Infantile status epilepticus disrupts myelin development

Temporal lobe epilepsy (TLE) is the most prevalent type of epilepsy in adults; it often starts in infancy or early childhood. Although TLE is primarily considered to be a grey matter pathology, a growing body of evidence links this disease with white matter abnormalities. In this study, we explore t...

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Autores principales:	Petra Bencurova, Hanne Laakso, Raimo A. Salo, Ekaterina Paasonen, Eppu Manninen, Jaakko Paasonen, Shalom Michaeli, Silvia Mangia, Martin Bares, Milan Brazdil, Hana Kubova, Olli Gröhn
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2022
Materias:	Animal model Status Epilepticus Temporal Lobe Epilepsy Myelin development White matter integrity MRI Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
Acceso en línea:	https://doaj.org/article/4e99dbbd9da8404ca9ff7abd8ac14b56
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spelling	oai:doaj.org-article:4e99dbbd9da8404ca9ff7abd8ac14b562021-12-02T04:59:16ZInfantile status epilepticus disrupts myelin development1095-953X10.1016/j.nbd.2021.105566https://doaj.org/article/4e99dbbd9da8404ca9ff7abd8ac14b562022-01-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0969996121003156https://doaj.org/toc/1095-953XTemporal lobe epilepsy (TLE) is the most prevalent type of epilepsy in adults; it often starts in infancy or early childhood. Although TLE is primarily considered to be a grey matter pathology, a growing body of evidence links this disease with white matter abnormalities. In this study, we explore the impact of TLE onset and progression in the immature brain on white matter integrity and development utilising the rat model of Li-pilocarpine-induced TLE at the 12th postnatal day (P). Diffusion tensor imaging (DTI) and Black-Gold II histology uncovered disruptions in major white matter tracks (corpus callosum, internal and external capsules, and deep cerebral white matter) spreading through the whole brain at P28. These abnormalities were mostly not present any longer at three months after TLE induction, with only limited abnormalities detectable in the external capsule and deep cerebral white matter. Relaxation Along a Fictitious Field in the rotating frame of rank 4 indicated that white matter changes observed at both timepoints, P28 and P72, are consistent with decreased myelin content. The animals affected by TLE-induced white matter abnormalities exhibited increased functional connectivity between the thalamus and medial prefrontal and somatosensory cortex in adulthood. Furthermore, histological analyses of additional animal groups at P15 and P18 showed only mild changes in white matter integrity, suggesting a gradual age-dependent impact of TLE progression. Taken together, TLE progression in the immature brain distorts white matter development with a peak around postnatal day 28, followed by substantial recovery in adulthood. This developmental delay might give rise to cognitive and behavioural comorbidities typical for early-onset TLE.Petra BencurovaHanne LaaksoRaimo A. SaloEkaterina PaasonenEppu ManninenJaakko PaasonenShalom MichaeliSilvia MangiaMartin BaresMilan BrazdilHana KubovaOlli GröhnElsevierarticleAnimal modelStatus EpilepticusTemporal Lobe EpilepsyMyelin developmentWhite matter integrityMRINeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENNeurobiology of Disease, Vol 162, Iss , Pp 105566- (2022)
institution	DOAJ
collection	DOAJ
language	EN
topic	Animal model Status Epilepticus Temporal Lobe Epilepsy Myelin development White matter integrity MRI Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571
spellingShingle	Animal model Status Epilepticus Temporal Lobe Epilepsy Myelin development White matter integrity MRI Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Petra Bencurova Hanne Laakso Raimo A. Salo Ekaterina Paasonen Eppu Manninen Jaakko Paasonen Shalom Michaeli Silvia Mangia Martin Bares Milan Brazdil Hana Kubova Olli Gröhn Infantile status epilepticus disrupts myelin development
description	Temporal lobe epilepsy (TLE) is the most prevalent type of epilepsy in adults; it often starts in infancy or early childhood. Although TLE is primarily considered to be a grey matter pathology, a growing body of evidence links this disease with white matter abnormalities. In this study, we explore the impact of TLE onset and progression in the immature brain on white matter integrity and development utilising the rat model of Li-pilocarpine-induced TLE at the 12th postnatal day (P). Diffusion tensor imaging (DTI) and Black-Gold II histology uncovered disruptions in major white matter tracks (corpus callosum, internal and external capsules, and deep cerebral white matter) spreading through the whole brain at P28. These abnormalities were mostly not present any longer at three months after TLE induction, with only limited abnormalities detectable in the external capsule and deep cerebral white matter. Relaxation Along a Fictitious Field in the rotating frame of rank 4 indicated that white matter changes observed at both timepoints, P28 and P72, are consistent with decreased myelin content. The animals affected by TLE-induced white matter abnormalities exhibited increased functional connectivity between the thalamus and medial prefrontal and somatosensory cortex in adulthood. Furthermore, histological analyses of additional animal groups at P15 and P18 showed only mild changes in white matter integrity, suggesting a gradual age-dependent impact of TLE progression. Taken together, TLE progression in the immature brain distorts white matter development with a peak around postnatal day 28, followed by substantial recovery in adulthood. This developmental delay might give rise to cognitive and behavioural comorbidities typical for early-onset TLE.
format	article
author	Petra Bencurova Hanne Laakso Raimo A. Salo Ekaterina Paasonen Eppu Manninen Jaakko Paasonen Shalom Michaeli Silvia Mangia Martin Bares Milan Brazdil Hana Kubova Olli Gröhn
author_facet	Petra Bencurova Hanne Laakso Raimo A. Salo Ekaterina Paasonen Eppu Manninen Jaakko Paasonen Shalom Michaeli Silvia Mangia Martin Bares Milan Brazdil Hana Kubova Olli Gröhn
author_sort	Petra Bencurova
title	Infantile status epilepticus disrupts myelin development
title_short	Infantile status epilepticus disrupts myelin development
title_full	Infantile status epilepticus disrupts myelin development
title_fullStr	Infantile status epilepticus disrupts myelin development
title_full_unstemmed	Infantile status epilepticus disrupts myelin development
title_sort	infantile status epilepticus disrupts myelin development
publisher	Elsevier
publishDate	2022
url	https://doaj.org/article/4e99dbbd9da8404ca9ff7abd8ac14b56
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Infantile status epilepticus disrupts myelin development

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