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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 ...
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.
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.
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.
Axon, endo-, peri-, and epineurium transected. Neurotmesis may be partial or complete. Other characteristics: 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)
This degeneration is due to an autoimmune response typically initiated by various infections. Two primary classifications exist: demyelinating (Schwann cell damage) and axonal (direct nerve fiber damage). [7] [16] Each of these then branches into additional sub-classifications depending on the exact manifestation. In all cases, however, the ...
To assess the location and severity of a nerve injury, clinical assessment is commonly combined with electrodiagnostic tests. [2] Injuries to the myelin are usually the least severe (neuropraxia), while injuries to the axons and supporting structures are more severe (axonotmesis is moderate injury, while neurotmesis is severe injury). [2]