Localizing non-epileptiform abnormal brain function in children using high density EEG: Electric Source Imaging of focal slowing.


Journal

Epilepsy research
ISSN: 1872-6844
Titre abrégé: Epilepsy Res
Pays: Netherlands
ID NLM: 8703089

Informations de publication

Date de publication:
01 2020
Historique:
received: 06 08 2019
revised: 01 11 2019
accepted: 22 11 2019
pubmed: 18 12 2019
medline: 1 7 2021
entrez: 18 12 2019
Statut: ppublish

Résumé

Electric Source Imaging (ESI) of interictal epileptiform discharges (IED) is increasingly validated for localizing epileptic activity. In children, IED can be absent or multifocal even in cases of a focal epileptogenic zone and additional electrophysiological markers are needed. Here, we investigated ESI of pathological focal slowing (FS) recorded on EEG as a new localizing marker in children with drug-resistant epilepsy. We selected 15 children (median: 12; range: 4-18yrs), with high-density EEG (hdEEG), presurgical evaluation and surgical resection. One patient had a non-lesional MRI. ESI of patient-specific focal slow activity was performed (distributed linear inverse solution and individual head model). The maximal average power in the band of interest was considered as the source of focal slowing (ESI-FS). The Euclidian distance between ESI-FS and the resection (5 mm margin) was compared to the localization of maximal ESI of interictal epileptiform discharges (ESI-IED), interictal FDG-PET and ictal SPECT/SISCOM. In 9/15 patients (60%), ESI of focal slowing (ESI-FS) was inside or ≤5 mm from resection margins. The remaining 6/15 cases had distances ≤15 mm. In 9/15 patients with interictal spikes, the ESI-IED was concordant with the resection. 6/15 patients with concordant ESI-FS showed also interictal concordant ESI of IED; in 3/15 patients, ESI-FS but not ESI-IED was concordant with the resection. In 10/15 patients, ESI-FS was concordant with MRI lesion and for ESI-IED this concordance was on 8/15 patients. Maximal hypometabolism and SISCOM were concordant with the resection for 7/15 and 7/12, respectively. These findings suggest that "non-epileptiform" EEG activity, such as focal slowing, could be a complementary useful marker to localize the epileptogenic zone. ESI-FS may notably be applied in young patients without focal interictal spikes or multifocal spikes. This potential new marker of brain dysfunction has potential applications to other neurological disorders associated with slow EEG activity.

Sections du résumé

BACKGROUND
Electric Source Imaging (ESI) of interictal epileptiform discharges (IED) is increasingly validated for localizing epileptic activity. In children, IED can be absent or multifocal even in cases of a focal epileptogenic zone and additional electrophysiological markers are needed. Here, we investigated ESI of pathological focal slowing (FS) recorded on EEG as a new localizing marker in children with drug-resistant epilepsy.
METHODS
We selected 15 children (median: 12; range: 4-18yrs), with high-density EEG (hdEEG), presurgical evaluation and surgical resection. One patient had a non-lesional MRI. ESI of patient-specific focal slow activity was performed (distributed linear inverse solution and individual head model). The maximal average power in the band of interest was considered as the source of focal slowing (ESI-FS). The Euclidian distance between ESI-FS and the resection (5 mm margin) was compared to the localization of maximal ESI of interictal epileptiform discharges (ESI-IED), interictal FDG-PET and ictal SPECT/SISCOM.
RESULTS
In 9/15 patients (60%), ESI of focal slowing (ESI-FS) was inside or ≤5 mm from resection margins. The remaining 6/15 cases had distances ≤15 mm. In 9/15 patients with interictal spikes, the ESI-IED was concordant with the resection. 6/15 patients with concordant ESI-FS showed also interictal concordant ESI of IED; in 3/15 patients, ESI-FS but not ESI-IED was concordant with the resection. In 10/15 patients, ESI-FS was concordant with MRI lesion and for ESI-IED this concordance was on 8/15 patients. Maximal hypometabolism and SISCOM were concordant with the resection for 7/15 and 7/12, respectively.
CONCLUSION
These findings suggest that "non-epileptiform" EEG activity, such as focal slowing, could be a complementary useful marker to localize the epileptogenic zone. ESI-FS may notably be applied in young patients without focal interictal spikes or multifocal spikes. This potential new marker of brain dysfunction has potential applications to other neurological disorders associated with slow EEG activity.

Identifiants

pubmed: 31846783
pii: S0920-1211(19)30437-1
doi: 10.1016/j.eplepsyres.2019.106245
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

106245

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Sara Baldini (S)

Neurology Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland; Clinical Unit of Neurology, Department of Medical Sciences, University Hospital and Health Services of Trieste, University of Trieste, Trieste, Italy.

Ana Coito (A)

Neurology Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland; Department of Neurology Cantonal Hospital Aarau, Aarau, Switzerland.

Christian M Korff (CM)

Pediatric Neurology Unit, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Valentina Garibotto (V)

Nuclear Medicine and Molecular Imaging, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Martin Ndenghera (M)

Neurology Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Laurent Spinelli (L)

Neurology Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Andrea Bartoli (A)

Neurosurgery Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Shahan Momjian (S)

Neurosurgery Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Karl Schaller (K)

Neurosurgery Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Margittta Seeck (M)

Neurology Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Francesca Pittau (F)

Neurology Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland.

Serge Vulliemoz (S)

Neurology Clinic, University Hospitals and Faculty of Medicine of Geneva, Geneva, Switzerland. Electronic address: Serge.Vulliemoz@hcuge.ch.

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