Evidence for Activation of the Coagulation System in Migraine with Aura

Abstract

Migraine with aura has been shown to be an independent risk factor for stroke. Although the precise mechanism of migraine-related stroke is not known, risk factors for hypercoagulability have been found in migraineurs. Prothrombin factor 1.2 (F1.2) is a cleavage product of prothrombin. Elevated plasma F1.2 has been shown to be a sensitive and a specific marker of ongoing thrombin generation, and thus may serve as an indicator of hypercoagulability. In this study we determined plasma F1.2 levels in 35 patients with migraine (22 with aura and 13 without aura) and in 24 healthy age- and sex-matched volunteers. Elevated F1.2 levels were found in 11 of 22 (50%) patients with migraine with aura (1.25-3.5 nmol/l). None of the patients with migraine without aura nor any of the healthy volunteers had elevated plasma F1.2 levels (normal < 1.1 nmol/l). We conclude that prothrombin F1.2 levels are elevated in a significant number of patients with migraine with aura but not in patients with migraine without aura. This finding suggests that there is activation of the clotting system in certain patients with migraine with aura.

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).…”

Identification of molecular genetic factors that influence migraine

“…A SNP in the MTHFR gene C677T causes an alanine to be replaced with a valine within the catalytic domain of the enzyme reportedly reducing the enzymatic capacity by up to 50% (Frosst et al 1995). This in turn may lead to mild hyperhomocysteinemia which has been associated with endothelial cell injury (Hering-Hanit et al 2001), reduced production of NO (Colson et al 2006b), oxidative stress and may contribute to the activation of the trigeminal fibres.…”

Current views of the risk of stroke for migraine with and migraine without aura

“…However, the frequency of cervical artery dissection among migraine patients seems too low to explain the overall association between migraine and ischemic stroke [33]. Furthermore, migraine has been associated with increases in prothrombotic or vasoactive factors, including von Willebrand factor [40], factor V Leiden [41], prothrombin factor 1.2 [42], and serotonin [43]. In addition, the release of vasoactive neuropeptides during migraine attacks that may stimulate inflammatory responses also has been observed [44].…”