title: Histological effects of residual compression sustained for 60 minutes at different depths in a novel rat spinal cord injury contusion model.
abstract: Spinal cord injuries are frequently accompanied by persisting residual compression of the spinal cord; however, it remains controversial as to what effect the sustained compression has on neurological damage. The objective of this study was to determine the influence of post-traumatic residual spinal cord compression on the extent and progression of tissue damage within a dynamic thoracic contusion rat model. Twenty-nine male Wistar rats were distributed into one of four groups: spinal cord contusion only, contusion with 40% residual compression, contusion with 90% residual compression, and a surgical control group. A moderate injury was performed (1 mm, 700 mm/sec) with our custom University of British Columbia (UBC) multimechanism apparatus, and the residual compression groups had the impactor tip maintained at 40% or 90% of the initial impact depth (1.0 mm) for 60 min post-injury. All animals were killed at 3 h post-injury, when the spinal cord was harvested and stained for hemorrhage, neuronal damage in the gray matter, and axonal disruption in the white matter. The initial contusion injury immediately damaged tissue beneath the impactor as evidenced by rapid relaxation of the reaction force on the spinal cord during the subsequent compression. Importantly, the rostral-caudal extent of intramedullary hemorrhage was 66% larger after 90% residual spinal cord compression compared to the 40% group (p=0.016). Similarly, the extent of neuronal nuclei lost in different gray matter regions was 60-86% greater after 90% residual compression compared with 40% (p<0.001). Thus, a high level of residual compression of the spinal cord following a moderate contusion injury has the potential to adversely increase the extent of tissue damage, whereas a lower level of residual compression may have little to no effect.
authors.affiliation: Orthopaedic and Injury Biomechanics Group, Departments of Orthopaedics and Mechanical Engineering, University of Pennsylvania , Philadelphia, Pennsylvania, USA.
authors.forename: Simon G
authors.initials: SG
authors.lastname: Sjovold
authors.forename: Stephen F E
authors.initials: SF
authors.lastname: Mattucci
authors.forename: Anthony M
authors.initials: AM
authors.lastname: Choo
authors.forename: Jie
authors.initials: J
authors.lastname: Liu
authors.forename: Marcel F
authors.initials: MF
authors.lastname: Dvorak
authors.forename: Brian K
authors.initials: BK
authors.lastname: Kwon
authors.forename: Wolfram
authors.initials: W
authors.lastname: Tetzlaff
authors.forename: Thomas R
authors.initials: TR
authors.lastname: Oxland
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013117:Spinal Cord Compression / Q000209:etiology* / Q000473:pathology*; D013119:Spinal Cord Injuries / Q000150:complications* / Q000473:pathology*; D013997:Time Factors