High risk of early neurological worsening of lacunar infarction.


Journal

Acta neurologica Scandinavica
ISSN: 1600-0404
Titre abrégé: Acta Neurol Scand
Pays: Denmark
ID NLM: 0370336

Informations de publication

Date de publication:
Feb 2019
Historique:
received: 01 03 2018
revised: 27 08 2018
accepted: 12 09 2018
pubmed: 20 9 2018
medline: 23 2 2019
entrez: 20 9 2018
Statut: ppublish

Résumé

We aimed to evaluate factors associated with neurological worsening among patients with lacunar or non-lacunar infarction admitted within 3 hours and between 3 and 24 hours after stroke onset. All patients admitted to Haukeland university hospital between 2006 and 2016 with acute cerebral infarction on MRI and admission within 24 hours were included. Repeated National Institute of Health Stroke Scale (NIHSS) scoring was performed in all patients whenever possible. Neurological worsening during the hospital stay was defined as NIHSS score increase ≥3 compared to NIHSS score on admission. In patients with lacunar infarction admitted within 3 hours of onset, neurological worsening was associated with low NIHSS score on admission, low body temperature, and leukoaraiosis, whereas only internal carotid artery stenosis or occlusion was associated with neurological worsening in non-lacunar infraction. For patients admitted 3-24 hours after onset, neurological worsening was associated with low body temperature, high systolic blood pressure, and short time from onset to admission in patients with lacunar infarction, whereas high systolic blood pressure, high NIHSS score on admission, middle cerebral artery occlusion, and high blood glucose were associated with neurological worsening in patients with non-lacunar infarction (all P < 0.05). Lacunar infarctions with minor neurological deficits within 3 hours of stroke onset are at high risk of neurological worsening especially if concomitant low body temperature and leukoaraiosis.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE
We aimed to evaluate factors associated with neurological worsening among patients with lacunar or non-lacunar infarction admitted within 3 hours and between 3 and 24 hours after stroke onset.
METHODS METHODS
All patients admitted to Haukeland university hospital between 2006 and 2016 with acute cerebral infarction on MRI and admission within 24 hours were included. Repeated National Institute of Health Stroke Scale (NIHSS) scoring was performed in all patients whenever possible. Neurological worsening during the hospital stay was defined as NIHSS score increase ≥3 compared to NIHSS score on admission.
RESULTS RESULTS
In patients with lacunar infarction admitted within 3 hours of onset, neurological worsening was associated with low NIHSS score on admission, low body temperature, and leukoaraiosis, whereas only internal carotid artery stenosis or occlusion was associated with neurological worsening in non-lacunar infraction. For patients admitted 3-24 hours after onset, neurological worsening was associated with low body temperature, high systolic blood pressure, and short time from onset to admission in patients with lacunar infarction, whereas high systolic blood pressure, high NIHSS score on admission, middle cerebral artery occlusion, and high blood glucose were associated with neurological worsening in patients with non-lacunar infarction (all P < 0.05).
CONCLUSIONS CONCLUSIONS
Lacunar infarctions with minor neurological deficits within 3 hours of stroke onset are at high risk of neurological worsening especially if concomitant low body temperature and leukoaraiosis.

Identifiants

pubmed: 30229856
doi: 10.1111/ane.13029
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

143-149

Informations de copyright

© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Auteurs

Halvor Naess (H)

Department of Neurology, Haukeland University Hospital, Bergen, Norway.
Department of Clinical Medicine, University of Bergen, Bergen, Norway.
Centre for age-related medicine, Stavanger University Hospital, Stavanger, Norway.

Lars Thomassen (L)

Department of Neurology, Haukeland University Hospital, Bergen, Norway.
Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Ulrike Waje-Andreassen (U)

Department of Neurology, Haukeland University Hospital, Bergen, Norway.
Department of Clinical Medicine, University of Bergen, Bergen, Norway.

Solveig Glad (S)

Department of Neurology, Haukeland University Hospital, Bergen, Norway.

Christopher E Kvistad (CE)

Department of Neurology, Haukeland University Hospital, Bergen, Norway.

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