Combining Transcranial Doppler and EEG Data to Predict Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.


Journal

Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060

Informations de publication

Date de publication:
01 02 2022
Historique:
received: 07 05 2021
accepted: 08 11 2021
pubmed: 1 12 2021
medline: 6 4 2022
entrez: 30 11 2021
Statut: ppublish

Résumé

Delayed cerebral ischemia (DCI) is the leading complication of subarachnoid hemorrhage (SAH). Because DCI was traditionally thought to be caused by large vessel vasospasm, transcranial Doppler ultrasounds (TCDs) have been the standard of care. Continuous EEG has emerged as a promising complementary monitoring modality and predicts increased DCI risk. Our objective was to determine whether combining EEG and TCD data improves prediction of DCI after SAH. We hypothesize that integrating these diagnostic modalities improves DCI prediction. We retrospectively assessed patients with moderate to severe SAH (2011-2015; Fisher 3-4 or Hunt-Hess 4-5) who had both prospective TCD and EEG acquisition during hospitalization. Middle cerebral artery (MCA) peak systolic velocities (PSVs) and the presence or absence of epileptiform abnormalities (EAs), defined as seizures, epileptiform discharges, and rhythmic/periodic activity, were recorded daily. Logistic regressions were used to identify significant covariates of EAs and TCD to predict DCI. Group-based trajectory modeling (GBTM) was used to account for changes over time by identifying distinct group trajectories of MCA PSV and EAs associated with DCI risk. We assessed 107 patients; DCI developed in 56 (51.9%). Univariate predictors of DCI are presence of high-MCA velocity (PSV ≥200 cm/s, sensitivity 27%, specificity 89%) and EAs (sensitivity 66%, specificity 62%) on or before day 3. Two univariate GBTM trajectories of EAs predicted DCI (sensitivity 64%, specificity 62.75%). Logistic regression and GBTM models using both TCD and EEG monitoring performed better. The best logistic regression and GBTM models used both TCD and EEG data, Hunt-Hess score at admission, and aneurysm treatment as predictors of DCI (logistic regression: sensitivity 90%, specificity 70%; GBTM: sensitivity 89%, specificity 67%). EEG and TCD biomarkers combined provide the best prediction of DCI. The conjunction of clinical variables with the timing of EAs and high MCA velocities improved model performance. These results suggest that TCD and cEEG are promising complementary monitoring modalities for DCI prediction. Our model has potential to serve as a decision support tool in SAH management. This study provides Class II evidence that combined TCD and EEG monitoring can identify delayed cerebral ischemia after SAH.

Sections du résumé

BACKGROUND AND OBJECTIVES
Delayed cerebral ischemia (DCI) is the leading complication of subarachnoid hemorrhage (SAH). Because DCI was traditionally thought to be caused by large vessel vasospasm, transcranial Doppler ultrasounds (TCDs) have been the standard of care. Continuous EEG has emerged as a promising complementary monitoring modality and predicts increased DCI risk. Our objective was to determine whether combining EEG and TCD data improves prediction of DCI after SAH. We hypothesize that integrating these diagnostic modalities improves DCI prediction.
METHODS
We retrospectively assessed patients with moderate to severe SAH (2011-2015; Fisher 3-4 or Hunt-Hess 4-5) who had both prospective TCD and EEG acquisition during hospitalization. Middle cerebral artery (MCA) peak systolic velocities (PSVs) and the presence or absence of epileptiform abnormalities (EAs), defined as seizures, epileptiform discharges, and rhythmic/periodic activity, were recorded daily. Logistic regressions were used to identify significant covariates of EAs and TCD to predict DCI. Group-based trajectory modeling (GBTM) was used to account for changes over time by identifying distinct group trajectories of MCA PSV and EAs associated with DCI risk.
RESULTS
We assessed 107 patients; DCI developed in 56 (51.9%). Univariate predictors of DCI are presence of high-MCA velocity (PSV ≥200 cm/s, sensitivity 27%, specificity 89%) and EAs (sensitivity 66%, specificity 62%) on or before day 3. Two univariate GBTM trajectories of EAs predicted DCI (sensitivity 64%, specificity 62.75%). Logistic regression and GBTM models using both TCD and EEG monitoring performed better. The best logistic regression and GBTM models used both TCD and EEG data, Hunt-Hess score at admission, and aneurysm treatment as predictors of DCI (logistic regression: sensitivity 90%, specificity 70%; GBTM: sensitivity 89%, specificity 67%).
DISCUSSION
EEG and TCD biomarkers combined provide the best prediction of DCI. The conjunction of clinical variables with the timing of EAs and high MCA velocities improved model performance. These results suggest that TCD and cEEG are promising complementary monitoring modalities for DCI prediction. Our model has potential to serve as a decision support tool in SAH management.
CLASSIFICATION OF EVIDENCE
This study provides Class II evidence that combined TCD and EEG monitoring can identify delayed cerebral ischemia after SAH.

Identifiants

pubmed: 34845057
pii: WNL.0000000000013126
doi: 10.1212/WNL.0000000000013126
pmc: PMC8826465
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

e459-e469

Subventions

Organisme : NINDS NIH HHS
ID : K23 NS110980
Pays : United States
Organisme : NINR NIH HHS
ID : R01 NR018335
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS102190
Pays : United States
Organisme : NINDS NIH HHS
ID : U24 NS107136
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS119825
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS112596
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG064312
Pays : United States
Organisme : NINDS NIH HHS
ID : R03 NS112859
Pays : United States
Organisme : NINDS NIH HHS
ID : U24 NS107215
Pays : United States
Organisme : NINDS NIH HHS
ID : U01 NS106513
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS102574
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS109062
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS107291
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS105950
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS097629
Pays : United States
Organisme : NINDS NIH HHS
ID : K23 NS114201
Pays : United States

Informations de copyright

© 2021 American Academy of Neurology.

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Auteurs

Hsin Yi Chen (HY)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Jonathan Elmer (J)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Sahar F Zafar (SF)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Manohar Ghanta (M)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Valdery Moura Junior (V)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Eric S Rosenthal (ES)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Emily J Gilmore (EJ)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Lawrence J Hirsch (LJ)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Hitten P Zaveri (HP)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Kevin N Sheth (KN)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Nils H Petersen (NH)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

M Brandon Westover (MB)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston.

Jennifer A Kim (JA)

From the Department of Neurology (H.Y.C., E.J.G., L.J.H., H.P.Z., K.N.S., N.H.P., J.A.K.), Yale University, New Haven, CT; Department of Critical Care Medicine (J.E.), University of Pittsburgh Medical Center, PA; and Department of Neurology (S.F.Z., M.G., V.M.J., E.S.R., M.B.W.), Massachusetts General Hospital, Boston. jennifer.a.kim@yale.edu.

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