Testing hypotheses about the underlying deficit of Apraxia of Speech (AOS) through computational neural modelling with the DIVA model

Purpose: A recent behavioural experiment featuring a noise masking paradigm suggests that Apraxia of Speech (AOS) reflects a disruption of feedforward control, whereas feedback control is spared and plays a more prominent role in achieving and maintaining segmental contrasts. The present study set out to validate the interpretation of AOS as a possible feedforward impairment using computational neural modelling with the DIVA (Directions Into Velocities of Articulators) model. Method: In a series of computational simulations with the DIVA model featuring a noise-masking paradigm mimicking the behavioural experiment, we investigated the effect of a feedforward, feedback, feedforward + feedback, and an upper motor neuron dysarthria impairment on average vowel spacing and dispersion in the production of six/bVt/speech targets. Result: The simulation results indicate that the output of the model with the simulated feedforward deficit resembled the group findings for the human speakers with AOS best. Conclusion: These results provide support to the interpretation of the human observations, corroborating the notion that AOS can be conceptualised as a deficit in feedforward control

Cognitive functions in Childhood Apraxia of Speech

Purpose: Childhood Apraxia of Speech (CAS) is diagnosed on the basis of specific speech characteristics, in the absence of problems in hearing, intelligence, and language comprehension. This does not preclude the possibility that children with this speech disorder might demonstrate additional problems. Method: Cognitive functions were investigated in three domains: complex sensory-motor and sequential memory functions, simple sensory-motor functions, and non-related control functions. Seventeen children with CAS were compared to 17 children with normal speech development at two occasions within 15 months. Results: The children with CAS showed overall lower scores but similar improvement at Occasion 2 compared to the typically developing controls, indicating an overall delay in the development of cognitive functions. However, a specific deviant development in sequential abilities was found as well, indicated by significantly lower scores at Occasion 2 as compared to (younger) control children at Occasion 1. Furthermore, the scores on the complex sensory-motor and sequential memory tasks were significantly correlated with the severity of the speech impairment. Conclusions: These results suggest that CAS involves a symptom complex that not only comprises errors of sequencing speech movements, but implicates comorbidity in nonverbal sequential functioning in most children with CAS