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首页> 外文期刊>Pain. >Abnormal processing of the nociceptive input in Parkinson's disease: A study with CO(2) laser evoked potentials.
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Abnormal processing of the nociceptive input in Parkinson's disease: A study with CO(2) laser evoked potentials.

机译:帕金森氏病伤害感受输入的异常处理:CO(2)激光诱发电位的研究。

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Since a number of patients with Parkinson's Disease (PD) complain of painful sensations, we studied whether the central processing of nociceptive inputs is abnormal in PD. To test this hypothesis, we recorded scalp CO(2) laser evoked potentials (LEPs) to hand skin stimulation in 18 pain-free PD patients with unilateral bradykinetic-rigid syndrome (hemiparkinson) during the off state and in 18 healthy subjects. This technique allows us to explore non-invasively the functional status of some cerebral structures involved in nociceptive input processing. In both PD patients and control subjects, CO(2) laser stimulation gave rise to a main negative N2 potential followed by a positive P2 response at vertex peaking at a latency of about 200 and 300ms, respectively. These potentials are thought to originate from several brain structures devoted to nociceptive input processing, including the cingulate gyrus and insula. PD patients and normal subjects showed comparable N2 and P2 latencies, whereas the N2/P2 peak-to-peak amplitude was significantly lower in PD patients (regardless of the clinically affected body side) than in controls. LEPs were even recorded after acute L-dopa administration in 7 additional PD patients. L-dopa administration yielded no significant change in N2/P2 amplitude as compared to the off state. These results suggest an abnormal nociceptive input processing in pain-free PD patients which appears to be independent of clinical expression of parkinsonian motor signs and is not affected by dopaminergic stimulation.
机译:由于许多帕金森氏病(PD)患者抱怨疼痛感,因此我们研究了伤害性输入的中央处理在PD中是否异常。为了验证该假设,我们在关闭状态下的18例健康受试者中记录了头皮CO(2)激光诱发电位(LEPs),以在18例无疼痛的PD单侧缓动-刚性综合征(hemiparkinson)的PD患者中进行手部皮肤刺激。这项技术使我们能够无创地探索参与伤害性输入处理的某些大脑结构的功能状态。在PD患者和对照组中,CO(2)激光刺激产生主要的负N2电位,然后在顶点峰值处分别以大约200ms和300ms的等待时间出现正P2反应。人们认为这些潜能来自于专门用于伤害性输入处理的几种大脑结构,包括扣带回和回肠。 PD患者和正常受试者表现出相当的N2和P2潜伏期,而PD患者中的N2 / P2峰峰值幅度(无论受临床影响的身体侧如何)明显低于对照组。在另外7名PD患者中,急性左旋多巴给药后甚至记录了LEP。与关闭状态相比,左旋多巴给药对N2 / P2振幅无明显影响。这些结果表明,无痛PD患者的伤害性输入异常,似乎与帕金森氏运动体征的临床表达无关,并且不受多巴胺能刺激的影响。

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