Background & Aims
Migraine is a neurological disease affecting around 14% of the world population, with a higher incidence in women than in men (1). Although the exact pathophysiology is not known, migraine is considered a neuronal excitability disorder where the trigeminovascular system appears to play a key role (2). The onset of a migraine attack is linked with an increase of pro-inflammatory molecules and neuropeptides, including Calcitonin Gene Related Peptide (CGRP); a potent vasodilator (3; 4). Published data is inconsistent in collection methods and analysis of CGRP levels in migraine patients (5). For neurobiological characterization, we compared CGRP levels in different sample types from patients with episodic and chronic migraine to those in healthy controls.
Methods
Here we present data from a monocentric observational study. Our analysis includes 159 subjects divided into three groups (HC: healthy controls; EM: episodic migraine; CM: chronic migraine). CGRP levels were analysed in tear fluid, saliva, plasma and serum. All samples were collected in a standardized way and stored at -80°C until analysed. For the quantitative determination of CGRP levels, we used an enzyme-linked immunosorbent assay (CUSABIO®, Wuhan, China).
Results
Our cohort is composed of 38 HC (median age: 42.5 years; 30 female, 8 male), 100 EM (median age: 38.5 years; 90 female, 1 divers, 9 male) and 21 CM patients (median age: 31 years; 19 female, 2 male). Median migraine days per month were 4 days for EM patients and 16 days for CM patients. There is a correlation between serum and plasma CGRP levels in all groups (EM: r = 0.82 p < 0.001, CM: r = 0.68; p = 0.001, HC: r = 0.72; p < 0.001). Plasma CGRP levels were higher in EM (p = 0.015) and CM patients (p = 0.004) compared to HC. Median CGRP levels in plasma were 3.5 pg/mL (1.2 – 21.3 pg/mL) for HC, 5.0 pg/mL (1.2 – 29.5 pg/mL) for EM patients and 6.4 pg/mL (1.4 – 14.9 pg/mL) for CM patients. Serum CGRP levels were higher in CM patients compared to HC (p = 0.027). Median CGRP values for serum were 4.1 pg/mL (1.7 – 22.5 pg/mL) for HC, 4.7 pg/mL (1.2 – 25.1 pg/mL) for EM and 5.7 pg/mL (3.1 – 31.4 pg/mL) for CM patients. Tear fluid and saliva did not show differences in CGRP between groups.
Conclusions
In this methodological study, we found that plasma and serum CGRP are comparable in migraine patients and are informative on a group level. Tear fluid and saliva were not informative as to differences in CGRP between groups.
References
(1)Stovner, L. J., Hagen, K., Linde, M., & Steiner, T. J. (2022). The global prevalence of headache: an update, with analysis of the influences of methodological factors on prevalence estimates. The journal of headache and pain, 23(1), 34.
(2) Maleki, N., & Gollub, R. L. (2016). What Have We Learned From Brain Functional Connectivity Studies in Migraine Headache? Headache, 56(3), 453–461.
(3) Edvinsson, L., Grell, A.-S., & Warfvinge, K. (2020). Expression of the CGRP Family of Neuropeptides and their Receptors in the Trigeminal Ganglion. Journal of Molecular Neuroscience, 70(6), 930–944.
(4) Ashina, M., Hansen, J. M., Do, T. P., Melo-Carrillo, A., Burstein, R., & Moskowitz, M. A. (2019). Migraine and the trigeminovascular system—40 years and counting. The Lancet Neurology, 18(8), 795–804.
(5) Kamm K. CGRP and Migraine: What Have We Learned From Measuring CGRP in Migraine Patients So Far? Front Neurol. 2022 Jul 27;13:930383.
(6)Gárate G, González-Quintanilla V, González A, Pascual M, Pérez-Pereda S, Madera J, Pascual J. Serum Alpha and Beta-CGRP Levels in Chronic Migraine Patients Before and After Monoclonal Antibodies Against CGRP or its Receptor. Ann Neurol. 2023 Aug;94(2):285-294.
Presenting Author
Morgane Paternoster
Poster Authors
Topics
- Specific Pain Conditions/Pain in Specific Populations: Migraine