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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 .
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 ...
N-cadherin agonists have been identified and observed to stimulate neurite growth and cell migration, key aspects of promoting axon growth and remyelination after injury or disease. [ 25 ] Immunomodulatory drugs such as fingolimod have been shown to reduce immune-mediated damage to the CNS, preventing further damage in patients with MS.
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 ...
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 regards to the pathophysiology of ulnar neuropathy:the axon, and myelin can be affected. Within the axon, fascicles to individual muscles could be involved, with subsequent motor unit loss and amplitude decrease. Conduction block means impaired transmission via a part of the nerve.
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]
The loss of axons because of lack of protection is what makes MS so debilitating. Degradation is considered to be worse than the effects of demyelination. [5] Once an axon is degenerated, it cannot regenerate like myelin, thus making research to promote remyelination that much more important.