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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 ...
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 disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating polyradiculoneuropathy (because it involves the nerve roots). [2] CIDP is closely related to Guillain–Barré syndrome and it is considered the chronic counterpart of that acute disease. [ 3 ]
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.
Organophosphate-induced delayed neuropathy (OPIDN), also called organophosphate-induced delayed polyneuropathy (OPIDP), is a neuropathy caused by killing of neurons in the central nervous system, especially in the spinal cord, as a result of acute or chronic organophosphate poisoning.
Treatment of early manifestations of sensorimotor polyneuropathy involves improving glycemic control. [18] Tight control of blood glucose can reverse the changes of diabetic neuropathy if the neuropathy and diabetes are recent in onset.