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NEUROLOGY 2006;67:1071-1073
© 2006 American Academy of Neurology
Brief Communications

CSF neurofilament levels: A potential prognostic marker in Guillain–Barré syndrome

A. Petzold, MD, PhD, N. Hinds, MRCP, NM F. Murray, FRCP, N. P. Hirsch, FRCP, D. Grant, MA, G. Keir, FRCPath, E. J. Thompson, DSc and M. M. Reilly, FRCP

From the Department of Neuroimmunology, Institute of Neurology and Tavistock Intensive Care Unit (A.P.), Department of Neurology and Clinical Neurophysiology (N.M.F.M.), Centre for Neuromuscular Disease and Department of Molecular Neuroscience (M.M.R.), Batten Harris Intensive Care Unit (N.P.H.), National Hospital for Neurology and Neurosurgery, London; Department of Neurophysiology (N.H.), Walton Centre, Liverpool; and Department of Neuroimmunology (D.G., G.K., E.J.T.), Institute of Neurology, London, UK.

Address correspondence and reprint requests to Dr. Axel Petzold, Institute of Neurology, Queen Square, London, UK WC1N 3BG; e-mail: a.petzold{at}ion.ucl.ac.uk.

Long-term morbidity from Guillain–Barré syndrome (GBS) is caused by axonal damage. This prospective study demonstrated that neurofilaments (NfHs), a biomarker for axonal damage, were of prognostic value in GBS. CSF NfH levels correlated with the F score and Medical Research Council summed score and were higher in patients with neurophysiologic evidence of axonal degeneration compared to those without. Pathologically high CSF NfH levels (>0.73 ng/mL) predicted worse motor and functional outcome.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the September 26 issue to find the title link for this article.

This study was presented in part at the 10th International Congress on Neuromuscular Diseases, Vancouver, British Columbia, Canada, July 7–12, 2002; the joint meeting of the American Association of Electrodiagnostic Medicine and the International Federation of Clinical Neurophysiology, San Francisco, September 16–20, 2003; the British Society of Clinical Neurophysiology, London, October 10, 2003; and the 7th Annual Meeting of the Peripheral Nerve Society, Pisa, Italy, July 9–13, 2005.

Disclosure: The authors report no conflicts of interest.

Received November 30, 2005. Accepted in final form May 11, 2006.






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