Our understanding of the neurobiological bases of stuttering remains limited, hampering development of effective treatments that are informed by basic science. Stuttering affects more than 5% of all preschool-age children and remains chronic in approximately 1% of adults worldwide. As a condition that affects a most fundamental human ability to engage in fluid and spontaneous verbal communication, stuttering can have substantial psychosocial, occupational, and educational impacts on those who are affected. This article summarizes invited talks and breakout sessions that were held in June 2023 as part of a 2-day workshop sponsored by the US National Institute on Deafness and Other Communication Disorders. The workshop encompassed topics including neurobiology, genetics, speech motor control, cognitive, social, and emotional impacts, and intervention. Updates on current research in these areas were summarized by each speaker, and critical gaps and priorities for future research were raised, and then discussed by participants. Research talks were followed by smaller, moderated breakout sessions intended to elicit diverse perspectives, including on the matter of defining therapeutic targets for stuttering. A major concern that emerged following participant discussion was whether priorities for treatment in older children and adults should focus on targeting core speech symptoms of stuttering, or on embracing effective communication regardless of whether the speaker exhibits overt stuttering. This article concludes with accumulated convergent points endorsed by most attendees on research and clinical priorities that may lead to breakthroughs with substantial potential to contribute to bettering the lives of those living with this complex speech disorder.

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 right pre-supplementary motor area (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.

People who stutter learn to anticipate many of their overt stuttering events. Despite the critical role of anticipation, particularly how responses to anticipation shape stuttering behaviors, the neural bases associated with anticipation are unknown. We used a novel approach to identify anticipated and unanticipated words, which were produced by 22 adult stutterers in a delayed-response task while hemodynamic activity was measured using functional near infrared spectroscopy (fNIRS). Twenty-two control participants were included such that each individualized set of anticipated and unanticipated words was produced by one stutterer and one control participant. We conducted an analysis on the right dorsolateral prefrontal cortex (R-DLPFC) based on converging lines of evidence from the stuttering and cognitive control literatures. We also assessed connectivity between the R-DLPFC and right supramarginal gyrus (R-SMG), two key nodes of the frontoparietal network (FPN), to assess the role of cognitive control, and particularly error-likelihood monitoring, in stuttering anticipation. All analyses focused on the five-second anticipation phase preceding the go signal to produce speech. The results indicate that anticipated words are associated with elevated activation in the R-DLPFC, and that compared to non-stutterers, stutterers exhibit greater activity in the R-DLPFC, irrespective of anticipation. Further, anticipated words are associated with reduced connectivity between the R-DLPFC and R-SMG. These findings highlight the potential roles of the R-DLPFC and the greater FPN as a neural substrate of stuttering anticipation. The results also support previous accounts of error-likelihood monitoring and action-stopping in stuttering anticipation. Overall, this work offers numerous directions for future research with clinical implications for targeted neuromodulation.