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Age-related changes are observed in fine structure of spindle nerve innervation in the form of axonal swelling and expanded/abnormal endplates. [6] When subject to a task of proprioception, the elderly show increased cocontraction of agonist-antagonist muscles, perhaps to increase gamma drive and spindle sensitivity. It is believed to be used ...
Alcoholic polyneuropathy is a neurological disorder in which peripheral nerves throughout the body malfunction simultaneously.It is defined by axonal degeneration in neurons of both the sensory and motor systems and initially occurs at the distal ends of the longest axons in the body.
Axonal transport can be disrupted by a variety of mechanisms including damage to: kinesin and cytoplasmic dynein, microtubules, cargoes, and mitochondria. [25] When axonal transport is severely disrupted a degenerative pathway known as Wallerian-like degeneration is often triggered. [71]
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.
Strich first proposed the idea in 1956, calling it diffuse degeneration of white matter; however, the more concise term "diffuse axonal injury" came to be preferred. [38] Strich was researching the relationship between dementia and head trauma [ 37 ] and asserted in 1956 that DAI played an integral role in the eventual development of dementia ...
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 ...
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.
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 ...