Serum Neurofilament Light Chain Concentration Correlates with Infarct Volume but Not Prognosis in Acute Ischemic Stroke.


Journal

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
ISSN: 1532-8511
Titre abrégé: J Stroke Cerebrovasc Dis
Pays: United States
ID NLM: 9111633

Informations de publication

Date de publication:
Aug 2019
Historique:
received: 11 02 2019
revised: 22 04 2019
accepted: 06 05 2019
pubmed: 4 6 2019
medline: 14 8 2019
entrez: 2 6 2019
Statut: ppublish

Résumé

We studied serum neurofilaments diagnostic value in patients with acute ischemic stroke (AIS) or TIA and evaluated any correlation with symptom severity, cerebral infarction volume, aetiology, and clinical outcome. One hundred and thirty-six patients (101 with AIS, and 35 with TIA) were included. Acute-phase serum neurofilament light chain (sNfL) was analyzed with a novel ultrasensitive single molecule array (Simoa). Cerebral infarction volume was measured from brain computed tomography in the subacute phase (>2 days). Stroke aetiology was defined by trial of ORG 10172 in acute stroke treatment classification, severity by National Institute of Health stroke scale (NIHSS) and the degree of disability by the Modified Rankin Scale (mRS) after 90 days. sNfL was markedly higher in patients with AIS (89.5 pg/mL [IQR: 44.7-195.3]) than with TIA (25.2 pg/mL [IQR: 14.6-48.0]), P= <.001), also after adjusting for age, NIHSS, and stroke volume (P= .003). In receiver operating characteristic analysis, sNfL concentration greater than or equal to 49 pg/mL proved to be the best cut-off value to differentiate between patients with stroke and those with TIA (sensitivity of 73% and specificity of 80%). sNfL concentration significantly correlated with cerebral infarction volume (r = .413, P= <.001), this association remained significant after adjusting for established predictors (P= .019). Patients with AIS due to cardioembolism or large artery atherosclerosis had the highest sNfL concentrations. NIHSS on admission (r = .343, P = <.001) and mRS scores after 3 months (r = .306, P = .004) correlated with sNfL concentration, however functional outcome 3 months after stroke was not associated with sNfL after adjusting for potential confounders. Cases with stroke were distinguishable from those with TIA following the determination of sNfL in the blood samples. The presence and amount of axonal damage estimated by sNfL correlated with the final cerebral infarction volume but was not predictive of degree of disability.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE
We studied serum neurofilaments diagnostic value in patients with acute ischemic stroke (AIS) or TIA and evaluated any correlation with symptom severity, cerebral infarction volume, aetiology, and clinical outcome.
METHODS METHODS
One hundred and thirty-six patients (101 with AIS, and 35 with TIA) were included. Acute-phase serum neurofilament light chain (sNfL) was analyzed with a novel ultrasensitive single molecule array (Simoa). Cerebral infarction volume was measured from brain computed tomography in the subacute phase (>2 days). Stroke aetiology was defined by trial of ORG 10172 in acute stroke treatment classification, severity by National Institute of Health stroke scale (NIHSS) and the degree of disability by the Modified Rankin Scale (mRS) after 90 days.
RESULTS RESULTS
sNfL was markedly higher in patients with AIS (89.5 pg/mL [IQR: 44.7-195.3]) than with TIA (25.2 pg/mL [IQR: 14.6-48.0]), P= <.001), also after adjusting for age, NIHSS, and stroke volume (P= .003). In receiver operating characteristic analysis, sNfL concentration greater than or equal to 49 pg/mL proved to be the best cut-off value to differentiate between patients with stroke and those with TIA (sensitivity of 73% and specificity of 80%). sNfL concentration significantly correlated with cerebral infarction volume (r = .413, P= <.001), this association remained significant after adjusting for established predictors (P= .019). Patients with AIS due to cardioembolism or large artery atherosclerosis had the highest sNfL concentrations. NIHSS on admission (r = .343, P = <.001) and mRS scores after 3 months (r = .306, P = .004) correlated with sNfL concentration, however functional outcome 3 months after stroke was not associated with sNfL after adjusting for potential confounders.
CONCLUSIONS CONCLUSIONS
Cases with stroke were distinguishable from those with TIA following the determination of sNfL in the blood samples. The presence and amount of axonal damage estimated by sNfL correlated with the final cerebral infarction volume but was not predictive of degree of disability.

Identifiants

pubmed: 31151840
pii: S1052-3057(19)30228-9
doi: 10.1016/j.jstrokecerebrovasdis.2019.05.008
pii:
doi:

Substances chimiques

Biomarkers 0
Neurofilament Proteins 0
neurofilament protein L 0

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

2242-2249

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Juha Onatsu (J)

Department of Neurology, NeuroCenter, Kuopio University Hospital, Kuopio, Finland. Electronic address: Juha.Onatsu@kuh.fi.

Ritva Vanninen (R)

Department of Clinical Radiology, Kuopio University Hospital, Kuopio, Finland; Department of Clinical Radiology, University of Eastern Finland, Kuopio Finland.

Pekka Jäkälä (P)

Department of Neurology, NeuroCenter, Kuopio University Hospital, Kuopio, Finland; Unit of Neurology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland.

Pirjo Mustonen (P)

Department of Cardiology, Keski-Suomi Central Hospital, Jyväskylä, Finland.

Kari Pulkki (K)

Department of Clinical Radiology and Clinical Chemistry, Kuopio, Finland; Eastern Finland Laboratory Center and Department of Clinical Chemistry, University of Eastern Finland, Kuopio, Finland.

Miika Korhonen (M)

Department of Clinical Radiology, Kuopio University Hospital, Kuopio, Finland.

Marja Hedman (M)

Department of Clinical Radiology, Kuopio University Hospital, Kuopio, Finland.

Henrik Zetterberg (H)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom; UK Dementia Research Institute, London, United Kingdom.

Kaj Blennow (K)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.

Kina Höglund (K)

Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.

Sanna-Kaisa Herukka (SK)

Department of Neurology, NeuroCenter, Kuopio University Hospital, Kuopio, Finland; Unit of Neurology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland.

Mikko Taina (M)

Department of Clinical Radiology, Kuopio University Hospital, Kuopio, Finland.

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