Title:

An Investigation of Motor Programming in Childhood Apraxia of Speech

The underlying nature of the motor programming disorder in apraxia of speech (AOS) has received extensive investigation. This is not the case for childhood apraxia of speech (CAS). CAS and AOS present with many of the same perceptual characteristics (increased intersegment and segment duration ((i.e., segmentation)), equal lexical stress, and speech sound distortions), however, little work has been done to investigate whether the disorders have the same mechanism of action. Previous studies investigating motor programming in AOS have utilized a two-stage model developed by Klapp (2003). This model breaks down the motor programming process into two stages. The first is INT which involves the organization of the internal spatiotemporal structure of a unit of movement and loading the unit into a motor buffer. The second is SEQ which involves the sequencing of the units in the motor buffer into their correct serial order. The present study investigates motor programming in CAS by utilizing a self-select paradigm which allows for the measurement of both INT and SEQ in each trial (Wright et al., 2009). The INT process is termed study time (ST) and reflects the amount of time that a participant takes to prepare their response. The SEQ process is termed reaction time (RT) and reflects the amount of time that it takes for a participant to execute their response after the presentation of a “go” signal. Maas et al. (2008) utilized this self-select paradigm in adults with AOS in comparison to typical controls and individuals with a language impairment (aphasia). They found that for participants with AOS the impairment was specific to the INT (ST) stage of motor programming. This translated to participants with AOS having overall longer ST in comparison to typical and aphasic controls. In contrast, participants with AOS demonstrated typical SEQ (RT) when compared to typical controls. These results were shown in both speech and nonspeech movements, indicating that AOS is due to a central, rather than modality-specific impairment (Maas et al., 2008). In this study, two experimental tasks were designed to investigate whether the nature of the impairment seen in CAS is that same as that observed in AOS, and whether the impairment is central or modality-specific. Experiment one tested non-speech motor movements (finger tapping) and experiment two tested speech motor movements (vocalization of the syllable /bɔ/). Again, like in Maas et al. (2008) three groups of participants were included in the study: children with a diagnosis of CAS, typically developing children (TD), and children with a language-based phonological impairment (PI). There were 26 participants in total ranging from ages 5-12: CAS (n=6), PI (n=9), TD (n=11). Participants across groups demonstrated substantial difficulty with accurately executing the finger-tapping motor responses in experiment one, therefore, testing was discontinued, and results were excluded from the analysis. Results from experiment two (vocalizations of the syllable /bɔ/) demonstrated a negative correlation of ST and RT with age for TD and PI participants. This was not the case for participants with CAS who did not demonstrate a decrease in ST and RT with age. This suggests that for participants with CAS, the motor programming process does not become more efficient as they get older. These findings provide insight into the underlying motor programming impairment in CAS and inform the need for theory-driven treatment approaches which specifically target the disorder. Another finding from experiment two demonstrates that as the experiment progresses, children with CAS demonstrate a dramatic increase in ST while TD and PI participants do not. Conversely, TD and CAS participants demonstrate similar patterns of RT across the experiment. These findings support the hypothesis that the impairment in CAS is localized to the INT stage of the motor programming process, while the SEQ phase is intact. Given that this finding is similar to what was found in Maas et al. (2008) with adults with AOS, these results also support the hypothesis that CAS and AOS arise from the same mechanism of action.

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