Early neurological deterioration following thrombolysis for minor stroke with isolated internal carotid artery occlusion.


Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
02 2021
Historique:
received: 02 06 2020
accepted: 09 09 2020
pubmed: 23 9 2020
medline: 13 8 2021
entrez: 22 9 2020
Statut: ppublish

Résumé

Better understanding the incidence, predictors and mechanisms of early neurological deterioration (END) following intravenous thrombolysis (IVT) for acute stroke with mild symptoms and isolated internal carotid artery occlusion (iICAo) may inform therapeutic decisions. From a multicenter retrospective database, we extracted all patients with both National Institutes of Health Stroke Scale (NIHSS) score <6 and iICAo (i.e. not involving the Willis circle) on admission imaging, intended for IVT alone. END was defined as ≥4 NIHSS points increase within 24 h. END and no-END patients were compared for (i) pre-treatment clinical and imaging variables and (ii) occurrence of intracranial occlusion, carotid recanalization and parenchymal hemorrhage on follow-up imaging. Seventy-four patients were included, amongst whom 22 (30%) patients experienced END. Amongst pre-treatment variables, suprabulbar carotid occlusion was the only admission predictor of END following stepwise variable selection (odds ratio = 4.0, 95% confidence interval: 1.3-12.2; P = 0.015). On follow-up imaging, there was no instance of parenchymal hemorrhage, but an intracranial occlusion was now present in 76% vs. 0% of END and no-END patients, respectively (P < 0.001), and there was a trend toward higher carotid recanalization rate in END patients (29% vs. 9%, P = 0.07). As compared to no-END, END was strongly associated with a poor 3-month outcome. Early neurological deterioration is a frequent and highly deleterious event after IVT for minor stroke with iICAo, and is of thromboembolic origin in three out of four patients. The strong association with iICAo site-largely a function of underlying stroke etiology-may point to a different response of the thrombus to IVT. These findings suggest END may be preventable in this setting.

Sections du résumé

BACKGROUND AND PURPOSE
Better understanding the incidence, predictors and mechanisms of early neurological deterioration (END) following intravenous thrombolysis (IVT) for acute stroke with mild symptoms and isolated internal carotid artery occlusion (iICAo) may inform therapeutic decisions.
METHODS
From a multicenter retrospective database, we extracted all patients with both National Institutes of Health Stroke Scale (NIHSS) score <6 and iICAo (i.e. not involving the Willis circle) on admission imaging, intended for IVT alone. END was defined as ≥4 NIHSS points increase within 24 h. END and no-END patients were compared for (i) pre-treatment clinical and imaging variables and (ii) occurrence of intracranial occlusion, carotid recanalization and parenchymal hemorrhage on follow-up imaging.
RESULTS
Seventy-four patients were included, amongst whom 22 (30%) patients experienced END. Amongst pre-treatment variables, suprabulbar carotid occlusion was the only admission predictor of END following stepwise variable selection (odds ratio = 4.0, 95% confidence interval: 1.3-12.2; P = 0.015). On follow-up imaging, there was no instance of parenchymal hemorrhage, but an intracranial occlusion was now present in 76% vs. 0% of END and no-END patients, respectively (P < 0.001), and there was a trend toward higher carotid recanalization rate in END patients (29% vs. 9%, P = 0.07). As compared to no-END, END was strongly associated with a poor 3-month outcome.
CONCLUSIONS
Early neurological deterioration is a frequent and highly deleterious event after IVT for minor stroke with iICAo, and is of thromboembolic origin in three out of four patients. The strong association with iICAo site-largely a function of underlying stroke etiology-may point to a different response of the thrombus to IVT. These findings suggest END may be preventable in this setting.

Identifiants

pubmed: 32959480
doi: 10.1111/ene.14541
doi:

Substances chimiques

Fibrinolytic Agents 0

Types de publication

Journal Article Multicenter Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

479-490

Investigateurs

Wagih Ben Hassen (W)
Bertrand Lapergue (B)
Chantal Lamy (C)
Ludovic Lucas (L)
Frédéric Philippeau (F)
Michael Obadia (M)
Michel Piotin (M)
Omar Bennani (O)
Laura Mechtouff (L)
Frédéric Klapczynski (F)
Olivier Detante (O)
Caroline Arquizan (C)
Gioia Mione (G)
Denis Sablot (D)
Sébastien Gazzola (S)
Séverine Debiais (S)
Serkan Cakmak (S)
Valer Grigoras (V)
Ruben Tamazyan (R)
Cécile Preterre (C)
Charlotte Rosso (C)
Philippe Niclot (P)
Pierre Garnier (P)
Sébastien Soize (S)
François Lun (F)
Amélie Tuffal (A)
Marion Boulanger (M)
Sébastien Gazzola (S)
Mathieu Zuber (M)
Fernando Pico (F)
Frédéric Clarençon (F)
Igor Sibon (I)
Sonia Alamowitch (S)
Laurie Fraticelli (L)
Anne-Evelyne Vallet (AE)
Vincent Costalat (V)
Catherine Oppenheim (C)
Jean-Philippe Cottier (JP)
Yves Berthezene (Y)
Hubert Desal (H)
Pierre Agius (P)
Claire Boutet (C)
Nicolas Bricout (N)
Didier Leys (D)
Mohamed Chbicheb (M)
Arnaud Malbranque (A)
Laurent Spelle (L)
Serge Bracard (S)
Mylène Masson (M)

Informations de copyright

© 2020 European Academy of Neurology.

Références

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Auteurs

N Boulenoir (N)

Neurology Department, GHU Paris Psychiatrie et Neurosciences, Sainte-Anne Hospital, INSERM UMR 1266, FHU NeuroVasc, Université de Paris, Paris, France.

G Turc (G)

Neurology Department, GHU Paris Psychiatrie et Neurosciences, Sainte-Anne Hospital, INSERM UMR 1266, FHU NeuroVasc, Université de Paris, Paris, France.

H Henon (H)

Inserm U1171, Degenerative and Vascular Cognitive Disorders, CHU Lille, Department of Neurology, Université de Lille, Lille, France.

N Laksiri (N)

Neurology Department, La Timone University Hospital, Marseille, France.

F Mounier-Véhier (F)

Neurology Department, Lens Hospital, Lens, France.

I Girard Buttaz (I)

Neurology Department, Valenciennes Hospital, Valenciennes, France.

D-L Duong (DL)

Neurology Department, Versailles University Hospital, Versailles, France.

J Papassin (J)

Stroke Unit, Grenoble University Hospital, Grenoble, France.
Neurology Department, Chambery Hospital, Chambery, France.

M Yger (M)

Neurology Department, Saint-Antoine Hospital, Paris, France.

A Triquenot (A)

Neurology Department, Rouen Hospital, Rouen, France.

A Lyoubi (A)

Neurology Department, Delafontaine Hospital, St. Denis, France.

A Ter Schiphorst (A)

Neurology Department, CHRU Gui de Chauliac, Montpellier, France.

C Denier (C)

Neurology Department, CHU Kremlin Bicêtre, Kremlin Bicêtre, France.

J-C Baron (JC)

Neurology Department, GHU Paris Psychiatrie et Neurosciences, Sainte-Anne Hospital, INSERM UMR 1266, FHU NeuroVasc, Université de Paris, Paris, France.

P Seners (P)

Neurology Department, GHU Paris Psychiatrie et Neurosciences, Sainte-Anne Hospital, INSERM UMR 1266, FHU NeuroVasc, Université de Paris, Paris, France.

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