Abstract
Epilepsy is characterized by recurrent spontaneous seizures due to hyperexcitability and hypersynchrony of brain neurons. Current theories of pathophysiology stress neuronal dysfunction and damage, and aberrant connections as relevant factors. Most antiepileptic drugs target neuronal mechanisms. However, nearly one-third of patients have seizures that are refractory to available medications; a deeper understanding of mechanisms may be required to conceive more effective therapies. Recent studies point to a significant contribution by non-neuronal cells, the glia--especially astrocytes and microglia--in the pathophysiology of epilepsy. This review critically evaluates the role of glia-induced hyperexcitability and inflammation in epilepsy.
Copyright © 2012 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Review
MeSH terms
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Action Potentials
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Animals
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Anticonvulsants / pharmacology
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Anticonvulsants / therapeutic use
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Blood-Brain Barrier
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Body Water / metabolism
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Calcium Signaling
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Cytokines / metabolism
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Drug Resistance
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Encephalitis / complications
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Encephalitis / physiopathology*
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Epilepsy / drug therapy
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Epilepsy / etiology
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Epilepsy / immunology
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Epilepsy / pathology
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Epilepsy / physiopathology*
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Extracellular Space / metabolism
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Gliosis / pathology
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Gliosis / physiopathology
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Glutamic Acid / metabolism
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Humans
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Inflammation Mediators / metabolism
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Ion Channels / physiology
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Microcirculation
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Models, Neurological
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Nerve Tissue Proteins / physiology
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Neuroglia / physiology*
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Neurons / metabolism
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Potassium / metabolism
Substances
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Anticonvulsants
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Cytokines
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Inflammation Mediators
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Ion Channels
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Nerve Tissue Proteins
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Glutamic Acid
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Potassium