Fondazione Ospedale San Camillo IRCCS, via Alberoni 70, 30126 Venice, Italy.
B.R.A.I.N. Center for Neuroscience, Department of Life Sciences, University of Trieste, via Fleming 22, 34100 Trieste, Italy.
Clin Neurophysiol. 2019 Jan;130(1):61-76. doi: 10.1016/j.clinph.2018.10.005. Epub 2018 Nov 10.
Brain dynamics in developmental stuttering (DS) are not well understood. The supplementary motor area (SMA) plays a crucial role, since it communicates with regions related to planning/execution of movements, and with sub-cortical regions involved in paced/voluntary acts (such as speech). We used TMS combined with EEG to shed light on connections in DS, stimulating the SMA.
TMS/EEG was recorded in adult DS and fluent speakers (FS), stimulating the SMA during rest. TMS-evoked potentials and source distribution were evaluated.
Compared to FS, stutterers showed lower activity of neural sources in early time windows: 66-82 ms in SMA, and 91-102 ms in the left inferior frontal cortex and left inferior parietal lobule. Stutterers, however, showed higher activations in later time windows (i.e. from 260-460 ms), in temporal/premotor regions of the right hemisphere.
These findings represent the functional counterpart to known white matter and cortico-basal-thalamo-cortical abnormalities in DS. They also explain how white matter abnormalities and cortico-basal-thalamo-cortical dysfunctions may be associated in DS. Finally, a mechanism is proposed in which compensatory activity of the non-dominant (right) hemisphere is recruited.
DS may be a disorder of neural timing that appears to be delayed compared to FS; new mechanisms that support stuttering symptoms are inferred; the SMA may be a promising target for neuro-rehabilitation.
发育性口吃(DS)患者的大脑动力学尚不清楚。辅助运动区(SMA)起着至关重要的作用,因为它与与运动的计划/执行有关的区域以及与参与有节奏/自愿行为(如言语)的皮质下区域进行交流。我们使用 TMS 结合 EEG 来研究 SMA 刺激下 DS 中的连接。
在休息期间,对成年 DS 患者和流利说话者(FS)进行 TMS/EEG 记录。评估 TMS 诱发的电位和源分布。
与 FS 相比,口吃者在早期时间窗口(66-82ms 在 SMA,91-102ms 在左侧额下回和左侧顶下小叶)中的神经源活性较低。然而,口吃者在较晚的时间窗口(即 260-460ms)显示出更高的激活,在右半球的颞叶/运动前区域。
这些发现代表了已知的 DS 中的白质和皮质基底节丘脑皮质异常的功能对应物。它们还解释了 DS 中白质异常和皮质基底节丘脑皮质功能障碍如何相关。最后,提出了一种机制,其中非优势(右)半球的代偿性活动被招募。
DS 可能是一种神经时间的紊乱,与 FS 相比似乎存在延迟;推断出支持口吃症状的新机制;SMA 可能是神经康复的一个有前途的靶点。