Guillain-Barré syndrome (GBS) is an acute postinfectious polyneuropathy characterized by symmetric and ascending flaccid paralysis. In affected patients, cross‑reactive autoantibodies attack the host's own axonal antigens, resulting in inflammatory and demyelinating polyneuropathy. Albuminocytologic dissociation, characterized by elevated protein levels and normal cell counts in cerebrospinal fluid (CSF), is a hallmark finding of GBS. Additionally, muscle and nerve electrophysiology are used to diagnose demyelinating processes. Symptomatic and supportive treatment results in disease remission in about 70% of cases. In severe cases or patients who do not respond to treatment, intravenous immunoglobulin (IVIG) administration and/or plasmapheresis may be used. Potentially acute life-threatening complications such as respiratory insufficiency, pulmonary embolism, and/or cardiac arrest increase mortality. Although GBS is associated with a good prognosis overall, up to 20% of patients remain severely disabled and approximately 5% of cases are fatal, despite immunotherapy.
- ∼ 1 case per 100,000 individuals
- Adults are affected more frequently than children.
- Sex: ♂ > ♀ (1.5:1) 
Epidemiological data refers to the US, unless otherwise specified.
- Associated pathogens 
- Postinfectious autoimmune reaction that generates cross-reactive antibodies (molecular mimicry)
- Infection triggers humoral response → formation of autoantibodies against gangliosides (e.g., GM1, GD1a) or other unknown antigens of peripheral Schwann cells → immune-mediated segmental demyelination → axonal degeneration of motor and sensory fibers in peripheral and cranial nerves (CN III–XII)
- Bilateral flaccid paralysis
- Spreads from the lower to the upper limbs in a “stocking‑glove” distribution
- Landry paralysis: involvement of the respiratory muscles → respiratory failure
- Reduced or absent
- Commonly beginning in the lower limbs
- Peripheral, symmetric
- Usually affecting hands and feet
- Neuropathic pain: develops in about ⅔ of affected individuals
- Blood pressure dysregulation: ↑ or ↓
- Voiding dysfunction
- Intestinal dysfunction
- Cranial nerve involvement
GBS paralysis affects the muscles of respiration, possibly leading to death due to respiratory failure.
Subtypes and variants
|Overview of subtypes and variants of Guillain-Barré syndrome|
|Acute inflammatory demyelinating polyneuropathy (AIDP) || |
|Chronic inflammatory demyelinating polyneuropathy (CIDP) || || |
|Miller-Fisher syndrome|| || |
|Multifocal motor neuropathy (MMN) || |
- Cerebrospinal fluid: albuminocytologic dissociation
- Serological screening
- ↓ Nerve conduction velocity (NCV) due to demyelination
- Signs of denervation: characteristic of axonal lesions
- Pathologic spontaneous activity (unfavorable prognostic sign)
- ECG: autonomic cardiac dysregulation → impaired heart frequency variation
- Supportive management
- Intravenous immunoglobulins 
- In adults: equivalent outcome as IV immunoglobulins
- In children: only recommended in children with rapidly progressing or severe disease
- ∼ 70% of patients with GBS have a good prognosis 
3–7% of patients with GBS die due to acute complications such as:
- Respiratory paralysis (apnea)
- Pulmonary infection/embolism
- Cardiac dysfunction
- 6 months after onset, ∼ 20% of affected individuals are still unable to walk unaided.
Death can occur as many as > 30 days after onset of symptoms, during the recovery phase.