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Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired autoimmune disease of the peripheral nervous system characterized by progressive weakness and impaired sensory function in the legs and arms. [1]
The demyelinating diseases of the peripheral nervous system include: [citation needed] Guillain–Barré syndrome and its chronic counterpart, chronic inflammatory demyelinating polyneuropathy; Anti-MAG peripheral neuropathy; Charcot–Marie–Tooth disease and its counterpart Hereditary neuropathy with liability to pressure palsy
The most common cause is acute inflammatory demyelinating polyneuropathy AIDP, the most common form of Guillain–Barré syndrome [13] (although other causes include chronic inflammatory demyelinating polyneuropathy) [14] Neuronopathy is the result of issues in the peripheral nervous system (PNS) neurons.
Inflammatory demyelinating diseases (IDDs), sometimes called Idiopathic (IIDDs) due to the unknown etiology of some of them, are a heterogenous group of demyelinating diseases - conditions that cause damage to myelin, the protective sheath of nerve fibers - that occur against the background of an acute or chronic inflammatory process.
Hypertrophic demyelinating type: affected individuals experience weakness and atrophy in the lower legs in adolescence, and later develop weakness in the hands. This is the most common type of CMT. HMSN2: Charcot–Marie–Tooth disease type 2: 2343 (multiple) Neuronal type: symptoms similar to type1, onset in adolescence. HMSN3
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Myelin-associated glycoprotein (MAG) is a glycoprotein that is specific to Schwann cells, which create myelin for nerve cells in the peripheral nervous system. Research through cloning of the rat MAG gene has shown that it is a type I transmembrane protein meaning that it contains domains both inside the cell membrane and outside the cell membrane.
Demyelinating lesions begin with the appearance of some areas named NAWM (normal appearing white matter) which despite its name, is abnormal in several parameters. These areas show axonal transections and stressed oligodendrocytes (the cells responsible for maintaining the myelin), and randomly, they show clusters of activated microglia named ...