Peripheral Nerve Injury Classification

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Peripheral nerve injury classification

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Classification of peripheral nerve injury assists in prognosis and determination of treatment strategy.
Classification of nerve injury was described by Seddon in 1943 and by Sunderland in 1951. The [1]
lowest degree of nerve injury in which the nerve remains intact but signaling ability is damaged is
called neurapraxia. The second degree in which the axon is damaged but the surrounding
connecting tissue remains intact is called axonotmesis. The last degree in which both the axon and
connective tissue are damaged is called neurotmesis.
Contents
 1Seddon's classification
o 1.1Neurapraxia (Class I)
o 1.2Axonotmesis (Class II)
o 1.3Neurotmesis (Class III)
 2Sunderland's classification
 3See also
 4References
Seddon's classification[edit]
In 1943, Seddon described three basic types of peripheral nerve injury that include:
[2]
Neurapraxia (Class I)[edit]

Main article: Neurapraxia
It is a temporary interruption of conduction without loss of axonal continuity. In neurapraxia, there is
[3]
a physiologic block of nerve conduction in the affected axons.

Other characteristics:
 It is the mildest type of peripheral nerve injury.

 There are sensory-motor problems distal to the site of injury.
 The endoneurium, perineurium, and the epineurium are intact.
 There is no wallerian degeneration.
 Conduction is intact in the distal segment and proximal segment, but no conduction occurs
across the area of injury. [4]
 Recovery of nerve conduction deficit is full, and requires days to weeks.

 EMG shows lack of fibrillation potentials (FP) and positive sharp waves.
Axonotmesis (Class II)[edit]
Main article: Axonotmesis
It involves loss of the relative continuity of the axon and its covering of myelin, but preservation of
the connective tissue framework of the nerve ( the encapsulating tissue, the epineurium and
perineurium, are preserved ). [5]
 Wallerian degeneration occurs distal to the site of injury.

 There are sensory and motor deficits distal to the site of lesion.
 There is no nerve conduction distal to the site of injury (3 to 4 days after injury).
 EMG shows fibrillation potentials (FP), and positive sharp waves (2 to 3 weeks postinjury).
 Axonal regeneration occurs and recovery is possible without surgical treatment.Sometimes
surgical intervention because of scar tissue formation is required.
Neurotmesis (Class III)[edit]
Main article: Neurotmesis
It is a total severance or disruption of the entire nerve fiber. A peripheral nerve fiber contains an
[6]
axon (Or long dendrite), myelin sheath (if existence), their schwann cells, and the endoneurium.
Neurotmesis may be partial or complete.
 Wallerian degeneration occurs distal to the site of injury.

