Neurofilament levels prognostic of outcome after cardiac arrest


REPORT FROM THE AMERICAN ACADEMY OF NEUROLOGY (AAN) ANNUAL MEETING, PHILADELPHIA PA, APRIL 26-MAY 3, 2014 – There is an increasing body of evidence suggesting that neurofilament (NFL) protein is a useful biomarker of axonal injury. The latest study examined the prognostic value of NFL in survivors of cardiac arrest (Rosen et al. AAN 2014; abstract P1.101).

Levels of NFL, tau, hyperphosphorylated tau and YKL-40 (Chitinase-3-like protein 1; a marker of inflammation and tissue remodelling) in CSF were measured in 21 patients about 14 days after cardiac arrest and compared to 21 age-matched healthy controls. Results were followed up at one year.

CSF levels of NFL, total tau and YKL-40 were elevated in patients after cardiac arrest compared to controls. Moreover, levels of NFL and total tau were significantly higher in patients with a poorer outcome at one year, as assessed by the Glasgow Outcome Scale and the MMSE. Thus, significant elevations in NFL appear to indicate more extensive neurological damage and NFL assessment could be a useful prognostic measure, in conjunction with clinical and radiological evaluations, in patients following cardiac arrest.

A number of studies have reported that neurofilament levels in blood or CSF are a good indicator of the extent of axonal damage in the setting of acute ischemic or hemorrhagic stroke (Cai et al. Clin Chim Acta 2013;424:182-186; Sellner et al. Neurochem Res 2011;36:2287-2291; Singh et al. J Neurol Sci 2011;304:117-121; Nylen et al. Neurosci Lett 2006;404:132-136).

It has also been suggested that NFL in CSF or serum is a potentially useful biomarker of axonal damage in a variety of neurodegenerative conditions such as Parkinson’s disease and multiple sclerosis (Su et al. Clin Neurol Neurosurg 2012;114:372-375; Gresle et al. J Neurol Neurosurg Psychiatry 2014; epub. March 17, 2014). In MS, NFL levels appear to be normal in relapsing-remitting MS patients without gadolinium-enhancing lesions, but become elevated in the weeks following a relapse, and are generally higher in patients with primary- and secondary-progressive MS (Burman et al. Acta Neurol Scand 2014; epub. February 24, 2014; Ehling et al. Mult Scler 2004;10:601-606).

Guest Reviewer: Dr. Daniel Selchen, Head of Neurology, St. Michael’s Hospital, Toronto, Canada

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