Behavioural Brain Research:帕金森病中皮质-运动相互作用的中断

2021-02-22 MedSci原创 MedSci原创

帕金森病(PD)是一种神经退行性疾病,表现为运动和非运动症状。帕金森病的主要运动特征包括运动迟缓、震颤和僵硬。帕金森病患者的运动能力受损被认为反映了运动回路的中断,运动回路是大脑皮层和皮层下神经结构的

帕金森病(PD)是一种神经退行性疾病,表现为运动和非运动症状。帕金森病的主要运动特征包括运动迟缓、震颤和僵硬。帕金森病患者的运动能力受损被认为反映了运动回路的中断,运动回路是大脑皮层和皮层下神经结构的网络。更具体地说,基底节多巴胺能传递受损会导致运动回路中断,从而影响运动的产生。这些干扰的影响可以在多个大脑结构、静止时的运动结果和运动任务中看到。脑电图(EEG)作为一种非侵入性检查手段被广泛用于探索PD病理性皮质特征与其相关症状结果之间的关系。在很多研究中证明PD中的苍白球DBS分别在低β和高β的情况下对局部和网络活动进行不同的调节。

上肢运动结果已记录使用多种范式和评估模式,以探讨病理模式在帕金森病。在有起搏和无起搏手指叩击任务中提取了叩击潜伏期、个体内变异性、叩击力和频率,以确定潜在的疾病标志物,并评估治疗和治疗的有效性。尽管许多研究试图描述皮质和运动结果的病理模式,但很少有人试图将这两者直接联系起来。迄今为止,皮层ß带活动在帕金森病运动产生中的作用,如运动特征所反映的,还没有很好的理解。尽管有希望成为帕金森病的一个可能的标志物。本文目的是探讨脑电图α和低/高-β带功率以及在无垫手指敲击任务中运动结果之间的关系,并在一组帕金森病参与者和一组健康对照者之间比较这些测量。

8例PD患者(年龄72.4±8.9,女性5例)和7例健康对照者(年龄65.4±9.1,女性5例)被纳入本研究。帕金森病组的症状包括运动减退、肌张力障碍、运动迟缓、震颤和步态异常。PD组的所有受试者在数据收集期间均处于服药状态没有患者在记录期间出现明显震颤或运动障碍。帕金森病组的所有参与者都完成了蒙特利尔认知评估(MOCA);帕金森病组除一名成员外,其他每个成员都有轻度认知障碍(MOCA评分<26)[34]。对照组参与者没有已知的神经紊乱病史。

每个参与者在一次持续约60分钟的实验中完成所有数据记录。脑电图和运动信号是从一次由五个试验组成的实验中同时记录的。每次试验包括10秒的休息,然后是10秒的自定节奏手指敲击。受试者就坐,并被要求以一种让他们感到舒服的速度反复地将右手食指与拇指相对,做一个大动作。在实验过程中,在参与者面前的显示器上显示的提示会提示每个任务(即休息或手指敲击)。脑电图信号记录来自13通道脑电图蒙太奇周围区域,包括运动皮层:Fc3,Fc4,C1,C2,C3,C4,Cp1,Cp2,Cp3,Cp4,P3和P4。随后对C3通道进行了分析,因为它位于执行任务的手的对侧运动皮质上。应用重复测量相关(rrm)分析将每个试验的PSD测量与相应的运动变量(包括平均峰值潜伏期、平均峰值振幅和SaEn)相关联。当每个个体贡献多个非独立观察值时,重复测量相关分析确定组内相关性。该分析被应用于探索每组中每个参与者重复变量之间的线性皮质运动学关系。每个试验都被当作一个衡量标准,每组的试验都被参与者标记,以说明个体对整体相关性的贡献。

Fig. 1

与帕金森病参与者相比,健康组在任务期间的运动相关频率(α和β波段频率)表现出更大的失调。两组的去同步在任务开始时最强,并持续了一段时间。健康组α带失同步平均值为-34.5±14.7%,低β带失同步平均值为-47.9±15.9%,高β带失同步平均为-30.5±11.4%。PD组α带失步率为-21.6±27.0%,低β带失步率为-28.1±19.5%,高β带失步率为-11.0±21.7%。相对于运动开始,健康组在0-7s时间窗内的低β(p=0.044)和高β(p=0.039)条带的失同步明显强于帕金森组。α带无显著性差异(p>0.05)。

Fig. 2

运动数据分析显示,健康组的平均波幅峰值为1.04±0.35mv,平均潜伏期为0.52±0.19s,平均熵值为0.20±0.068。PD组平均波幅峰值为0.97±0.29mv,平均潜伏期峰值为0.50±0.11s,平均熵值为0.16±0.08。然而,在手指敲击幅度、潜伏期和样本熵的平均值之间,两组之间没有统计学意义的差异(p>0.05)。两组中α、低β和高βEEG频带功率和运动峰值潜伏期测量之间的重复测量相关性(rrm)。在健康组中,高β带(rrm=0.46,p=0.04)的功率与平均潜伏期显著相关,而α带(rrm=0.15,p=0.54)和低β带(rrm=0.13,p=0.59)的功率与平均潜伏期无关。在PD组,α带功率(rrm=0.01,p=0.97)、低β带功率(rrm=0.08,p=0.72)和高β带功率(rrm=0.26,p=0.24)与潜伏期测量值之间无显著相关性。这意味着高-β功率和敲击峰值潜伏期之间存在直接关系。在两组中,运动峰值振幅与上述频带之间均未观察到显著相关性。

本研究以两组帕金森病患者和健康对照者为研究对象,通过同时记录脑电和运动信号,探讨了自定节奏手指叩击任务中皮层振荡变化与运动结果之间的相互作用。总的来说,证明在PD组中,高ß带皮层振荡和运动测量之间的关系被破坏。研究结果还表明,在健康人群中,运动皮质高频带功率与运动复杂度呈负相关,而在帕金森病患者中,这种负相关并不存在。这些结果表明,帕金森病患者的皮层ß带振荡及其在正常运动中的功能被破坏。本文研究结果有助于更好地理解帕金森病患者大脑皮层运动功能和运动输出之间相互作用受损的机制。

J. McLinden, R.J. Deligani, M.R. Abtahi, U. Akbar, K. Mankodiya, Y. Shahriari,Disruptions of cortico-kinematic interactions in Parkinson’s disease,Behavioural Brain Research,Volume 404,

 

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    2021-02-24 ylz8405
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    2021-02-24 qjddjq
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    2021-02-24 yangshch
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    2021-02-22 raxiedavid

    😁

    0

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    2021-02-22 ms2000001051330459

    学习了,涨知识了!

    0

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