Highlights & Basics
- Guillain-Barre syndrome (GBS) is an acute inflammatory polyneuropathy that is classified according to symptoms and divided into axonal and demyelinating forms.
- Two-thirds of patients have a history of gastroenteritis or influenza-like illness weeks before onset of neurologic symptoms.
- GBS is associated with outbreaks of Zika virus. As with other viral infections, there are occasional reports of GBS associated with coronavirus disease 2019 (COVID-19) infection, although this is very rare.
- Approximately 20% to 30% of patients with GBS will develop respiratory muscle weakness requiring ventilation.
- Neurophysiology is confirmatory and is abnormal in most patients, even early in the disease.
- Lumbar puncture is useful, and the classic finding is elevated protein with normal cell count (albuminocytologic dissociation).
- Treatment combines supportive and disease-modifying therapy (high-dose immune globulin or plasma exchange).
Quick Reference
History & Exam
Key Factors
muscle weakness
paresthesia
back/leg pain
respiratory distress
speech problems
areflexia/hyporeflexia
facial weakness
bulbar dysfunction causing oropharyngeal weakness
extraocular muscle weakness
facial droop
diplopia
dysarthria
dysphagia
dysautonomia
pupillary dysfunction
ophthalmoplegia
Other Factors
ptosis
altered level of consciousness
ataxia
Diagnostics Tests
1st Tests to Order
nerve conduction studies
lumbar puncture
LFTs
spirometry
Other Tests to consider
antiganglioside antibody
serology
stool culture
HIV antibodies
spinal MRI
Borrelia burgdorferi serology
cerebrospinal fluid (CSF) meningococcal polymerase chain reaction
CSF cytology
CSF angiotensin-converting enzyme
chest x-ray
CSF VDRL
CSF West Nile polymerase chain reaction
Emerging Tests
ultrasound imaging of peripheral nerves
Treatment Options
acute
ambulatory within 2 weeks of onset or nonambulatory within 4 weeks of onset
without IgA deficiency or renal failure
with IgA deficiency or renal failure
Definition
Classifications
Variants of Guillain-Barre
- Sensory and motor: AIDP (most common) or AMSAN.[5]
- Motor: acute motor demyelinating neuropathy or AMAN.[5]
- Miller-Fisher syndrome: ophthalmoplegia, ataxia, and areflexia (also referred to as Fisher syndrome).
- Bickerstaff brainstem encephalitis: similar to Miller-Fisher syndrome but also includes altered consciousness (encephalopathy) or hyperreflexia, or both.[6]
- Pharyngeal-cervical-brachial: acute arm weakness, swallowing dysfunction, and facial weakness.[5]
- Pure sensory: acute sensory loss, sensory ataxia, and areflexia but no motor involvement.[9]
Vignette
Common Vignette
Epidemiology
Etiology
Pathophysiology
Diagnostic Approach
History
Symptoms and signs: general
Symptoms and signs: acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
Symptoms and signs: acute motor axonal neuropathy (AMAN)
Symptoms and signs: acute motor-sensory axonal neuropathy (AMSAN)
Symptoms and signs: Miller-Fisher syndrome (MFS)
Symptoms and signs: Bickerstaff brainstem encephalitis (BBE)
Symptoms and signs: pharyngeal-cervical-brachial
Symptoms and signs: acute pandysautonomia
Symptoms and signs: pure sensory
Investigations
Neurophysiologic evaluation
Cerebrospinal fluid analysis
Spirometry
Serology and stool culture
Antiganglioside antibodies
Hepatic aminotransferases
Imaging
Risk Factors
History & Exam
Tests
Differential Diagnosis
Transverse myelitis
Differentiating Signs/Symptoms
- Spinal cord disorders including transverse myelitis present with asymmetric motor or sensory loss usually involving lower extremities, early bowel or bladder dysfunction with persistent incontinence, and segmental radicular pain.
- Physical exam demonstrates upper motor neuron signs (hyper-reflexia, positive Babinski response) and a sensory level.
Differentiating Tests
- Cerebrospinal fluid analysis: pleocytosis with modest number of lymphocytes and increase in total protein.
- MRI shows focal demyelination with possible enhancement at the appropriate level.
Myasthenia gravis
Differentiating Signs/Symptoms
- Early involvement of muscle groups including extraocular, levator, pharyngeal jaw, neck, and respiratory muscles. Sometimes presents without limb weakness.
- Excessive fatigability and variation of symptoms and signs through the day is common.
- Reflexes are preserved, and sensory features, dysautonomia, and bladder dysfunction are absent.
