基于大脑感觉门控理论对rTMS治疗持续性躯体形式疼痛障碍的机理研究

发布时间：2018-06-04 16:20

本文选题：持续性躯体形式疼痛障碍 + 重复经颅磁刺激　；参考：《成都中医药大学》2015年硕士论文

【摘要】：目的：探讨重复经颅磁刺激治疗持续性躯体形式疼痛障碍的机理。从大脑感觉门控功能入手,初步探讨大脑感觉门控功能在持续性躯体形式疼痛障碍(persistent somatoform pain disorder, PSPD)中的发病机制,进而探讨重复经颅磁刺激(repetitive transcranial magnetic stimulation, rTMS)治疗PSPD的机理,明确rTMS治疗PSPD的有效性。方法：1、以30例PSPD患者以及30例正常受试者为研究对象,检查其感觉门控电位P50、痛觉相关电位(Pain-related evoked potentials,PREP),并进行分析比较,观察PSPD患者与正常受试者P50及PREP的差异。2、以30例PSPD患者以及30例正常受试者为研究对象,对30例PSPD患者组进行15次rTMS治疗,在rTMS治疗前后进行P50及PREP检查以及疼痛视觉模拟评分量表(VAS)评定,并进行比较,观察rTMS治疗前后及治疗后与正常受试者相比P50及PREP的差异。结果：1、PSPD患者P50抑制异常百分率均高于正常组(P0.05),与正常受试者相比,PSPD患者S1-P50波幅无明显改变(P0.05),S2-P50波幅增高,S1-S2值(即S1-P50与S2-P50波幅差)降低,S2/S1(P50抑制)值增高(P0.05)；PSPD患者PREP各成分波(除P6波外)潜伏期均显著提前(P0.05)。2、PSPD患者PERP各成分波潜伏期与S2/S1成负相关,与S1-P50波幅及S1-S2成正相关(均P0.05),与S2-P50波幅无直线相关关系(均P0.05)。3、与rTMS治疗前比较,治疗后PSPD患者S2-P50波幅、S2/S1值、P50抑制异常百分率均显著降低(P0.05),S1-P50波幅无明显改变,S1-S2值有增高趋势,但增高无统计学意义(P0.05); PREP异常成分波中P1、N1、P2、N2、P4、N4、P5波潜伏期均显著延后(P0.05)；VAS评分显著降低(P0.05)。4、PSPD患者经rTMS治疗后,P50以及PREP各成分波与正常受试者比较均无显著差异(均P0.05)。结论：1、PSPD患者痛觉信息的传递速度加快。PREP可反映PSPD患者大脑对痛觉刺激信息的心理反应及痛觉信息处理过程,因此可能应用于疼痛症状程度的评估。2、PSPD患者门控缺损程度与疼痛症状显著相关,感觉门控缺损可能是PSPD精神病学发病机制。3、rTMS可能通过神经可塑效应调节大脑信息处理过程,改善PSPD患者感觉门控功能,进而改善认知过程及疼痛症状。
[Abstract]:Objective: to explore the mechanism of repeated transcranial magnetic stimulation in the treatment of persistent somatoform pain disorder. The mechanism of sensory gating function in persistent somatoform pain disorder (somatoform pain disorder, PSPD) was discussed from the perspective of sensory gating function in the brain, and the mechanism of repeated transcranial magnetic stimulation (TMS) repetive transcranial magnetic stimulation, rTMS) in the treatment of PSPD was discussed. To determine the efficacy of rTMS in the treatment of PSPD. Methods: the sensory gated potential (P50), pain associated potential (Pain-related evoked potentialsn) of 30 patients with PSPD and 30 normal subjects were examined and compared. The difference of P50 and PREP between PSPD patients and normal subjects was observed. 30 patients with PSPD and 30 normal subjects were treated with rTMS for 15 times. P50, PREP and pain visual analogue scale (VAS) were assessed before and after rTMS treatment, and the differences of P50 and PREP before and after rTMS treatment were observed. Results the percentage of abnormal P50 inhibition in the patients with PSPD was higher than that in the normal controls. There was no significant change in the amplitude of S1-P50 in the patients with PSPD compared with the normal subjects. The increase of S1-S2 (the difference between the amplitude of S1-P50 and S2-P50) and the decrease of the inhibition of P50 in the patients with PSPD were higher than those in the patients with PSPD, and the PREP of the patients with PSPD was higher than that of the patients with PSPD. The latent period of partial wave (except P6 wave) was significantly earlier than that of P0.050.2in patients with PSPD, the latency of each component of PERP was negatively correlated with S2/S1. There was a positive correlation with the amplitude of S1-P50 and S1-S2 (all P0.05A, but no linear correlation with the amplitude of S2-P50 (all P0.05U. 3). Compared with that before rTMS treatment, the percentage of abnormal inhibition of S2-P50 amplitudes S2 / S1 and P50 in PSPD patients decreased significantly after treatment, and the amplitude of S1-P50 did not change with the increase of S1-S2. However, there was no statistical significance in the increase of P0. 05%, and there was no significant difference in the latency of P1 + N1, P2, N2, P4, N4, P4, P5, P0. 05 and P0. 05 in patients with PREP after rTMS treatment. There was no significant difference in the P0. 05 and P0. 05 components of PREP between P0. 05 and normal subjects (both P0. 05 and P0. 05) after rTMS treatment, there was no significant difference between P0. 05 and P0. 05. Conclusion the rapid transmission of pain information in patients with PSPD can reflect the psychological response of the brain to the information of pain stimulation and the process of processing the information of pain in the brain of patients with PSPD. Therefore, the degree of gated defect in patients with PSPD may be significantly correlated with the severity of pain symptoms, and sensory gated defect may be the pathogenesis of PSPD psychiatry. 3rTMS may regulate the process of brain information processing through neuroplastic effect. To improve sensory gated function, cognitive process and pain symptoms in patients with PSPD.
【学位授予单位】：成都中医药大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R402

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