Computational modeling of stuttering caused by impairments in a basal ganglia thalamo-cortical circuit involved in syllable selection and initiation

• We examine the roles of dopamine excess and atypical white matter in stuttering.
• We simulate “neurally impaired” versions of the neurocomputational model GODIVA.
• Each abnormality causes stuttering by affecting the same BG–thalamus–vPMC circuit.
• The circuit selects/initiates the next syllable too late, resulting in dysfluency.
• The results account for brain imaging findings during dysfluent speech production.

Atypical white-matter integrity and elevated dopamine levels have been reported for individuals who stutter. We investigated how such abnormalities may lead to speech dysfluencies due to their effects on a syllable-sequencing circuit that consists of basal ganglia (BG), thalamus, and left ventral premotor cortex (vPMC). “Neurally impaired” versions of the neurocomputational speech production model GODIVA were utilized to test two hypotheses: (1) that white-matter abnormalities disturb the circuit via corticostriatal projections carrying copies of executed motor commands and (2) that dopaminergic abnormalities disturb the circuit via the striatum. Simulation results support both hypotheses: in both scenarios, the neural abnormalities delay readout of the next syllable’s motor program, leading to dysfluency. The results also account for brain imaging findings during dysfluent speech. It is concluded that each of the two abnormality types can cause stuttering moments, probably by affecting the same BG–thalamus–vPMC circuit.