ture oligodendrocytes, already in the spinal cord, migrate short distances to the site of injury, where they can differentiate into mature oligodendrocytes and produce myelin (Gensert and Goldman, 1997). It bears remembering, however, that oligodendrocyte precursor cells can also mature into oligodendrocytes that do the opposite: inhibit axon regrowth through the release of inhibitory substances (see above). What triggers their development into inhibitory cells versus beneficial cells is not yet known.

It is also possible that demyelinated axons within the injured spinal cord may reorganize at the molecular level to acquire the ability to conduct nerve impulses without myelin insulation. This type of recovery is known to occur not only in animal models but also in humans with multiple sclerosis, in whom demyelinated spinal cord axons produce additional sodium channels to support impulse conduction after damage to the myelin (Craner et al., 2004).

Limited regrowth of axons and sprouting of new branches from the tips of existing axons to form new synapses are part of yet another mechanism of functional recovery (Raineteau and Schwab, 2001). The fact that limited regrowth and sprouting do occur reveals that axons possess the capacity for some degree of regrowth, a capacity that can be cultivated with better knowledge of what governs it. Numerous studies with animals have demonstrated the ways in which axonal regrowth from central neurons can be improved, particularly across the area of injury. Research indicates that, after injury, the surviving cells continue to produce certain molecules and release them into the extracellular milieu that bathes the sprouting axons. Some of the molecules are growth factors—members of a family of molecules called neurotrophins (Raineteau and Schwab, 2001). Others are guidance molecules that guide axons to their destination (Walsh and Doherty, 1997; Willson et al., 2002). This area of research is still in its early phases, and much of the information on axonal guidance gained to date involves the developing nervous system. Research is needed to determine if the same or similar mechanisms are involved in axon guidance following injury in the adult CNS.


No daily activity can be taken for granted for someone with a spinal cord injury. A range of functions—getting out of bed, walking, dressing, eating, controlling the bladder and the bowel, and breathing—can be severely compromised, and their loss has a staggering effect. To develop the technological or medical means to restore function and to improve quality of life, it is vital to understand the neurological basis of dysfunction. The emphasis in this section is on the nervous system’s role in generating movements and how injury to the spinal cord results in functional loss.

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