Galcanezumab, a monoclonal antibody against calcitonin gene-related peptide, is an emerging migraine preventative. We hypothesized that the preventive effects are conveyed via modulation of somatosensory processing and that certain sensory profiles may hence be associated with different clinical responses. We recruited migraine patients (n=26), who underwent quantitative sensory tests (QST) over the right V1 dermatome and forearm at baseline (T0), 2-3 weeks (T1), and one year (T12) after monthly galcanezumab treatment. The clinical response was defined as a reduction of ≥30% in headache frequency based on the headache diary. Predictors for clinical response were calculated using binary logistical regression models. After galcanezumab (T1 vs. T0), the heat pain threshold (HPT) (°C, 44.9 ± 3.4 vs. 43.0 ± 3.3, p=0.013) and mechanical pain threshold (MPT) (log mN, 1.60 ± 0.31 vs. 1.45 ± 0.26, p=0.042) were increased exclusively in the V1 dermatome, but not the forearm. These changes were immediate, did not differ between responders and non-responders, and did not last in one year of follow-up (T12 vs. T0). However, baseline HPT (OR: 2.13, 95% CI: 1.08-4.19, p = 0.029) on the forearm was a robust predictor for a clinical response three months later. In summary, our data demonstrated that galcanezumab modulates pain thresholds specifically in the V1 dermatome, but this modulation is short-lasting and irrelevant to clinical response. Instead, the clinical response may be determined by individual sensibility even before the administration of medication.
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