Normobaric Hypoxia and Nitroglycerin as Trigger Factors for Migraine

Abstract

Migraine prevalence is increased in high-altitude populations and symptoms of acute mountain sickness mimic migraine symptoms. Here we tested whether normobaric hypoxia may trigger migraine attacks. As positive control we used nitrolgycerin (NTG), which has been shown to induce migraine attacks in up to 80% of migraineurs. Sixteen patients (12 females, mean age 28.9 +/- 7.2 years) suffering from migraine with (n = 8) and without aura (n = 8) underwent three different provocations (normobaric hypoxia, NTG and placebo) in a randomized, cross-over, double dummy design. Each provocation was performed on a separate day. The primary outcome measure was the proportion of patients developing a migraine attack according to the criteria of the International Headache Society within 8 h after provocation onset. Fourteen patients completed all three provocations. Migraine was provoked in six (42%) patients by hypoxia, in three (21%) by NTG and in two (14%) by placebo. The differences among groups were not significant (P = 0.197). The median time to attacks was 5 h. In conclusion, the (remarkably) low response rate to NTG is surprising in view of previous data. Further studies are required to establish fully the potency of hypoxia in triggering migraine attacks.

Role of endothelial cells in antihyperalgesia induced by a triptan and β-blocker

“…For example, one of the diagnostic tests for migraine headache has been the precipitation of a headache by the administration of nitroglycerin, a potent vasodilator, which increases nitric oxide (NO) in the endothelial cell (Greco et al, 2011). One of the unusual characteristic features of the nitroglycerin provocation test is that in patients with migraine headache, there is a distinct delay from the administration of nitroglycerin and the onset of the migraine headache (Schoonman et al, 2006). We suggest that such a delay might be explained by an indirect mechanism of action, such as by its action to increase NO in endothelial cells, leading to the release of mediators that act on nociceptors to produce headache pain.…”

Reactive Oxygen Species Induce Procalcitonin Expression in Trigeminal Ganglia Glia

“…A combination of hypoxia with paracrine signals may be required for full induction in the organ culture. Also, while hypoxia is unlikely to occur within the trigeminal nerve under physiological conditions, a prolonged hypoxia occurs in the cortex following CSD 67 , and hypoxia is an established trigger of migraine 68 …”

Right-to-left shunts and micro-embolization in migraine

“…Furthermore, resting hypoxemia related to (left-to-right) shunting across a PFO has been reported [40]. Mild arterial desaturation due to a RLS, therefore, should be considered as a possible mechanism linking RLS with migraine, as hypoxia is a known trigger of migraine [41].…”