Stuttering: Our Current Knowledge, Research Opportunities, and Ways to Address Critical Gaps

Abstract

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.

Keywords: genetics; intervention; neurobiology; research priorities; speech disorder; treatment.

Figure 1.

Key areas of research highlighted in the National Institute on Deafness and Other Communication Disorders sponsored workshop on stuttering. Stuttering occurs during communicative speech and is often exacerbated by social, cognitive, and linguistic contexts. Like many complex disorders, the neurobiological bases of stuttering have been difficult to uncover to date. Emerging research findings in the areas of genetics, animal research, and neuroimaging research probing brain function and anatomy in children and adults may pave the way for novel treatment development. Newer intervention approaches involving neuromodulation (i.e., brain stimulation) guided by an updated understanding of neural circuits affected in stuttering may help modulate brain function toward alleviation of core speech symptoms. Shifts in perspectives on the treatment goals for stuttering that include a greater emphasis on confident, authentic communication, and societal acceptance toward stuttering were also topics of interest (more details in the text). Adapted from the University of Delaware Neurobiology of Speech and Language Lab’s web page “Research Strategies” (; available at sites.udel.edu/brainspeak/research/), with permission from Dr. Ho Ming Chow.

Figure 2.

Simplified qualitative summary of the imaging literature. Reorganization potential depends on multiple factors, and evidence levels vary across individual brain regions. Brain correlates for speech motor memory formation and usage (A) and brain correlates for structural reorganization associated with spontaneous recovery in children and for functional reorganization associated with therapy-induced improvement of speech fluency in adults who stutter (B). Abbreviations: Ac = nucleus accumbens; AF = arcuate fasciculus; aSTG = anterior superior temporal gyrus; Ca = caudate nucleus; Cb = cerebellum; CC = corpus callosum; dMC = dorsal primary motor cortex; DN = dentate nucleus; dPMC = dorsal premotor cortex; FAT = frontal aslant tract; FO = frontal operculum; Gp = globus pallidus; Gpi = globus pallidus internal segment; IFG = inferior frontal gyrus; IFGorb = inferior frontal gyrus pars orbitalis; IFS = inferior frontal sulcus; ILF = inferior longitudinal fasciculus; MC = primary motor cortex; MN = vocal tract motor neurons; pIFS = posterior inferior frontal sulcus; PMC = premotor cortex; PN = pontine nuclei; PO = parietal operculum; preSMA = presupplementary motor area; pSTG = posterior superior temporal gyrus; Pu = putamen; SC = primary somatosensory cortex; SLF = superior longitudinal fasciculus; SMA = supplementary motor area; SMG = supramarginal gyrus; SNr = substantia nigra pars reticulata; STG = superior temporal gyrus; Th = Thalamus; vMC = ventral primary motor cortex; vPMC = ventral premotor cortex. Adapted from Neef and Chang (2024).