Burden of Epileptiform Activity Predicts Discharge Neurologic Outcomes in Severe Acute Ischemic Stroke.


Journal

Neurocritical care
ISSN: 1556-0961
Titre abrégé: Neurocrit Care
Pays: United States
ID NLM: 101156086

Informations de publication

Date de publication:
06 2020
Historique:
pubmed: 5 4 2020
medline: 8 6 2021
entrez: 5 4 2020
Statut: ppublish

Résumé

Clinical seizures following acute ischemic stroke (AIS) appear to contribute to worse neurologic outcomes. However, the effect of electrographic epileptiform abnormalities (EAs) more broadly is less clear. Here, we evaluate the impact of EAs, including electrographic seizures and periodic and rhythmic patterns, on outcomes in patients with AIS. This is a retrospective study of all patients with AIS aged ≥ 18 years who underwent at least 18 h of continuous electroencephalogram (EEG) monitoring at a single center between 2012 and 2017. EAs were classified according to American Clinical Neurophysiology Society (ACNS) nomenclature and included seizures and periodic and rhythmic patterns. EA burden for each 24-h epoch was defined using the following cutoffs: EA presence, maximum daily burden < 10% versus > 10%, maximum daily burden < 50% versus > 50%, and maximum daily burden using categories from ACNS nomenclature ("rare" < 1%; "occasional" 1-9%; "frequent" 10-49%; "abundant" 50-89%; "continuous" > 90%). Maximum EA frequency for each epoch was dichotomized into ≥ 1.5 Hz versus < 1.5 Hz. Poor neurologic outcome was defined as a modified Rankin Scale score of 4-6 (vs. 0-3 as good outcome) at hospital discharge. One hundred and forty-three patients met study inclusion criteria. Sixty-seven patients (46.9%) had EAs. One hundred and twenty-four patients (86.7%) had poor outcome. On univariate analysis, the presence of EAs (OR 3.87 [1.27-11.71], p = 0.024) and maximum daily burden > 10% (OR 12.34 [2.34-210], p = 0.001) and > 50% (OR 8.26 [1.34-122], p = 0.035) were associated with worse outcomes. On multivariate analysis, after adjusting for clinical covariates (age, gender, NIHSS, APACHE II, stroke location, stroke treatment, hemorrhagic transformation, Charlson comorbidity index, history of epilepsy), EA presence (OR 5.78 [1.36-24.56], p = 0.017), maximum daily burden > 10% (OR 23.69 [2.43-230.7], p = 0.006), and maximum daily burden > 50% (OR 9.34 [1.01-86.72], p = 0.049) were associated with worse outcomes. After adjusting for covariates, we also found a dose-dependent association between increasing EA burden and increasing probability of poor outcomes (OR 1.89 [1.18-3.03] p = 0.009). We did not find an independent association between EA frequency and outcomes (OR: 4.43 [.98-20.03] p = 0.053). However, the combined effect of increasing EA burden and frequency ≥ 1.5 Hz (EA burden * frequency) was significantly associated with worse outcomes (OR 1.64 [1.03-2.63] p = 0.039). Electrographic seizures and periodic and rhythmic patterns in patients with AIS are associated with worse outcomes in a dose-dependent manner. Future studies are needed to assess whether treatment of this EEG activity can improve outcomes.

Sections du résumé

BACKGROUND/OBJECTIVES
Clinical seizures following acute ischemic stroke (AIS) appear to contribute to worse neurologic outcomes. However, the effect of electrographic epileptiform abnormalities (EAs) more broadly is less clear. Here, we evaluate the impact of EAs, including electrographic seizures and periodic and rhythmic patterns, on outcomes in patients with AIS.
METHODS
This is a retrospective study of all patients with AIS aged ≥ 18 years who underwent at least 18 h of continuous electroencephalogram (EEG) monitoring at a single center between 2012 and 2017. EAs were classified according to American Clinical Neurophysiology Society (ACNS) nomenclature and included seizures and periodic and rhythmic patterns. EA burden for each 24-h epoch was defined using the following cutoffs: EA presence, maximum daily burden < 10% versus > 10%, maximum daily burden < 50% versus > 50%, and maximum daily burden using categories from ACNS nomenclature ("rare" < 1%; "occasional" 1-9%; "frequent" 10-49%; "abundant" 50-89%; "continuous" > 90%). Maximum EA frequency for each epoch was dichotomized into ≥ 1.5 Hz versus < 1.5 Hz. Poor neurologic outcome was defined as a modified Rankin Scale score of 4-6 (vs. 0-3 as good outcome) at hospital discharge.
RESULTS
One hundred and forty-three patients met study inclusion criteria. Sixty-seven patients (46.9%) had EAs. One hundred and twenty-four patients (86.7%) had poor outcome. On univariate analysis, the presence of EAs (OR 3.87 [1.27-11.71], p = 0.024) and maximum daily burden > 10% (OR 12.34 [2.34-210], p = 0.001) and > 50% (OR 8.26 [1.34-122], p = 0.035) were associated with worse outcomes. On multivariate analysis, after adjusting for clinical covariates (age, gender, NIHSS, APACHE II, stroke location, stroke treatment, hemorrhagic transformation, Charlson comorbidity index, history of epilepsy), EA presence (OR 5.78 [1.36-24.56], p = 0.017), maximum daily burden > 10% (OR 23.69 [2.43-230.7], p = 0.006), and maximum daily burden > 50% (OR 9.34 [1.01-86.72], p = 0.049) were associated with worse outcomes. After adjusting for covariates, we also found a dose-dependent association between increasing EA burden and increasing probability of poor outcomes (OR 1.89 [1.18-3.03] p = 0.009). We did not find an independent association between EA frequency and outcomes (OR: 4.43 [.98-20.03] p = 0.053). However, the combined effect of increasing EA burden and frequency ≥ 1.5 Hz (EA burden * frequency) was significantly associated with worse outcomes (OR 1.64 [1.03-2.63] p = 0.039).
CONCLUSIONS
Electrographic seizures and periodic and rhythmic patterns in patients with AIS are associated with worse outcomes in a dose-dependent manner. Future studies are needed to assess whether treatment of this EEG activity can improve outcomes.

Identifiants

pubmed: 32246435
doi: 10.1007/s12028-020-00944-0
pii: 10.1007/s12028-020-00944-0
pmc: PMC7416505
mid: NIHMS1581967
doi:

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

697-706

Subventions

Organisme : NINDS NIH HHS
ID : K23 NS090900
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS105950
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS114201
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS102190
Pays : United States

Commentaires et corrections

Type : CommentIn

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Auteurs

Mohammad Tabaeizadeh (M)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Hassan Aboul Nour (H)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Maryum Shoukat (M)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Haoqi Sun (H)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Jing Jin (J)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Farrukh Javed (F)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Solomon Kassa (S)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Muhammad Edhi (M)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Elahe Bordbar (E)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Justin Gallagher (J)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Valdery Junior Moura (VJ)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Manohar Ghanta (M)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Yu-Ping Shao (YP)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Andrew J Cole (AJ)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Eric S Rosenthal (ES)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

M Brandon Westover (MB)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA.

Sahar F Zafar (SF)

Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA. sfzafar@mgh.harvard.edu.

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