Mild traumatic brain injury impairs the coordination of intrinsic and motor-related neural dynamics.

Mild traumatic brain injury impairs the coordination of intrinsic and motor-related neural dynamics.
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DOI:
10.1016/j.nicl.2021.102841
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发表时间:
2021
期刊:
NeuroImage. Clinical
影响因子:
--
通讯作者:
Dunkley BT
Dunkley BT
中科院分区:
其他
文献类型:
--
作者:
Rier L;Zamyadi R;Zhang J;Emami Z;Seedat ZA;Mocanu S;Gascoyne LE;Allen CM;Scadding JW;Furlong PL;Gooding-Williams G;Woolrich MW;Evangelou N;Brookes MJ;Dunkley BT

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MTBI了解甚少,缺乏客观的诊断和预后工具。在有mTBI病史的受试者中发现异常神经振荡。我们使用隐马尔可夫模型来识别MEG数据中的瞬时爆发。我们解释了赤字的β连通性和权力方面的瞬态突发。数据驱动的特征选择识别与数据相关的功能连接。轻度创伤性脑损伤(mTBI)给医疗保健系统带来了相当大的负担。虽然大多数患者恢复迅速,但相当多的患者患有后遗症,这些后遗症并不伴有可测量的结构性损伤。了解这些衰弱效应的神经基础并开发检测损伤的方法,将解决一个重要的未满足的临床需求。它可以为干预措施提供信息,并有助于预测预后。脑磁图(MEG)在探测神经功能方面具有出色的灵敏度,并为评估mTBI提供了重要的前景,异常神经振荡是一种潜在的特异性生物标志物。然而,越来越多的证据表明,神经动力学(至少部分)驱动的瞬态,泛谱爆发,在本文中,我们采用这种模式来调查mTBI。我们应用隐马尔可夫模型的MEG数据记录在休息状态和运动任务,并表明,以前的研究结果与mTBI的个人减少内在β振幅在很大程度上是由于减少β波段的频谱内容的爆发,并减少β连接的结果从突发状态的时间重合的损失。在运动任务中,mTBI导致爆发振幅减小,运动期间爆发概率的调制改变,以及运动网络连接的丧失。这些结果表明,从机制上讲,mTBI破坏了神经同步的结构框架,从而损害了网络功能。虽然损伤可能太细微,结构成像无法看到,但功能后果是可检测的,并且在损伤后持续存在。我们的工作表明,mTBI损害神经网络活动的动态协调,并提出了一个有效的新方法来理解mTBI。
MTBI is poorly understood and lacks objective diagnostic and prognostic tools. Abnormal neural oscillations are found in subjects with a history of mTBI. We identify transient bursts in MEG data using a Hidden Markov Model. We explain a deficit in beta connectivity and power in terms of transient bursts. Data-driven feature selection identifies symptom-relevant functional connections. Mild traumatic brain injury (mTBI) poses a considerable burden on healthcare systems. Whilst most patients recover quickly, a significant number suffer from sequelae that are not accompanied by measurable structural damage. Understanding the neural underpinnings of these debilitating effects and developing a means to detect injury, would address an important unmet clinical need. It could inform interventions and help predict prognosis. Magnetoencephalography (MEG) affords excellent sensitivity in probing neural function and presents significant promise for assessing mTBI, with abnormal neural oscillations being a potential specific biomarker. However, growing evidence suggests that neural dynamics are (at least in part) driven by transient, pan-spectral bursting and in this paper, we employ this model to investigate mTBI. We applied a Hidden Markov Model to MEG data recorded during resting state and a motor task and show that previous findings of diminished intrinsic beta amplitude in individuals with mTBI are largely due to the reduced beta band spectral content of bursts, and that diminished beta connectivity results from a loss in the temporal coincidence of burst states. In a motor task, mTBI results in diminished burst amplitude, altered modulation of burst probability during movement, and a loss in connectivity in motor networks. These results suggest that, mechanistically, mTBI disrupts the structural framework underlying neural synchrony, which impairs network function. Whilst the damage may be too subtle for structural imaging to see, the functional consequences are detectable and persist after injury. Our work shows that mTBI impairs the dynamic coordination of neural network activity and proposes a potent new method for understanding mTBI.
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