secreted by astrocytes themselves, and they directly inhibit axon growth (Fawcett and Asher, 1999). The role of astrocytes has perplexed researchers because, in addition to their inhibitory role, they can also play a growth-promoting role under different circumstances (Jones et al., 2003).
Syringomyelia is a complication that arises as early as 2 months or as late as 30 years after the injury. It results from the formation of a cyst in the center of the spinal cord. This cyst expands and elongates over time, significantly damaging the center of the spinal cord. About 4 percent of individuals with spinal cord injuries develop syringomyelia (Schurch et al., 1996; Terre et al., 2000). Individuals with syringomyelia can present with multiple symptoms, including pain, weakness, headaches, and stiffness of the limbs and the back. The pathogenesis of syringomyelia, however, is not well understood. It may even lie dormant for many years before symptoms arise. Detection was especially difficult because of the wide range of other complications and sensory deficits that result from spinal cord injuries; however, the advent of magnetic resonance imaging (MRI) technologies has greatly enhanced the ability of clinicians to detect syringomyelia.
Often overlooked amid the litany of pathological changes that occur after a spinal cord injury is the natural ability of the spinal cord to heal itself. In fact, most individuals with spinal cord injuries, especially those with incomplete injuries, show some degree of functional recovery, and some show substantial degrees of recovery (Tator et al., 1998). Conventional wisdom had been that although some recovery is possible, it is limited in time and extent. A change of thinking has emerged in recent years, however. It is now well accepted that the spinal cord has the capacity to recover in several unforeseen ways starting at about 24 hours after injury and continuing for years. That capacity has become so well recognized that new treatments are being designed to marshal its potential.
Mature nerve cells lack the capacity to divide once they are injured. Whatever recovery of function that occurs naturally after a spinal cord injury is largely the product of plasticity in the surviving neurons. Plasticity is a generic term that denotes the body’s natural capacity to react to changing conditions in numerous ways, from regrowth to gene up-regulation. The surviving neurons can adapt to compensate for injury; however, for many years it was thought that within limits the axons of neurons in mammals do not spontaneously regrow more than a few millimeters (Raineteau and Schwab, 2001). However, groundbreaking discoveries in