The Relationship between Localized Subarachnoid Inflammation and Parenchymal Pathophysiology after Spinal Cord Injury

• DOI: 10.1089/neu.2012.2354
• Publication Date: 2012-06-01T14:50:44Z
• Authors: James W. Austin; Mehdi Afshar; Michael G. Fehlings
• Keywords: Arachnoiditis; Pathophysiology; Parenchyma

Subarachnoid inflammation following spinal cord injury (SCI) can lead to the formation of localized subarachnoid scarring and development post-traumatic syringomyelia (PTS). While PTS is a devastating complication SCI, its relative rarity (occurring symptomatically in about 5% clinical cases), lack fundamental physiological insights, have led us examine an animal model traumatic SCI with induced arachnoiditis. We hypothesized that arachnoiditis associated would potentiate early parenchymal pathophysiology. To test this theory, we examined spatial pathophysiology four groups: (1) sham (non-injured controls), (2) (intrathecal injection kaolin), (3) (35-g clip contusion/compression injury), (4) kaolin+SCI). Overall, there was greater group group. This demonstrated by significant increases cytokine (IL-1α IL-1β) chemokine (MCP-1, GRO/KC, MIP-1α) production, MPO activity, blood-spinal barrier (BSCB) permeability, MMP-9 activity. However, inflammatory mediator production (acute IL-1α IL-1β, subacute chemokines), BSCB fibrous were larger than sum combined, suggesting does indeed Accordingly, these findings suggest exacerbation injury, potentially impacting outcome condition.