Cross-frequency cortex-muscle interactions are abnormal in young people with dystonia
Cross-frequency cortex-muscle interactions are abnormal in young people with dystonia
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DOI：
10.1093/braincomms/fcae061
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发表时间：
2024-03-14
影响因子：
4.8
通讯作者：
McClelland，Verity M.
中科院分区：
文献类型：
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作者：
Guo，Zhenghao;Lin，Jean-Pierre;McClelland，Verity M.
肌张力障碍患者的感觉处理和感觉运动整合异常，包括β-皮质肌肉一致性调节受损。然而，很少描述任一方向的皮质-肌肉相互作用，报告主要限于使用皮质肌肉相干性或格兰杰因果关系研究线性耦合。诸如传递熵之类的信息理论工具可以检测进程之间的线性和非线性相互作用。这项观察性病例对照研究应用传递熵来确定肌张力障碍/肌张力障碍性脑瘫年轻人的同频和跨频皮质-肌肉耦合。 15 名患有肌张力障碍/肌张力障碍性脑瘫的儿童和 13 名年龄为 12-18 岁的对照组儿童用惯用手执行抓握任务。机械扰动由机电攻丝机提供。记录对侧感觉运动皮层的双极头皮脑电图和第一背侧骨间的表面肌电图。应用多尺度小波传递熵将信号分解为振荡活动的功能频带，并量化大脑和肌肉之间的同频和跨频耦合。建立了针对零转移熵零假设的统计显着性，设定了个体 95% 的置信阈值。使用 Fisher 精确检验比较每组中每个频率组合/方向显示显着转移熵的个体比例，并校正多重比较。在所有参与者中，在 β (16–32 Hz) 范围内双向检测到频率内传递熵，在大多数参与者中，从脑电图到肌电图在 α (8–16 Hz) 范围内检测到频率内传递熵。跨多个频带的跨频率转移熵在各组之间基本相似，但肌张力障碍中从低频 EMG 到 β EEG 的特定耦合显着降低 [P = 0.0061（校正）]。肌张力障碍中双向皮层-肌肉通讯的演示强调了转移熵对于探索神经系统疾病中神经通讯的价值。肌张力障碍中低频肌电图与β脑电图耦合减弱的新发现表明，具有特定频率特征的本体感觉信息的皮层反馈受损，这可能与肌肉过度低频驱动的起源有关。
Sensory processing and sensorimotor integration are abnormal in dystonia, including impaired modulation of beta-corticomuscular coherence. However, cortex–muscle interactions in either direction are rarely described, with reports limited predominantly to investigation of linear coupling, using corticomuscular coherence or Granger causality. Information-theoretic tools such as transfer entropy detect both linear and non-linear interactions between processes. This observational case–control study applies transfer entropy to determine intra- and cross-frequency cortex–muscle coupling in young people with dystonia/dystonic cerebral palsy. Fifteen children with dystonia/dystonic cerebral palsy and 13 controls, aged 12–18 years, performed a grasp task with their dominant hand. Mechanical perturbations were provided by an electromechanical tapper. Bipolar scalp EEG over contralateral sensorimotor cortex and surface EMG over first dorsal interosseous were recorded. Multi-scale wavelet transfer entropy was applied to decompose signals into functional frequency bands of oscillatory activity and to quantify intra- and cross-frequency coupling between brain and muscle. Statistical significance against the null hypothesis of zero transfer entropy was established, setting individual 95% confidence thresholds. The proportion of individuals in each group showing significant transfer entropy for each frequency combination/direction was compared using Fisher's exact test, correcting for multiple comparisons. Intra-frequency transfer entropy was detected in all participants bidirectionally in the beta (16–32 Hz) range and in most participants from EEG to EMG in the alpha (8–16 Hz) range. Cross-frequency transfer entropy across multiple frequency bands was largely similar between groups, but a specific coupling from low-frequency EMG to beta EEG was significantly reduced in dystonia [P= 0.0061 (corrected)]. The demonstration of bidirectional cortex–muscle communication in dystonia emphasizes the value of transfer entropy for exploring neural communications in neurological disorders. The novel finding of diminished coupling from low-frequency EMG to beta EEG in dystonia suggests impaired cortical feedback of proprioceptive information with a specific frequency signature that could be relevant to the origin of the excessive low-frequency drive to muscle.