Differentiating Tests
- Electrophysiologic study shows normal nerve conduction and presence of decremental response to repetitive nerve stimulation.
- Electromyogram shows abnormal jitter and blocking.
Lambert-Eaton myasthenic syndrome (LEMS)
Differentiating Signs/Symptoms
- Can be difficult to differentiate because of similar clinical characteristics.
- Characteristics more typical of LEMS include slower development of clinical symptoms, dry mouth, lack of objective sensory loss, rare involvement of respiratory muscle group, and potentiation of reflexes after exercise or contraction.[147]
Differentiating Tests
- Electrophysiologic study: hallmark is a low amplitude compound muscle action potential (CMAP) after single nerve stimulus, increase in CMAP amplitude after voluntary contraction, or repetitive stimulation at high frequencies.[147]
Botulism
Differentiating Signs/Symptoms
- History of ingesting food tainted with botulinum toxin.
- Descending paralysis begins in the bulbar muscles then the limbs, face, neck, and respiratory muscles.
- Respiratory muscles are involved with mild limb weakness, and reflexes are usually preserved.
- Ptosis, dilated nonreactive pupils are present. Dilated nonreactive pupils are uncommon in GBS, but more common in botulism.
- Constipation is also a characteristic feature of botulism.[147]
Differentiating Tests
- Electrophysiologic study: reduced amplitude of evoked muscle potentials, increase in amplitude with repetitive nerve stimulation and increased number of myopathic units, which is atypical for GBS.[147]
Polymyositis
Differentiating Signs/Symptoms
- Presence of pain and muscle tenderness usually in the shoulder and upper arm, involvement of flexor neck muscle disproportionate to limb weakness, absence of sensory symptoms, preservation of reflexes, absence of dysautonomia, and presence of skin lesions, which are uncommon presentation for GBS.[147]
Differentiating Tests
- Elevated erythrocyte sedimentation rate and creatine kinase, normal nerve conduction study, and myopathic changes with fibrillation on electromyogram.
- Muscle biopsy shows muscle fiber destruction and regeneration, and lymphocyte infiltrates.[147]
Differentiating Signs/Symptoms
- Common features include painful asymmetric presentation of muscle weakness, uncommon involvement of cranial nerves, respiratory paralysis, and sphincter dysfunction.
- Usually patients report fever, fatigue, weakness, and arthralgia.[147]
Differentiating Tests
- May have elevated erythrocyte sedimentation rate.
- Cerebrospinal fluid does not show albuminocytologic dissociation.
- Electrophysiologic study shows evidence of denervation.
- Nerve biopsy shows signs of inflammation and scarring.[147]
Criteria
- Progressive weakness in both arms and legs
- Areflexia (or hyporeflexia).
- Progression of symptoms over days to 4 weeks
- Relative symmetry
- Mild sensory signs or symptoms
- Cranial nerve involvement, especially bilateral facial weakness
- Recovery beginning 2 to 4 weeks after progression ceases
- Autonomic dysfunction
- Absence of fever at onset
- Typical cerebrospinal fluid (CSF) and electromyogram/nerve conduction studies features.
- Asymmetric weakness
- Persistent bladder and bowel dysfunction
- Bladder or bowel dysfunction at onset
- >50 mononuclear leukocytes/mm³ or presence of polymorphonuclear leukocytes in CSF
- Distinct sensory level.
- Hexacarbon abuse
- Abnormal porphyrin metabolism
- Recent diphtheria infection
- Lead intoxication
- Other similar conditions: poliomyelitis, botulism, hysterical paralysis, toxic neuropathy.
- Motor conduction velocity <90% LLN (85% if dCMAP <50% LLN)
- Distal motor latency >110% upper limit of normal (ULN) (>120% if dCMAP <100% LLN)
- Proximal compound muscle action potential (pCMAP)/dCMAP ratio <0.5 and dCMAP >20% LLN
- F-response latency >120% ULN.
- At least 1 of the following in at least 2 nerves: mean corpuscular volume <70% LLN; distal motor latency >150% ULN; F-response latency >120% ULN, or >150% ULN (if distal CMAP <50% of LLN); or
- F-wave absence in 2 nerves with dCMAP ≥20% LLN or greater, with an additional parameter, in 1 other nerve; or
- pCMAP/dCMAP ratio <0.7 (excluding the tibial nerve) in 2 nerves, with an additional parameter in 1 other nerve.
- Diminution of muscle and sensory action potentials[64]
- None of the features of AIDP except 1 demyelinating feature allowed in 1 nerve if dCMAP <10% LLN
- Sensory action potential amplitudes less than LLN.
