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Such lesions give rise to extensive astrocyte loss, which may occur in part in the absence of any other tissue injury, such as demyelination or axonal degeneration (lesion type 5). Finally, lesions with a variable degree of astrocyte clasmatodendrosis are found, which show plaque-like primary demyelination that is associated with ...
The axon and encapsulating connective tissue lose their continuity. The last (extreme) degree of neurotmesis is transsection, but most neurotmetic injuries do not produce gross loss of continuity of the nerve but rather internal disruption of nerve structures sufficient to involve perineurium and endoneurium as well as axons and their covering.
[1] Alcoholic polyneuropathy usually has a gradual onset over months or even years, although axonal degeneration often begins before an individual experiences any symptoms. [2] The disease typically involves sensory issues and motor loss, as well as painful physical perceptions, though all sensory modalities may be involved. [3]
Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically , there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier .
The axon's survival depends on its connection with the cell body, supported by the axonal transport mechanisms to carry cellular material. [4] The axonal transport system carries material along the axon in both directions (anterograde and retrograde) at different speeds (fast and slow). [4] [5] The fast transport travels at up to 400 mm/day.
Neurapraxia is a temporary interruption of conduction without loss of axonal continuity. [3] Neurapraxia involves a physiologic block of nerve conduction in the affected axons. Other characteristics: mildest type of nerve injury; sensory-motor problems present distal to the site of injury; intact endoneurium, perineurium, and the epineurium
In the 1950s, further classification occurred and separated patients into two distinct groups. Group one was characterized by slow nerve conduction velocities and demyelinating neuropathy. Group two was characterized by mostly normal nerve conduction velocities and degeneration of axons. In 1968, HMSN were classified again into seven groups: [1 ...
When a nerve axon is severed, the end still attached to the cell body is labeled the proximal segment, while the other end is called the distal segment. After injury, the proximal end swells and experiences some retrograde degeneration, but once the debris is cleared, it begins to sprout axons and the presence of growth cones can be detected.