Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease.
Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease.
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帕金森氏病临床上有效的丘脑深脑刺激临床有效的深层脑刺激过程中皮质的潜伏潜伏期激活。
DOI：
10.1002/mds.25025
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发表时间：
2012-06
影响因子：
8.6
通讯作者：
Watts, Ray L.
中科院分区：
文献类型：
--
作者：
Walker, Harrison C.;Huang, He;Gonzalez, Christopher L.;Bryant, James E.;Killen, Jeffrey;Cutter, Gary R.;Knowlton, Robert C.;Montgomery, Erwin B.;Guthrie, Bart L.;Watts, Ray L.
关键词：
对于晚期帕金森病的运动症状，丘脑底脑深部电刺激上级优于药物治疗，另外的证据表明，它可以改善原发性震颤、原发性全身性肌张力障碍和强迫症的难治性症状。尽管如此，其治疗机制尚不清楚。我们假设，在帕金森病的临床有效刺激过程中，丘脑底核刺激在刺激开始后的短潜伏期激活大脑皮层。在5名受试者（6个半球）中，脑电图测量了在一系列刺激电压和频率范围内丘脑底核刺激时皮质的反应。新的分析技术颠倒了阳极和阴极电极接触，并将所得的事件相关电位对相加，以抑制刺激伪影。20赫兹的丘脑底脑刺激在离散潜伏期激活体感皮层（平均潜伏期分别为1.0 ± 0.4、5.7 ± 1.1和22.2 ± 1.8毫秒，分别表示为R1、R2和R3）。在临床有效的高频刺激期间，短潜伏期峰值（R1）的幅度非线性地依赖于刺激电压（p < 0.001，重复测量方差分析），并且其潜伏期的变化小于R3（1.02与19.46毫秒，p < 0.001，Levene检验）。在帕金森病患者中，临床有效的丘脑底脑刺激在刺激开始后1毫秒激活大脑皮层，最有可能是通过逆向激活。我们的研究结果表明，改变皮层神经元的轴突投射到丘脑底区的动作电位的精确时间是丘脑底脑刺激的治疗机制的重要组成部分。
Subthalamic deep brain stimulation is superior to medical therapy for the motor symptoms of advanced Parkinson’s disease, and additional evidence suggests that it improves refractory symptoms of essential tremor, primary generalized dystonia, and obsessive-compulsive disorder. Despite this, its therapeutic mechanism is unknown. We hypothesized that subthalamic stimulation activates cerebral cortex at short latencies after stimulus onset during clinically effective stimulation for Parkinson disease. In 5 subjects (6 hemispheres) electroencephalography measured the response of cortex to subthalamic stimulation across a range of stimulation voltages and frequencies. Novel analytical techniques reversed the anode and cathode electrode contacts and summed the resulting pair of event related potentials to suppress the stimulation artifact. Subthalamic brain stimulation at 20 Hertz activates somatosensory cortex at discrete latencies (mean latencies 1.0 ± 0.4, 5.7 ± 1.1, and 22.2 ± 1.8 milliseconds, denoted R1, R2, and R3, respectively). The amplitude of the short latency peak (R1) during clinically effective high frequency stimulation is nonlinearly dependent on stimulation voltage (p < 0.001, repeated measures analysis of variance), and its latency is less variable than that of R3 (1.02 versus 19.46 milliseconds, p < 0.001, Levene’s test). Clinically effective subthalamic brain stimulation in humans with Parkinson disease activates cerebral cortex at one millisecond after stimulus onset, most likely by antidromic activation. Our findings suggest that alteration of the precise timing of action potentials in cortical neurons with axonal projections to the subthalamic region is an important component of the therapeutic mechanism of subthalamic brain stimulation.
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影响因子：
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通讯作者：
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