OUP accepted manuscript

脑深部刺激 丘脑底核 初级运动皮层 运动皮层 神经科学 步态 帕金森病 刺激 心理学 物理医学与康复 冻结行为 皮质(解剖学)
作者
Zixiao Yin,Guanyu Zhu,Yuye Liu,Baotian Zhao,Defeng Liu,Yutong Bai,Quan Zhang,Lin Shi,Tao Feng,Anchao Yang,Huanguang Liu,Fangang Meng,Wolf-Julian Neumann,Andrea A Kühn,Yin Jiang,Jianguo Zhang
出处
期刊:Brain [Oxford University Press]
标识
DOI:10.1093/brain/awac121
摘要

Freezing of gait is a debilitating symptom in advanced Parkinson's disease and responds heterogeneously to treatments such as deep brain stimulation. Recent studies indicated that cortical dysfunction is involved in the development of freezing, while evidence depicting the specific role of the primary motor cortex in the multi-circuit pathology of freezing is lacking. Since abnormal beta-gamma phase-amplitude coupling recorded from the primary motor cortex in patients with Parkinson's disease indicates parkinsonian state and responses to therapeutic deep brain stimulation, we hypothesized this metric might reveal unique information on understanding and improving therapy on freezing of gait. Here we directly recorded potentials in the primary motor cortex using subdural electrocorticography and synchronously captured gait freezing using optoelectronic motion-tracking systems in 16 freely-walking patients with Parkinson's disease who received subthalamic nucleus deep brain stimulation surgery. Overall, we recorded 451 timed up-and-go walking trials, and quantified 7,073 s of stable walking and 3,384 s of gait freezing in conditions of ON/OFF-stimulation and with/without dual-tasking. We found that (i) high beta-gamma phase-amplitude coupling in the primary motor cortex was detected in freezing trials (i.e., walking trials that contained freezing), but not nonfreezing trials, and the high coupling in freezing trials was not caused by dual-tasking or the lack of movement; (ii) nonfreezing episodes within freezing trials also demonstrated abnormally high couplings, which predicted freezing severity; (iii) deep brain stimulation of subthalamic nucleus reduced these abnormal couplings and simultaneously improved freezing; and (iv) in trials that were at similar coupling levels, stimulation trials still demonstrated lower freezing severity than no-stimulation trials. These findings suggest that elevated phase-amplitude coupling in the primary motor cortex indicates higher probabilities of freezing. Therapeutic deep brain stimulation alleviates freezing by both decoupling cortical oscillations and enhancing cortical resistance to abnormal coupling. We formalized these findings to a novel "bandwidth model," which specifies the role of cortical dysfunction, cognitive burden, and therapeutic stimulation on the emergence of freezing. By targeting key elements in the model, we may develop next-generation deep brain stimulation approaches for freezing of gait.
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