3. Therapy after acute SCI

In recent years, neuroprotective or neuroregenerative strategies regarding the injury site have been chosen to mitigate autodestructive events following a SCI. These strategies include: preservation or regeneration of damaged neural tissue, neutralization of toxic mediators, and increasing tissue resistance to toxicity [74].

Although there is a substantial evidence showing new preclinical strategies that aim to promote neuroprotection, achieved with certain efficiency in murine SCI models [75], there are few clinically approved treatments available to patients with SCI. Currently, clinical treatments are limited to surgical decompression, blood pressure control, and the possible use of methylprednisolone (MP), which is not recommended due to its secondary effects [76].

However, for each treatment strategy, it is important to consider the time elapsed between the injury and the initial treatments, in order to promote a beneficial effect by inhibiting or diminishing secondary damage as rapidly as possible. Despite the promising results shown by several treatments, there is currently no therapy that satisfies all the requirements necessary for an optimal recovery [77].
