Tilley Dana M, Vallejo Ricardo, Kelley Courtney A, Benyamin Ramsin, Cedeño David L
Basic Science, Millennium Pain Center, Bloomington, IL, USA; School of Biological Sciences, Illinois State University, Normal, IL, USA.
Neuromodulation. 2015 Apr;18(3):171-6; discussion 176. doi: 10.1111/ner.12280. Epub 2015 Feb 13.
Models that simulate clinical conditions are needed to gain an understanding of the mechanism involved during spinal cord stimulation (SCS) treatment of chronic neuropathic pain. An animal model has been developed for continuous SCS in which animals that have been injured to develop neuropathic pain behavior were allowed to carry on with regular daily activities while being stimulated for 72 hours.
Sprague-Dawley rats were randomized into each of six different groups (N = 10-13). Three groups included animals in which the spared nerve injury (SNI) was induced. Animals in two of these groups were implanted with a four-contact electrode in the epidural space. Animals in one of these groups received stimulation for 72 hours continuously. Three corresponding sham groups (no SNI) were included. Mechanical and cold-thermal allodynia were evaluated using von Frey filaments and acetone drops, respectively. Mean withdrawal thresholds were compared. Statistical significance was established using one-way ANOVAs followed by Holm-Sidak post hoc analysis.
Continuous SCS attenuates mechanical allodynia in animals with neuropathic pain behavior. Mechanical withdrawal threshold increases significantly in SNI animals after 24 and 72 hours stimulation vs. SNI no stimulation (p = 0.007 and p < 0.001, respectively). SCS for 24 and 72 hours provides significant increase in mechanical withdrawal thresholds relative to values before stimulation (p = 0.001 and p < 0.001, respectively). Stimulation did not provide recovery to baseline values. SCS did not seem to attenuate cold-thermal allodynia.
A continuous SCS model has been developed. Animals with neuropathic pain behavior that were continuously stimulated showed significant increase in withdrawal thresholds proportional to stimulation time.
需要建立能够模拟临床情况的模型,以了解脊髓刺激(SCS)治疗慢性神经性疼痛的机制。已开发出一种用于持续SCS的动物模型,在该模型中,已受伤并出现神经性疼痛行为的动物在接受72小时刺激的同时可进行日常活动。
将Sprague-Dawley大鼠随机分为六个不同组(每组n = 10 - 13)。其中三组诱导了保留神经损伤(SNI)。这三组中的两组动物在硬膜外间隙植入了四触点电极。其中一组动物接受了72小时的持续刺激。还包括三个相应的假手术组(无SNI)。分别使用von Frey细丝和丙酮滴评估机械性和冷-热痛觉过敏。比较平均撤针阈值。采用单因素方差分析及Holm-Sidak事后分析确定统计学意义。
持续SCS可减轻有神经性疼痛行为动物的机械性痛觉过敏。与未刺激的SNI动物相比,SNI动物在刺激24小时和72小时后的机械撤针阈值显著升高(分别为p = 0.007和p < 0.001)。与刺激前的值相比,24小时和72小时的SCS使机械撤针阈值显著升高(分别为p = 0.001和p < 0.001)。刺激并未使恢复至基线值。SCS似乎并未减轻冷-热痛觉过敏。
已建立了一种持续SCS模型。持续接受刺激的有神经性疼痛行为的动物,其撤针阈值随刺激时间的延长而显著升高。