Volume 14, Issue 3 pp. 248-254

Ventricular cerebrospinal fluid neurofilament protein levels decrease in parallel with white matter pathology after shunt surgery in normal pressure hydrocephalus

M. Tullberg

M. Tullberg

Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden

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K. Blennow

K. Blennow

Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden

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J.-E. Månsson

J.-E. Månsson

Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden

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P. Fredman

P. Fredman

Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden

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M. Tisell

M. Tisell

Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden

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C. Wikkelsö

C. Wikkelsö

Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden

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First published: 23 February 2007
Citations: 58
Dr Mats Tullberg, Institute of Clinical Neuroscience, Sahlgrenska University Hospital, SE 413 45 Göteborg, Sweden (tel.: + 46 31 342 10 00; fax: + 46 31 342 24 67; e-mail: [email protected]).

Abstract

Normal pressure hydrocephalus (NPH) is characterized by disturbed cerebrospinal fluid (CSF) dynamics and white matter lesions (WML). Although the morphology of these lesions is described, little is known about the biochemistry. Our aim was to explore the relationship between ventricular CSF markers, periventricular WML and postoperative clinical outcome in patients with NPH. We analysed lumbar and ventricular concentrations of 10 CSF markers, 12 clinical symptoms and signs, magnetic resonance imaging (MRI) periventricular white matter hyperintensities (PVH) and ventricular size before and 3 months after shunt surgery in 35 patients with NPH. Higher ventricular CSF neurofilament protein (NFL), an axonal marker, correlated with more extensive PVH. A larger postoperative reduction in NFL correlated with larger reduction in PVH and a more pronounced overall improvement. Albumin ratio, HMPG, NPY, VIP and GD3 increased postoperatively whereas NFL, tau and HVA decreased. Variations in ventricular size were not associated with CSF concentrations of any marker. We conclude that NPH is characterized by an ongoing periventricular neuronal dysfunction seen on MRI as PVH. Clinical improvement after shunt surgery is associated with CSF changes indicating a restitution of axonal function. Other biochemical effects of shunting may include increased monoaminergic and peptidergic neurotransmission, breakdown of blood brain barrier function, and gliosis.

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