局灶性肌张力障碍的躯体-认知行为网络

IF 7.6 1区 医学 Q1 CLINICAL NEUROLOGY
Yuchao Wang, Baothy Huynh, Jianxun Ren, Mo Chen, Wei Zhang, Dan Hu, Shasha Li, Hesheng Liu, Teresa J. Kimberley
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引用次数: 0

摘要

背景:引起特发性局灶性肌张力障碍的主要病理机制尚不清楚。最近发现的躯体-认知行为网络(SCAN)也涉及其中。目的:我们测试是否效应不可知的扫描可能构成跨肌张力障碍亚型共享的中心病理,而初级感觉运动皮层中的效应特异性区域可能显示出肌张力障碍身体部位特有的明显功能变化。方法收集局灶性肌张力障碍患者(喉肌张力障碍[LD], N = 24;局灶性手肌张力障碍[FHD], N = 18)和健康对照组(N = 21)的功能磁共振成像(MRI)。在基底神经节-丘脑-皮质和小脑-丘脑-皮质感觉运动通路中预先选择感兴趣的区域。我们研究了肌张力障碍依赖的静息状态连通性变化:扫描和相关皮质区域之间、皮质和非皮质区域之间以及非皮质区域之间。皮层网络边界根据静息状态数据个性化。另外,个性化的手和嘴/喉区域也由基于任务的MRI(分别是手指敲击和发声)生成,以进行比较。结果与对照组相比,两种局灶性肌张力障碍亚型均表现出显著的功能变化(LD为P = 0.048, FHD为P = 0.017),这是由于SCAN与基于任务的口/喉区域的功能连通性较高,而与扣眼网络的连通性较低。当LD和FHD作为独立组建模时,未观察到明显的皮质下或小脑变化。然而,结合LD和FHD的探索性分析表明,SCAN和感觉运动小脑之间存在张力障碍依赖的异步化(P = 0.010),这可能表明这是一种病理过程,而不是代偿过程。结论:我们证明SCAN与局灶性肌张力障碍的独特关联超越了肌张力障碍效应区,为病理生理学和治疗提供了见解。©2025作者。Wiley期刊有限责任公司代表国际帕金森和运动障碍学会出版的《运动障碍》。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Somato‐Cognitive Action Network in Focal Dystonia
BackgroundThe central pathology causing idiopathic focal dystonia remains unclear. The recently identified somato‐cognitive action network (SCAN) has been implicated.ObjectiveWe tested whether the effector‐agnostic SCAN may constitute a central pathology shared across dystonia subtypes, whereas the effector‐specific regions in the primary sensorimotor cortex may show distinct functional changes specific to the dystonic body part.MethodsWe collected functional magnetic resonance imaging (MRI) from patients with focal dystonia (laryngeal dystonia [LD], N = 24; focal hand dystonia [FHD], N = 18) and healthy control participants (N = 21). Regions of interest were selected a priori within the basal ganglia‐thalamo‐cortical and cerebello‐thalamo‐cortical sensorimotor pathways. We investigated dystonia‐dependent resting‐state connectivity changes: between SCAN and related cortical regions, between cortical and noncortical regions, and among noncortical regions. Cortical network boundaries were individualized based on resting‐state data. Separately, individualized hand and mouth/larynx regions were also generated from task‐based MRI (finger‐tapping and phonation, respectively) for comparison.ResultsBoth focal dystonia subtypes showed significant functional changes (P = 0.048 for LD, P = 0.017 for FHD) compared to controls, driven by SCAN's higher functional connectivity to task‐based mouth/larynx region and concomitantly lower connectivity to the cingulo‐opercular network. No significant subcortical or cerebellar changes were observed when LD and FHD were modeled as independent groups. However, exploratory analysis combining LD and FHD suggested a dystonia‐dependent asynchronization between SCAN and sensorimotor cerebellum (P = 0.010) that may indicate a pathological rather than compensatory process.ConclusionsWe demonstrate that SCAN is uniquely associated with focal dystonia dysfunction beyond the dystonic effector regions, offering insights into pathophysiology and treatments. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
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来源期刊
Movement Disorders
Movement Disorders 医学-临床神经学
CiteScore
13.30
自引率
8.10%
发文量
371
审稿时长
12 months
期刊介绍: Movement Disorders publishes a variety of content types including Reviews, Viewpoints, Full Length Articles, Historical Reports, Brief Reports, and Letters. The journal considers original manuscripts on topics related to the diagnosis, therapeutics, pharmacology, biochemistry, physiology, etiology, genetics, and epidemiology of movement disorders. Appropriate topics include Parkinsonism, Chorea, Tremors, Dystonia, Myoclonus, Tics, Tardive Dyskinesia, Spasticity, and Ataxia.
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