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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.
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.
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
Hemorrhage into the basal ganglia or thalamus causes contralateral hemiplegia due to damage to the internal capsule. [7] Other possible symptoms include gaze palsies or hemisensory loss. [7] Intracerebral hemorrhage into the cerebellum may cause ataxia, vertigo, incoordination of limbs and vomiting. [7]
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]
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.
Non-traumatic causes of hemorrhage includes: hypertension, cerebral amyloid angiopathy, hemorrhagic conversion of ischemic infarction, cerebral aneurysms, dural arteriovenous fistulae, cerebral venous sinus thrombosis, cerebral vasculitis and mycotic aneurysm. [3] More than half of all cases of intracranial hemorrhage are the result of ...