title: Neurological recovery is impaired by concurrent but not by asymptomatic pre-existing spinal cord compression after traumatic spinal cord injury.
abstract: METHODS
  An in vivo animal study to examine the influence of pre-existing or concurrent spinal canal stenosis (SCS) on the functional recovery after spinal cord injury (SCI).
  
  
  OBJECTIVE
  To clarify whether spinal cord compression before or after SCI results in less favorable neurological recovery.
  
  
  BACKGROUND
  The influence of spinal cord compression on the neurological recovery after SCI remains unclear.
  
  
  METHODS
  We created mice with SCS using an extradural spacer before or after producing SCI and statistically analyzed the correlation between the extent of SCS and neurological outcomes. The extent of SCS was calculated by micro-computed tomography, and the spinal cord blood flow (SCBF) was measured serially with laser Doppler flowmetry. Molecular and immunohistochemical examinations were performed to evaluate the neovascularization at the site of cord compression.
  
  
  RESULTS
  Spacer placement (<300 μm) alone in the control mouse resulted in no neurological deficits. Even with spacer placement that caused asymptomatic SCS, the functional recovery after SCI was progressively impaired as spacer sizes increased in the mice with SCS co-occurring with SCI, whereas no significant impact was observed in the mice with pre-existing SCS, irrespective of the spacer sizes. The SCBF progressively decreased immediately after SCS was produced, but it fully recovered at the later time points. Angiogenesis-related genes were upregulated, and neovascular vessels were observed after producing the SCS. We found that concurrent SCS resulted in a significant reduction and impaired the subsequent recovery of the SCBF, whereas pre-existing SCS did not affect the hemodynamics of the spinal cord after SCI.
  
  
  CONCLUSIONS
  The dynamic reduction of the SCBF occurring immediately after spinal cord compression is a significant factor that impairs the neurological recovery after SCI, whereas pre-existing SCS is not always an impediment due to the potentially restructured SCBF.
authors.affiliation: Departments of Orthopaedic Surgery and Advanced Medical Initiatives, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Kensuke
authors.initials: K
authors.lastname: Kubota
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Saiwai
authors.forename: Hiromi
authors.initials: H
authors.lastname: Kumamaru
authors.forename: Kazu
authors.initials: K
authors.lastname: Kobayakawa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Maeda
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Matsumoto
authors.forename: Katsumi
authors.initials: K
authors.lastname: Harimaya
authors.forename: Yukihide
authors.initials: Y
authors.lastname: Iwamoto
authors.forename: Seiji
authors.initials: S
authors.lastname: Okada
mesh_terms: D042702:Angiopoietin-2 / Q000235:genetics; D000818:Animals; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000235:genetics; D015870:Gene Expression; D017078:Laser-Doppler Flowmetry; D051379:Mice; D008810:Mice, Inbred C57BL; D020127:Recovery of Function; D012039:Regional Blood Flow; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013116:Spinal Cord / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology*; D013117:Spinal Cord Compression / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013130:Spinal Stenosis / Q000503:physiopathology; D016212:Transforming Growth Factor beta / Q000235:genetics
chemical_list: D042702:Angiopoietin-2; D016212:Transforming Growth Factor beta; D016222:Fibroblast Growth Factor 2