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Wallerian degeneration is named after Augustus Volney Waller.Waller experimented on frogs in 1850, by severing their glossopharyngeal and hypoglossal nerves. He then observed the distal nerves from the site of injury, which were separated from their cell bodies in the brain stem. [5]
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 ...
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.
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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]
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In a preganglionic lesion, the sensory fibre remain attached to the cell body of the sensory ganglion, thus there is no wallerian degeneration of the sensory fibre, thus sensory action potential can still be detected at the distal end of the spinal nerve. However, those who get this type of lesion have sensory loss over the affected nerve roots.
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