- None of the features of AIDP except 1 demyelinating feature allowed in 1 nerve if dCMAP <10% LLN
- Sensory action potential amplitudes normal.
- dCMAP absent in all nerves or present in only 1 nerve with dCMAP <10%.
- Reduced or absent sensory action potential response without slowing of sensory conduction velocity.[149]
- 150% prolongation of motor distal latency above ULN
- 70% slowing of motor conduction velocity below LLN
- 125% (150% if the distal negative-peak CMAP amplitude was 80% of LLN) prolongation of F wave latency above ULN
- Abnormal temporal dispersion (peak CMAP duration increase) in ≥2 nerves.
- Vital capacity <20 mL/kg (odds ratio 15.0)
- Maximal inspiratory pressure worse than -30 cmH₂O
- Maximal expiratory pressure <40 cmH₂O
- Reduction of 30% or more of vital capacity, maximal inspiratory pressure, or maximal expiratory pressure.
Treatment Approach
Supportive therapy: respiratory management
- Vital capacity is <20 mL/kg
- Maximal inspiratory pressure is worse than -30 cmH₂O (negative inspiratory force)
- Maximal expiratory pressure is <40 cmH₂O
- Vital capacity, maximal inspiratory pressure, or maximal expiratory pressure is reduced by 30% or more from baseline.[125]
Supportive therapy: cardiovascular management
Supportive therapy: deep vein thrombosis (DVT) prophylaxis
Supportive therapy: pain management
Choice of immunotherapy
- Mean time to recover walking with aid (primary outcome)
- Shorter time to onset of recovery (primary outcome)
- Improvement by one disability grade by 4 weeks (secondary outcome).
Intravenous immune globulin (IVIG)
- ambulatory patients ≤2 weeks from the onset of neurologic symptoms
- patients who require help to walk within 2 to 4 weeks from the onset of neurologic symptoms.
Plasma exchange (plasmapheresis)
- Within 4 weeks of symptom onset for nonambulatory patients
- Within 2 weeks of symptom onset for ambulatory patients.
Rehabilitation
Treatment Options
ambulatory within 2 weeks of onset or nonambulatory within 4 weeks of onset
without IgA deficiency or renal failure
intravenous immune globulin (IVIG)
Primary Options
- immune globulin (human)
400 mg/kg/day intravenously for 5 days
- immune globulin (human)
Comments
- IVIG is a pooled blood product and is associated with the risk of pathogen transmission (e.g., HIV, hepatitis B or C, Creutzfeldt-Jakob disease), although low. IVIG can precipitate anaphylaxis in an IgA-deficient person. However, it is much easier to administer than plasma exchange because it is a peripheral intravenous infusion. Treatment-related complications occur less frequently with IVIG than with plasma exchange.[158]
- A randomized controlled trial found no evidence of any benefit of a second IVIG course for patients with GBS with a poor prognosis, and there was a risk of serious adverse events. Therefore a second course of IVIG is not recommended.[165]
supportive treatment
Comments
- All patients with severe disease should have their pulse and blood pressure (BP) monitored until they are off ventilator support and have begun to recover.
- Deep vein thrombosis prophylaxis: appropriate prophylactic anticoagulation (e.g., a direct oral anticoagulant, subcutaneous unfractionated heparin, or a low molecular weight heparin) and support stockings are recommended for nonambulatory patients until they are able to walk independently.[152]
- Respiratory management: risk factors for progression to mechanical ventilation include short time from symptom onset to hospital admission, bulbar, neck, or facial weakness, severe muscle weakness at hospital admission, and autonomic instability.[128] [129] Algorithms or tools that predict a patient's risk of respiratory failure at admission (e.g., the Erasmus GBS Respiratory Insufficiency Score [EGRIS]) may be more reliable than individual variables.[128] [129] [11] Pulse oximetry and arterial blood gases should not be relied on, as hypoxia or hypercapnia is a late sign and patients will decompensate very quickly. Early intubation should be performed for patients with bulbar dysfunction, high risk of aspiration, and new atelectasis on chest x-ray. Elective intubation should be considered for patients with no or mild bulbar dysfunction if any of the following is present: vital capacity is <20 mL/kg; maximal inspiratory pressure is worse than -30 cmH₂O; maximal expiratory pressure is <40 cmH₂O; or vital capacity, maximal inspiratory pressure, or maximal expiratory pressure is reduced by 30% or more from baseline.[125] Once the patient is intubated, the need for tracheostomy should be addressed from week 2 onward. If there is no improvement of pulmonary function tests (PFTs), percutaneous tracheostomy should be performed. If there is improvement of PFT above baseline, tracheostomy may be delayed for an additional week before reassessment.[152]
- Hypotension: can be managed with fluid boluses. Intra-arterial BP monitoring should be started if BP is very labile.
