Ion Channels and Migraine

Yan, Jin; Dussor, Gregory

doi:10.1111/head.12323

Cited by 40 publications

(42 citation statements)

References 201 publications

(275 reference statements)

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“…Meningeal afferents express numerous ion channels including transient receptor potential (TRP) channels, acid-sensing ion channels (ASICS), glutamate-gated channels, ATP-gated channel, and K + channels that when activated may contribute to the pain of migraine (for revew see Yan and Dussor, 2014). Among the stimuli capable of activating or sensitizing dural afferents are capsaicin (via TRPV1), mustard oil (via TRPA1), hypotonic solutions (via TRPV4), or an inflammatory soup (Strassman et al, 1996; Bove and Moskowitz, 1997; Wei et al, 2011; Edelmayer et al, 2012).…”

Section: 1 Meningeal Afferentsmentioning

confidence: 99%

Neurovascular contributions to migraine: Moving beyond vasodilation

2016

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Migraine is the third most common disease worldwide, the most common neurological disorder, and one of the most common pain conditions. Despite its prevalence, the basic physiology and underlying mechanisms contributing to the development of migraine is still poorly understood and development of new therapeutic targets is long overdue. Until recently, the major contributing pathophysiological event thought to initiate migraine was cerebral and meningeal arterial vasodilation. However, the role of vasodilation in migraine is unclear and recent findings challenge its necessity. While vasodilation itself may not contribute to migraine, it remains possible that vessels play a role in migraine pathophysiology in the absence of vasodilation. Blood vessels consist of a variety of cell types that both release and respond to numerous mediators including growth factors, cytokines, adenosine triphosphate (ATP), and nitric oxide (NO). Many of these mediators have actions on neurons that can contribute to migraine. Conversely, neurons release factors such as norepinephrine and calcitonin gene-related peptide (CGRP) that act on cells native to blood vessels. Both normal and pathological events occurring within and between vascular cells could thus mediate bi-directional communication between vessels and the nervous system, without the need for changes in vascular tone. This review will discuss the potential contribution of the vasculature, specifically endothelial cells, to current neuronal mechanisms hypothesized to play a role in migraine. Hypothalamic activity, cortical spreading depression (CSD), and dural afferent input from the cranial meninges will be reviewed with a focus on how these mechanisms can influence or be impacted by blood vessels. Together, the data discussed will provide a framework by which vessels can be viewed as important potential contributors to migraine pathophysiology, even in light of the current uncertainty over the role of vasodilation in this disorder.

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Section: 1 Meningeal Afferentsmentioning

confidence: 99%

Neurovascular contributions to migraine: Moving beyond vasodilation

2016

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“…These are found on a variety of intra‐ and extracranial neurons as well as other cell types and respond a variety of stimuli by admitting Na+ and Ca++, thus producing depolarization. They have also been implicated in the release of calcitonin gene‐related peptide and are thus implicated in vasodilatation that is probably in some way related to the pain of migraine …”

Section: Mechanisms Of Migraine and Epilepsymentioning

confidence: 99%

“…They have also been implicated in the release of calcitonin gene-related peptide and are thus implicated in vasodilatation that is probably in some way related to the pain of migraine. 72 Brain Imaging and Electrophysiology in Epilepsy. -In about a third of patients, the epilepsy is idiopathic; that is to say, there is no obvious structural lesion or other brain disease to account for it, although there may be subtle changes in brain architecture.…”

Section: Mechanisms Of Migraine and Epilepsymentioning

confidence: 99%

Migraine and Epilepsy: Review of the Literature

2015

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Migraine and epilepsy are disorders that are common, paroxysmal, and chronic. In many ways they are clearly different diseases, yet there are some pathophysiological overlaps, and overlaps in clinical symptomatology, particularly with regard to visual and other sensory disturbances, pain, and alterations of consciousness. Epidemiological studies have revealed that the two diseases are comorbid in a number of individuals. Both are now recognized as originating from electrical disturbances in the brain, although their wider manifestations involve the recruitment of multiple pathogenic mechanisms. An initial excess of neuronal activity in migraine leads to cortical spreading depression and aura, with the subsequent recruitment of the trigeminal nucleus leading to central sensitization and pain. In epilepsy, neuronal overactivity leads to the recruitment of larger populations of neurons firing in a rhythmic manner that constitutes an epileptic seizure. Migraine aura and headaches may act as a trigger for epileptic seizures. Epilepsy is not infrequently accompanied by preictal, ictal, and postictal headaches that often have migrainous features. Genetic links are also apparent between the two disorders, and are particularly evident in the familial hemiplegic migraine syndromes where different mutations can produce either migraine, epilepsy, or both. Also, various medications are found to be effective for both migraine and epilepsy, again pointing to a commonality and overlap between the two disorders.

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“…Cortical spreading depression (CSD) underlies the aura, although its precise relationship to headache is unclear. Activation and sensitization of trigeminal neurons (TG) leading to the release of pro-inflammatory peptides is likely a key component in pain initiation and transmission in migraine (Noseda and Burstein, 2013;Yan and Dussor, 2014).…”

Section: Introductionmentioning

confidence: 99%