Endothelin 1 in migraine and tension-type headache

Abstract

We determined the plasma levels of ET1, both interictally and ictally, in 50 migraine patients, 20 with aura (MPA) and 30 without aura (MPWA), comparing them with the levels of 40 age‐matched tension‐type headache patients (20 episodic and 20 chronic) (ETTHP and CTTHP) and the levels of a group of 20 healthy control subjects (CS). No statistically significant difference was evident between the mean ET1 plasma levels of MPA and those of MPWA, assessed in headache‐free periods. The mean ET1 plasma levels of MPA and MPWA, assessed interictally, were significantly higher than those of CS. However, the values of plasma ET1 in ETTP and in CTTHP did not differ statistically from those of CS. MPA and MPWA ET1 plasma levels increased significantly within 2 h from the onset of attacks (p<0.0001) and remained significantly higher between 4 and 6 h from the onset. The ET1 plasma levels of ETTHP and CTTHP assessed during attacks did not differ statistically from those of the same patients assessed in the headache‐free periods. The increase in ET1 levels in MPA and MPWA patients when assessed ictally, suggests that this peptide is involved in the haemodynamic changes and vascular tone modifications observed during migraine attacks, particularly in the first phase of the ictal period.

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

“…In contrast, a slight constriction of penetrating arterioles embedded in cortical tissue through which the SD propagates can explain the reduction in CBF (344). Interestingly, elevated plasma endothelin-1 levels have been reported during the first few hours of migraine attacks with or without aura that may provide a mechanism for increased parenchymal cerebrovascular resistance (125,139).…”

Ischemic stroke subtypes and migraine with visual aura in the ARIC study

“…Taken together, it is possible that migraine with visual aura may promote vasospasm, activate platelet aggregation, [24][25][26] and increased concentration of procoagulant factors. [27][28][29][30] Directly or indirectly in the setting of PFO, these vasoactive substances could gain access to coronary artery as well as cerebral vasculature, Table 3 Hazard ratios (95% confidence intervals [CI]) for the association of migraine with visual aura compared to migraine without visual aura and risk of verified ischemic stroke (all types) where they induce visual aura symptoms, and subsequently may result in brain ischemic injury if larger emboli are formed. Our data suggest that migraine without visual aura is not an isolated risk factor for stroke, in our sample, when compared to healthy controls without any headache history; any association identified can be explained by the traditional stroke risk factors (it is also possible that the number of participants with migraine without visual aura is too low, and the study is underpowered to detect an association with stroke).…”

Migraine and Biomarkers of Endothelial Activation in Young Women

“…31,32 This study finding of endothelial activation in migraine leads to speculation regarding the nature of the relation. Ictal studies of migraine that have documented increased vWF, 25 endothelin-1, 33 soluble intercellular adhesion molecule, tissue necrosis factor, 34 transforming growth factor-␤1, 35 and matrix metalloproteinase-9 36 suggest that migraine may directly activate the endothelium. An alternative and not mutually exclusive hypothesis is that endothelial dysfunction causes migraine.…”