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Transient Cognitive Impairment in Epilepsy

Impairments of the dialog between excitation and inhibition (E/I) is commonly associated to neuropsychiatric disorders like autism, bipolar disorders and epilepsy. Moderate levels of hyperexcitability can lead to mild alterations of the EEG and are often associated with cognitive deficits even in th...

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Autores principales: Landi, Silvia, Petrucco, Luigi, Sicca, Federico, Ratto, Gian Michele
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330286/
https://www.ncbi.nlm.nih.gov/pubmed/30666185
http://dx.doi.org/10.3389/fnmol.2018.00458
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author Landi, Silvia
Petrucco, Luigi
Sicca, Federico
Ratto, Gian Michele
author_facet Landi, Silvia
Petrucco, Luigi
Sicca, Federico
Ratto, Gian Michele
author_sort Landi, Silvia
collection PubMed
description Impairments of the dialog between excitation and inhibition (E/I) is commonly associated to neuropsychiatric disorders like autism, bipolar disorders and epilepsy. Moderate levels of hyperexcitability can lead to mild alterations of the EEG and are often associated with cognitive deficits even in the absence of overt seizures. Indeed, various testing paradigms have shown degraded performances in presence of acute or chronic non-ictal epileptiform activity. Evidences from both animal models and the clinics suggest that anomalous activity can cause cognitive deficits by transiently disrupting cortical processing, independently from the underlying etiology of the disease. Here, we will review our understanding of the influence of an abnormal EEG activity on brain computation in the context of the available clinical data and in genetic or pharmacological animal models.
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spelling pubmed-63302862019-01-21 Transient Cognitive Impairment in Epilepsy Landi, Silvia Petrucco, Luigi Sicca, Federico Ratto, Gian Michele Front Mol Neurosci Neuroscience Impairments of the dialog between excitation and inhibition (E/I) is commonly associated to neuropsychiatric disorders like autism, bipolar disorders and epilepsy. Moderate levels of hyperexcitability can lead to mild alterations of the EEG and are often associated with cognitive deficits even in the absence of overt seizures. Indeed, various testing paradigms have shown degraded performances in presence of acute or chronic non-ictal epileptiform activity. Evidences from both animal models and the clinics suggest that anomalous activity can cause cognitive deficits by transiently disrupting cortical processing, independently from the underlying etiology of the disease. Here, we will review our understanding of the influence of an abnormal EEG activity on brain computation in the context of the available clinical data and in genetic or pharmacological animal models. Frontiers Media S.A. 2019-01-07 /pmc/articles/PMC6330286/ /pubmed/30666185 http://dx.doi.org/10.3389/fnmol.2018.00458 Text en Copyright © 2019 Landi, Petrucco, Sicca and Ratto. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Landi, Silvia
Petrucco, Luigi
Sicca, Federico
Ratto, Gian Michele
Transient Cognitive Impairment in Epilepsy
title Transient Cognitive Impairment in Epilepsy
title_full Transient Cognitive Impairment in Epilepsy
title_fullStr Transient Cognitive Impairment in Epilepsy
title_full_unstemmed Transient Cognitive Impairment in Epilepsy
title_short Transient Cognitive Impairment in Epilepsy
title_sort transient cognitive impairment in epilepsy
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330286/
https://www.ncbi.nlm.nih.gov/pubmed/30666185
http://dx.doi.org/10.3389/fnmol.2018.00458
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