Zhang Yi, Lian Yajun, Zhang Haifeng, Xie Nanchang, Chen Yuan
Department of Neurology, Zhengzhou University First Affiliated Hospital, Henan, China.
Pain Med. 2020 Aug 1;21(8):1611-1615. doi: 10.1093/pm/pnaa028.
The aim of this study was to investigate the changes of calcitonin gene-related peptide (CGRP) plasma levels in patients with classical trigeminal neuralgia (TN) and if plasma CGRP concentrations could be used to predict the response to botulinum toxin type A (BTX-A).
Forty-seven patients with classical TN were recruited and treated with BTX-A. A patient was considered a responder when the visual analog scale (VAS) score and number of episodes were reduced by at least 50% compared with baseline data. Matched healthy subjects with no headache history served as controls. CGRP levels were measured by the enzyme-linked immunosorbent assay.
A total of 45 patients and 30 healthy controls completed the study. Plasma CGRP concentrations after treatment with BTX-A (median [interquartile range {IQR}] = 28.86 [14.75-61.23] pg/mL) were significantly lower than before treatment (median [IQR] = 55.38 [22.59-71.67] pg/mL, P < 0.001). Plasma CGRP concentrations in responders after treatment with BTX-A (median [IQR] = 28.02 [12.78-57.28] pg/mL) were significantly lower than before treatment (median [IQR] = 50.57 [24.30-70.09] pg/mL, P < 0.001). In nonresponders, there were no significant differences between the levels before and after treatment (P = 0.938). Age, gender, VAS score, taking/not taking carbamazepine, and the number of trigeminal nerve branches involved had no significant influence on the median difference between plasma CGRP concentrations. The concentration of CGRP before treatment was not predictive of the treatment result.
CGRP levels decrease significantly in patients with classical TN after treatment with BTX-A. Plasma levels of CGRP cannot be used to predict the response to BTX-A. This study indicates that CGRP is likely to be involved in the pathophysiology of classical TN. Moreover, the analgesic mechanism of BTX-A may be related to the inhibition of CGRP release.
本研究旨在调查经典三叉神经痛（TN）患者降钙素基因相关肽（CGRP）血浆水平的变化，以及血浆CGRP浓度是否可用于预测A型肉毒毒素（BTX-A）的治疗反应。
招募47例经典TN患者并接受BTX-A治疗。当视觉模拟量表（VAS）评分和发作次数与基线数据相比至少降低50%时，该患者被视为治疗有效。选取无头痛病史的匹配健康受试者作为对照。采用酶联免疫吸附测定法测量CGRP水平。
共有45例患者和30例健康对照完成了研究。BTX-A治疗后血浆CGRP浓度（中位数[四分位间距{IQR}]=28.86[14.75 - 61.23] pg/mL）显著低于治疗前（中位数[IQR]=55.38[22.59 - 71.67] pg/mL，P < 0.001）。BTX-A治疗后治疗有效的患者血浆CGRP浓度（中位数[IQR]=28.02[12.78 - 57.28] pg/mL）显著低于治疗前（中位数[IQR]=50.57[24.30 - 70.09] pg/mL，P < 0.001）。在治疗无效的患者中，治疗前后水平无显著差异（P = 0.938）。年龄、性别、VAS评分、是否服用卡马西平以及受累三叉神经分支数量对血浆CGRP浓度的中位数差异无显著影响。治疗前CGRP浓度不能预测治疗结果。
经典TN患者经BTX-A治疗后CGRP水平显著降低。血浆CGRP水平不能用于预测BTX-A的治疗反应。本研究表明CGRP可能参与经典TN的病理生理过程。此外，BTX-A的镇痛机制可能与抑制CGRP释放有关。
