Neuropathic pain (NP) is common after spinal cord injury/disorder (SCI/D). Hyperexcitable nociceptors contribute to development and maintenance of SCI/D-induced NP. Calcitonin gene–related peptide (CGRP), a neuropeptide expressed in C-fibers and Aδ afferents, transmits pain to the dorsal root ganglion. Aberrant CGRP fiber sprouting within the dorsal horn after SCI is thought to facilitate nociception. CGRP inhibitors (CGRPi) were recently FDA-approved for migraine prevention. This study accessed deidentified electronic medical record data via the TriNetX global federated health research network. Queries were built using diagnosis codes related to SCI/D and presence or exclusion of migraine prophylactic agents. Three cohorts were created for comparison with primary outcome being the presence of gabapentinoid prescription in the timeframe 30-days following initiation of topiramate/CGRPi/propranolol. CGRPi were found to be associated with reduced odds of gabapentinoid prescription after 30 days compared to propranolol (N=3,527; OR 0.75, 95% CI 0.62–0.91, ARR 4.41%) and to topiramate (N=4,890; OR 0.62, 95% CI 0.53–0.73, ARR 7.41%). No significant difference was observed between propranolol and topiramate (N=13,210; OR 0.87, 95% CI 0.83–0.96, ARR 2.12%). Given the extensive expression of CGRP receptors, CGRPi may also be useful for treatment of SCI/D-induced NP.
Shields et al. (2026) studied this question.