Acquired peripheral neuropathies are broadly classified into acute and chronic inflammatory demyelinating neuropathies (AIDP and CIDP, respectively). Clinical forms of these neuropathies are many, and all of them proceed with sensory abnormalities or motor weaknesses, or a combination of both. Pathogenetically inflammatory neuropathies belong to autoimmune diseases; the actual neuropathy usually follows viral infection; the latter triggers an immune response, which turns into an autoimmune reaction aimed at myelin or protein components of Schwann cells. Important roles are played by antibodies against viral oligosaccharide components, which are, incidentally, identical to gangliosides (GM1 or GD1a) of the peripheral nerve; as a result, antibodies produced against viruses attack the body's own tissue. In addition, certain infections may produce antibodies against myelin proteins, most frequently against protein PMP22.
The autoreactive T cells, bearing the autoantibodies, migrate towards the peripheral nerve, and (by release of cytokines and chemokines) recruit macrophages, which attack both Schwann cells and myelin sheaths. Initially, macrophages form infiltrations within the peripheral nerve, and destroy the myelin; subsequently, they phagocytose the remnants of the glial cells and demyelinated axons.
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