Myelin secondary demyelination

Secondary demyelination is the loss of myelin secondary to loss of axons. Axonal trophic factors sustain myelin. When the axon is severed or not sustained by its neuron of origin, the axon and then its myelin degenerates. This can happen secondary to infarcts, trauma, toxic, metabolic, or degenerative nervous system diseases. In contrast to primary demyelination, straight and long NF-positive axons are not seen in secondary demyelination. Acutely, the axons crumble into short pieces, and in a few days they are eaten by macrophages and disappear. NF stains thus distinguish secondary from primary demyelination. 

O MS symptoms are a function of the position of lesions within the CNS. Because myelin increases the speed of nerve impulse transmission, demyelination slows the speed of transmission. No impulses can be transmitted if the axon is transected. The primary symptoms of MS are caused by this delay or cessation of impulses. Secondary symptoms of MS result from the primary symptoms. 

MS is an autoimmune disease that attacks the myelin sheath of oligodendrocytes around the neuronal axons. This allows the axonal cytoskeleton to be damaged, bringing about secondary axonal loss and persisting neurological dysfunction. The characteristic pathology is of a lesion or plaque in the CNS white matter, formed by inflammation and demyelination and these can be classified into active, chronic active, or chronic silent plaques [86]. 

Diphtheria toxin, inorganic lead, and tellurium are considered toxicants that cause demyelination through injury to the myelinating cell. The mechanism of action of diphtheria toxin was discussed in Section 30.1. The mechanism by which inorganic lead causes Schwann cell injury and demyelination is not well understood, but may be related to uncoupling or inhibition of oxidative phosphorylation secondary to interference of lead with some aspect of ion transport across the mitochondrial membrane. 

Axonal damage secondary to myelin loss is a major cause of sensory, motor, and cognitive disabilities in adult MS (Bjartmar and Trapp, 2001). The lack of myelin recovery may be due primarily to deficiency in the genesis of OPCs and in their maturation in the adult CNS (Franklin, 2002 Stangel and Hartung, 2002). Limited myelin regeneration is observed in early demyelinating lesions in MS (Wolswijk,... 

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