CGRP Plasma Levels Decrease in Classical Trigeminal Neuralgia Patients Treated with Botulinum Toxin Type A: A Pilot Study.

[OBJECTIVE] 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).

[METHODS] 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.

[RESULTS] 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.

[CONCLUSIONS] 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.