These common neuropathies are presumed to be immune disorders in which antibodies reacting with antigens present on peripheral nerves elicit an inflammatory and macrophage reaction that destroys myelin and axons. The strongest evidence of a humoral immune reaction in these neuropathies is that plasma exchange results in significant clinical improvement. However, a cell mediated response probably plays a role also. EAN is a cell-mediated immune reaction. It begins with paresthesias in the toes and fingertips, followed by rapidly advancing weakness and areflexia.
Weakness reaches a plateau within four weeks, after which recovery begins.
Some cases are fulminant, evolving in one or two days. Axonal damage is variable and may be severe. The pathology is most severe in spinal roots and plexuses and less pronounced in more distal nerves. In the phase of recovery, there are thin myelin sheaths, indicating myelin regeneration. About 20 to 30 percent of GBS cases are preceded by an infection with Campylobacter Jejuni.