Inflammatory pain is the most common type of pain that is treated clinically. The use of currently available treatments (classic analgesics - NSAIDs, paracetamol and opioids) is limited by insufficient efficacy and/or side effects/tolerance development. Antiepileptic drugs (AEDs) are widely used in neuropathic pain treatment, but there is substantial preclinical evidence on their efficacy against inflammatory pain, too. In this review we focus on gabapentinoids (gabapentin and pregabalin) and dibenzazepine AEDs (carbamazepine, oxcarbazepine, and recently introduced eslicarbazepine acetate) and their potential for relieving inflammatory pain. In models of somatic, visceral and trigeminal inflammatory pain, that have a translational value for inflammatory conditions in locomotor system, viscera and head/face, AEDs have demonstrated analgesic activity. This activity was mostly consistent, dependent on the dose and largely independent on the site of inflammation and method of its induction, nociceptive stimuli, species, specific drug used, its route of administration and dosing schedule. AEDs exerted comparable efficacy with classic analgesics. Effective doses of AEDs are lower than toxic doses in animals and, when expressed as equivalent human doses, they are largely overlapping with AEDs doses already used in humans for treating epilepsy/neuropathic pain. The main mechanism of antinociceptive/antihyperalgesic action of gabapentinoids in inflammatory pain models seems to be α₂δ-dependent suppression of voltage-gated calcium channels in primary sensory neurons that leads to reduced release of neurotransmitters in the spinal/medullar dorsal horn. The suppression of NMDA receptors via co-agonist binding site primarily at spinal sites, activation of various types of K⁺ channels at spinal and peripheral sites, and activation of noradrenergic and serotonergic descending pain modulatory pathways may also contribute. Inhibition of voltage-gated sodium channels along the pain pathway is probably the main mechanism of antinociceptive/antihyperalgesic effects of dibenzazepines. The recruitment of peripheral adrenergic and purinergic mechanisms and central GABAergic mechanisms may also contribute. When co-administered with classic/other alternative analgesics, AEDs exerted synergistic/additive interactions. Reviewed data could serve as a basis for clinical studies on the efficacy/safety of AEDs as analgesics/adjuvants in patients with inflammatory pain, and contribute to the improvement of the treatment of various inflammatory pain states.

炎性疼痛是临床上最常见的疼痛类型。由于疗效和/或副作用/耐受性不足，限制了目前可用的治疗方法（经典镇痛药-NSAID，对乙酰氨基酚和阿片类药物）的使用。抗癫痫药（AED）被广泛用于神经性疼痛的治疗，但也有大量的临床前证据表明它们可抗炎性疼痛。在这篇综述中，我们重点研究加巴喷丁类药物（加巴喷丁和普瑞巴林）和地苯并ze庚因类抗癫痫药（卡马西平，奥卡西平，以及最近推出的醋酸埃斯卡西平）及其缓解炎性疼痛的潜力。在躯体，内脏和三叉神经炎性疼痛的模型中，对于运动系统，内脏和头部/面部的炎性疾病具有转化价值，AED具有镇痛作用。该活性基本上是一致的，取决于剂量，并且基本上不依赖于炎症的部位及其诱导方法，伤害性刺激，种类，所用的特定药物，其给药途径和给药方案。AEDs具有与传统止痛药相当的功效。AED的有效剂量低于动物的毒性剂量，当以等效的人类剂量表示时，它们与已经用于治疗癫痫/神经性疼痛的人类AED剂量大为重叠。加巴喷丁胺类药物在炎性疼痛模型中的抗伤害性/抗痛觉过敏作用的主要机制似乎是α 使用的具体药物，给药途径和给药时间表。AEDs具有与传统止痛药相当的功效。AED的有效剂量低于动物的毒性剂量，当以等效的人类剂量表示时，它们与已经用于治疗癫痫/神经性疼痛的人类AED剂量大为重叠。加巴喷丁胺类药物在炎性疼痛模型中的抗伤害性/抗痛觉过敏作用的主要机制似乎是α 使用的具体药物，给药途径和给药时间表。AEDs具有与传统止痛药相当的功效。AED的有效剂量低于动物的毒性剂量，当以等效的人类剂量表示时，它们与已经用于治疗癫痫/神经性疼痛的人类AED剂量大为重叠。加巴喷丁胺类药物在炎性疼痛模型中的抗伤害性/抗痛觉过敏作用的主要机制似乎是α₂在初级感觉神经元的电压门控钙通道的δ依赖性抑制，导致减少在脊柱/骨髓背角神经递质的释放。NMDA受体主要通过在脊髓位点的激动剂结合位点来抑制，激活各种类型的K ⁺脊髓和周围部位的通道，以及去甲肾上腺素能和血清素能下降的疼痛调节途径的激活也可能起作用。抑制沿疼痛途径的电压门控钠通道可能是地苯扎西平抗伤害性/抗痛觉过敏作用的主要机制。周围肾上腺素能和嘌呤能机制以及中枢GABA能机制的募集也可能有贡献。当与经典/其他替代镇痛药合用时，AED发挥了协同/加性相互作用。复习的数据可以作为临床研究，作为AED在炎性疼痛患者中作为镇痛药/佐剂的功效/安全性的基础，并有助于改善各种炎性疼痛状态的治疗。