title: Intrathecal decompression versus epidural decompression in the treatment of severe spinal cord injury in rat model: a randomized, controlled preclinical research.
abstract: BACKGROUND
  In the setting of severe spinal cord injury (SCI), there is no markedly efficacious clinical therapeutic regimen to improve neurological function. After epidural decompression, as is shown in animal models, the swollen cord against non-elastic dura and elevation of intrathecal pressure may be the main causes of aggravated neurologic function. We performed an intrathecal decompression by longitudinal durotomy to evaluate the neuroprotective effect after severe SCI by comparing with epidural decompression.
  
  
  METHODS
  Eighty-four adult male Sprague-Dawley rats were assigned to three groups: sham group (group S), epidural decompression (group C), and intrathecal decompression group (group D). A weight-drop model was performed at T9. The Basso-Beattie-Bresnahan (BBB) score was used to evaluate neurological function. Animals were sacrificed at corresponding time points, and we performed pathohistological examinations including HE staining and immunohistochemical staining (IHC) of glial fibrillary acidic protein (GFAP), neurocan, and ED1 at the epicenter of injured cords. Finally, the lesions were quantitatively analyzed by SPSS 22.0.
  
  
  RESULTS
  The mortality rates were, respectively, 5.55 % (2/36) and 13.9 % (5/36) in groups C and D, and there was no significant difference between groups C and D (P = 0.214). Compared with epidural decompression, intrathecal decompression could obviously improve BBB scores after SCI. HE staining indicated that more white matter was spared, and fewer vacuoles and less axon degradation were observed. The expression peak of GFAP, neurocan, and ED1 occurred at an earlier time and was down-regulated in group D compared to group C.
  
  
  CONCLUSIONS
  Our findings based on rat SCI model suggest that intrathecal decompression by longitudinal durotomy can prompt recovery of neurological function, and this neuroprotective mechanism may be related to the down-regulation of GFAP, neurocan, and ED1.
authors.affiliation: No.1 Department of Orthopedic Surgery, Tianjin Baodi Hospital, No.8, Guangchuan Road, Baodi District, Tianjin, 301800, China. zhajian@umich.edu.
authors.forename: Jian
authors.initials: J
authors.lastname: Zhang
authors.affiliation: No.1 Department of Orthopedic Surgery, Tianjin Baodi Hospital, No.8, Guangchuan Road, Baodi District, Tianjin, 301800, China.
authors.forename: Huili
authors.initials: H
authors.lastname: Wang
authors.affiliation: Institute of Radiation and Radiation Medicine, Academy of Military Medical Sciences, No.27, Taiping Road, Haidian District, Beijing, 100850, China.
authors.forename: Chenggang
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Institute of Radiation and Radiation Medicine, Academy of Military Medical Sciences, No.27, Taiping Road, Haidian District, Beijing, 100850, China.
authors.forename: Weiguang
authors.initials: W
authors.lastname: Li
mesh_terms: D000818:Animals; D019299:Decompression, Surgical / Q000379:methods*; D004195:Disease Models, Animal; D004388:Dura Mater / Q000601:surgery; D053331:Ectodysplasins / Q000378:metabolism; D004824:Epidural Space; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D008297:Male; D009043:Motor Activity; D058580:Neurocan / Q000378:metabolism; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D013119:Spinal Cord Injuries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000601:surgery*; D016019:Survival Analysis
chemical_list: D053331:Ectodysplasins; D005904:Glial Fibrillary Acidic Protein; D058580:Neurocan
keywords: Animal model; Basso-Beattie-Bresnahan score; Decompression; Pathophysiology; Spinal cord injury