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Three questions were addressed in this study: (a) Do mothers of stuttering children talk faster than mothers of nonstuttering children, (b) do stuttering children talk faster than nonstuttering children, and (c) is there a relationship between child's rate of speech and mother's rate of speech in dyadic conversation? Twelve nonstuttering preschool boys and their mothers were matched with 12 stutterers and their mothers. Ten min of free-play interaction between alternated mother—child dyads were video recorded. Speech rates, defined as syllables per second in fluent utterances, were calculated. Results demonstrated that mothers of stutterers talked significantly faster to all children. Stutterers spoke slower than nonstutterers, and severe stutterers spoke slower than moderate stutterers. A correlational analysis revealed that the more the child stuttered, the slower he talked during fluent speech. Further, the slower the child talked during fluent speech, the faster the mother interacting with him talked. The results reveal an interactive and complex relationship between mother and child speech rates. The interpretation of results relating to child speech rates was complicated by post hoc analyses revealing a significant relationship between speech rates and utterance length.

Laryngeal muscle activity during fluent and stuttered utterances was investigated via electromyography. Analysis revealed that stuttering was accompanied by high levels of laryngeal muscle activity and disruption of normal reciprocity between abductor and adductor muscle groups. Results are interpreted as demonstrating the existence of a laryngeal component in stuttering and showing a strong correlation between abnormal laryngeal muscle activity and moments of stuttering.

Vocal symptoms in spasmodic dysphonia (SD) range from strain-strangle phonation and glottal-stop phonatory breaks of adductor SD to breathy phonation and aspirate phonatory breaks of abductor SD. Many SD subjects show both symptom types. Heterogeneity in vocal symptoms contributes to controversy surrounding the etiology(s) of SD. Acoustic/perceptual analyses of vocal symptoms are inconclusive in resolving this controversy. This investigation moves the search for distinguishing features of adductor and abductor SD to the level of neuromuscular control and analysis of intrinsic laryngeal muscle (adductor and abductor) activity. Subjects rated perceptually as primarily adductor or abductor SD sustained production of vegetative gestures and isolated speech sounds (/i/ and /s/). Qualitative and quantitative analyses of electromyographic signals recorded from thyroarytenoid (TA) failed to differentiate SD subjects by symptom type. Analysis of TA and posterior cricoarytenoid (PCA) activity in one abductor SD revealed high levels in both muscles during production of the voiced vowel. Data suggest that a possible explanation for symptom heterogeneity in SD is the relation between disrupted neuromotor input to laryngeal muscles and reflexive or conscious compensations constrained by laryngeal biomechanics.

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