guillainbarré

Guillain-Barré syndrome (GBS) is an acute autoimmune disorder of the peripheral nervous system. It most often follows a viral or bacterial infection by one to three weeks. The immune system targets peripheral nerves, causing inflammation and damage to the myelin sheath or the nerve axon.

The hallmark is sudden weakness that typically starts in the legs and ascends to the upper body, sometimes with numbness or tingling. Deep tendon reflexes are usually reduced or absent. Autonomic dysfunction and, in severe cases, respiratory failure may occur, requiring close medical monitoring and support.

Diagnosis is based on clinical presentation supported by tests. Nerve conduction studies can reveal demyelination or axonal loss, and cerebrospinal fluid often shows albuminocytologic dissociation (high protein with normal cell count). Other causes of acute weakness are ruled out through examination and testing.

Treatment options include intravenous immunoglobulin (IVIG) or plasma exchange, both of which can hasten recovery if started early. Most patients require hospitalization for monitoring of breathing and autonomic function, and rehabilitation is important. Recovery typically occurs over weeks to months, with many patients achieving substantial or complete recovery, though some may have lasting weakness or fatigue. Relapse is uncommon.

GBS affects about 1–2 people per 100,000 each year, with no strong gender bias and incidence increasing with age. It is autoimmune in origin; molecular mimicry after infection triggers an immune attack on myelin or axons. Variants include the demyelinating form (AIDP) and axonal forms (AMAN, AMSAN), with prognosis varying by variant. The condition was first described in 1916 by Georges Guillain and Jean Barré, with Alexis Strohl.