Department of Clinical Sciences, Faculté de médecine vétérinaire, Université de Montréal, Saint-Hyacinthe, Québec, Canada.
Faculté de médecine vétérinaire, Université de Montréal, Saint-Hyacinthe, Québec, Canada.
PLoS One. 2020 Nov 30;15(11):e0237121. doi: 10.1371/journal.pone.0237121. eCollection 2020.
Canine neuropathic pain (NeuP) has been poorly investigated. This study aimed to evaluate the pain burden, sensory profile and inflammatory cytokines in dogs with naturally-occurring NeuP. Twenty-nine client-owned dogs with NeuP were included in a prospective, partially masked, randomized crossover clinical trial, and treated with gabapentin/placebo/gabapentin-meloxicam or gabapentin-meloxicam/placebo/gabapentin (each treatment block of 7 days; total 21 days). Pain scores, mechanical (MNT) and electrical (ENT) nociceptive thresholds and descending noxious inhibitory controls (DNIC) were assessed at baseline, days 7, 14, and 21. DNIC was evaluated using ΔMNT (after-before conditioning stimulus). Positive or negative ΔMNT corresponded to inhibitory or facilitatory pain profiles, respectively. Pain scores were recorded using the Client Specific Outcome Measures (CSOM), Canine Brief Pain Inventory (CBPI), and short-form Glasgow Composite Measure Pain Scale (CMPS-SF). Data from baseline were compared to those of sixteen healthy controls. ΔMNT, but not MNT and ENT, was significantly larger in controls (2.3 ± 0.9 N) than in NeuP (-0.2 ± 0.7 N). The percentage of dogs with facilitatory sensory profile was similar at baseline and after placebo (61.5-63%), and between controls and after gabapentin (33.3-34.6%). The CBPI scores were significantly different between gabapentin (CBPI pain and CBPI overall impression) and/or gabapentin-meloxicam (CBPI pain and interference) when compared with baseline, but not placebo. The CBPI scores were not significantly different between placebo and baseline. The concentration of cytokines was not different between groups or treatments. Dogs with NeuP have deficient inhibitory pain mechanisms. Pain burden was reduced after gabapentin and/or gabapentin-meloxicam when compared with baseline using CBPI and CMPS-SF scores. However, these scores were not superior than placebo, nor placebo was superior to baseline evaluations. A caregiver placebo effect may have biased the results.
犬神经病理性疼痛（NeuP）研究甚少。本研究旨在评估自然发生 NeuP 的犬的疼痛负担、感觉特征和炎症细胞因子。29 只 NeuP 犬纳入一项前瞻性、部分盲法、随机交叉临床试验，并接受加巴喷丁/安慰剂/加巴喷丁-美洛昔康或加巴喷丁-美洛昔康/安慰剂/加巴喷丁治疗（每治疗 7 天，共 21 天）。在基线、第 7、14 和 21 天评估疼痛评分、机械（MNT）和电（ENT）伤害感受阈值和下行抑制性伤害控制（DNIC）。使用 ΔMNT（条件刺激前后）评估 DNIC。正或负 ΔMNT 分别对应抑制或促进疼痛特征。使用特定于客户的结果测量（CSOM）、犬简要疼痛量表（CBPI）和简短格拉斯哥复合疼痛量表（CMPS-SF）记录疼痛评分。将基线数据与 16 名健康对照进行比较。与 NeuP 犬（-0.2±0.7 N）相比，对照组的 ΔMNT（2.3±0.9 N）显著更大，但 MNT 和 ENT 无差异。基线时和安慰剂后具有促发感觉特征的犬的百分比相似（61.5%-63%），且对照组与加巴喷丁后相似（33.3%-34.6%）。与基线相比，加巴喷丁（CBPI 疼痛和 CBPI 总体印象）和/或加巴喷丁-美洛昔康（CBPI 疼痛和干扰）时 CBPI 评分显著不同，但安慰剂时无差异。与基线相比，安慰剂时 CBPI 评分无显著差异。各组或各治疗之间细胞因子浓度无差异。NeuP 犬存在抑制性疼痛机制缺陷。与基线相比，使用 CBPI 和 CMPS-SF 评分，加巴喷丁和/或加巴喷丁-美洛昔康治疗后疼痛负担减轻。然而，这些评分并不优于安慰剂，安慰剂也不优于基线评估。照顾者安慰剂效应可能影响了结果。
