Valálik István, Emri Miklós, Lengyel Zsolt, Mikecz Pál, Trón Lajos, Csókay András, Márián Teréz
Department of Neurosurgery, St. John's Hospital, Budapest, Hungary.
J Neuroimaging. 2009 Jul;19(3):253-8. doi: 10.1111/j.1552-6569.2008.00304.x. Epub 2008 Oct 22.
BACKGROUND AND PURPOSE The antiakinetic effect of internal Globus pallidus deep brain stimulation (Gpi-DBS) in Parkinson's disease is not clear and not either how this effect is modulated by L-dopa. METHODS Left Gpi-DBS and/or L-dopa effect was studied with auditory paced right-handed sequential movements on (15)O-butanol positron emission tomography (PET) in five patients. Rest and for conditions during movements (DBS off/L-dopa off; DBS on/L-dopa off; DBS off/L-dopa on; DBS on/L-dopa on) were compared with statistical parametric mapping. RESULTS Gpi-DBS activated the right supplementary motor area/premotor (SMA/PMC), and right insular cortex (IC), and as L-dopa decreased the left sensorimotor cortex (M1/S1) activity. L-dopa increased the left ventrolateral thalamus (VLTH), and decreased the left superior parietal cortex (PC) activity. Gpi-DBS and L-dopa interaction showed right SMA/PMC, IC, and left PC activation, decrease of left VLTH, PMC, and dorsolateral prefrontal cortex (PFC) activity. CONCLUSIONS The improvement of bradykinesia with Gpi-DBS is secondary and contributed to the regress of M1/S1-related rigidity and compensatory SMA/PMC, and IC activation. L-dopa and Gpi-DBS alone each reduces M1/S1 overactivity. Interaction ignores this effect, moreover has akinetic effect in the left VLTH, PMC, and PFC. Motor improvement possibly related to left PC and compensatory right SMA/PMC, and IC activation.
背景与目的 帕金森病中内侧苍白球深部脑刺激(Gpi-DBS)的抗运动不能作用尚不清楚,L-多巴对该作用的调节方式也不明确。方法 对5例患者进行了(15)O-丁醇正电子发射断层扫描(PET),通过听觉节奏的右手连续运动研究左侧Gpi-DBS和/或L-多巴的作用。将静息状态以及运动期间的不同情况(DBS关闭/L-多巴关闭;DBS开启/L-多巴关闭;DBS关闭/L-多巴开启;DBS开启/L-多巴开启)进行统计参数映射比较。结果 Gpi-DBS激活了右侧辅助运动区/运动前区(SMA/PMC)、右侧岛叶皮质(IC),且L-多巴降低了左侧感觉运动皮质(M1/S1)的活性。L-多巴增加了左侧腹外侧丘脑(VLTH)的活性,并降低了左侧顶上叶皮质(PC)的活性。Gpi-DBS与L-多巴的相互作用表现为右侧SMA/PMC、IC以及左侧PC激活,左侧VLTH、PMC和背外侧前额叶皮质(PFC)活性降低。结论 Gpi-DBS对运动迟缓的改善是继发性的,与M1/S1相关的强直减退以及代偿性SMA/PMC和IC激活有关。单独使用L-多巴和Gpi-DBS均可降低M1/S1的过度活动。两者相互作用时忽略了这种效应,而且在左侧VLTH、PMC和PFC产生运动不能作用。运动功能的改善可能与左侧PC以及代偿性右侧SMA/PMC和IC激活有关。