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J Neurol Neurosurg Psychiatry 2009;80:1130-1133 doi:10.1136/jnnp.2008.171686
  • Research paper

The longitudinal profile of CSF markers during external lumbar drainage

  1. A Tarnaris1,
  2. A K Toma1,
  3. M D Chapman2,
  4. A Petzold2,
  5. N D Kitchen1,
  6. G Keir2,
  7. L D Watkins1
  1. 1
    Victor Horsley Department of Neurosurgery, National Hospital for Neurology and Neurosurgery, Queen Square, London, UK
  2. 2
    Department of Neuroimmunology, Institute of Neurology, Queen Square, London, UK
  1. Correspondence to Dr A Tarnaris, Department of Neurosurgery, National Hospital for Neurology & Neurosurgery, Box 32, Queen Square, London WC1N 3BG, UK; andrewtarnaris{at}gmail.com
  • Received 31 December 2008
  • Revised 3 May 2009
  • Accepted 27 May 2009
  • Published Online First 16 June 2009

Abstract

Background: External lumbar drainage (ELD) is known as a good predictor of favourable outcome in shunting patients suffering from idiopathic normal pressure hydrocephalus (iNPH).

Methods: Eleven patients suffering from iNPH had a lumbar drain (LD) inserted for 72 h and participated in a research study to quantify any improvement in their clinical symptoms. The lumbar cerebrospinal fluid (CSF) levels of lactate, 8-isoprostane, vascular endothelial growth factor (VEGF), glial fibrillar acidic protein (GFAP), neurofilament (heavy chain) protein (NF (h)), Aβ1–42 (β-amyloid) and total tau were assayed samples from all three time points.

Results: The concentrations of lactate, VEGF, GFAP and tau increased significantly during the 72 h of drainage. There were also increases in 8-isoprostane and Aβ1–42 (non significant). The concentration of NF (h) was reduced significantly following 72 h of drainage. There was a significant positive correlation between Aβ1–42 and total tau in the first sample. GFAP was negatively correlated in a significant fashion with both Aβ1–42 and total tau. NF (h) was negatively correlated with VEGF.

Conclusion: Evidence is provided that ELD is producing measurable changes in the CSF composition of patients with iNPH. The present paper discusses how such changes may be implicated in the pathophysiology of the condition.

Footnotes

  • Funding AT and AKT are supported by a grant from B Braun/Aesculap.

  • Competing interests None.

  • Ethics approval Ethics approval was provided by GOSH, LREC.

  • Patient consent Obtained.

  • Provenance and Peer review Not commissioned; externally peer reviewed.

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