PM scores and speech, prosody, and voice precision-stability data were obtained for participants with CAS in idiopathic, neurogenetic, and complex neurodevelopmental disorders; adult-onset apraxia of speech consequent to stroke and primary progressive apraxia; and idiopathic speech delay. Three studies were completed including criterion and concurrent validity studies of the PMI and a temporal stability study of the PMI using retrospective case studies. Results: PM scores were significantly correlated with other signs of CAS precision and stability. The best fit of the distribution of PM scores to index CAS severity was obtained by dividing scores into 4 ordinal severity classifications: mild, mild-moderate, moderate-severe, and severe. Severity findings for the 4 classifications and retrospective longitudinal findings from 8 participants with CAS supported the validity and stability of the PMI. Conclusion: Findings support research and clinical use of the PMI to scale the severity of CAS.

Purpose: The aim of this study was to examine 2 aspects of treatment intensity in treatment for childhood apraxia of speech (CAS): practice amount and practice distribution. Method: Using an alternating-treatments single-subject design with multiple baselines, we compared high versus low amount of practice, and massed versus distributed practice, in 6 children with CAS. Conditions were manipulated in the context of integral stimulation treatment. Changes in perceptual accuracy, scored by blinded analysts, were quantified with effect sizes. Results: Four children showed an advantage for high amount of practice, 1 showed an opposite effect, and 1 showed no condition difference. For distribution, 4 children showed a clear advantage for massed over distributed practice post treatment; 1 showed an opposite pattern, and 1 showed no clear difference. Follow-up revealed a similar pattern. All children demonstrated treatment effects (larger gains for treated than untreated items). Conclusions: High practice amount and massed practice were associated with more robust speech motor learning in most children with CAS, compared to low amount and distributed practice, respectively. Variation in effects across children warrants further research to determine factors that predict optimal treatment conditions. Finally, this study adds to the evidence base supporting the efficacy of integral stimulation treatment for CAS. Supplemental Material: https://doi.org/10.23641/asha. 9630599, Parents of children with childhood apraxia of speech (CAS), and speech-language pathologists (SLPs) who work with these children, often ask how much treatment is needed for meaningful improvement and how [...]

We report clinical findings that extend the phenotype of the ∼550 kb 16p11.2 microdeletion syndrome to include a rare, severe, and persistent pediatric speech sound disorder termed Childhood Apraxia of Speech (CAS). CAS is the speech disorder identified in a multigenerational pedigree ('KE') in which half of the members have a mutation in FOXP2 that co-segregates with CAS, oromotor apraxia, and low scores on a nonword repetition task. Each of the two patients in the current report completed a 2-h assessment protocol that provided information on their cognitive, language, speech, oral mechanism, motor, and developmental histories and performance. Their histories and standard scores on perceptual and acoustic speech tasks met clinical and research criteria for CAS. Array comparative genomic hybridization analyses identified deletions at chromosome 16p11.2 in each patient. These are the first reported cases with well-characterized CAS in the 16p11.2 syndrome literature and the first report of this microdeletion in CAS genetics research. We discuss implications of findings for issues in both literatures. [ABSTRACT FROM AUTHOR]

This paper reviews current trends in treatment for childhood apraxia of speech (CAS), with a particular emphasis on motor-based intervention protocols. The paper first briefly discusses how CAS fits into the typology of speech sound disorders, followed by a discussion of the potential relevance of principles derived from the motor learning literature for CAS treatment. Next, different motor-based treatment protocols are reviewed, along with their evidence base. The paper concludes with a summary and discussion of future research needs.