Search

Converging evidence supports the hypothesis that the most common subtype of childhood speech sound disorder (SSD) of currently unknown origin is genetically transmitted. We report the first findings toward a set of diagnostic markers to differentiate this proposed etiological subtype (provisionally termed speech delay-genetic) from other proposed subtypes of SSD of unknown origin. Conversational speech samples from 72 preschool children with speech delay of unknown origin from 3 research centers were selected from an audio archive. Participants differed on the number of biological, nuclear family members (0 or 2+) classified as positive for current and/or prior speech-language disorder. Although participants in the 2 groups were found to have similar speech competence, as indexed by their Percentage of Consonants Correct scores, their speech error patterns differed significantly in 3 ways. Compared with children who may have reduced genetic load for speech delay (no affected nuclear family members), children with possibly higher genetic load (2+ affected members) had (a) a significantly higher proportion of relative omission errors on the Late-8 consonants; (b) a significantly lower proportion of relative distortion errors on these consonants, particularly on the sibilant fricatives /s/, /z/, and //; and (c) a significantly lower proportion of backed /s/ distortions, as assessed by both perceptual and acoustic methods. Machine learning routines identified a 3-part classification rule that included differential weightings of these variables. The classification rule had diagnostic accuracy value of 0.83 (95% confidence limits = 0.74-0.92), with positive and negative likelihood ratios of 9.6 (95% confidence limits = 3.1-29.9) and 0.40 (95% confidence limits = 0.24-0.68), respectively. The diagnostic accuracy findings are viewed as promising. The error pattern for this proposed subtype of SSD is viewed as consistent with the cognitive-linguistic processing deficits that have been reported for genetically transmitted verbal disorders.

Terms such as isochrony, syllable segregation, scanning speech and staccato-like rhythmic quality have been used to characterize the temporal regularity that may be a core feature of apraxia of speech. The present report describes a procedure to quantify temporal regularity in children with suspected apraxia of speech (sAOS). Conversational speech samples from 15 such children, together with samples from 30 3-6-year-old children with normal speech acquisition and 30 3-6-year-old children with moderate to severe speech delay of unknown origin, were selected from an audio archive. Signal processing routines were developed to identify and measure the duration of speech and pause events in 24 utterances from the speech samples of each of the 75 speakers. A value termed the coefficient of variation expressed the normalized variability in the durations of each participant's speech events and pause events within each utterance. A metric termed the coefficient of variation ratio, derived by dividing the coefficient of variation for pause events by the coefficient of variation for speech events, expressed a speaker's relative temporal variation in the two domains. The 15 children with sAOS had higher coefficient of variation ratios than the 30 children in each of the two comparison groups, indicating that the children with sAOS had proportionally more variation in the duration of pause events and/or less variation in the duration of speech events. Findings are interpreted as supporting the view that a constraint in speech timing is a core feature of the praxis disorder that defines a developmental form of apraxia of speech.