Provision of nutrients after acute spinal cord injury: the implications of feast and famine.

Traumatic spinal cord injury (SCI) often leaves patients with devastating neurological deficits. The traumatic event – or primary injury – can be due to mechanisms such as compression, distraction, shear, laceration or (rarely) even transection. Thereafter SCI patients are vulnerable to progressive, delayed damage as a result of secondary insults and secondary injury. Secondary insults such as hypoxia and hypotension occur at the level of the organism from a myriad of causes. Secondary injury occurs at the molecular level and includes processes such as ischemia, excitotoxicity, ionic dysregulation, free radical formation, inflammation, oxidative damage, and activation of necrotic and apoptotic cell death signaling events. Despite the great progress we have made in understanding delayed insults that follow SCI, physicians have little to offer save for supportive care, especially now that methylprednisolone administration has become controversial. This supportive care is largely focused upon optimizing nutrient delivery to the injured spinal cord.