Discovery Research, Biological Sciences, Allergan, 2525 Dupont Drive, Irvine, CA 92612-1599, USA.
Parkinsonism Relat Disord. 2011 Nov;17 Suppl 1:S28-33. doi: 10.1016/j.parkreldis.2011.06.013.
Botulinum toxin A has been traditionally viewed as a motor nerve specific treatment. However, clinical uses for botulinum toxin A have continued to expand, with increased use in conditions implicating sensory pain nerve dysfunction. Chronic pain is associated with excess pain fiber activity. When the site of this excess activity resides in the peripheral portion of the pain pathway, a condition of peripheral sensitization can establish. During this state, excess pain signaling reaches the central nervous system, which can then lead to a condition of central sensitization, manifesting as the symptoms associated with chronic pain (i.e. burning, electric pain, lowered pain threshold to normal stimuli, etc). Experimentally, botulinum toxin type A has been shown to reduce neuropeptides and neurotransmitter release from treated cells or nerve endings and to attenuate nociception in both neuropathic and non-neuropathic pain models. This review summarizes the literature to update the hypothesis for the mechanism by which botulinum toxin type A can modulate chronic pain.
肉毒毒素 A 传统上被视为一种运动神经特异性治疗药物。然而，肉毒毒素 A 的临床应用不断扩大，在涉及感觉疼痛神经功能障碍的情况下增加了使用。慢性疼痛与疼痛纤维活动过度有关。当这种过度活动的部位位于疼痛通路的外周部分时，就会出现外周致敏状态。在这种状态下，过多的疼痛信号到达中枢神经系统，这可能导致中枢敏化，表现为与慢性疼痛相关的症状（即烧灼感、电击样疼痛、对正常刺激的疼痛阈值降低等）。实验表明，肉毒毒素 A 可减少治疗细胞或神经末梢的神经肽和神经递质的释放，并减轻神经病理性和非神经病理性疼痛模型中的伤害感受。本综述总结了文献，更新了肉毒毒素 A 调节慢性疼痛的机制假说。
