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Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy

Epilepsy is a network disease. The primary somatosensory cortex (S1) is usually considered to be intact, but could be subclinically disturbed based on abnormal functional connectivity in patients with temporal lobe epilepsy (TLE). We aimed to investigate if the S1 of TLE is abnormally modulated. Som...

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Autores principales: Ishida, Makoto, Jin, Kazutaka, Kakisaka, Yosuke, Kanno, Akitake, Kawashima, Ryuta, Nakasato, Nobukazu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7523010/
https://www.ncbi.nlm.nih.gov/pubmed/32985579
http://dx.doi.org/10.1038/s41598-020-73051-x
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author Ishida, Makoto
Jin, Kazutaka
Kakisaka, Yosuke
Kanno, Akitake
Kawashima, Ryuta
Nakasato, Nobukazu
author_facet Ishida, Makoto
Jin, Kazutaka
Kakisaka, Yosuke
Kanno, Akitake
Kawashima, Ryuta
Nakasato, Nobukazu
author_sort Ishida, Makoto
collection PubMed
description Epilepsy is a network disease. The primary somatosensory cortex (S1) is usually considered to be intact, but could be subclinically disturbed based on abnormal functional connectivity in patients with temporal lobe epilepsy (TLE). We aimed to investigate if the S1 of TLE is abnormally modulated. Somatosensory evoked magnetic fields (SEFs) evoked by median nerve stimulation were recorded in each hemisphere of 15 TLE patients and 28 normal subjects. All responses were separately averaged in the awake state and light sleep using background magnetoencephalography. Latency and strength of the equivalent current dipole (ECD) was compared between the groups for the first (M1) and second peaks. Latencies showed no significant differences between the groups in either wakefulness or light sleep. ECD strengths were significantly lower in TLE patients than in controls only during wakefulness. The reduction of M1 ECD strength in the awake state is significantly correlated with duration of epilepsy. SEFs of TLE patients showed pure ECD strength reduction without latency delay. The phenomenon occurred exclusively during wakefulness, suggesting that a wakefulness-specific modulator of S1 is abnormal in TLE. Repetitive seizures may gradually insult the modulator of S1 distant from the epileptogenic network.
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spelling pubmed-75230102020-09-29 Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy Ishida, Makoto Jin, Kazutaka Kakisaka, Yosuke Kanno, Akitake Kawashima, Ryuta Nakasato, Nobukazu Sci Rep Article Epilepsy is a network disease. The primary somatosensory cortex (S1) is usually considered to be intact, but could be subclinically disturbed based on abnormal functional connectivity in patients with temporal lobe epilepsy (TLE). We aimed to investigate if the S1 of TLE is abnormally modulated. Somatosensory evoked magnetic fields (SEFs) evoked by median nerve stimulation were recorded in each hemisphere of 15 TLE patients and 28 normal subjects. All responses were separately averaged in the awake state and light sleep using background magnetoencephalography. Latency and strength of the equivalent current dipole (ECD) was compared between the groups for the first (M1) and second peaks. Latencies showed no significant differences between the groups in either wakefulness or light sleep. ECD strengths were significantly lower in TLE patients than in controls only during wakefulness. The reduction of M1 ECD strength in the awake state is significantly correlated with duration of epilepsy. SEFs of TLE patients showed pure ECD strength reduction without latency delay. The phenomenon occurred exclusively during wakefulness, suggesting that a wakefulness-specific modulator of S1 is abnormal in TLE. Repetitive seizures may gradually insult the modulator of S1 distant from the epileptogenic network. Nature Publishing Group UK 2020-09-28 /pmc/articles/PMC7523010/ /pubmed/32985579 http://dx.doi.org/10.1038/s41598-020-73051-x Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Ishida, Makoto
Jin, Kazutaka
Kakisaka, Yosuke
Kanno, Akitake
Kawashima, Ryuta
Nakasato, Nobukazu
Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy
title Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy
title_full Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy
title_fullStr Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy
title_full_unstemmed Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy
title_short Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy
title_sort awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7523010/
https://www.ncbi.nlm.nih.gov/pubmed/32985579
http://dx.doi.org/10.1038/s41598-020-73051-x
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