Guillain Barre Syndrome

Aka: Guillain Barre Syndrome, Guillain-Barre Syndrome, Landry-Guillain-Barre Syndrome, Guillain-Barre-Strohl Syndrome, Acute Inflammatory Demyelinating Polyradiculoneuropathy, Acute Motor Axonal Neuropathy, Acute Motor Sensory Axonal Neuropathy, Miller Fisher Syndrome

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II. Definition

  1. Progressive, idiopathic, symmetrical weakness and loss of Deep Tendon Reflexes reaching maximal intensity within 4 weeks

III. Epidemiology

  1. Incidence
    1. Annual Incidence: 1-3 cases per 100,000
    2. Incidence increases with advancing age
  2. Gender
    1. Male to female ratio: 3 to 2

IV. Precautions

  1. Presentation may have subtle, non-specific findings early in the course
    1. Focal Paresthesias
    2. Perception of weakness without motor weakness on exam
    3. Deep Tendon Reflexes may initially be preserved, and may appear to be asymmetric

V. Pathophysiology

  1. Inflammatory Neuropathy with cross reactivity between antibodies to infectious agents and neural antigens
  2. Lipooligosaccharides in Bacterial cell wall resemble gangliosides
  3. Anti-ganglioside antibodies form in response to acute infections (e.g. Diarrhea with Campylobacter jejuni)

VI. Types: Most Common Subtypes

  1. Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP)
    1. Most common subtype in the United States (90% of cases)
    2. Multifocal peripheral demyelination with slow remyelination
      1. Presents with progressive symmetrical weakness and hyporeflexia
      2. Symptoms start in legs in 90% of cases
      3. Myelin predominantly injured
  2. Acute Motor Axonal Neuropathy (AMAN)
    1. Accounts for 5-10% of Guillain-Barre Syndrome cases in U.S.
    2. Anti-ganglioside antibodies (GM1, GD1a, GalNAc-GD1a, GD1b) bind in peripheral Motor Nerve axons
    3. Most associated with Campylobacter jejuni infection (esp. younger patients, summer, China and Japan)
    4. Pure motor Neuropathy
    5. No demyelination (contrast with AIDP)
    6. Nodes of Ranvier predominantly injured
  3. Acute Motor Sensory Axonal Neuropathy (AMSCAN)
    1. Similar to AMAN subtype, but sensory Neuropathy predominates

VII. Types: Rare Subtypes

  1. Miller Fisher Syndrome (3% of cases)
    1. Anti-ganglioside antibodies (GQ1b, GD3, GT1a)
    2. Bilateral Ophthalmoplegia, Ataxia and areflexia
    3. Facial or bulbar weakness (50% of cases)
    4. Trunk and extremity weakness (50% of cases)
  2. Acute Panautonomic Neuropathy (rarest)
    1. Autonomic symptoms (cardiovascular and visual)
    2. Sensory loss
    3. Slow, often incomplete recovery

VIII. Risk Factors

  1. Acute infection precedes Guillain-Barre in 66% of cases
    1. Campylobacter jejuni (most common)
      1. Guillain-Barre occurs in one in 1000 patient infected with Campylobacter jejuni
    2. Epstein-Barr Virus (Mononucleosis)
      1. Associated with milder forms of Guillain-Barre
    3. Mycoplasma pneumoniae
    4. HaemophilusInfluenzae
    5. Cytomegalovirus
    6. HIV Infection
    7. Varicella Zoster Virus
    8. Vector-Borne Infections (Mosquito borne)
      1. West Nile Virus
      2. Zika Virus
  2. Vaccinations are associated with no significant increased risk
    1. H1N1 Influenza Vaccine was associated with a risk of 1-2 cases per 1 Million
    2. Tetanus Vaccine and hepatitis Vaccines also have minimal increased risk
    3. De Wals (2012) JAMA 308(2): 175-81 [PubMed]

IX. Course

  1. Peak timing
    1. Peaks by 2 weeks in 50% of cases
    2. Peaks by 3 weeks in 80% of cases
    3. Peaks by 4 weeks in 100% of cases
  2. Respiratory Failure requiring Mechanical Ventilation (25% of hospitalized cases)
    1. Onset within 1-2 weeks of symptoms

