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Restoring
motor
function following spinal cord injury The
failure of adult
spinal cord axons to regenerate through the lesion site is likely
caused by
multiple factors, such as the inability of the differentiated adult
neurons and
their axons to regrow along the correct pathway, the environment around
the
lesion site lacking the necessary growth facilitating signals, and the
inhibitory nature of the glial scar (Caroni, 1988; Bovolenta, 1992;
Behar,
2000, Zheng, 2003, Chen, 2000). To encourage axon regeneration
following SCI,
the hostile environment around the site of the injury needs to be
converted to
a permissive one that will enable lesioned axons to regenerate across
the
lesion site. Additionally, once the axons extend through the glial scar
and
into the adjacent tissue, they then need to reach appropriate targets
that can
restore function. Consequently, we seek to use cellular and
pharmacological techniques to encourage spinal cord regrowth or repair
following injury.
Of the technological solutions,
functional electrical stimulation promises to be an effective
technique
to restore function. In the case of
locomotion, FES systems seek to replace or augment the injured spinal
cord’s
pattern-generating capacity with an artificial signal generator. The
form of
this signal generator varies (Abbas and Chizeck, 1995; Davoodi and
Andrews,
2004; Riener et al., 2000), but considering the complexity of the
musculoskeletal system future generations of controllers are likely to
require
a model of the segment of the musculoskeletal system they are designed
to
control. |