Guillain-Barré syndrome historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Priyamvada Singh, MBBS [2]
Overview
Guillain-Barré syndrome (GBS) is an acute, autoimmune, polyradiculoneuropathy affecting the peripheral nervous system, usually triggered by an acute infectious process. It is included in the wider group of peripheral neuropathies. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, acute inflammatory demyelinating polyneuropathy (AIDP). It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment of plasmapheresis followed by immunoglobulins and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and dysautonomia are present.
Historical perspective
The disease was first described by the French physician Jean Landry in 1859. In 1916, Georges Guillain, Jean Alexandre Barré and Andre Strohl who diagnosed two soldiers with a discovered the key diagnostic abnormality of increased spinal fluid protein production, but normal cell count.[1]
GBS is also known as acute inflammatory demyelinating polyneuropathy, acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis, French Polio and Landry's ascending paralysis.