Association of epileptiform abnormalities and seizures in Alzheimer disease.
Journal
Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060
Informations de publication
Date de publication:
20 10 2020
20 10 2020
Historique:
received:
18
11
2019
accepted:
14
05
2020
pubmed:
9
8
2020
medline:
18
11
2020
entrez:
9
8
2020
Statut:
ppublish
Résumé
To examine the relationship between scalp EEG biomarkers of hyperexcitability in Alzheimer disease (AD) and to determine how these electric biomarkers relate to the clinical expression of seizures in AD. In this cross-sectional study, we performed 24-hour ambulatory scalp EEGs on 43 cognitively normal elderly healthy controls (HC), 41 participants with early-stage AD with no history or risk factors for epilepsy (AD-NoEp), and 15 participants with early-stage AD with late-onset epilepsy related to AD (AD-Ep). Two epileptologists blinded to diagnosis visually reviewed all EEGs and annotated all potential epileptiform abnormalities. A panel of 9 epileptologists blinded to diagnosis was then surveyed to generate a consensus interpretation of epileptiform abnormalities in each EEG. Epileptiform abnormalities were seen in 53% of AD-Ep, 22% of AD-NoEp, and 4.7% of HC. Specific features of epileptiform discharges, including high frequency, robust morphology, right temporal location, and occurrence during wakefulness and REM, were associated with clinical seizures in AD. Multiple EEG biomarkers concordantly demonstrated a pattern of left temporal lobe hyperexcitability in early stages of AD, whereas clinical seizures in AD were often associated with bitemporal hyperexcitability. Frequent small sharp spikes were specifically associated with epileptiform EEGs and thus identified as a potential biomarker of hyperexcitability in AD. Epileptiform abnormalities are common in AD but not all equivalent. Specific features of epileptiform discharges are associated with clinical seizures in AD. Given the difficulty recognizing clinical seizures in AD, these EEG features could provide guidance on which patients with AD are at high risk for clinical seizures.
Identifiants
pubmed: 32764101
pii: WNL.0000000000010612
doi: 10.1212/WNL.0000000000010612
pmc: PMC7713786
doi:
Substances chimiques
Biomarkers
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2259-e2270Subventions
Organisme : NINDS NIH HHS
ID : R01 NS062092
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS102190
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG062421
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS090900
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS101037
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS102574
Pays : United States
Organisme : NINDS NIH HHS
ID : R25 NS065743
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS107291
Pays : United States
Organisme : NINDS NIH HHS
ID : K24 NS088568
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2020 American Academy of Neurology.
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