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Neurochem Int. 2016 Feb;93:1-5. doi: 10.1016/j.neuint.2015.12.003. Epub 2015 Dec 10.

Total-tau and neurofilament light in CSF reflect spinal cord ischaemia after endovascular aortic repair.

Author information

1
Department of Clinical Sciences Malmö, Anaesthesiology and Intensive Care Medicine, Lund University, Skåne University Hospital, Malmö, Sweden. Electronic address: edyta.merisson@skane.se.
2
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA; Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
3
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden; UCL Institute of Neurology, London, UK.
4
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Skåne University Hospital, SE-20502 Malmö, Sweden.
5
Department of Clinical Sciences Malmö, Anaesthesiology and Intensive Care Medicine, Lund University, Skåne University Hospital, Malmö, Sweden; Center for Clinical Research Sörmland, Uppsala University, Eskilstuna, Sweden.
6
Department of Clinical Sciences Malmö, Vascular Center, Skåne University Hospital, Malmö, Sweden.
7
Department of Clinical Sciences Malmö, Anaesthesiology and Intensive Care Medicine, Lund University, Skåne University Hospital, Malmö, Sweden.

Abstract

BACKGROUND:

Repair of extensive aortic disease may be associated with spinal cord ischaemia (SCI). Here we test if levels of cerebrospinal fluid (CSF) biomarkers for neuronal injury are altered in patients with SCI after advanced endovascular repair in extensive aortic disease.

METHODS:

CSF was sampled for up to 48 h in ten patients undergoing endovascular aortic repair and analyzed for the axonal damage markers total-tau (T-tau) and neurofilament light (NFL).

RESULTS:

Six of ten patients developed SCI (clinically present within 3-6 h). CSF levels of NFL increased up to 37-fold in patients with, but were stable in patients without, SCI. CSF levels of T-tau also increased in patients with SCI, but with some overlap with patients without SCI. Levels of NFL and T-tau did not increase until after the appearance of clinical signs of neurological dysfunction (12-48 h after aortic repair).

CONCLUSIONS:

The CSF biomarkers NFL and T-tau both reflect development of SCI after endovascular aortic repair, but do not rise until after clinical signs of SCI appear. Future studies are desirable to further evaluate potential use of these biomarkers for assessment of the severity of SCI, and also to identify earlier biomarkers of SCI.

KEYWORDS:

Aortic disease; Biomarker; Cerebrospinal fluid; Endovascular; NFL; Tau

PMID:
26682901
DOI:
10.1016/j.neuint.2015.12.003
[Indexed for MEDLINE]

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