Frequency-dependent effects of electrical stimulation in the globus pallidus of dystonia patients

Frequency-dependent effects of electrical stimulation in the globus pallidus of dystonia patients
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DOI:
10.1152/jn.00527.2011
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发表时间:
2012-07-01
影响因子:
2.5
通讯作者:
Hutchison, William D.
Hutchison, William D.
中科院分区:
医学3区
文献类型:
--
作者:
Liu, D. Liu;Prescott, Ian A.;Hutchison, William D.

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Liu LD,Prescott IA,Dostrovsky JO,Hodaie M,Lozano AM,Hutchison WD.肌张力障碍患者苍白球电刺激的频率依赖性效应。J Neurophysiol 108:5-17,2012.首次发表于2012年3月28日; doi:10.1152/jn.00527.2011.-苍白球内(GPi)的深部脑刺激(DBS)已被证明可以改善肌张力障碍,这是一种重复扭转运动和姿势的运动障碍。频率高于60 Hz的DBS可改善肌张力障碍,但这种频率依赖性的机制尚不清楚。在接受GPi双微电极标测的患者中,微刺激已被证明可以减少神经元放电,可能是由于突触GABA释放。本研究探讨了不同的微刺激频率(1-100 Hz)和列车长度(0.5-20 s),有和没有事先高频刺激(HFS)对神经元放电和诱发场电位(fEP)的影响,在13名肌张力障碍患者。在HFS前,平均放电随着刺激频率的增加而减少,并且在50 Hz以上被沉默。平均fEP振幅增加到20-30 Hz的频率,但随后下降,在50 Hz时,仅为基线的75%。在某些情况下,观察到短潜伏期纤维齐射和逆向样尖峰,并遵循高频率。后HFS,整体放电减少相比,前HFS,和fEP振幅在低频率增强,提供证据的抑制性突触可塑性的GPi。在已经植入GPi的DBS电极的患者中,丘脑底核中四个神经元的记录显示,使用临床有效但非临床无效的刺激参数几乎完全抑制了放电。这些数据提供了额外的支持刺激诱发GABA从传入突触末梢释放和DBS过程中神经元放电减少的假设,此外,涉及兴奋GPi轴突纤维和神经元和增强抑制性突触传递的高频GPi DBS作为额外的推定机制DBS在肌张力障碍的临床受益。
Liu LD, Prescott IA, Dostrovsky JO, Hodaie M, Lozano AM, Hutchison WD. Frequency-dependent effects of electrical stimulation in the globus pallidus of dystonia patients. J Neurophysiol 108: 5-17, 2012. First published March 28, 2012; doi:10.1152/jn.00527.2011.-Deep brain stimulation (DBS) in the globus pallidus internus (GPi) has been shown to improve dystonia, a movement disorder of repetitive twisting movements and postures. DBS at frequencies above 60 Hz improves dystonia, but the mechanisms underlying this frequency dependence are unclear. In patients undergoing dual-microelectrode mapping of the GPi, microstimulation has been shown to reduce neuronal firing, presumably due to synaptic GABA release. This study examined the effects of different microstimulation frequencies (1-100 Hz) and train length (0.5-20 s), with and without prior high-frequency stimulation (HFS) on neuronal firing and evoked field potentials (fEPs) in 13 dystonia patients. Pre-HFS, the average firing decreased as stimulation frequency increased and was silenced above 50 Hz. The average fEP amplitudes increased up to frequencies of 20-30 Hz but then declined and at 50 Hz, were only at 75% of baseline. In some cases, short latency fiber volleys and antidromic-like spikes were observed and followed high frequencies. Post-HFS, overall firing was reduced compared with pre-HFS, and the fEP amplitudes were enhanced at low frequencies, providing evidence of inhibitory synaptic plasticity in the GPi. In a patient with DBS electrodes already implanted in the GPi, recordings from four neurons in the subthalamic nucleus showed almost complete inhibition of firing with clinically effective but not clinically ineffective stimulation parameters. These data provide additional support for the hypothesis of stimulation-evoked GABA release from afferent synaptic terminals and reduction of neuronal firing during DBS and additionally, implicate excitation of GPi axon fibers and neurons and enhancement of inhibitory synaptic transmission by high-frequency GPi DBS as additional putative mechanisms underlying the clinical benefits of DBS in dystonia.