CALCA and migraine disorder: While exact pathophysiological mechanisms remain elusive, increased (sub)cortical excitability, trigeminovascular activation, and release of the neuropeptide calcitonin-gene related peptide (CGRP) — a member of the larger calcitonin family [5] — have been consistently demonstrated to play a pivotal and causative role in the pathogenesis of migraine [6, 7, 8].