There are two acute phases of SCI, namely primary (at the moment of injury and immediately thereafter) and secondary (i.e. minutes to weeks or months post injury). The initial mechanical insult to the spinal cord is considered to be the primary injury; currently, damage incurred from this trauma cannot be reversed with pharmaceuticals. The primary injury is the strongest predictor of overall prognosis (Oyinbo, 2011). Within minutes after the initial insult, physiological and molecular changes occur that amplify the injury and enlarge the lesion site; these subsequent reactions are referred to as secondary injuries.
The primary injury is manifested by neuron death at the impact site and hemorrhaging. Secondary injuries also include continued neuron death and hemorrhaging, but also extend to encompass edema and inflammation, vascular alterations (e.g., neurogenic shock, ischemia), and biochemical reactions (e.g., production of toxic reactive oxygen species and neurotransmitters). The majority of the secondary injury is determined within days to a week and is the time frame during which neuroprotective strategies should be initiated. Secondary injuries continue to mount for weeks to months after injury (Fleming et al. 2006) and can substantially worsen the injury sustained from the initial trauma.
Traditionally, the medical care of those impacted by SCI focused on keeping the patient alive and later addressing complications (e.g., spasticity, pain, bladder dysfunction) that arose from the initial injury. Recently, efforts have been placed on protecting neurons from additional damage caused by secondary injuries (Sadowsky et al. 2002), and also on comprehensive and intensive rehabilitation. This concept of ‘neuroprotection’ has initiated medical research to develop pharmaceuticals that target the imminent vascular and biochemical reactions that occur after SCI.