Guillain-Barré syndrome (GBS) is an autoimmune acute peripheral polyneuropathy, which often follows an infectious process. The most common microorganisms associated with GBS are the bacteria Campylobacter jejuni and Mycoplasma pneumoniae. Viruses such as cytomegalovirus and the Zika virus have also been associated with GBS. The incidence of GBS ranges between 0.5 and 2 cases per 100,000 population per year. The pathophysiology of GBS most likely involves molecular mimicry, in which an autoantibody against a microorganism cross-reacts with host molecules, such as GD1a, GM1, and GM1/GD1 complex located at the terminal nerves and anterior roots, and GQ1b located on oculomotor nerves and primary sensory neurons. The classical complement system has also been implicated in facilitating the development of GBS. GBS usually presents with numbness, paresthesia, and progressive weakness, but there are several clinical variants, including acute motor axonal neuropathy (AMAN), acute inflammatory demyelinating polyneuropathy (AIDP), acute motor and sensory axonal neuropathy (AMSAM), Miller-Fisher syndrome (MFS), a pharyngeal-cervical-brachial variant, a paraparetic variant, and others. Treatment of GBS mostly targets the immune response through the use of IVIg, plasma exchange, and other forms of immunomodulatory therapy.
