Affecting 1% of the general population, stuttering impairs the normally effortless process of speech production, which requires precise coordination of sequential movement occurring among the articulatory, respiratory, and resonance systems, all within millisecond time scales. Those afflicted experience frequent disfluencies during ongoing speech, often leading to negative psychosocial consequences. The aetiology of stuttering remains unclear; compared to other neurodevelopmental disorders, few studies to date have examined the neural bases of childhood stuttering. Here we report, for the first time, results from functional (resting state functional magnetic resonance imaging) and structural connectivity analyses (probabilistic tractography) of multimodal neuroimaging data examining neural networks in children who stutter. We examined how synchronized brain activity occurring among brain areas associated with speech production, and white matter tracts that interconnect them, differ in young children who stutter (aged 3–9 years) compared with age-matched peers. Results showed that children who stutter have attenuated connectivity in neural networks that support timing of self-paced movement control. The results suggest that auditory-motor and basal ganglia-thalamocortical networks develop differently in stuttering children, which may in turn affect speech planning and execution processes needed to achieve fluent speech motor control. These results provide important initial evidence of neurological differences in the early phases of symptom onset in children who stutter.

* Abbreviations
 : BGTC
 : basal ganglia-thalamocortical
 DTI
 : diffusion tensor imaging
 M1
 : primary motor cortex
 SMA
 : supplementary motor area

Neural network connectivity differences in children who stutter

Primary objective: Communication impairments associated with acquired brain injury (ABI) are devastating in their impact on family, community, social, academic, and vocational participation. Despit...

https://www.tandfonline.com/doi/pdf/10.1080/02699052.2017.1379613

Introducing the model of cognitive-communication competence: A model to guide evidence-based communication interventions after brain injury

The fluent production of speech requires accurately timed movements. In this article, we propose that a deficit in brain timing networks is the core neurophysiological deficit in stuttering. We first discuss the experimental evidence supporting the involvement of the basal ganglia and supplementary motor area in stuttering and the involvement of the cerebellum as a mechanism for compensating for the neural deficits that underlie stuttering. Next, we outline the involvement of the right inferior frontal gyrus as another putative compensatory locus in stuttering and suggest a role for this structure in an expanded core timing-network. Subsequently, we review behavioral studies of timing in people who stutter and examine their behavioral performance as compared to people who do not stutter. Finally, we highlight challenges to existing research and provide avenues for future research with specific hypotheses.

/pdf/behavioral-and-multimodal-neuroimaging-evidence-for-a-yjdiuqpgra.pdf

Behavioral and multimodal neuroimaging evidence for a deficit in brain timing networks in stuttering: a hypothesis and theory.

The neural correlates of stuttering are to date incompletely understood. Although the possible involvement of the basal ganglia, the cerebellum and certain parts of the cerebral cortex in this speech disorder has previously been reported, there are still not many studies investigating the role of white matter fibers in stuttering. Axonal stimulation during awake surgery provides a unique opportunity to study the functional role of structural connectivity. Here, our goal was to investigate the white matter tracts implicated in stuttering, by combining direct electrostimulation mapping and postoperative tractography imaging, with a special focus on the left frontal aslant tract. Eight patients with no preoperative stuttering underwent awake surgery for a left frontal low-grade glioma. Intraoperative cortical and axonal electrical mapping was used to interfere in speech processing and subsequently provoke stuttering. We further assessed the relationship between the subcortical sites leading to stuttering and the spatial course of the frontal aslant tract. All patients experienced intraoperative stuttering during axonal electrostimulation. On postsurgical tractographies, the subcortical distribution of stimulated sites matched the topographical position of the left frontal aslant tract. This white matter pathway was preserved during surgery, and no patients had postoperative stuttering. For the first time to our knowledge, by using direct axonal stimulation combined with postoperative tractography, we provide original data supporting a pivotal role of the left frontal aslant tract in stuttering. We propose that this speech disorder could be the result of a disconnection within a large-scale cortico-subcortical circuit subserving speech motor control.

Role of the left frontal aslant tract in stuttering: a brain stimulation and tractographic study

Stuttering is a complex neurodevelopmental disorder that has to date eluded a clear explication of its pathophysiological bases. In this review, we utilize the Directions Into Velocities of Articulators (DIVA) neurocomputational modeling framework to mechanistically interpret relevant findings from the behavioral and neurological literatures on stuttering. Within this theoretical framework, we propose that the primary impairment underlying stuttering behavior is malfunction in the cortico-basal ganglia-thalamocortical (hereafter, cortico-BG) loop that is responsible for initiating speech motor programs. This theoretical perspective predicts three possible loci of impaired neural processing within the cortico-BG loop that could lead to stuttering behaviors: impairment within the basal ganglia proper; impairment of axonal projections between cerebral cortex, basal ganglia, and thalamus; and impairment in cortical processing. These theoretical perspectives are presented in detail, followed by a review of empirical data that make reference to these three possibilities. We also highlight any differences that are present in the literature based on examining adults versus children, which give important insights into potential core deficits associated with stuttering versus compensatory changes that occur in the brain as a result of having stuttered for many years in the case of adults who stutter. We conclude with outstanding questions in the field and promising areas for future studies that have the potential to further advance mechanistic understanding of neural deficits underlying persistent developmental stuttering.

Involvement of the Cortico-Basal Ganglia-Thalamocortical Loop in Developmental Stuttering.

https://isiarticles.com/bundles/Article/pre/pdf/33522.pdf

Nancy Helm-Estabrooks

Papers

Stuttering following acquired brain damage: A review of the literature