X. Symptoms

  1. Typically follows acute infectious illness
    1. Acute respiratory illness (fever, cough, Sore Throat)
    2. Acute gastrointestinal illness (Vomiting, Diarrhea)
      1. More likely to be associated with longer recovery and greater Disability (AMAN, AMSCAN subtypes)
  2. Progressive and ascending neurologic changes
    1. See signs below for more detailed description
    2. Tingling Paresthesias in distal extremities
    3. Proximal Muscle Weakness
  3. Myalgias (50% of cases)
    1. Deep, often severe aching pain in weak muscles
    2. Worse with movement, and at night
    3. Distribution (most common sites)
      1. Shoulder
      2. Back
      3. Posterior thighs

XI. Signs

  1. Progressive, symmetric neurologic symptoms
    1. Classically starts in distal extremities and ascends
      1. However lesions are random and patients may present first with Cranial Nerve deficit
    2. Progresses proximally over days to weeks (peaking by 2 to 4 weeks)
      1. Paresthesias (tingling) in distal extremities
      2. Proximal Muscle Weakness
      3. Cranial Nerves may be affected
        1. Facial muscles and eye movements may be affected (30-50% of cases)
        2. Ophthalmoplegia is rare except for in the Miller Fisher subtype
        3. Swallowing may be difficult
  2. Progressive, symmetric proximal Muscle Weakness
    1. Legs are affected more than arms (due to longer Neurons more apt to accumulate damage)
    2. Often onset in the legs and ascends to involve arms
    3. Observe patient standing and walking if possible
  3. Severe weakness (10-30% of cases)
    1. Quadriparesis
    2. Respiratory arrest requiring Ventilator support
    3. Bulbar failure (e.g. Dysphagia)
  4. Loss of Deep Tendon Reflexes within first few days
  5. Variable sensory losses
    1. Most prevalent in AMSCAN subtype
  6. Autonomic Dysfunction
    1. Hyperhidrosis
    2. Postural Hypotension and Blood Pressure fluctuation
    3. Tachycardia
    4. Urinary Retention
    5. Gastrointestinal pseudo-obstruction

XII. Diagnostics

  1. Cerebrospinal fluid (CSF)
    1. Albuminocytologic dissociation
      1. CSF Protein increased without increase in CSF White Blood Cells
    2. Increased CSF Protein >0.55 g/dl
      1. Increased by week 2 of symptoms in 90% of cases
    3. Normal CSF White Blood Cells Count (<10 cells/mm3)
      1. If increased, then consider other diagnosis
      2. Differential diagnosis if CSF WBCs increased
        1. Lyme Disease
        2. Cancer
        3. Human Immunodeficiency Virus (HIV Infection)
        4. Sarcoid Meningitis
  2. Electromyogram (EMG)
    1. Slowing of nerve conduction to <60% of normal velocity within weeks of onset in 80% of cases
    2. Specific findings
      1. Absent H reflex
      2. Low to absent sensory action potential amplitudes
      3. F wave response prolonged
  3. Evaluate respiratory function in all suspected cases
    1. Pulmonary Function Testing
    2. Arterial Blood Gas

XIII. Diagnosis: Major Criteria

  1. Bilateral, relatively symmetrical weakness or sensory deficit (typically with onset in legs)
  2. Decreased or absent Deep Tendon Reflexes
  3. Progressive and peaks within 4 weeks
  4. Not due to other cause

XIV. Differential Diagnosis: General

  1. See Acute Motor Weakness Causes
  2. See Symmetric Peripheral Neuropathy
  3. See Peripheral Neuropathy
  4. See Acute Motor Weakness Causes
  5. See Drug-Induced Polyneuropathy
  6. Brainstem Conditions
    1. Cerebrovascular Accident
    2. Encephalitis
    3. Meningitis
  7. Spinal Conditions
    1. Cord Compression (e.g. central spinal stenosis)
    2. Myelopathy
    3. Poliomyelitis
    4. Transverse Myelitis
  8. Muscular (and neuromuscular) Conditions
    1. Hypokalemia (includes periodic paralysis)
    2. Hypohosphatemia
    3. Myopathy
    4. Rhabdomyolysis
    5. Myasthenia Gravis
  9. Polyneuropathy conditions
    1. Arsenic
    2. Botulism
    3. Chronic inflammatory demyelinating Polyneuropathy
    4. Diabetes Mellitus
    5. Diphtheria
    6. Lyme Disease
    7. Lymphoma
    8. n-hexane (exposure with Inhalant Abuse)
    9. Paraneoplastic conditions
    10. Porphyria
    11. Sarcoidosis
    12. Uremia
    13. Vasculitis

