2020年9月28日
Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy.
Scientific reports
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- 巻
- 10
- 号
- 1
- 開始ページ
- 15895
- 終了ページ
- 15895
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1038/s41598-020-73051-x
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.
- リンク情報
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- DOI
- https://doi.org/10.1038/s41598-020-73051-x
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/32985579
- PubMed Central
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7523010
- Scopus
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85091663825&origin=inward 本文へのリンクあり
- Scopus Citedby
- https://www.scopus.com/inward/citedby.uri?partnerID=HzOxMe3b&scp=85091663825&origin=inward
- ID情報
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- DOI : 10.1038/s41598-020-73051-x
- eISSN : 2045-2322
- PubMed ID : 32985579
- PubMed Central 記事ID : PMC7523010
- SCOPUS ID : 85091663825