- Hypertension: should be treated with short-acting agents (e.g., labetalol, esmolol, or nitroprusside) to prevent abrupt hypotension.
- Rehabilitation: all patients should undergo an individual program of rehabilitation in the acute phase, comprising gentle strengthening involving isometric, isotonic, isokinetic, and manual resistive and progressive resistive exercises. The focus is on proper limb positioning, posture, orthotics, and nutrition.[168] [11] A multidisciplinary approach has been shown to improve disability and quality of life, as well as reduce fatigue.[167]
plasma exchange
Comments
- Two to five plasma exchanges are often needed, depending on the severity of GBS.[50]
- The dose for plasma exchange, given through a central venous catheter, is 50 mL/kg bodyweight every other day for 7 to 14 days.[169]
- During administration, patients should be closely monitored for electrolyte abnormalities and coagulopathies.
supportive treatment
Comments
- All patients with severe disease should have their pulse and blood pressure (BP) monitored until they are off ventilator support and have begun to recover.
- Deep vein thrombosis prophylaxis: appropriate prophylactic anticoagulation (e.g., a direct oral anticoagulant, subcutaneous unfractionated heparin, or a low molecular weight heparin) and support stockings are recommended for nonambulatory patients until they are able to walk independently.[152]
- Respiratory management: risk factors for progression to mechanical ventilation include short time from symptom onset to hospital admission, bulbar, neck, or facial weakness, severe muscle weakness at hospital admission, and autonomic instability.[128] [129] Algorithms or tools that predict a patient's risk of respiratory failure at admission (e.g., the Erasmus GBS Respiratory Insufficiency Score [EGRIS]) may be more reliable than individual variables.[128] [129] [11] Pulse oximetry and arterial blood gases should not be relied on, as hypoxia or hypercapnia is a late sign and patients will decompensate very quickly. Early intubation should be performed for patients with bulbar dysfunction, high risk of aspiration, and new atelectasis on chest x-ray. Elective intubation should be considered for patients with no or mild bulbar dysfunction if any of the following is present: vital capacity is <20 mL/kg; maximal inspiratory pressure is worse than -30 cmH₂O; maximal expiratory pressure is <40 cmH₂O; or vital capacity, maximal inspiratory pressure, or maximal expiratory pressure is reduced by 30% or more from baseline.[125] Once the patient is intubated, the need for tracheostomy should be addressed from week 2 onward. If there is no improvement of pulmonary function test (PFT), percutaneous tracheostomy should be performed. If there is improvement of PFT above baseline, tracheostomy may be delayed for an additional week before reassessment.[152]
- Hypotension: can be managed with fluid boluses. Intra-arterial BP monitoring should be started if BP is very labile.
- Hypertension: should be treated with short-acting agents (e.g., labetalol, esmolol, or nitroprusside) to prevent abrupt hypotension.
- Rehabilitation: all patients should undergo an individual program of rehabilitation in the acute phase, comprising gentle strengthening involving isometric, isotonic, isokinetic, and manual resistive and progressive resistive exercises. The focus is on proper limb positioning, posture, orthotics, and nutrition.[152] [11] A multidisciplinary approach has been shown to improve disability and quality of life, as well as reduce fatigue.[167]
with IgA deficiency or renal failure
plasma exchange
Comments
- If there is a contraindication to intravenous immune globulin - namely, IgA deficiency or ongoing renal failure - plasma exchange is preferred over IVIG.
- Ambulatory patients: plasma exchange is recommended within 2 weeks from the onset of neurologic symptoms.
- Nonambulatory patients: plasma exchange is recommended within 4 weeks from onset.[158]
- Two to five plasma exchanges are often needed, depending on the severity of GBS.[50]
- The dose for plasma exchange, given through a central venous catheter (Mahurkar), is 50 mL/kg bodyweight every other day for 7 to 14 days.[169] During administration, patients should be closely monitored for electrolyte abnormalities and coagulopathies.
supportive treatment
Comments
- All patients with severe disease should have their pulse and blood pressure (BP) monitored until they are off ventilator support and have begun to recover.
