Abstract
Within the last decades significant progress has been made in the understanding of the underlying pathophysiological mechanisms of migraine. There is a general agreement now that migraine is not only a vascular phenomenon but also a genetically determined heterogenic ion-channelopathy resulting in cortical-spreading-depression-like events, the temporary impairment of antinociceptive structures of the brainstem and the activation of the trigeminal-vascular system. The development and use of drugs targeting ion-channels and subsequently reducing cortical excitability appears as a promising avenue for both the acute treatment of migraine and migraine prevention. This review summarizes the current knowledge and evidence for GABAergic drugs in the treatment of migraine.
MeSH terms
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Acute Disease
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Amines / therapeutic use
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Animals
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Cyclohexanecarboxylic Acids / therapeutic use
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Fructose / analogs & derivatives
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Fructose / therapeutic use
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GABA Agents / therapeutic use*
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GABA Antagonists / therapeutic use
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Gabapentin
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Humans
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Migraine Disorders / drug therapy*
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Migraine Disorders / prevention & control
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Neuroprotective Agents / therapeutic use
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Pregabalin
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Receptors, GABA / drug effects
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Receptors, GABA / physiology*
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Receptors, GABA-A / drug effects
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Receptors, GABA-A / physiology
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Receptors, GABA-B / drug effects
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Receptors, GABA-B / physiology
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Topiramate
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Valproic Acid / therapeutic use
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gamma-Aminobutyric Acid / analogs & derivatives
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gamma-Aminobutyric Acid / physiology*
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gamma-Aminobutyric Acid / therapeutic use
Substances
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Amines
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Cyclohexanecarboxylic Acids
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GABA Agents
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GABA Antagonists
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Neuroprotective Agents
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Receptors, GABA
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Receptors, GABA-A
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Receptors, GABA-B
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Topiramate
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Fructose
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Pregabalin
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gamma-Aminobutyric Acid
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Valproic Acid
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Gabapentin