title: Destructive pathological changes in the rat spinal cord due to chronic mechanical compression. Laboratory investigation.
abstract: OBJECTIVE
  Chronic mechanical compression of the spinal cord, which is commonly caused by degeneration of the spine, impairs motor and sensory functions insidiously and progressively. Yet the exact mechanisms of chronic spinal cord compression (SCC) remain to be elucidated. To study the pathophysiology of this condition, the authors developed a simple animal experimental model that reproduced the clinical course of mechanical compression of the spinal cord.
  
  
  METHODS
  A custom-designed compression device was implanted on the exposed spinal cord of female Wistar rats between the T-7 and T-9 vertebrae. A root canal screw attached to a plastic plate was tightened 1 complete turn (1 pitch) every 7 days for 6 weeks. The placement of the compression device and the degree of compression were validated every week using radiography. Furthermore, a motor sensory deficit index was also calculated every week. After 3, 6, 9, or 12 weeks, the compressed T7-9 spinal cords were harvested and examined histologically.
  
  
  RESULTS
  Lateral projection of the thoracic spine showed a progressively increasing rate of mean spinal cord narrowing in the compression group. Motor and sensory deficiencies were observed from Week 3 onward; paralysis was observed in 2 rats at Week 12. Motor deficiency appeared earlier than sensory deficiency. Obvious pathological changes were observed starting at Week 6. The number of neurons in the gray matter of rats with chronic compression of the spinal cord decreased progressively in the 6- and 9-week compression groups. In the white matter, myelin destruction and loss of axons and glia were noted. The number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive neurons increased in the ventral-to-dorsal direction. The number of TUNEL-positive cells increased from Week 6 onward and peaked at Week 9.
  
  
  CONCLUSIONS
  This practical model accurately reproduces characteristic features of clinical chronic SCC, including progressive motor and sensory disturbances after a latency and insidious neuronal loss.
authors.affiliation: 1 Shandong University, Jinan, Shandong Province, People's Republic of China.
authors.forename: Peng
authors.initials: P
authors.lastname: Xu
authors.forename: Wei-Ming
authors.initials: WM
authors.lastname: Gong
authors.forename: Yao
authors.initials: Y
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Zhang
authors.forename: Kai
authors.initials: K
authors.lastname: Zhang
authors.forename: De-Zhen
authors.initials: DZ
authors.lastname: Yin
authors.forename: Tang-Hong
authors.initials: TH
authors.lastname: Jia
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology; D005260:Female; D007796:Laminectomy; D009186:Myelin Sheath / Q000473:pathology; D019636:Neurodegenerative Diseases / Q000209:etiology* / Q000473:pathology* / Q000601:surgery; D051381:Rats; D017208:Rats, Wistar; D013117:Spinal Cord Compression / Q000150:complications* / Q000601:surgery; D013119:Spinal Cord Injuries / Q000209:etiology* / Q000473:pathology* / Q000601:surgery; D013314:Stress, Mechanical