Guillain-Barré syndrome (GBS) is an acute immune-mediated polyneuropathy that typically manifests with bilateral ascending flaccid paralysis and sensory involvement, e.g., paresthesia. The pathogenesis of GBS involves autoantibodies against antigens in the myelin sheath, other Schwann-cell antigens, and axon membranes. Approximately 65% of patients have an upper respiratory tract or gastrointestinal infection before the onset of GBS symptoms. Diagnosis is primarily clinical; alternative diagnoses should be considered especially in patients with atypical presentations. Cerebrospinal fluid (CSF) analysis showing albuminocytologic dissociation and electrodiagnostic study findings help support the diagnosis. Medical treatment depends on the severity of symptoms; available treatment options are intravenous immunoglobulin (IVIg) and plasmapheresis. Close monitoring is required for all patients. Complications such as respiratory failure, pulmonary embolism, and/or cardiac arrest increase mortality. Up to 20% of patients remain severely disabled and approximately 5% of patients die despite medical treatment.
- 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) 
Typical disease progression
- Onset is acute or subacute, and symptoms progress rapidly.
- Symptoms peak at ∼ 2–4 weeks and then plateau over months or years, followed by partial or complete resolution. 
- Limb involvement: typically bilateral and ascending from the lower limbs
- Back and limb pain (often an early symptom)
- Cardiac arrhythmias, blood pressure fluctuations 
- and/or intestinal dysfunction
- Respiratory muscle involvement may lead to respiratory failure.
- Cranial nerve involvement
Subtypes and variants
Subtypes of Guillain-Barré syndrome
|Overview of subtypes of Guillain-Barré syndrome|
|Acute inflammatory demyelinating polyneuropathy (AIDP)|| |
|Axonal loss||Acute motor axonal neuropathy (AMAN)|| || |
|Acute motor and sensory axonal neuropathy (AMSAN)|
Classification into subtypes does not affect treatment decisions but may inform prognosis. 
Variants of Guillain-Barré syndrome
Variants of the classic sensorimotor presentation are characterized by the involvement of a specific group of muscles or nerves; overlap between variants is common.
- Miller-Fisher syndrome (MFS) ; 
- Other variants include:
General principles 
- A diagnosis of GBS is based on:
- Diagnostic criteria may be considered to support the diagnosis, e.g., the National Institute of Neurological Disorders and Stroke or Brighton criteria. 
- Evaluate patients for , especially those with atypical presentations. 
- Consult a neurologist for all patients.
A complete neurological examination is required for all patients.
CSF analysis 
- Obtained to support diagnosis and rule out infectious and malignant causes
Nerve conduction studies 
- Obtained to support diagnosis and/or to classify GBS into subtypes
- Findings vary according to the subtype of GBS and may be normal during the early stages of disease.
- Findings help differentiate between neuropathy and myopathy.
- Pathological spontaneous activity is a sign of an unfavorable prognosis.
- See “ .”
Additional studies 
- Routine laboratory studies
- Serological studies may be obtained to: 
Imaging studies: not routinely required but may help rule out differential diagnoses 
- MRI spine with contrast
- MRI brain with contrast: Consider in patients with suspected CNS involvement.
Differential diagnoses of Guillain-Barré syndrome 
See “” and “ ” for further details.
- Peripheral polyneuropathies
- Metabolic or electrolyte disorders
|Clinical features of Guillain-Barré syndrome vs. transverse myelitis|
|Guillain-Barré syndrome||Transverse myelitis|
|Symptom onset|| |
|Motor findings|| |
|Cranial nerve involvement|| |
|Imaging and findings|| |
|Electrophysiological findings|| || |
The differential diagnoses listed here are not exhaustive.
- Consult neurology.
- Admit all patients for close monitoring and supportive management.
- Start medical treatment (IVIg or plasmapheresis) promptly in patients with indications.
- Monitor for symptom progression and provide management as needed, e.g., bradycardia, dysphagia. ,
Medical treatment 
- Indications 
- Special considerations: patients with clinical variants of GBS 
The frequency of reassessment should be based on clinical severity; follow local protocols when available.
- Monitor frequently.
- Monitor autonomic function.
- Frequently assess paresis and/or paralysis progression and swallowing function.
Predictors of respiratory failure in GBS 
- Clinical features at presentation
- Rapid progression (e.g., onset-to-peak disability interval < 7 days)
- (especially bilateral)
- Neck weakness
- Bedside PFTs
- or < 20 mL/kg> 30% decline from baseline
- -30 cm H2O or > 30% decline from baseline less negative than
- or < 40 cm H2O> 30% decline from baseline
- Clinical features at presentation
- Clinical prediction rule: The Erasmus GBS Respiratory Insufficiency Score (EGRIS) can be used to predict the need for mechanical ventilation. 
- Management: See “ ” for a general approach.
Classic GBS. Identify as early as possible.  and typically occur late in
Supportive management 
- Manage neuropathic pain.
- Prevent complications.
- Approx. 80% of patients with GBS regain the ability to walk unaided 6 months after symptom onset. 
- Consider calculating the modified Erasmus GBS Outcome Score (mEGOS) to predict the patient's ability to walk unaided.
- 3–7% of patients with GBS die as a result of complications, e.g.: 
- Patient factors associated with an increased risk of long-term disability include: 
- Rapid symptom progression
- Severe symptoms at peak of the disease
- Older age
- Axonal damage (e.g., in AMAN)
- It may take > 5 years for symptoms to improve and/or resolve. 
Death can occur as many as > 30 days after onset of symptoms, during the recovery phase.