Deep Brain Stimulation Does Not Silence Neurons in Subthalamic Nucleus in Parkinson's Patients
Deep Brain Stimulation Does Not Silence Neurons in Subthalamic Nucleus in Parkinson's Patients
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DOI：
10.1152/jn.00363.2009
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发表时间：
2010-02-01
影响因子：
2.5
通讯作者：
Burchiel, Kim J.
中科院分区：
文献类型：
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作者：
Carlson, Jonathan D.;Cleary, Daniel R.;Burchiel, Kim J.
Carlson JD，Cleary DR，Cetas JS，Heinricher MM，Burchiel KJ.脑深部电刺激不会使帕金森病患者的丘脑底核神经元沉默。J Neurophysiol 103：962-967，2010.首次发表于2009年12月2日; doi：10.1152/jn.00363.2009。已经提出了两个广泛的假设来解释丘脑底核（DBS）脑深部电刺激（DBS）治疗帕金森病的临床疗效。一种是刺激会使海马神经元失活，产生功能性损伤。另一种是电刺激激活了突触输出，从而“干扰”了基底节-皮质丘脑回路中的病理活动。与这两个概念相一致的证据已经从建模和动物研究以及患者的记录中被引用。然而，许多记录研究中使用的刺激参数与临床使用的刺激参数并不匹配。在这项研究中，我们记录了帕金森病患者在通过临床DBS电极使用标准治疗刺激参数进行刺激期间的脑电活动。使用微电极记录DBS期间单个神经元的放电（3-5 V，80-200 Hz，90- 200 μ s脉冲; 33个神经元/11例患者）。放电率在刺激串期间不变，并且记录的神经元在刺激终止时没有显示放电率的延长变化。然而，一个简短的（类似于1毫秒），短潜伏期（6毫秒）脉冲后抑制被认为是在10的14个神经元分析。一个神经元子集显示出改变的放电模式，主要转向随机放电。这些数据并不支持DBS使丘脑失活的观点，而是与这种刺激向基底节-皮质丘脑回路提供零信号的假设更一致，该基底节-皮质丘脑回路已被改变为帕金森病的一部分。
Carlson JD, Cleary DR, Cetas JS, Heinricher MM, Burchiel KJ. Deep brain stimulation does not silence neurons in subthalamic nucleus in Parkinson's patients. J Neurophysiol 103: 962-967, 2010. First published December 2, 2009; doi:10.1152/jn.00363.2009. Two broad hypotheses have been advanced to explain the clinical efficacy of deep brain stimulation (DBS) in the subthalamic nucleus (STN) for treatment of Parkinson's disease. One is that stimulation inactivates STN neurons, producing a functional lesion. The other is that electrical stimulation activates the STN output, thus "jamming" pathological activity in basal ganglia-corticothalamic circuits. Evidence consistent with both concepts has been adduced from modeling and animal studies, as well as from recordings in patients. However, the stimulation parameters used in many recording studies have not been well matched to those used clinically. In this study, we recorded STN activity in patients with Parkinson's disease during stimulation delivered through a clinical DBS electrode using standard therapeutic stimulus parameters. A microelectrode was used to record the firing of a single STN neuron during DBS (3-5 V, 80-200 Hz, 90- to 200-mu s pulses; 33 neurons/11 patients). Firing rate was unchanged during the stimulus trains, and the recorded neurons did not show prolonged (s) changes in firing rate on termination of the stimulation. However, a brief (similar to 1 ms), short-latency (6 ms) postpulse inhibition was seen in 10 of 14 neurons analyzed. A subset of neurons displayed altered firing patterns, with a predominant shift toward random firing. These data do not support the idea that DBS inactivates the STN and are instead more consistent with the hypothesis that this stimulation provides a null signal to basal ganglia-corticothalamic circuitry that has been altered as part of Parkinson's disease.