title: Dural repair reduces connective tissue scar invasion and cystic cavity formation after acute spinal cord laceration injury in adult rats.
abstract: This study examined whether duraplasty after acute cervical laceration spinal cord injury (SCI) in a rat model could (1) improve cerebrospinal fluid (CSF) circulation adjacent to the injury; (2) minimize connective tissue scarring; and (3) reduce post-traumatic inflammation and cystic cavitation. Following a transverse dural/arachnoid incision and C5-6 dorsal spinal hemisection, a 5-mm2 cadaveric dura mater allograft was placed over the lesion and fixed with fibrin glue (n=12). Control animals received an identical dural/arachnoid incision and cervical dorsal hemisection without dural repair (n=12). At 1, 5, and 10 weeks post-injury, plain film myelograms were obtained to characterize CSF circulation, and stereological methods were used to compare the extent of tissue sparing between the two groups. Immunohistochemical studies were performed to assess the degree of inflammation (ED-1), connective tissue scarring (laminin and type IV collagen), and reactive astrogliosis (GFAP). Our results indicate that dural allograft can improve CSF flow adjacent to the site of injury, which may be due to reduced meningeal fibrosis/scarring at the lesion site. Stereological analysis demonstrated that duraplasty resulted in a significant reduction in lesion volume at each time-point (p<0.01) associated with a nearly complete attenuation of post-traumatic cystic cavitation (p<0.001). Immunofluorescence studies demonstrated that duraplasty reduced the infiltration of ED-1-positive macrophages/microglia into and surrounding the lesion site, which may be responsible for the marked reduction in secondary injury following duraplasty. We conclude that duraplasty following acute spinal cord laceration may (1) improve CSF flow by limiting meningeal fibrosis; (2) reduce connective tissue scar formation; and (3) attenuate macrophage accumulation and progressive secondary injury.
authors.affiliation: Kentucky Spinal Cord Injury Research Center, Department of Neurological Surgery, University of Louisville School of Medicine Louisville, Kentucky 40292, USA.
authors.forename: Christopher
authors.initials: C
authors.lastname: Iannotti
authors.forename: Y Ping
authors.initials: YP
authors.lastname: Zhang
authors.forename: Lisa B E
authors.initials: LB
authors.lastname: Shields
authors.forename: Yingchun
authors.initials: Y
authors.lastname: Han
authors.forename: Darlene A
authors.initials: DA
authors.lastname: Burke
authors.forename: Xiao-Ming
authors.initials: XM
authors.lastname: Xu
authors.forename: Christopher B
authors.initials: CB
authors.lastname: Shields
mesh_terms: D000208:Acute Disease; D000818:Animals; D003238:Connective Tissue / Q000473:pathology*; D003560:Cysts / Q000473:pathology*; D004388:Dura Mater / Q000637:transplantation*; D005109:Extracellular Matrix / Q000473:pathology; D005260:Female; D005455:Fluorescent Antibody Technique; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000473:pathology; D007150:Immunohistochemistry; D007797:Laminin / Q000378:metabolism; D008264:Macrophages / Q000502:physiology; D019635:Neurosurgical Procedures; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000134:cerebrospinal fluid / Q000473:pathology* / Q000601:surgery*
chemical_list: D005904:Glial Fibrillary Acidic Protein; D007797:Laminin