本文選題：持續(xù)性軀體形式疼痛障礙 + 重復經(jīng)顱磁刺激�。� 參考：《成都中醫(yī)藥大學》2015年碩士論文

【摘要】：目的：探討重復經(jīng)顱磁刺激治療持續(xù)性軀體形式疼痛障礙的機理。從大腦感覺門控功能入手,初步探討大腦感覺門控功能在持續(xù)性軀體形式疼痛障礙(persistent somatoform pain disorder, PSPD)中的發(fā)病機制,進而探討重復經(jīng)顱磁刺激(repetitive transcranial magnetic stimulation, rTMS)治療PSPD的機理,明確rTMS治療PSPD的有效性。方法：1、以30例PSPD患者以及30例正常受試者為研究對象,檢查其感覺門控電位P50、痛覺相關電位(Pain-related evoked potentials,PREP),并進行分析比較,觀察PSPD患者與正常受試者P50及PREP的差異。2、以30例PSPD患者以及30例正常受試者為研究對象,對30例PSPD患者組進行15次rTMS治療,在rTMS治療前后進行P50及PREP檢查以及疼痛視覺模擬評分量表(VAS)評定,并進行比較,觀察rTMS治療前后及治療后與正常受試者相比P50及PREP的差異。結果：1、PSPD患者P50抑制異常百分率均高于正常組(P0.05),與正常受試者相比,PSPD患者S1-P50波幅無明顯改變(P0.05),S2-P50波幅增高,S1-S2值(即S1-P50與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)潛伏期均顯著提前(P0.05)。2、PSPD患者PERP各成分波潛伏期與S2/S1成負相關,與S1-P50波幅及S1-S2成正相關(均P0.05),與S2-P50波幅無直線相關關系(均P0.05)。3、與rTMS治療前比較,治療后PSPD患者S2-P50波幅、S2/S1值、P50抑制異常百分率均顯著降低(P0.05),S1-P50波幅無明顯改變,S1-S2值有增高趨勢,但增高無統(tǒng)計學意義(P0.05); PREP異常成分波中P1、N1、P2、N2、P4、N4、P5波潛伏期均顯著延后(P0.05)；VAS評分顯著降低(P0.05)。4、PSPD患者經(jīng)rTMS治療后,P50以及PREP各成分波與正常受試者比較均無顯著差異(均P0.05)。結論：1、PSPD患者痛覺信息的傳遞速度加快。PREP可反映PSPD患者大腦對痛覺刺激信息的心理反應及痛覺信息處理過程,因此可能應用于疼痛癥狀程度的評估。2、PSPD患者門控缺損程度與疼痛癥狀顯著相關,感覺門控缺損可能是PSPD精神病學發(fā)病機制。3、rTMS可能通過神經(jīng)可塑效應調(diào)節(jié)大腦信息處理過程,改善PSPD患者感覺門控功能,進而改善認知過程及疼痛癥狀。
[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.
【學位授予單位】：成都中醫(yī)藥大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R402

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