Abstract 10- 1415-1430
Category: Basic Science

At the end of the session,
participants will be able to:

  1. Mechanisms of astrogliosis involved in the CNS reaction to the neurotrauma in the model of the SCI.
  2. Novel interpretation of the role of astrogliosis in histologic analysis of neurotrauma including the SCI.



Dr. Jacek M. Kwiecien

Education: DVM: University of Agriculture, Lublin, Poland, 1983; MSc, PhD: University of Guelph, 1991, 1995; fellow NMSS, Univ. of Wisconsin-Madison, 1994-1996; Habilitated Doctorate, Medical University of Lublin, Poland, 2018. Research: pathogenesis of neurotrauma, neuroprotective treatments, neuroregenerative treatments.


Jacek M. Kwiecien.

Department of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada.

Target Audience:
Pathologists, Residents, Medical Students

Medical Expert (the integrating role),  Leader, Scholar

Hail to astrogliosis! The unsung hero of the CNS tissue reaction to the spinal cord injury


Spinal trauma results in a localized spinal cord injury (SCI) with an area of hemorrhage and necrosis surrounded by edema in Acute Phase that lasts 2 days followed by an Inflammatory Phase beginning on day 3 with infiltration of necrosis by inflammatory CD68+/CD163- macrophages whose numbers rapidly increase and persist at high levels for 4 weeks and then decline but are still present in low numbers at 16 weeks. This destructive inflammation is fuelled by myelin-rich necrotic debris and the macrophage activation causes ongoing damage to the surrounding spinal cord and further damaged myelin to sustain a mechanism of vicious cycle. The severity of post-SCI inflammation becomes inhibited and eliminated by a spinal cord tissue response in the 3rd Phase, Resolution. Astrogliosis is a hallmark of reaction to SCI. In the 1st week astrocytes surrounding the lesion hypertrophy and define a cavity of injury (COI) containing macrophage-rich inflammation and accumulation of water. Progression of severity of astrogliosis around the COI coincides with the reduction of numbers of macrophages and leads to formation of quiescent syrinx. While the inflammation in the COI leads to damage of blood vessel in the surrounding spinal cord resulting in vasogenic edema beyond 16 weeks post-SCI, astrocytes equipped with aquaporin-4 pass excess edema water to 4 extra-spinal spaces; (1) the sub-arachnoid, (2) the central canal, (3) the blood vessels, and (4) the COI, a novel mechanism. Astrogliosis is a beneficial element in neuroplasticity following the SCI and should not be inhibited in anti-inflammatory treatments effecting neuroprotection.