*3.1.1.1 Sodium*

*Neuroprotection - New Approaches and Prospects*

blood flow was disrupted [10, 11].

improve the quality of life of patients.

**3. Neuroprotective therapy after acute SCI**

pharmacological and nonpharmacological treatments.

The Spinal Cord Injury could be divided by its etiology in traumatic and nontraumatic. The traumatic type is caused by physical damage (traffic accident, sportive, and fall), whereas nontraumatic is occasioned by an illness/sickness, such as tumors, infections or degenerative diseases which directly affect the SC [8]. In

Primary injury is caused at the moment of physical damage and leads to irreversible affection on gray matter during the first hour post-lesion. There are three main mechanisms of injury: contusion, when there is not a visible alteration in its morphology, producing a necrotic region at the injury area; laceration or transection, when there is an extreme trauma or penetration, affecting SC conduction of nervous impulses depending on whether the tissue is partial or totally transected; compression from vertebral fractures leading ischemic damage in the area where

After injury, superficial blood vessels undergo to vasospasm which provokes damage in the microvasculature of gray matter [12]. Reduction in the perfusion has two important implications: hypoxia and ischemia; which may involve to neurogenic shock characterized by arterial hypotension, bradycardia, arrhythmia, and intraparenchymal hemorrhage that causes neuronal death by necrosis. Afterwards, primary injury provokes the rupture of blood brain barrier and a cascade of

destructive secondary phenomena leading to a further damage in SC and neurological dysfunction [1, 13]. Therefore, the primary lesion results in the development of a succession of cellular and molecular changes that alter gene expression patterns, which are processes that are already part of the secondary injury [11, 12]. During the acute phase, injury to the blood vessels and severe hemorrhages cause massive influx of inflammatory cells, cytokines, and vasoactive peptides. This phase is almost characterized by ionic deregulation that leads to edema, thus interrupting the conduction of nerve impulses. Following, subacute phase involves a sequence of events like ischemia, vasospasm, thrombosis, inflammatory response, free radicals (FR) production, lipid peroxidation (LPO), and activation of autoimmune responses causing apoptosis. The huge inflammatory responses after the acute and subacute phase, together with the disruption of the blood-brain barrier (BBB), contribute to the progressively swelling of the SC. This generalized edema may increase

To counteract all these acute effects after SCI, neuroprotective strategies have been investigated to rapidly intervene decreasing the neuronal death occurring after damage mechanisms. Many pharmacological and nonpharmacological therapies have been developed, and others are still under investigation, this in order to

As we review previously, SCI leads to motor and sensory dysfunction, first with the primary mechanical injury and then with the complex cascade of secondary damaging events [15]. For several years, basic science, preclinical, and clinical studies are focused in overcoming elements involved in accurate recovery from SCI [1]. An ideal neuroprotective therapy must reduce neurological symptoms including degenerative changes; starting from there, we can discriminate between potential clinical therapies, which could have a better effect [16]. While these therapies are being searched, there are many preclinical and clinical investigations exploring

the mechanical pressure of the SC, aggravating the injury [1, 11, 14].

addition, SCI can be divided into primary and secondary injury [1, 9].

**2. Pathophysiology**

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