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The diagnosis of polyneuropathy begins with a history (anamnesis) and physical examination to ascertain the pattern of the disease process (such as arms, legs, distal, proximal), if they fluctuate, and what deficits and pain are involved. If pain is a factor, determining where and how long it has been present is important; one also needs to ...
It was thought that the polyneuropathy was a direct result of the toxic effect alcohol had on peripheral nerves when used excessively. In 1928, George C. Shattuck argued that the polyneuropathy resulted from a vitamin B deficiency commonly found in alcoholics and he claimed that alcoholic polyneuropathy should be related to beriberi. This ...
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).
Diabetes most commonly causes damage to the long nerves that supply the feet and lower legs, causing numbness, tingling and pain (diabetic polyneuropathy). Although these symptoms may also be present, the pain and weakness of proximal diabetic neuropathy often onset more quickly and affect nerves closer to the torso. [citation needed]
Diabetic peripheral neuropathy can be diagnosed with a history and physical examination. The diagnosis is considered in people who develop pain or numbness in a leg or foot with a history of diabetes. Muscle weakness, pain, balance loss, and lower limb dysfunction are the most common clinical manifestations. [7]
The Therapeutic Goods Administration requires a label warning about peripheral neuropathy if the daily dose is predicted to exceed 10 mg/day. [47] [48] U.S. Institute of Medicine - Food and Nutrition Board 100 mg/day The adult UL was set in 1998 and has not been updated as of 2024 [24]