- Deep vein thrombosis prophylaxis: appropriate prophylactic anticoagulation (e.g., a direct oral anticoagulant, subcutaneous unfractionated heparin, or a low molecular weight heparin) and support stockings are recommended for nonambulatory patients until they are able to walk independently.[152]
- Respiratory management: risk factors for progression to mechanical ventilation include short time from symptom onset to hospital admission, bulbar, neck, or facial weakness, severe muscle weakness at hospital admission, and autonomic instability.[128] [129] Algorithms or tools that predict a patient's risk of respiratory failure at admission (e.g., the Erasmus GBS Respiratory Insufficiency Score [EGRIS]) may be more reliable than individual variables.[128] [129] [11] Pulse oximetry and arterial blood gases should not be relied on, as hypoxia or hypercapnia is a late sign and patients will decompensate very quickly. Early intubation should be performed for patients with bulbar dysfunction, high risk of aspiration, and new atelectasis on chest x-ray. Elective intubation should be considered for patients with no or mild bulbar dysfunction if any of the following is present: vital capacity is <20 mL/kg; maximal inspiratory pressure is worse than -30 cmH₂O; maximal expiratory pressure is <40 cmH₂O; or vital capacity, maximal inspiratory pressure, or maximal expiratory pressure is reduced by 30% or more from baseline.[125] Once the patient is intubated, the need for tracheostomy should be addressed from week 2 onward. If there is no improvement of pulmonary function test (PFT), percutaneous tracheostomy should be performed. If there is improvement of PFT above baseline, tracheostomy may be delayed for an additional week before reassessment.[152]
- Hypotension: this can be managed with fluid boluses. Intra-arterial BP monitoring should be started if BP is very labile.
- Hypertension: should be treated with short-acting agents (e.g., labetalol, esmolol, or nitroprusside) to prevent abrupt hypotension.
- Rehabilitation: all patients should undergo an individual program of rehabilitation in the acute phase, comprising gentle strengthening involving isometric, isotonic, isokinetic, and manual resistive and progressive resistive exercises. The focus is on proper limb positioning, posture, orthotics, and nutrition.[152] [11] A multidisciplinary approach has been shown to improve disability and quality of life, as well as reduce fatigue.[167]
Emerging Tx
Complement activation inhibitors
Other therapies
Prevention
Secondary Prevention
Follow-Up Overview
Prognosis
Monitoring
Complications
Citations
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Guidelines
Diagnostic
Summary
Includes recommendations on the early recognition and diagnosis of GBS, including diagnostic criteria, clinical variants and differential diagnoses.Published by
ZikaPLAN
Published
2019
Summary
Interim guidance on the case definition of GBS and strategies to manage the syndrome, in the context of Zika virus.Published by
World Health Organization
Published
2016
Summary
Includes recommendations on the diagnosis of GBS in children and adolescents.Published by
German-Speaking Society of Neuropediatrics (GNP); Association of Scientific Medical Societies (AWMF)
Published
2020
Summary
Discusses the diagnostic evaluation of Guillain-Barré syndrome in the context of Zika virus infection.Published by
Public Health England
Published
2017
Summary
Diagnostic criteria for clinical diagnosis.Published by
GBS-consensus group of the Dutch Neuromuscular Research Support Centre
Published
2001
Summary
Neurophysiologic criteria for acute inflammatory demyelinating polyradiculoneuropathy, acute motor-sensory axonal neuropathy, and acute motor axonal neuropathy.Published by
Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group
Published
1998
Treatment
Summary
Includes recommendations on the management of GBS.Plasma exchange is recommended for nonambulatory patients within 4 weeks of onset and for ambulatory patients within 2 weeks of onset.Intravenous immune globulin (IVIG) is recommended within 2 to 4 weeks from onset for patients requiring help to walk.Combination treatment with plasma exchange followed by IVIG is not recommended.Published by
American Academy of Neurology
Published
2003 (reaffirmed 2022)
Summary
Includes recommendations on the management of GBS.Published by
ZikaPLAN
Published
2019
Summary
Includes recommendations on the management of GBS.Published by
World Health Organization
Published
2016
Summary
Includes recommendations on the management of GBS.Published by
Public Health England
Published
2017
Summary
Includes recommendations on the treatment of GBS in children and adolescents.Published by
German-Speaking Society of Neuropediatrics (GNP); Association of Scientific Medical Societies (AWMF)
Published
2020
Credits
Patient Instructions
- Advise patients to call their neurologist straight away with any worsening symptoms of weakness, numbness, paresthesia, facial weakness, difficulty with swallowing or breathing, or worsening bladder function.
- Advise patients to continue with physical therapy and occupational therapy.
- Provide information about possible long-term effects of GBS, such as fatigue, pain, and psychological problems, and encourage the patient to contact their neurologist if they experience any of these problems.
- Provide information about patient organisations, such as GBS/CIDP Foundation International (the international patient association for GBS).CBS/CIPD Foundation: International patient association for GBS