Cerebrospinal Fluid Levels of Vascular Endothelial Growth Factor Correlate With Reported Pain and Are Reduced by Spinal Cord Stimulation in Patients With Failed Back Surgery Syndrome

Kevin F. McCarthy*, Thomas J. Connor, Connail McCrory

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Objectives Spinal cord stimulation (SCS) is an efficacious therapy for chronic neuropathic pain whose precise mechanism of action is unclear. Mediators produced by glial and immune cells are now believed to modulate neuronal transmission and promote chronic neuropathic pain. We postulated a relationship between cerebrospinal fluid (CSF) concentrations of neuroimmune mediators and SCS.

Materials and Methods We measured CSF concentrations of the chemokine, monocyte chemotactic protein-1 (MCP-1), and the growth factors, brain-derived neurotrophic factor (BDNF), and vascular endothelial growth factor (VEGF) and tested for relationships with stimulation parameters and clinical response in nine patients with failed back surgery syndrome (FBSS).

Results Patients with FBSS had higher CSF concentrations of BDNF (p = 0.01) and MCP-1 (p = 0.0001) than matched controls. CSF concentrations of BDNF and VEGF correlated with reported pain (p = 0.04). Five minutes of SCS resulted in a reduction in median VEGF concentrations (p = 0.01).

Conclusions Patients with FBSS have altered CSF levels of BDNF and MCP-1. CSF VEGF correlates with pain and is reduced by SCS. This may offer novel insights into both the mechanism of action of SCS in FBSS and the variation in clinical response that may be encountered.

Original languageEnglish
Pages (from-to)519-522
Number of pages4
JournalNeuromodulation: Technology at the Neural Interface
Volume16
Issue number6
DOIs
Publication statusPublished - Nov 2013

Keywords / Materials (for Non-textual outputs)

  • basic science
  • failed back surgery syndrome
  • mechanisms of action
  • nonrandomized study
  • prospective
  • spinal cord stimulation
  • NEUROPATHIC PAIN
  • RECEPTOR
  • RATS
  • GABA
  • VEGF
  • BDNF
  • INHIBITION
  • MODULATION
  • ACTIVATION
  • EXPRESSION

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