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[4] [6] [8] [11] Dr. Daniel LaChance, a physician at both the Austin Medical Center and the Mayo Clinic in nearby Rochester, Minnesota, was notified. He launched a request to area physicians to refer other patients with similar symptoms to him. [11] The Minnesota Department of Health was notified and began an investigation into the "outbreak."
The characteristics are typical of demyelinating neuropathy with antimyelin-associated glycoprotein (MAG) antibodies; however, anti-MAG neuropathy is not included in the CIDP criteria according to the EFNS/PNS criteria, primarily due to the presence of a particular antibody and a different response to treatment.
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.
Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., inflammation (), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy).
The signs and symptoms of Peripheral mononeuropathy and neuropathy vary as a result of the types of individual and/or nerve areas affected. There are three types of nerve damage, including: "motor nerve damage, sensory nerve damage, and autonomic nerve damage". [2]
The signs and symptoms of hereditary sensory neuropathy type 1 typically appear during a person's teens or twenties. While the features of this disorder tend to worsen over time, affected individuals have a normal life expectancy if signs and symptoms are properly treated. Type 1 is the most common form among the 5 types of HSAN.
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