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These symptoms are a result of severe muscular weakness and atrophy. In patients with demyelinating neuropathy, symptoms are due to slow nerve conduction velocities; however people with axonal degradation have average-to-normal nerve conduction velocities. [citation needed]
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.
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).
Acute motor axonal neuropathy (AMAN) is a variant of Guillain–Barré syndrome. It is characterized by acute paralysis and loss of reflexes without sensory loss. Pathologically , there is motor axonal degeneration with antibody-mediated attacks of motor nerves and nodes of Ranvier .
Additionally, BP control in those with diabetes is helpful, while intravenous immunoglobulin is used for multifocal motor neuropathy. [ 1 ] According to Lopate, et al., methylprednisolone is a viable treatment for chronic inflammatory demyelinative polyneuropathy (which can also be treated with intravenous immunoglobulin).
Symptoms of sensory neuropathy may sometimes precede the cancer diagnosis by several months. Immune mediated sensory neuronopathy is commonly associated with Sjogrens syndrome. [5] Sjogren's is most commonly affected by a length dependent axonal sensorimotor neuropathy characterized by symptoms in the extremities.
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.
See Anti-neurofascin demyelinating diseases. Some anti-neurofascin demyelinating diseases were previously considered a subtype of Multiple Sclerosis but now they are considered a separate entity, as it happened before to anti-MOG and anti-AQP4 cases. Around 10% of MS cases are now thought to be anti-Neurofascin disease in reality. [34]
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