The Body's Secondary Response to Spinal Cord Injuries
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Secondary injury: Secondary injury is the injury to the spinal cord and related structures following the primary injury. Although it continues for hours after the initial damage, it can be advantageous by providing time periods in which treatment can reduce the extent of overall damage and disability (21). It begins when immune cells enter the damaged area. The first cells to respond to the injury are neutrophils, which enter the central nervous system about twelve hours after injury and remain for about a day. Following the neutrophils and around three days after injury, T cells enter the central nervous system. They help to monitor immune response and kill infected cells. Two of the most important types of immune cells appear to be macrophages and monocytes, which rid the area of cellular debris. They also release regulatory substances which may either aid or interfere with recovery (13, 19, 21). The secondary injury process is composed of many theories of explanation:

1. Ischemia theory- ischemia following an injury to the spinal cord develops from the damage and rupture of the microcirculation of the compressed neural tissue (13). Ischemia leads to an increase in lactate concentration and a decrease in the amount of oxygen, ATP, and pyruvate (21). Dysfunction of the autonomic nervous system, hypotension, bradycardia, and reliance on systemic circulation further impair the spinal cord, thus leading to ischemia (10, 21).

2. Calcium theory- arises from the fact that following spinal cord injury there is a decrease in the amount of extracellular calcium but a large increase in the amount of intracellular calcium. The changes in calcium concentrations lead to disruption of the neuronal cytoskeleton, enzyme function, and intracellular transport (13). Calcium ions stimulate phospholipases, phosphatases, and proteases, which disrupt cell membranes and interfere with mitochondrial functioning causing the activation of free-radicals (13) which can rupture cell membranes resulting in the death of previously undamaged cells (20). It has been theorized that glutamate, an amino acid that has been identified as the substance causing apoptosis , causes the influx of calcium ions following injury (13) Glutamate also allows ions such as sodium and chloride to enter cells which then causes water to enter the cells, thus leading to swelling (21).

3. Free-radical theory- proposes that oxygen free radicals aggregate in the injured spinal tissue as a result of depletions in antioxidants (10). Free radicals are a product of normal metabolism. Following injury, the restoration of normal blood flow rate to the brain and spinal cord, which have a high metabolism, may increase the number of free radicals produced. Inflammation may also contribute to the increased number of free radicals (13,20). The free radicals break down proteins, lipids, and nucleic acids leading to the formation of lipid peroxides and the destruction of cell membranes (10, 13).

4. Inflammatory theory- is based on the fact that inflammatory substances including prostaglandins, leukotrienes, platelet-activating factors, and serotonin concentrate at the injury site and damage neural structures (13). Several weeks after the injury, microphages from the immune system, and microglia from the central nervous system have cleared away the debris and damaged tissues from the injury site. At this area a syrinx, a fluid filled cavity called, forms and impedes the two sides of the injury from reconnecting. A glial scar also forms at the site of injury and surrounds the syrinx (2). It is composed of astrocytes that have undergone both a morphological and biological transformation; the morphological transformation prevents the physical regrowth of axons and other nervous tissue, and the biological changes create an environment that prevents regeneration (15).

Quick Facts
Cells of the Spinal Cord
Impulse Transmission

Anatomy of the Spinal Cord

Physiology of the Spinal Cord

Spinal Cord Injuries (Overview)

Types of Spinal Cord Injuries

The Body's Primary Response to a SCI

The Body's Secondary Response to a SCI

Effects of SCIs

Initial Treatment of SCIs
Recent Advances in SCI Research

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References

 

 
   

Picture provided by The National Institutes of Health

Picture provided by The National Institutes of Health

    This MRI of the cervical spine of a paraplegic patient shows the syrinx (dark area) that has formed at the injury site. The continuity of the white matter shows that the spinal cord was crushed, not severed. This micrograph shows the syrinx (dark cavern) in the spinal cord of an adult rat. A few weeks after injury the syrinx forms and replaces the damaged tissues. It is surrounded by the glial scar, and together they prevent the axons from regenerating. Here the glial scar and syrinx prevent the corticospinal cord (descending group of white fibers), which normally controls voluntary movement, from regenerating.