Humans have a distinguishing ability for fine motor control that is subserved by a highly evolved cortico-motor neuronal network. The acquisition of a particular motor skill involves a long series of practice movements, trial and error, adjustment and refinement. At the cortical level, this acquisition begins in the parieto-temporal sensory regions and is subsequently consolidated and stratified in the premotor-motor cortex. Task-specific dystonia can be viewed as a corruption or loss of motor control confined to a single motor skill. Using a multimodal experimental approach combining neuroimaging and non-invasive brain stimulation, we explored interactions between the principal nodes of the fine motor control network in patients with writer’s cramp and healthy matched controls. Patients and healthy volunteers underwent clinical assessment, diffusion-weighted MRI for tractography, and functional MRI during a finger tapping task. Activation maps from the task-functional MRI scans were used for target selection and neuro-navigation of the transcranial magnetic stimulation. Single- and double-pulse TMS evaluation included measurement of the input-output recruitment curve, cortical silent period, and amplitude of the motor evoked potentials conditioned by cortico-cortical interactions between premotor ventral (PMv)-motor cortex (M1), anterior inferior parietal lobule (aIPL)-M1, and dorsal inferior parietal lobule (dIPL)-M1 before and after inducing a long term depression-like plastic change to dIPL node with continuous theta-burst transcranial magnetic stimulation in a randomized, sham-controlled design. Baseline dIPL-M1 and aIPL-M1 cortico-cortical interactions were facilitatory and inhibitory, respectively, in healthy volunteers, whereas the interactions were converse and significantly different in writer’s cramp. Baseline PMv-M1 interactions were inhibitory and similar between the groups. The dIPL-PMv resting state functional connectivity was increased in patients compared to controls, but no differences in structural connectivity between the nodes were observed. Cortical silent period was significantly prolonged in writer’s cramp. Making a long term depression-like plastic change to dIPL node transformed the aIPL-M1 interaction to inhibitory (similar to healthy volunteers) and cancelled the PMv-M1 inhibition only in the writer’s cramp group. These findings suggest that the parietal multimodal sensory association region could have an aberrant downstream influence on the fine motor control network in writer’s cramp, which could be artificially restored to its normal function.

中文翻译：

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下顶叶在作家抽筋中的作用。

人类具有良好的精细运动控制能力，这是高度进化的皮质运动神经元网络所具有的。学习特定的运动技能需要进行一系列的练习动作，反复试验，调整和完善。在皮层水平上，这种获取开始于顶颞感觉区域，随后在运动前皮层中巩固和分层。特定于任务的肌张力障碍可以被视为仅限于一项运动技能的运动控制受损或丧失。使用结合神经影像学和非侵入性脑刺激的多模式实验方法，我们探讨了作者抽筋患者和健康匹配对照者的精细运动控制网络的主要节点之间的相互作用。患者和健康志愿者接受了临床评估，磁共振加权弥散加权成像（MRI），用于物镜检查，在手指敲击任务期间进行功能性MRI检查。来自任务功能MRI扫描的激活图用于经颅磁刺激的目标选择和神经导航。单脉冲和双脉冲TMS评估包括输入-输出补充曲线，皮质静默期的测量，以及由运动前腹（PMv）-运动皮质（M1）之间，前下皮质之间的皮质-皮质相互作用调节的运动诱发电位的幅度顶叶小叶（aIPL）-M1和背侧下顶叶小叶（dIPL）-M1之前和之后，通过连续的经颅爆破经颅磁刺激，以随机，假对照设计，长期凹陷样塑性改变至dIPL结节，并持续经θ爆破经颅磁刺激。基线dIPL-M1和aIPL-M1皮质-皮质相互作用在健康志愿者中分别是促进和抑制，而相互作用在作者抽筋时是相反的，并且有显着差异。两组之间的基线PMv-M1相互作用具有抑制作用，且相似。与对照组相比，患者的dIPL-PMv静息状态功能连接性增加，但未观察到结点之间的结构连接性差异。皮质寂静期显着延长了作家的抽筋。对dIPL节点进行长期抑郁样的塑性改变，将aIPL-M1相互作用转化为抑制性（类似于健康志愿者），并且仅在作者的抽筋组中取消了PMv-M1抑制。