Computational Modeling of the Neural Substrates of Stuttering and Induced Fluency

Stuttering is a speech motor control disorder of unknown etiology whose hallmark is part-syllable repetition. The principal aim of this dissertation is to understand the neural mechanisms underlying stuttering through computational modeling with DIVA and GODIVA, neural network models of speech acquisition and production. The first part of the dissertation investigates the hypothesis that stuttering may result in part from impaired readout of feedforward commands for speech, which forces persons who stutter (PWS) to produce speech with a motor strategy that is weighted too much toward auditory feedback control. Over-reliance on feedback control leads to sensory errors which, if they grow large enough, can cause the motor system to “reset” and repeat the current syllable. This hypothesis is investigated by impairing the feedforward control subsystem of the DIVA model. The model’s outputs are compared to published acoustic data from PWS’ fluent speech, and to combined acoustic and articulatory-movement data collected from the dysfluent speech of one PWS. The viii simulations mimic the errors observed in the PWS subject’s speech, as well as the repairs of these errors. Additional simulations were able to account for enhancements of fluency gained by slowed/prolonged speech and masking noise. The second part of the dissertation explores the role of the basal ganglia (BG) – left ventral premotor cortex (vPMC) loop in the impaired readout of feedforward control. Two hypotheses are put to test: 1) due to structural abnormality in the corticostriatal projections carrying corollary discharge of motor commands, the BG fail to detect the context for initiating the next syllable, and 2) due to increased dopamine binding in the striatum leading to a ceiling effect, the BG are unable to bias cortical competition in favor of the correct syllable. Simulations of a neurally impaired version of the extended GODIVA model show that both hypotheses can explain dysfluent speech and associated abnormal brain activations. Further simulations account for the alleviation of stuttering with D2 antagonists. Together these results support the hypothesis that many dysfluencies in stuttering are due to abnormalities interfering with normal BG-vPMC loop operation, which ultimately biases the system away from feedforward control and toward feedback control.