 There is connective tissue lesion that may be partial or complete.
 Sensory-motor problems and autonomic function defect are severe.
 There is no nerve conduction distal to the site of injury (3 to 4 days after lesion).
 EMG and NCV findings are as axonotmesis.
 Because of lack of nerve, surgical intervention is necessary.
Sunderland's classification[edit]
In 1951, Sunderland expanded Seddon's classification to five degrees of peripheral nerve injury:
First-degree (Class I)
Seddon's neurapraxia and first-degree are the same.
Second-degree (Class II)
Seddon's axonotmesis and second-degree are the same.
Third-degree (Class III)
Third-degree is included within Seddon's Neurotmesis.
Sunderland's third-degree is a nerve fiber interruption. In third-degree injury, there is a
lesion of the endoneurium, but the epineurium and perineurium remain intact. Recovery
from a third-degree injury is possible, but surgical intervention may be required.
Fourth-degree (Class III)
Fourth-degree is included within Seddon's Neurotmesis.
In fourth-degree injury, only the epineurium remain intact. In this case, surgical
repair is required.
Fifth-degree (Class III)
Fifth-degree is included within Seddon's Neurotmesis.
Fifth-degree lesion is a complete transection of the nerve. Recovery is not
possible without an appropriate surgical treatment.
See also[edit]
 Nerve
 Nerve fiber
 Peripheral nerve injury (Nerve injury)
 Connective tissue in the peripheral nervous system
 Neuroregeneration
 Wallerian degeneration
References[edit]
1. ^ "Peripheral Nerve Injuries".
2. ^ "Seddon classification of nerve injuries".
3. ^ Otto D.Payton & Richard P.Di Fabio et al.Manual of physical therapy. Churchill Livingstone Inc. ISBN 0-443-08499-8
4. ^ "ELECTRODIAGNOSTIC STUDIES OF THE HAND".
5. ^ "Classification of Nerve Injuries". Archived from the original on 2009-09-25.
6. ^ Otto D.Payton & Richard P.Di Fabio et al.Manual of physical therapy. Churchill Livingstone Inc. Page:24. ISBN 0-443-08499-8
Wallerian degeneration
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Nerve injury
Fluorescent micrographs (100x) of Wallerian degeneration in cut and crushed peripheral nerves. Left column is proximal to the
injury, right is distal. A and B: 37 hours post cut. C and D: 40 hours post crush. E and F: 42 hours post cut. G and H: 44 hours
post crush.
Wallerian degeneration is an active process of degeneration that results when a nerve fiber is cut
or crushed and the part of the axondistal to the injury (i.e. farther from the neuron's cell body)
degenerates. A related process of dying back or retrograde degeneration known as 'Wallerian-like
[1]
degeneration' occurs in many neurodegenerative diseases, especially those where axonal

transport is impaired. Primary culture studies suggest that a failure to deliver sufficient quantities of
[2]
the essential axonal protein NMNAT2 is a key initiating event. [3]
Wallerian degeneration occurs after axonal injury in both the peripheral nervous system (PNS)
and central nervous system (CNS). It occurs in the section of the axon distal to the site of injury and
usually begins within 24–36 hours of a lesion. Prior to degeneration, the distal section of the axon
tends to remain electrically excitable. After injury, the axonal skeleton disintegrates, and the axonal
membrane breaks apart. Axonal degeneration is followed by degradation of the myelin sheath and
infiltration by macrophages. The macrophages, accompanied by Schwann cells, serve to clear the
debris from the degeneration. [4][5]
Schwann cells respond to loss of axons by extrusion of their myelin sheaths, downregulation of
myelin genes, dedifferentiation and proliferation. They finally align in tubes (Büngner bands) and
express surface molecules that guide regenerating fibers. Within 4 days of the injury, the distal end
[6]
of the portion of the nerve fiber proximal to the lesion sends out sprouts towards those tubes and
these sprouts are attracted by growth factors produced by Schwann cells in the tubes. If a sprout
reaches the tube, it grows into it and advances about 1 mm per day, eventually reaching and
reinnervating the target tissue. If the sprouts cannot reach the tube, for instance because the gap is
too wide or scar tissue has formed, surgery can help to guide the sprouts into the tubes.
Regeneration is efficient in the PNS, with near complete recovery in case of lesions that occur close
to the distal nerve terminal. However recovery is hardly observed at all in the spinal cord. One
crucial difference is that in the CNS, including the spinal cord, myelin sheaths are produced
by oligodendrocytes and not by Schwann cells.

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https://www.youtube.com/watch?

Peripheral nerve injury classification

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Neurapraxia (Class I)[edit]

a physiologic block of nerve conduction in the affected axons.

 It is the mildest type of peripheral nerve injury.

 Recovery of nerve conduction deficit is full, and requires days to weeks.

 Wallerian degeneration occurs distal to the site of injury.

 Wallerian degeneration occurs distal to the site of injury.

2. ^ "Seddon classification of nerve injuries".

4. ^ "ELECTRODIAGNOSTIC STUDIES OF THE HAND".

5. ^ "Classification of Nerve Injuries". Archived from the original on 2009-09-25.

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degeneration' occurs in many neurodegenerative diseases, especially those where axonal

the essential axonal protein NMNAT2 is a key initiating event. [3]

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