GuillainBarrésyndroomassa

Guillain-Barré syndrome (GBS) is an acute autoimmune disorder of the peripheral nervous system. It typically follows an infectious illness and is characterized by rapidly developing weakness and diminished or absent reflexes. The immune system is believed to attack nerve components, leading to demyelination or, in some variants, direct axonal injury. It is not contagious.

Most people with GBS experience symmetric weakness that starts in the legs and ascends over hours to days, often with numbness or pain. Cranial nerves may be involved, leading to facial weakness or difficulties with swallowing. Autonomic dysfunction, such as unstable heart rate or blood pressure, can occur. In about a minority, the respiratory muscles are affected, requiring ventilatory support.

Pathology varies by subtype. The most common form is acute inflammatory demyelinating polyradiculoneuropathy (AIDP); other forms include axonal variants such as AMAN and AMSAN. Triggers include infections with Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and Zika virus. Diagnosis relies on clinical features supported by nerve conduction studies and cerebrospinal fluid analysis, which may show elevated protein with normal cell count (albuminocytologic dissociation) after the first week.

Treatment aims to modulate the immune response and provide supportive care. First-line therapies are intravenous immunoglobulin (IVIG) or plasma exchange, both of which can shorten recovery when started early. Recovery typically begins within weeks and can take months; most patients regain much or all function, though some have residual weakness or fatigue. Severe cases require intensive monitoring and rehabilitation, and mortality is relatively low with current care.

Prevention and prognosis depend on prompt recognition, access to supportive medical care, and the underlying triggers.