Buscher H C J L, van Goor H, Wilder-Smith O H G
Department of General Surgery, Radboud University Nijmegen Medical Centre, P.O.B. 9101, Internal 520, 6500 HB Nijmegen, The Netherlands.
Eur J Pain. 2007 May;11(4):437-43. doi: 10.1016/j.ejpain.2006.06.001. Epub 2006 Jul 13.
Central sensitisation due to visceral pancreatic nociceptive input may play an important role in chronic pancreatitis pain. Using quantitative sensory testing (QST), this first study investigates whether thoracoscopic splanchnic denervation (TSD), performed to reduce nociceptive visceral input, affects central sensitisation in chronic pancreatitis patients.
We studied 19 chronic pancreatitis patients (11 men, 8 women on stable opioid medication) and 18 healthy volunteers as preoperative controls. Preoperatively and 6 weeks after TSD, pain numeric rating scores, opioid medication, and thresholds to electric skin stimulation and pressure pain (measured in dermatomes T10 (pancreas), C5, T4, L1, L4) were documented. Treatment success was defined as cessation of opioids 6 weeks after TSD.
Six weeks after TSD, there was a trend towards lower pain scores, only 10 patients were still on opioids (P<0.05 vs. preoperatively) and thresholds overall were significantly higher than preoperatively (pressure pain: +25%, P<0.001; electric: sensation +55%, pain detection +34%, pain tolerance +21%, P<0.05). Gender-specific differences in hypoalgesia patterns were seen. Preoperatively, TSD treatment successes consumed significantly less opioids than failures, without significant differences in preoperative patterns of neuroplasticity.
TSD for chronic pancreatitis pain resulted in fewer patients on opioids and overall increases in pain thresholds. Our results suggest that TSD for reducing visceral nociceptive input may be effective in reducing resulting central sensitisation. Although patients benefiting from TSD consume less opioids preoperatively, we were unable to clearly link treatment success with specific perioperative patterns of neuroplasticity such as the presence or absence of hyperalgesia.
内脏胰腺伤害性输入引起的中枢敏化可能在慢性胰腺炎疼痛中起重要作用。本第一项研究采用定量感觉测试(QST),调查为减少伤害性内脏输入而进行的胸腔镜内脏神经切除术(TSD)是否会影响慢性胰腺炎患者的中枢敏化。
我们研究了19例慢性胰腺炎患者(11例男性,8例女性,均服用稳定剂量的阿片类药物)和18名健康志愿者作为术前对照。在术前以及TSD术后6周,记录疼痛数字评分、阿片类药物使用情况以及皮肤电刺激和压力疼痛阈值(在T10皮节(胰腺)、C5、T4、L1、L4测量)。治疗成功定义为TSD术后6周停用阿片类药物。
TSD术后6周,疼痛评分有降低趋势,仅10例患者仍在服用阿片类药物(与术前相比P<0.05),总体阈值显著高于术前(压力疼痛:升高25%,P<0.001;电刺激:感觉升高55%,疼痛检测升高34%,疼痛耐受升高21%,P<0.05)。观察到痛觉减退模式存在性别差异。术前,TSD治疗成功的患者服用的阿片类药物明显少于治疗失败的患者,术前神经可塑性模式无显著差异。
TSD治疗慢性胰腺炎疼痛使服用阿片类药物的患者减少,疼痛阈值总体升高。我们的结果表明,TSD减少内脏伤害性输入可能有效降低由此引起的中枢敏化。尽管从TSD中获益的患者术前服用的阿片类药物较少,但我们无法明确将治疗成功与特定的围手术期神经可塑性模式(如是否存在痛觉过敏)联系起来。