XV. Differential Diagnosis: Findings suggestive of alternative diagnosis

  1. Neurotoxic findings
    1. Porphyria
    2. Diphtheria
    3. Botulism
    4. Toxic Neuropathy
    5. Inhalant Abuse
    6. Occupational exposures
    7. Lead Poisoning
  2. Exam and lab findings not suggestive of Guillain-Barre
    1. Pure sensory deficits (sensory-only GBS is rare)
    2. Significant asymmetric neurologic symptoms or findings
    3. Well demarcated line of senory deficit
    4. Bowel or Bladder symptoms predominate
    5. CSF Leukocytosis (see diagnostics)

XVI. Management: Criteria for ICU admission (risk of Respiratory Failure)

  1. Pulmonary Function Test abnormalities
    1. Vital Capacity < 20 ml/kg (or <60% of predicted)
    2. Peak inspiratory pressure <30 cm H2O
    3. Peak expiratory pressure <40 cm H2O
  2. Poor swallowing
  3. Ineffective cough
  4. Aspiration Pneumonia
  5. Autonomic Dysfunction
  6. Increased Respiratory Rate
  7. Dyspnea
  8. Severe Muscle Weakness
    1. Unable to lift elbows above bed or flex arms
    2. Unable to lift head above bed
    3. Unable to stand
  9. Other predictors of Respiratory Failure and Mechanical Ventilation
    1. Rapid progression of symptoms over <7 days
    2. Arm weakness
    3. Elevated Liver Function Tests
    4. Bulbar palsy

XVII. Management: Indications for Intubation

  1. Consider when patient reports Dyspnea
  2. Forced Vital Capacity <20 ml/kg
    1. Some criteria differentiate with bulbar weakness
    2. Vital Capacity 15-18 ml/kg with bulbar weakness
    3. Vital Capacity <15 ml/kg without bulbar weakness
  3. Pressure measurement criteria
    1. Maximal inspiratory pressure <30 cm H2O
    2. Maximal expiratory pressure <40 cm H2O

XVIII. Management: Supportive care

  1. Monitor for Respiratory Failure (25%)
    1. Incentive Spirometry
    2. Control Secretions
  2. Monitor for autonomic failure
    1. Arrhythmias
    2. Blood Pressure abnormalities
  3. Turn patient frequently (prevents Decubitus Ulcers)
  4. Subcutaneous Heparin (prevents Pulmonary Embolism)
  5. Fluid management (Observe for SIADH with low Sodium)
  6. Nutrition
  7. Monitor for infections (Urinary Tract Infection in 20%)
  8. Prevent exposure Keratitis
  9. Physical therapy reduces pain
    1. Gentle massage
    2. Range of motion
    3. Position changes
  10. Pain management (significant pain in affected muscles)
    1. See physical therapy above
    2. NSAIDs
    3. Narcotics (use caution due to ileus)
    4. Carbamazepine (Tegretol)
    5. Gabapentin (Neurontin)
    6. Corticosteroids are no longer recommended
      1. Van Der Meche (1992) N Engl J Med 326:1123-9 [PubMed]
  11. Ventilatory management
    1. Indicators to start weaning
      1. Vital Capacity > 15 ml/kg (if no lung disease)
    2. Weaning
      1. First: Change to IMV
      2. Later: lower the Respiratory Rate

XIX. Management: Specific Treatment

  1. General
    1. Best efficacy if treatment given within first 2 weeks
    2. Both plasma exchange and IV-Ig are equally effective (choose one)
    3. Corticosteroids are not recommended
      1. No evidence of improved outcome
      2. Risk of delayed recovery
  2. Plasma Exchange (Plasmapheresis)
    1. Protocol
      1. Number of exchanges depends on severity (up to five exchanges total)
        1. Mild Guillain-Barre: 2 exchanges
        2. Moderate to severe Guillain-Barre: 4-5 exchanges
      2. Perform one exchange every other day for 4 to 10 days (2-5 exchanges)
      3. Best outcomes if started within first 7 days from onset
    2. Special Indications
      1. Pregnancy
      2. Renal Insufficiency
      3. IgA deficient
      4. Has not been studied in children
  3. IV Immunoglobulin
    1. Easier management with fewer complications than plasma exchange
    2. Dose
      1. Standard: IV-Ig 400 mg/kg daily for 5-7 days
      2. Alternative: IV-Ig 2g/kg total with divided dosing over 2 days
    3. Special Indications
      1. Children
      2. Poor venous access
      3. Autonomic instability

