Role of Fcγ Receptor Mediated Inflammation in Immune Neuropathies

Peripheral neuropathies are among the most common diseases encountered in clinical neurology. Autoimmunity and inflammation are implicated in a small but important group of peripheral nerve disorders because they are potentially treatable. These include the acute inflammatory neuropathies grouped under Guillain-Barré syndrome (GBS) and the chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). GBS is the commonest cause of acute flaccid paralysis worldwide, and a life-threatening acute, monophasic, autoimmune peripheral neuropathy. GBS is subdivided into two major subtypes, i.e., axonal and demyelinating (acute inflammatory demyelinating polyradiculoneuropathy (AIDP)) variants [1-3]. CIDP and its variants are considered as the most common chronic inflammatory/immune neuropathy. It is believed that there is a temporal continuum between AIDP, the demyelinating form of GBS, and CIDP and some view CIDP as the chronic counterpart of AIDP form of GBS.