Department of Neuropsychology, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany.
Department of Clinical Neurophysiology, University Medical Center Göttingen, Göttingen, Germany.
Brain. 2018 Jan 1;141(1):191-204. doi: 10.1093/brain/awx316.
A neuronal sign of persistent developmental stuttering is the magnified coactivation of right frontal brain regions during speech production. Whether and how stuttering severity relates to the connection strength of these hyperactive right frontal areas to other brain areas is an open question. Scrutinizing such brain-behaviour and structure-function relationships aims at disentangling suspected underlying neuronal mechanisms of stuttering. Here, we acquired diffusion-weighted and functional images from 31 adults who stutter and 34 matched control participants. Using a newly developed structural connectivity measure, we calculated voxel-wise correlations between connection strength and stuttering severity within tract volumes that originated from functionally hyperactive right frontal regions. Correlation analyses revealed that with increasing speech motor deficits the connection strength increased in the right frontal aslant tract, the right anterior thalamic radiation, and in U-shaped projections underneath the right precentral sulcus. In contrast, with decreasing speech motor deficits connection strength increased in the right uncinate fasciculus. Additional group comparisons of whole-brain white matter skeletons replicated the previously reported reduction of fractional anisotropy in the left and right superior longitudinal fasciculus as well as at the junction of right frontal aslant tract and right superior longitudinal fasciculus in adults who stutter compared to control participants. Overall, our investigation suggests that right fronto-temporal networks play a compensatory role as a fluency enhancing mechanism. In contrast, the increased connection strength within subcortical-cortical pathways may be implied in an overly active global response suppression mechanism in stuttering. Altogether, this combined functional MRI-diffusion tensor imaging study disentangles different networks involved in the neuronal underpinnings of the speech motor deficit in persistent developmental stuttering.
持续性发展性口吃的一个神经学标志是,在言语产生过程中,右侧额区大脑区域的过度协同激活。口吃的严重程度与这些过度活跃的右侧额区与其他大脑区域的连接强度之间的关系如何,这是一个悬而未决的问题。仔细研究这些大脑-行为和结构-功能关系的目的是为了厘清口吃潜在的神经学机制。在这里,我们从 31 名口吃者和 34 名匹配的对照组参与者中获取了弥散加权和功能图像。使用一种新开发的结构连接度量方法,我们在起源于功能上活跃的右侧额区的束容积内计算了连接强度与口吃严重程度之间的体素相关性。相关分析表明,随着言语运动缺陷的增加,右侧额斜束、右侧前丘脑辐射以及右侧中央前回下的 U 形投射中的连接强度增加。相反,随着言语运动缺陷的减少,连接强度在右侧钩束中增加。全脑白质骨架的额外组间比较复制了之前报道的口吃者与对照组参与者相比,左侧和右侧上纵束以及右侧额斜束与右侧上纵束交界处的各向异性分数减少。总的来说,我们的研究表明,右侧额颞网络起着增强流畅性的补偿作用。相比之下,皮质下-皮质通路内连接强度的增加可能与口吃者过度活跃的全局反应抑制机制有关。总的来说,这项功能磁共振成像-弥散张量成像的联合研究,厘清了持续性发展性口吃言语运动缺陷的神经学基础中涉及的不同网络。