XX. Prognosis

  1. Full recovery within 6-12 months in 85% of cases
  2. Neurologic sequelae in up to 15-20%
    1. Foot drop
    2. Hand intrinsic Muscle Weakness
    3. Sensory Ataxia
  3. Median hospitalization duration: 7 days
  4. Relapse rate <3-5%
  5. Mortality rate <3-5% overall
    1. Mortality approaches 20% in some studies if Mechanical Ventilation required
  6. Predictors of poor prognosis or longterm Disability
    1. Age over 60 years
    2. Rapidly progressive, severe disease
    3. EMG showing axonal loss
    4. Prolonged Mechanical Ventilation >1 month
    5. Absence of motor response
    6. Inability to walk at 14 days
  7. Trigger conditions associated with worse outcomes
    1. Preceding Diarrheal illness (often Campylobacter jejuni)
    2. Cytomegalovirus infection

XXI. Resources

  1. National Institute of Neurological Disorders and Stroke (NINDS)
    1. http://www.ninds.nih.gov/disorders/gbs/gbs.htm
  2. Guillain-Barre and Chronic Inflammatory Demyelinating Polyneuropathy Foundation International
    1. http://www.gbs-cidp.org/

XXII. References

  1. Gallagher in Marx (2002) Rosen's Emergency Med, p. 1510
  2. Shields in Goetz (2003) Neurology, p. 1085-90
  3. Weinstock et al. in Herbert (2015) EM:Rap 15(1): 7
  4. Alshekhlee (2008) Neurology 70(18): 1608-13 [PubMed]
  5. Cornblath (2009) Ann Nuerol 66(5): 569-70 [PubMed]
  6. Joseph (2002) Adolesc Med 13:487-94 [PubMed]
  7. Newswanger (2004) Am Fam Physician 69(10):2405-10 [PubMed]
  8. van Doorn (2008) Lancet Neurol 7(10): 939-50 [PubMed]
  9. Walling (2013) Am Fam Physician 87(3): 191-7 [PubMed]

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Ontology: Guillain-Barre Syndrome (C0018378)

Definition (MEDLINEPLUS)

Guillain-Barre syndrome is a rare disorder that causes your immune system to attack your peripheral nervous system (PNS). The PNS nerves connect your brain and spinal cord with the rest of your body. Damage to these nerves makes it hard for them to transmit signals. As a result, your muscles have trouble responding to your brain. No one knows what causes the syndrome. Sometimes it is triggered by an infection, surgery, or a vaccination.

The first symptom is usually weakness or a tingling feeling in your legs. The feeling can spread to your upper body. In severe cases, you become almost paralyzed. This is life-threatening. You might need a respirator to breathe. Symptoms usually worsen over a period of weeks and then stabilize.

Guillain-Barre can be hard to diagnose. Possible tests include nerve tests and a spinal tap. Most people recover. Recovery can take a few weeks to a few years. Treatment can help symptoms, and may include medicines or a procedure called plasma exchange.

