This study aims to improve the management migraine by providing a more profound understanding of the interactions of pain disinhibition on the brain stem level and calcitonin gene-related peptide as a main mediator in the generation of migraine headaches. For this purpose, this observational study investigates established neurophysiological and blood biomarkers parameters in association with the clinical phenotype.

The study's focus is the investigation of mechanisms that are directly related to the pain generation in migraine. In this context, the primary endpoint is an enhancement of trigeminal stimulation evoked calcitonin gene-related peptide (CGRP). The stimulation is normalized using an established protocol to elicit the nociceptive blink reflex, which is a brain stem reflex to study the trigemino-spinal system. We expect CGRP levels to rise more in patients affected by migraine as compared to controls, based on the observation that painful stimulation elicits migraine attacks. Furthermore, baseline CGRP levels and their association with markers of brainstem excitability are probed.

Inclusion Criteria:

• Migraine according to ICHD-3 criteria (cases)
• No headaches or tension-type headache frequency <1x/year (controls)

Exclusion Criteria:

• other chronic pain disorder

Patients will be recruited through the outpatient headache department and through public adverstisement. Patients are consecutively recruited and inclusion/exclusion criteria are minimzied to avoid selection bias.

IPD can be shared upon reasonable request. Data protection regulation preclude public sharing of data.