17 General introduction 1 24 hours after taking attack medication despite an initial response). 10, 20 As a result, repetitive use of acute medication is necessary during a single attack, increasing the risk of medication overuse in women with menstrual migraine. Interestingly, while acute migraine treatments are not less effective for perimenstrual attacks, as indicated by a similar 2-hour response rate after triptan use, recurrence rates are higher.20 Additionally, differences in attack duration also exist between migraine attacks in women and those in men, with perimenstrual attacks lasting the longest.8 Although smaller, there are also differences in duration between non-perimenstrual migraine attacks in women and attacks in men, despite women being more likely to use long-acting triptans.8 Clinicians should be aware of the longer attack duration in women, particularly the increased risk of recurrence during the perimenstrual window. Women also more often experience accompanying symptoms during a migraine attack compared to men, increasing the severity of an attack.8 Further research is needed to determine the extent to which the differences between men and women are attributable to biological factors.21 PATHOPHYSIOLOGY OF MIGRAINE The headache that occurs during a migraine attack is caused by the activation of the trigeminovascular system. This system consists of nociceptive trigeminal afferents and the cranial blood vessels that they surround. The exact mechanism of how this system is activated remains largely unknown, but changes in the brainstem and hypothalamus likely play an important role.22 The trigeminovascular system can be activated by CSD, considered the electrophysiological substrate for migraine aura. Upon activation of the trigeminovascular system, the trigeminal afferents, trigeminal ganglion, and trigeminal nucleus caudalis (TNC) in the brainstem are stimulated (Figure 4). Calcitonin gene-related peptide (CGRP) is a key neurotransmitter in this signal transmission. Sensory information is then transmitted from the TNC to the thalamus, where all sensory information converges. The processing of this information is influenced by pain-modulating systems that can either facilitate or inhibit nociception. CGRP is a potent vasodilator and a modulator of cerebrovascular nociception. Moreover, an infusion of CGRP in patients with migraine may trigger migrainous headache.23 For these reasons, CGRP is believed to play a crucial role in the pathophysiology of migraine.
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