Joan Orpella

Research points to neurofunctional differences underlying fluent speech between stutterers and non-stutterers. Considerably less work has focused on processes that underlie stuttered vs. fluent speech. Additionally, most of this research has focused on speech motor processes despite contributions from cognitive processes prior to the onset of stuttered speech. We used MEG to test the hypothesis that reactive inhibitory control is triggered prior to stuttered speech. Twenty-nine stutterers completed a delayed-response task that featured a cue (prior to a go cue) signaling the imminent requirement to produce a word that was either stuttered or fluent. Consistent with our hypothesis, we observed increased beta power likely emanating from the R-preSMA—an area implicated in reactive inhibitory control—in response to the cue preceding stuttered vs. fluent productions. Beta power differences between stuttered and fluent trials correlated with stuttering severity and participants' percentage of trials stuttered increased exponentially with beta power in the R-preSMA. Trial-by-trial beta power modulations in the R-preSMA following the cue predicted whether a trial would be stuttered or fluent. Stuttered trials were also associated with delayed speech onset suggesting an overall slowing or freezing of the speech motor system that may be a consequence of inhibitory control. Post-hoc analyses revealed that independently-generated anticipated words were associated with greater beta power and more stuttering than researcher-assisted anticipated words, pointing to a relationship between self-perceived likelihood of stuttering (i.e., anticipation) and inhibitory control. This work offers a neurocognitive account of stuttering by characterizing cognitive processes that precede overt stuttering events.