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migraine disorders/hypoxia
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Effect of hypoxia on BOLD fMRI response and total cerebral blood flow in migraine with aura patients.
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Experimentally induced hypoxia triggers migraine and aura attacks in patients suffering from migraine with aura (MA). We investigated the blood oxygenation level-dependent (BOLD) signal response to visual stimulation during hypoxia in MA patients and healthy volunteers. In a randomized double-blind
Hypoxia triggers high-altitude headache with migraine features: A prospective trial.
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BACKGROUND
Given the high prevalence and clinical impact of high-altitude headache (HAH), a better understanding of risk factors and headache characteristics may give new insights into the understanding of hypoxia being a trigger for HAH or even migraine attacks.
METHODS
In this prospective trial,
Hypoxia facilitates neurogenic dural plasma protein extravasation in mice: a novel animal model for migraine pathophysiology.
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Migraine animal models generally mimic the onset of attacks and acute treatment processes. A guinea pig model used the application of meta-chlorophenylpiperazine (mCPP) to trigger immediate dural plasma protein extravasation (PPE) mediated by 5-HT2B receptors. This model has predictive value for
Migraine and aura triggered by normobaric hypoxia
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Background: For future experimental studies or the development of targeted pharmaceutical agents, a deeper insight into the pathophysiology of migraine is of utmost interest. Reliable methods to trigger migraine attacks including aura are
The effect of intermittent hypoxia training on migraine: a randomized controlled trial
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Objective: To study the effect of intermittent hypoxia training (IHT) for migraine.
Design: A single-blind, randomized controlled trial. All participants were recruited from a
Normobaric hypoxia and nitroglycerin as trigger factors for migraine.
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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
Migraine and cerebral hypoxia: a hypothesis with pharmacotherapeutic implications.
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It is postulated that a migraine attack is a specific reaction pattern to an episode of focal cerebral hypoxia. This hypothesis holds that any type of focal brain hypoxia (and thus not only a vasospasm) may provoke a migraine attack. Indeed, as hypoxia is a result of an imbalance between energy
Pathogenesis of migraine: the biobehavioural and hypoxia theories reconciled.
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The recent pathophysiological data obtained in migraine patients during and between attacks are reviewed in this article. They suggest that the headache in migraine is due to activation of the trigemino-vascular system. While this can be found in other headache disorders, the process leading
Migraine induced by hypoxia: an MRI spectroscopy and angiography study.
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Migraine with aura is prevalent in high-altitude populations suggesting an association between migraine aura and hypoxia. We investigated whether experimental hypoxia triggers migraine and aura attacks in patients suffering from migraine with aura. We also investigated the metabolic and vascular
Brain hypoxia: the turning-point in the genesis of the migraine attack?
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The hypothesis postulates that a brief episode of focal cerebral hypoxia occurs in every attack of migraine. Clinical biochemical and technical (EEG and CT scans) evidence is summarized suggesting that cerebral hypoxia is seen as the turning-point in the pathogenesis of the attack. It may be
Migraine at altitude--is it due to hypoxia or hypobaria?
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Brain hypoxia in migraine: pathophysiologic and therapeutic implications.
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Hypoxia, a turning point in migraine pathogenesis?
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The effects of flunarizine in experimental models related to the pathogenesis of migraine.
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Two new hypotheses suggest that the key pathology in migraine has a neuronal origin. A pivotal role is assigned to brain hypoxia (1) and spreading depression (SD) (neuronal depolarization spreading gradually over the cortex) (2). Flunarizine has been tested both against brain hypoxia and SD. Its
[Calcium antagonists in the prophylactic treatment of migraine].
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Calcium channel antagonists have been employed in the prophylactic treatment of migraine. Their major action is the inhibition of Ca2+ influx into smooth muscle cells that is mediated through high voltage-sensitive Ca2+ channels. These drugs had been introduced for the treatment of migraine mainly
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