Guillain-Barre syndrome, clinical features, pathophysiology and advances in management

Guillain-Barré syndrome (GBS) is an umbrella term that describes several clinically and electrophysiologically heterogeneous disorders that share the common feature of acute onset regional or generalised flaccid paralysis with or without sensory loss. Among the reported antibodies, anti-GM1 and anti-GQ1B have been reported to be responsible for attacking and damaging either the neuromuscular junctions or peripheral nerves. Moreover, it has been found that the anti-GD1a antibodies in patients binds to the neuromuscular junction and also binds to the nodes of Ranvier of the peripheral nerves and the paranodal myelin of the affected nerves. Reports have shown that this disease is identified as a special form of neuropathies that develop in immune-mediated, post-infection sequelae. Furthermore, in another study it was reported that Molecular mimicry has been previously reported to predispose to the development of GBS in humans. However, scientists have found that plasma exchange and intravenous immunoglobulins (IVIG) remain the most significant and efficacious factors in managing the disease. Nevertheless, recent trails have investigated other approaches that are less efficacious and can lead to serious adverse events and complications.