GuillainBarrén

Guillain-Barré syndrome (GBS) is an acute autoimmune disorder of the peripheral nervous system characterized by rapid-onset muscle weakness and areflexia. It is typically preceded by an infection and involves immune-mediated demyelination or, in some variants, axonal damage to peripheral nerves. The main variants are acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor-sensory axonal neuropathy (AMSAN).

Clinically, GBS usually presents with symmetric weakness that begins in the legs and ascends over hours to days, often with numbness or tingling. Autonomic dysfunction and facial or bulbar weakness can occur, and a fraction of patients develop respiratory failure requiring intensive care. The course is variable, but progression tends to halt within a few weeks, followed by gradual recovery over weeks to months.

Diagnosis is based on history and examination, supported by tests. Nerve conduction studies help distinguish demyelinating from axonal forms. Cerebrospinal fluid obtained after the first week often shows albuminocytologic dissociation, meaning elevated protein with a normal cell count. Other causes of acute weakness are ruled out.

Treatment emphasizes monitoring and supportive care, particularly for respiratory and cardiovascular stability. Intravenous immunoglobulin (IVIG) or plasma exchange (plasmapheresis) are first-line disease-modifying therapies; corticosteroids alone are not effective. Most patients recover, though residual weakness can persist for months to years. Mortality is low with modern intensive care, and relapses are uncommon, though some patients may develop chronic inflammatory demyelinating polyneuropathy in rare cases.