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Page 4 Fracaro et al. Neuroimmunol Neuroinflammation 2020;7:1-12 I http://dx.doi.org/10.20517/2347-8659.2019.009

sense, repair cells act and try to reverse the damage caused, expressing factors responsible for the formation
[5]
of new vessels, eliminating cell debris, and remodeling damaged neurons .

Treatment of the injury is limited by the low regenerative potential of the central nervous system, but spinal
cord plasticity may support the recovery of some lost mechanisms after the injury. Spinal cord plasticity
[12]
is related to factors such as synaptic reorganization, axonal sprouting, and neurogenesis . There is little
evidence of spontaneous axon regeneration after SCI but there is evidence for axonal sprouting as synaptic
compensation. Regeneration is the growth of new axons, while sprouting involves the growth of collateral
branches of the fibers. Due to the formation of a glial scar, which is a physical and chemical barrier to
axonal regeneration, axonal sprouting is an alternative found because it can occur around a glial scar. To
support SCI repair, studies have shown that functional exercise, neurotrophic factors, and cell therapy can
effectively improve spinal cord neural plasticity response [12,13] .

TREATMENTS
[14]
After SCI, mammals are unable to regenerate nervous tissue, which can lead to lifelong disability .
Some treatments may be used after SCI to try to reduce side effects and protect injured nerve tissue.
Decompression surgery is one of the treatments used to relieve pressure, reducing hypoxia and ischemia
caused by edema and hemorrhage [15,16] . Studies have shown that patients who underwent decompression
surgery before 24 h after SCI showed an improvement compared to patients who underwent surgery more
[17]
than 24 h after SCI [16-18] . Fehlings et al. showed that more than half of the patients who underwent surgery
(before or after 24 h) had at least one grade of improvement on the American Spinal Injury Association
Impairment Scale (AIS) without statistical difference between the groups. However, a higher percentage of
patients had two or three grade improvement on the AIS scale in the group who underwent surgery before
[18]
24 h after 6 months of follow-up. Sewell et al. observed that patients with spinal cord injury (cervical
level) who underwent surgery before and after 24 h showed no neurological improvement on the AIS scale
with significant difference after 6 months of follow-up. However, there is a tendency for improvement in
patients with early surgery, particularly in patients experiencing > 2-grade AIS improvement.

Another commonly used treatment after SCI is the intravenous application of methylprednisolone sodium
succinate (MPSS). The central MPSS effect on SCI is the inhibition of posttraumatic lipid peroxidation
occurring in neurons and blood vessels, directly compromising the function and integrity of neuronal
and axonal membranes, causing microvascular damage and secondary ischemia that indirectly contribute
to secondary neuronal injury. In addition to inhibiting lipid peroxidation, MPSS inhibits post-traumatic
spinal cord ischemia, supports aerobic energy metabolism, and attenuates the neurofilaments loss [19,20] .
However, the use of MPSS is not a consensus among professionals, because, even with improvement when
applied up to eight hours after injury, this drug can cause gastrointestinal bleeding and infection [16,21] . Due
to these associated complications, MPSS should be used with caution.

Neuroprotective agents are also a treatment option for spinal cord injury. These agents aim to prevent
neuronal cell death by reducing side events that result in cell dysfunction and death [16,22] . Many of these
neuroprotective agents have been studied, but without positive results for thoracic spinal cord injury
patients [23,24] . Riluzole, a sodium channel blocker, and hypothermia, which decreases central nervous
system metabolism, have been shown to be effective neuroprotective agents for the treatment of
[28]
spinal cord injury [16,25-27] . Mu et al. associated riluzole and MPSS in rats with spinal cord injury. The
combined treatment preserved the tissue at the epicenter of the lesion but did not have a clear effect on
the myelination index. The results of this study clearly demonstrate the potential beneficial effects of a
combined approach in treating spinal cord injury.