It looks like firm, white fat; nerves extend out from the cord to the muscles, skin and bones, to control movement, receive sensations and regulate bodily excretions and secretions.
What happens within the body when the spinal cord is injured?
When synaptic connections are interrupted. A sequence of 3 stages rapidly ensues:
1. The impact of force that exceeds the backbone's protective design damages nerve cells.
2. Acute: loss of normal blood flow, swelling of tissue, breakdown of cell structure, and loss of myelin sheath. The flow of ionic current is disrupted when the higher concentrated calcium ions on the exterior of the nerve cells break through their respective cell membranes to flood the interior of these neurons.
In the process of regaining a balance of pressures in the ionic concentrations, calcium sets off a series of self-destructive cellular events. Phospholipase enzymes, that digest tissue, are released from the broken cell membrane. This results in the release of free radicals that satisfy the imbalance by attacking nearby "good" cells. This sets off a process called lipid peroxidation.
Since this oxygen breakdown of essential cell lipids will lead to more swelling by water entering tissue from the blood and cerebrospinal fluids, cell breakdown accelerates with the release of toxic substances that affect blood flow.
Glutamate, the main excitatory transmitter, is an amino acid messenger in normal neuronal communication, but in large doses glutamate expresses its toxicity by overloading neuronal circuits.
Other neural substances are released by injury, such as serotonin, catecholamines, and endorphins.
Some studies suggest that astrocytes emit a growth inhibiting effector molecule that prevents regrowth of axons.
What is the immediate axonal reaction to "transection" of the spinal cord?
The very first event after disruption of an axon (whether by spinal cord transection or contusion) is the instantaneous escape of axoplasm from both the proximal and distal ends of the axon. The axons will naturally become swollen, but axoplasmic transport attempts to prepare axons to regenerate. This regeneration is common in the PNS, but not in the CNS.
Other factors influenced by the transection of axons are found in the myelin sheath, supporting glial cells, and in the microvasculature. The interaction of factors affecting axonal regeneration can be observed at the axonal tip.
The axoplasmic leakage creates an almost immediate gap in the axoplasmic column within the otherwise intact myelin sheath tube. Within a few hours of transection the axonal tips of large fibers are set back from the injury site leaving smaller fibers at the cut end.
The leakage of axoplasm stops within a few hours of transection as the axon tip is lined by axolemma within an hour, and layers of collapsed myelin form a septum in front of the axonal tip.
The process of "axonal autotomy" begins approximately one day after transection and continues for about a week. It is a process whereby the tips of axons degenerate by a means of terminal club rupture, and then retrograde as much as 1 cm from the point of original transection.
The terminal club rupture is significant. Among the axoplasmic contents that build up and escape, are lysosomes (which contain more than 50 enzymes, all hydrolytic and with acid pH optima). The escaping lysosomes could be activated and lead to autolysis of the surrounding spinal cord tissue resulting in the destruction of the heretofore smaller intact fibers passing near the ruptured terminal clubs.
After the one week period the final terminal club is formed at a distance of 1 to 2 mm or more from the site of transection and does not rupture again.
As there are antagonistic forces at work between the force of the axonal transport and the encasing myelin barrier, the only mechanism that could result in axonal regeneration seems to be the removal of the myelin encasement without rupture of the terminal club. This is precisely what occurs in the CNS of lower vertebrates that exhibit axonal elongation after transection.
The crucial difference in sheath structure is the presence of the neurilemmal basal lamina in the PNS and its absence in the CNS. In the PNS the basal lamina tube covers the myelin and the node, thus providing a continuous channel for the terminal club to pass through. It may be possible that the expanding force of the terminal club could be converted by the restraint of the basal lamina into a forward movement. Axonal regeneration could then begin.
What are some of the demyelinating agents that could possibly be used to clear the path for axonal regeneration? Possibilities: trypsin.
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