Biology Reference
In-Depth Information
Seddon's axonotmesis grade into three types, depending on the degree of
connective tissue involvement:
i.
Type 1 injury corresponds to Seddon's neurapraxia with conduction
block and completely intact stroma.
ii.
Type 2 injury corresponds to Seddon's axonotmesis. The end-
oneurium, perineurium, and epineurium are still intact, but the axons
are physiologically disrupted. Recovery can occur by axonal regrowth
along endoneurial tubes, and complete functional recovery can be
expected. The time for recovery depends on the level of injury, usually
months.
iii.
In type 3 injury, the endoneurium is also disrupted, but the surround-
ing perineurium and epineurium are intact. Recovery is incomplete
and depends upon how well the axons can cross the site of the lesion
and find endoneurial tubes.
iv.
In type 4 injury, individual nerve fascicles are transected, and the con-
tinuity of the nerve trunk is maintained only by the surrounding epi-
neurium. This type of injury requires surgical repair or reconstruction
of the nerve.
Type 5 injury is equivalent to Seddon's neurotmesis (complete nerve
disruption), and spontaneous recovery is negligible.
Although Sunderland's classification provides a concise and anatomic
description of nerve injury, the clinical utility of this system is debatable since
a nerve may undergo a combination of different degrees of injury. There-
fore, a sixth degree of nerve injury has been introduced to define a combi-
nation of the other degrees of injuries (
Mackinnon, 1989
).
After a peripheral nerve traumatic injury, complex pathophysiologic
changes, including morphologic and metabolic changes, occur at the injury
site almost immediately. The interruption of a peripheral nerve causes sig-
nificant changes in normal morphology and tissue organization both prox-
imally and distally to the lesion site.
The nerve stump distal to the lesion undergoes a degeneration that is now
known as “Wallerian degeneration” in honor of Augustus Volney Waller,
who first characterized the disintegration of the frog glossopharyngeal and
hypoglossal nerves after axotomy 160 years ago (
Stoll, Jander, & Myers,
2002
). The process involves a number of phases, some concurrent, others
consecutive, in which the distal portions of all affected axons degenerate.
The sequence begins with prompt degradation of axoplasm, axolemma,
and myelin sheath due to proteolysis (
Lubinska, 1982; Schlaepfer, 1977;
Vial, 1958
). Then, the degraded myelin is phagocytized by the recruited
v.
