Seizures

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Abstract

A brief introduction to the pathology of epilepsy is presented. Seizure-prone areas of the brain are always accompanied by reactive gliosis. These reactive astrocytes exhibit loss of domain organization, a phenomenon not seen in any other brain pathology. There is no evidence that astrocytic mutations are causing idiopathic seizures, although this remains a theoretical possibility. A different matter, however, is acquired epilepsy. The question is if the primary injury, which leads eventually to the seizures, is acting through reactive astrocytes to change neuronal excitability or if the primary injury directly affects neuronal excitation and this in turn causes reactive astrogliosis. The issue has not been addressed directly, but most (but not all) of the existing indirect evidence points to neuronal seizures causing gliosis rather than the other way around. In most animal models (but not all), initiating astrocytic calcium waves releases massive amounts of glutamate and this causes seizures as does any interference with astrocytic glutamate clearance. Another evidence, this time from human patients, points to genetic defects in the astrocytic potassium channel Kir4.1 interfering with potassium clearance and therefore lowering the neuronal firing threshold. There is evidence that, early in epileptogenesis, microglia secretions contribute to astrocyte transformation into a proconvulsive phenotype. The lost domain organization of reactive astrocytes in epileptic areas is an enigma. Not much research has focused on the functional properties of reactive astrocytes from epileptic brains versus those from brains afflicted with other pathologies.

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Walz, W. (2023). Seizures. In: The Gliocentric Brain. Springer, Cham. https://doi.org/10.1007/978-3-031-48105-5_15

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  • DOI: https://doi.org/10.1007/978-3-031-48105-5_15

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