Page 43 - Read Online

Page 338 Crozier-Shaw et al. Neuroimmunol Neuroinflammation 2020;7:335-44 I http://dx.doi.org/10.20517/2347-8659.2019.005

Figure 2. Treatment algorithm for acute traumatic spinal cord Injury. Adapted from Vale et al. [35]

following injury with inflammatory cells becoming absent from CSF then to reflect the end of ongoing
[9]
secondary damage .

Cellular role
Remyelination plays an important role in the recovery of axons after SCI. While pro-inflammatory
cytokines mediate inflammation and cell damage in SCI, there is a parallel action of proliferation-orientated
cells.

Microglia are a key cellular component of the scar that develops after SCI to protect neural tissue. They
are dynamic and proliferate extensively during the first two weeks, accumulating around the lesion. There,
microglia move to the interface between infiltrating leukocytes and astrocytes, where they proliferate and
[14]
form a scar .

Oligodendrocyte precursor cells (OPCs) regulate the inflammatory reaction after SCI. After injury, OPCs
migrate to the injury site and rapidly proliferate. From the day of injury to day 7, the number of OPCs
persistently increases.

Activated astrocytes influence proliferation, differentiation, and maturation of inflammatory reactions after
injury. Astrocytes are also involved in synaptogenesis and control the immune response. It is these factors
[15]
that play a fundamental role in remyelination after acute SCI . After trauma, astrocytes surrounding
the lesion become reactive and become hypertrophic. They migrate centripetally to the epicentre of the
lesion and help with the tissue repair process. These reactive astrocytes do eventually become scar-forming