NIH: National Institute of Neurological Disorders and Stroke
Definition (MSHCZE) Zánětlivé onemocnění nervových kořenů, které se projevuje porušenou citlivostí a hybností končetin. Kromě míšních kořenů mohou být postiženy i hlavové nervy, popř. i další části CNS. Podle postižení a průběhu se rozlišují různé formy (např. ascendentní, descendentní, pseudomyopatická s nápadnými svalovými atrofiemi aj.). Vzniká sekundárně, předpokládá se, že patogeneticky se uplatňují autoimunitní procesy charakteru vaskulitidy v oblasti míšních kořenů. Obv. následuje po chřipkovém onemocnění či jiné infekci (např. při Lymeské borrelióze), které zřejmě chorobu iniciují. Po několika týdnech dochází většinou k uzdravení, jen někdy choroba postupuje dále a postihuje i dýchací svaly (Landryho vzestupná paralýza). Terapie je zaměřena imunosupresivně (kortikoidy, imunosupresiva, plasmaferéza), podávají se rovněž vitaminy skupiny B, významná je rehabilitace. Syn. polyradikuloneuritida. (cit. Velký lékařský slovník online, 2013 http://lekarske.slovniky.cz/ )
Definition (NCI) An acute, autoimmune inflammatory process affecting the peripheral nervous system and nerve roots. It results in demyelination. It is often caused by an acute viral or bacterial infection.
Definition (MSH) An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)
Definition (CSP) progressive ascending motor neuron paralysis of unknown etiology, frequently following an enteric or respiratory infection.
Concepts Disease or Syndrome (T047)
MSH D020275
ICD9 357.0
ICD10 G61.0
SnomedCT 40956001, 155082001, 193173004, 267707000, 193176007, 314091000009101, 128085000, 129131007, 193174005
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Italian Sindrome di Guillain-Barre, Paralisi ascendente, Polineurite infettiva acuta, Polineuropatia infiammatoria acuta, Poliradicoloneuropatia infiammatoria acuta demielinizzante, AIDP, Neuropatia immunomediata acuta, Poliradicoloneuropatia infiammatoria acuta, Sindrome di Landry-Guillain-Barré, GBS, Sindrome di Guillain-Barré
Dutch paralyse opstijgend, Guillain Barré syndroom, acute infectieuze polyneuritis, syndroom Guillain-Barré, acute inflammatoire demyeliniserende polyradiculoneuropathie, Landry; paralyse, ascendans; paralyse, infectieus; polyneuritis, multipel; neuritis, infectieus, acuut, neuritis; multipel, infectieus, acuut, paralyse; Landry, paralyse; ascendans, polyneuritis; acuut, polyneuritis; infectieus, polyneuritis; postinfectieus, postinfectieus; polyneuritis, Syndroom van Guillain-Barrs, AIDP, Acute auto-immuunneuropathie, Acute inflammatoire demyeliniserende polyradiculoneuropathie, Acute inflammatoire polyneuropathie, Polyradiculoneuropathie, acute inflammatoire, Guillain-Barré-syndroom, Landry-Guillain-Barré-syndroom, Syndroom, Guillain-Barré-
