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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.
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.
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) no distal conduction (EMG and NCV (nerve conduction velocity) surgical intervention is necessary to restore function
Wallerian degeneration is a process that occurs before nerve regeneration and can be described as a cleaning or clearing process that essentially prepares the distal stump for reinnervation. [2] Schwann cells are glial cells in the peripheral nervous system that support neurons by forming myelin that encases nerves.
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 ...
When an axon is damaged, the distal segment undergoes Wallerian degeneration, losing its myelin sheath. The proximal segment can either die by apoptosis or undergo the chromatolytic reaction, which is an attempt at repair. In the CNS, synaptic stripping occurs as glial foot processes invade the dead synapse. [1]
Loss of NMNAT2 initiates Wallerian degeneration. [9] By contrast, NMNAT2 enhancement opposes the actions of SARM1 which would lead to axon degeneration, [10] but this effect is not due to preventing SARM1 depletion of NAD+. [9] Mice lacking NMNAT2 die before birth, [11] but are completely rescued by SARM1 deletion. [12]
Wallerian degeneration outside the lesions has been reported. [ 34 ] In general, during the acute phase, the plaques of lesions were characterized by massive demyelination with relatively axonal preservation associated with reactive astrocytosis and infiltration of macrophages.