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Diffuse axonal injury after a motorcycle accident. MRI after 3 days: on T1-weighted images the injury is barely visible. On the FLAIR, DWI and T2*-weighted images a small bleed is identifiable. DAI is difficult to detect since it does not show up well on CT scans or with other macroscopic imaging techniques, though it shows up microscopically. [9]
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.
Slower degeneration of the distal segment than that which occurs in the peripheral nervous system also contributes to the inhibitory environment because inhibitory myelin and axonal debris are not cleared away as quickly. All these factors contribute to the formation of what is known as a glial scar, which axons cannot grow across. [9]
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
Sensory neuronopathy differs from the more common length dependent axonal polyneuropathies (such as diabetic sensorimotor polyneuropathy) in that the symptoms do not progress in a distal to proximal pattern (starting in the feet and progressing to the legs and hands), rather symptoms develop in a multifocal, asymmetric, and non-length dependent ...
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 ...
Two different mechanisms of axon destruction are acting in MS. First of all, there is a diffuse axon degeneration, probably related to the NAWM appearance. Later, there is a second axonal damage mechanism localized in old demyelinating lesions, probably produced by B-Cells.