Shared and independent roles of CGRP and PACAP in migraine pathophysiology

Table 1 Comparison of migraine frequencies after infusion of CGRP, PACAP, and other triggers in humans

Trigger^a	Migraine Frequency^b	References
CGRP	63% (50–77%)	50%^c, [34] 57%, [36] 75%, [35] 63%, [37, 38]^d 77%, [39] 56%, [40]
PACAP-38	68% (58–73%)	58%, [18] 73%, [17] 72%, [38, 41]^d
PACAP-27	55%	[25]
VIP (20 min infusion)	9% (0–18%)	0%, [44] 18%, [17]
VIP (2 h infusion)	71%	[45]
Pramlintide (amylin analog)	41%	[40]
Adrenomedullin	55%	[46]
Glyceryl trinitrate (GTN)	70% (67–80%)	67%, [47] 80%, [48] 50%, [49] 75%, [50] 77%^e, [51]
Sildenafil (PDE5^f inhibitor)	83%	[52]
Dipyridamole (PDE5^f inhibitor)	50%	[53]
Cilostazol (PDE3^f inhibitor)	86%	[54]
Levcromakalim (K_ATP channel opener)	91% (82–100%)	100% [55], 82%, [56]
Histamine	70%	[57]
Prostaglandin E₂	58%	[58]
Prostaglandin I₂	50%	[59]

^aAdministrations were by intravenous infusion (~ 20 min), except for sublingual GTN in two studies [47, 51] and oral delivery of sildenafil and cilostazol
^bThe average frequency and range of all migraine attacks are combined from migraine patients with and without aura. Data do not include familial hemiplegic migraine, traumatic brain injury, or control subjects
^cWhile originally reported as 33%, this was subsequently revised to 50% [36]
^dFurther descriptions of the same patients as in [38]
^eAverage frequency from both the migraine without and with aura cohorts
^fPDE = phosphodiesterase

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