Decreased thalamocortical connectivity in resolved Rolandic epilepsy.


Journal

Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
ISSN: 1872-8952
Titre abrégé: Clin Neurophysiol
Pays: Netherlands
ID NLM: 100883319

Informations de publication

Date de publication:
09 2023
Historique:
received: 28 03 2023
revised: 09 05 2023
accepted: 24 05 2023
pmc-release: 01 09 2024
medline: 21 8 2023
pubmed: 8 7 2023
entrez: 7 7 2023
Statut: ppublish

Résumé

Median nerve somatosensory evoked fields (SEFs) conduction times reflect the integrity of neural transmission across the thalamocortical circuit. We hypothesized median nerve SEF conduction time would be abnormal in children with Rolandic epilepsy (RE). 22 children with RE (10 active; 12 resolved) and 13 age-matched controls underwent structural and diffusion MRI and median nerve and visual stimulation during magnetoencephalography (MEG). N20 SEF responses were identified in contralateral somatosensory cortices. P100 were identified in contralateral occipital cortices as controls. Conduction times were compared between groups in linear models controlling for height. N20 conduction time was also compared to thalamic volume and Rolandic thalamocortical structural connectivity inferred using probabilistic tractography. The RE group had slower N20 conduction compared to controls (p = 0.042, effect size 0.6 ms) and this difference was driven by the resolved RE group (p = 0.046). There was no difference in P100 conduction time between groups (p = 0.83). Ventral thalamic volume positively correlated with N20 conduction time (p = 0.014). Children with resolved RE have focally decreased Rolandic thalamocortical connectivity. These results identify a persistent focal thalamocortical circuit abnormality in resolved RE and suggest that decreased Rolandic thalamocortical connectivity may support symptom resolution in this self-limited epilepsy.

Identifiants

pubmed: 37419052
pii: S1388-2457(23)00644-2
doi: 10.1016/j.clinph.2023.05.013
pmc: PMC10520846
mid: NIHMS1911882
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

21-27

Subventions

Organisme : NINDS NIH HHS
ID : K23 NS092923
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS115868
Pays : United States

Informations de copyright

Copyright © 2023 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.

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Auteurs

Dhinakaran M Chinappen (DM)

Massachusetts General Hospital, Department of Neurology, Boston, MA 02114, USA; Graduate Program in Neuroscience, Boston University, Boston, MA 02215, USA. Electronic address: dchinappen@mgh.harvard.edu.

Lauren M Ostrowski (LM)

Massachusetts General Hospital, Department of Neurology, Boston, MA 02114, USA.

Elizabeth R Spencer (ER)

Massachusetts General Hospital, Department of Neurology, Boston, MA 02114, USA; Graduate Program in Neuroscience, Boston University, Boston, MA 02215, USA.

Hunki Kwon (H)

Massachusetts General Hospital, Department of Neurology, Boston, MA 02114, USA.

Mark A Kramer (MA)

Department of Mathematics and Statistics and Center for Systems Neuroscience, Boston University, Boston, MA 02215, USA.

Matti S Hämäläinen (MS)

Massachusetts General Hospital, Department of Radiology, Boston, MA 02114, USA; Athinoula A, Martinos Center for Biomedical Imaging, Charlestown, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA.

Catherine J Chu (CJ)

Massachusetts General Hospital, Department of Neurology, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA. Electronic address: cjchu@mgh.harvard.edu.

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Classifications MeSH