Alalami Kareem, Goff Jenna, Grimson Hannah, Martin Oliver, McDonald Eloise, Mirza Thonima, Mistry Dhruvi, Ofodile Adanma, Raja Sara, Shaker Tooba, Sleibi Danah, Forget Patrice
School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Polwarth Building, Foresterhill Health Campus, Aberdeen AB24 3FX, UK.
Epidemiology Group, Institute of Applied Health Sciences, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Polwarth Building, Foresterhill Health Campus, Aberdeen AB25 2ZN, UK.
Pharmaceuticals (Basel). 2024 Jun 27;17(7):842. doi: 10.3390/ph17070842.
Research has been conducted investigating the neuronal pathways responsible for the generation of chronic neuropathic pain, including the components of it in conditions such as chronic post-surgical pain, phantom limb pain, and cluster headaches. Forming part of the management of such conditions, capsaicin as a molecule has proven effective. This review has investigated the central nervous system modifications exhibited in such conditions and the pharmacological mechanisms of capsaicin relevant to this. The current paradigm for explaining topical capsaicin-induced analgesia is that TRPV1-mediated calcium ion influx induces calpain, in turn causing axonal ablation and functional defunctionalisation in the PNS (Peripheral Nervous System). Demonstrated through the analysis of existing data, this review demonstrates the changes seen in the CNS (Central Nervous System) in chronic neuropathic pain, as well as some of the evidence for capsaicin modulation on the CNS. Further supporting this, the specific molecular mechanisms of capsaicin-induced analgesia will also be explored, including the action of TRPV1, as well as discussing the further need for clinical research into this area of uncertainty due to the limited specific data with suitable parameters. Further research this review identified as potentially useful in this field included fMRI (functional Magnetic Resonance Imaging) studies, though more specific observational studies of patients who have already been administered capsaicin as a current treatment may prove helpful in studying the modification of the CNS in the long term.
已有研究对导致慢性神经性疼痛产生的神经通路进行了调查,包括慢性术后疼痛、幻肢痛和丛集性头痛等病症中的相关组成部分。辣椒素作为一种分子,已被证明在这类病症的治疗中有效。本综述研究了这些病症中表现出的中枢神经系统变化以及与之相关的辣椒素药理机制。目前用于解释局部辣椒素诱导镇痛的范例是,TRPV1介导的钙离子内流诱导钙蛋白酶,进而导致外周神经系统(PNS)中的轴突消融和功能失活。通过对现有数据的分析表明,本综述展示了慢性神经性疼痛中中枢神经系统(CNS)的变化,以及辣椒素对中枢神经系统调节的一些证据。进一步支持这一点的是,还将探索辣椒素诱导镇痛的具体分子机制,包括TRPV1的作用,并讨论由于具有合适参数的具体数据有限,该不确定领域临床研究的进一步必要性。本综述确定在该领域可能有用的进一步研究包括功能磁共振成像(fMRI)研究,不过对已经接受辣椒素作为当前治疗的患者进行更具体的观察性研究,可能有助于长期研究中枢神经系统的变化。