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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.
Human axon growth rates can reach 2 mm/day in small nerves and 5 mm/day in large nerves. [4] The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, but the endoneurium remains. In the later stages of regeneration the remaining endoneurial tube directs axon growth back to the ...
When the axon is torn, Wallerian degeneration, in which the part of the axon distal to the break degrades, takes place within one to two days after injury. [26] The axolemma disintegrates, [ 26 ] myelin breaks down and begins to detach from the cell in an anterograde direction (from the body of the cell toward the end of the axon), [ 27 ] and ...
Axon, endo-, peri-, and epineurium transected. Neurotmesis may be partial or complete. Other characteristics: distal Wallerian degeneration; partial or complete connective tissue lesion; severe sensory-motor problems and autonomic function defect; nerve conduction distal to the site of injury absent (3 to 4 days after lesion)
If an axon is injured, the axonal transport system may not function. Since the axon depends on its connection to the cell body, the disrupted axonal transport will cause segmental death of the axon distal to the injury site in a process called Wallerian degeneration. [4]
To assess the location and severity of a nerve injury, clinical assessment is commonly combined with electrodiagnostic tests. [2] Injuries to the myelin are usually the least severe (neuropraxia), while injuries to the axons and supporting structures are more severe (axonotmesis is moderate injury, while neurotmesis is severe injury). [2]
Motor and sensory functions distal to the point of injury are completely lost over time leading to Wallerian degeneration due to ischemia, or loss of blood supply. Axonotmesis is usually the result of a more severe crush or contusion than neurapraxia. [1] Axonotmesis mainly follows a stretch injury.
When an axon is crushed, an active process of axonal degeneration takes place at the part of the axon furthest from the cell body. This degeneration takes place quickly following the injury, with the part of the axon being sealed off at the membranes and broken down by macrophages. This is known as Wallerian degeneration. [54]
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