This article presents a theoretical perspective on stuttering based on numerous findings regarding speech and nonspeech neuromotor control in individuals who stutter in combination with recent empirical data and theoretical models from the literature on the neuroscience of motor control. Specifically, this perspective on stuttering relies heavily on recent work regarding feedforward and feedback control schemes; the formation, consolidation, and updating of inverse and forward internal models of the motor systems; and cortical, subcortical, and cerebellar activation patterns during speech and nonspeech motor tasks. Against this background, we propose that stuttering may result when producing speech (a) with unstable or insufficiently activated internal models or (b) with a motor E

A typical 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.

Stuttering is associated with atypical structural and functional connectivity in sensorimotor brain areas, in particular premotor, motor, and auditory regions. It remains unknown, however, which specific mechanisms of speech planning and execution are affected by these neurological abnormalities. To investigate pre-movement sensory modulation, we recorded 12 stuttering and 12 nonstuttering adults’ auditory evoked potentials in response to probe tones presented prior to speech onset in a delayed-response speaking condition vs. no-speaking control conditions (silent reading; seeing nonlinguistic symbols). Findings indicate that, during speech movement planning, the nonstuttering group showed a statistically significant modulation of auditory processing (reduced N1 amplitude) that was not observed in the stuttering group. Thus, the obtained results provide electrophysiological evidence in support of the hypothesis that stuttering is associated with deficiencies in modulating the cortical auditory system during speech movement planning. This specific sensorimotor integration deficiency may contribute to inefficient feedback monitoring and, consequently, speech dysfluencies.