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Pathology
After nerve damage, the pathologic changes depend on the nature of the injury, which
also affects the regenerative response and the prognosis for recovery.
According to Seddon (1954), mechanical nerve injuries are classified as follows: (1)
complete severing of a nerve ( neurotmesis), (2) axonal interruption with distal
degeneration but an intact endoneurium ( axonotmesis), or (3) conduction block at the
site of the lesion but normal distal conduction without degeneration of distal
fibers (neurapraxia).
Within the first 24 hours of injury, focal swelling occurs adjacent to the damaged site
with fragmentation of endoplasmic reticulum, neurotubules, and neurofilaments,
and accumulation of organelles. The axolemma becomes discontinuous; axons swell at
some sites and narrow at others to give a beaded appearance. This process
begins between the nodes of Ranvier and appears first in smaller fibers. Changes in
myelin sheaths lag behind those in axons but progress in a similar way along the
entire distal stump, again affecting small fibers first. The myelin surrounding the
fragmented axons breaks up to form rows of elliptoids. Finally, Schwann cells and
macrophages degrade the axon and myelin debris. In addition to these distal nerve
changes, a retrograde axon reaction or chromatolysis is seen, with retraction of
axons proximal to the lesion and alterations in the somata of neurons, such as cell body
swelling, disruption of Nissl substance, migration of the cell nucleus, and
increase in the size of the nucleolus. Presynaptic terminals gradually withdraw from the
soma and dendrites; synaptic transmission is reduced until dorsal root
stimulation fails to excite the motor neuron and evoke a reflex discharge in the ventral
root. The pathologic distal changes of degeneration and retrograde axon
reaction are similar in crush injury or complete nerve transection.
If a nerve has been completely severed, the orderly process just described is interfered
with in proportion to the length of the discontinuity between proximal and distal
ends. If this distance is great, regeneration is not possible, unless the ends are apposed
at operation. If the distance is small, the fine processes of the axon penetrate
the fibrin and connective tissue in the scar and enter the distal end of the nerve. Some
of these may be deflected from the proper path by the scar and become
entangled to form a neuroma.
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