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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 ...
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.
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 .
A demyelinating disease refers to any disease affecting the nervous system where the myelin sheath surrounding neurons is damaged. [1] This damage disrupts the transmission of signals through the affected nerves, resulting in a decrease in their conduction ability.
[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]
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 ...
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.
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 ...