French Polynévrite aiguë infectieuse, Paralysie ascendante, Polyradiculonévrite démyélinisante inflammatoire aigüe, PARALYSIE ASCENDANTE, SYNDROME DE GUILLAIN-BARRE, Polyradiculoneuropathie inflammatoire démyélinisante aiguë, Syndrome de Guillain-Barre, Polyradiculonévrite aiguë inflammatoire, Polyradiculonévrite de Guillain-Barré, Syndrome de Guillain-Barré, Syndrome de Landry-Guillain-Barré, Polyradiculonévrite démyélinisante inflammatoire aiguë, SGB (Syndrome de Guillain-Barré)
German Guillain Barre Syndrom, Syndrom, Guillain-Barre, akute infektioese Polyneuritis, Paralyse, aufsteigend, akut inflammatorische demyelinisierende Polyradikulpathie, GUILLAIN-BARRE SYNDROM, Guillain-Barre-Syndrom, LAEHMUNG AUFSTEIGEND, AIDP, Akute autoimmune Neuropathie, Akute entzündliche demyelinisierende Polyradikuloneuropathie, Akute entzündliche Polyneuropathie, Guillain-Barré-Syndrom, Landry-Guillain-Barré-Syndrom, Polyradikuloneuritis Typ Guillain-Barré, Polyradikuloneuropathie, akute entzündliche
Portuguese Paralisia ascendente, Polinevrite infecciosa aguda, PARALISIA ASCENDENTE, SINDROME DE GUILLAIN BARRE, Poliradiculoneuropatia inflamatória desmielinizante aguda, Neuropatia Autoimune Aguda, Polineuropatia Inflamatória Aguda, Polirradiculoneuropatia Desmielinizante Inflamatória Aguda, Polirradiculoneuropatia Inflamatória Aguda, Síndrome de Guillain-Barré, Síndrome de Landry-Guillain-Barré
Japanese ギラン・バレー症候群, 上行性麻痺, ｼﾞｮｳｺｳｾｲﾏﾋ, ｷﾞﾗﾝﾊﾞﾚｰｼｮｳｺｳｸﾞﾝ, ｷｭｳｾｲｶﾝｾﾝｾｲﾀﾊﾂｼﾝｹｲｴﾝ, ｷｭｳｾｲｴﾝｼｮｳｾｲﾀﾞﾂｽﾞｲｾｲﾀﾊﾂｺﾝﾆｭｰﾛﾊﾟﾁｰ, 急性炎症性脱髄性多発根ニューロパチー, ギラン-バレー症候群, 急性自己免疫性神経障害, 急性特発性多発性神経炎, 自己免疫性神経障害-急性, 自己免疫性ニューロパシー-急性, 多発神経炎-感染性-急性, バレー-ギラン症候群, 急性炎症性脱髄性多発根神経炎, 急性感染性多発性神経炎, 急性上行性脊髄麻痺, ギラン-バレ多発性神経炎, 自己免疫性神経異常症-急性, 感染後多発性神経炎, 急性感染後多発性神経炎, 急性特発性多発神経炎, 急性熱性多発性神経炎, ギラン-バレ多発神経炎, 多発神経炎-感染後, 多発神経障害-炎症性-急性, 多発性根神経障害-脱髄性-炎症性-急性, 多発性神経炎-感染後-急性, Guillain-Barre症候群, 感染後多発性神経障害-急性, 急性炎症性脱髄多発根神経障害, 急性炎症性ポリニューロパシー, ギラン･バレ症候群, 多発神経炎-感染後-急性, 多発性神経炎-感染後, ポリニューロパシー-炎症性-急性, ランドリー症候群, 炎症性ポリニューロパシー-急性, 急性炎症性多発神経障害, 急性感染後多発神経障害, 急性熱性多発神経炎, バレ-ギラン症候群, 炎症性多発神経障害-急性, 感染後多発神経炎, 感染後多発神経炎-急性, 感染後多発神経障害-急性, 感染性多発性神経炎-急性, 急性自己免疫性ニューロパシー, ギラン-バレー多発性神経炎, 神経障害-自己免疫性-急性, 脊髄麻痺-上行性-急性, 多発性神経炎-感染性-急性, 脱髄性多発根神経炎-炎症性-急性, ニューロパシー-自己免疫性-急性, 炎症性多発性神経障害-急性, 炎症性脱髄性多発根神経炎-急性, 炎症性脱髄性多発性根神経障害-急性, 感染後多発性神経炎-急性, 急性感染後多発性神経障害, 急性自己免疫性神経異常症, ギラン-バレ症候群, 神経異常症-自己免疫性-急性, 上行性脊髄麻痺-急性, 多発性神経障害-感染後-急性, 脱髄性多発性根神経障害-炎症性-急性, 急性炎症性脱髄性多発性根神経障害, 感染性多発神経炎-急性, 急性炎症性多発性神経障害, 急性感染後多発神経炎, 急性感染性多発神経炎, ギラン-バレー多発神経炎, ギラン･バレー症候群, 多発神経障害-感染後-急性, 多発性神経障害-炎症性-急性, ランドリー麻痺
Swedish Guillain-Barres syndrom
Czech Guillainův-Barrého syndrom, Landryho-Guillainův-Barrého syndrom, akutní zánětlivá demyelinizační polyradikuloneuropatie, akutní autoimunitní neuropatie, akutní zánětlivá polyneuropatie, AIDP, Akutní infekční polyneuritida, Guillain-Barre syndrom, Syndrom Guillain-Barre, Akutní zánětová demyelinizační polyradikuloneuropatie, Obrna vzestupná, Guillainův-Barréův syndrom
Finnish Polyradikuliitti
Russian NEVROPATIIA AUTOIMMUNNAIA OSTRAIA, POLIRADIKULONEVROPATIIA VOSPALITEL'NAIA OSTRAIA, POLIRADIKULONEVROPATIIA DEMIELINIZIRUIUSHCHAIA VOSPALITEL'NAIA OSTRAIA, GIIENA-BARRE SINDROM, ГИЙЕНА-БАРРЕ СИНДРОМ, НЕВРОПАТИЯ АУТОИММУННАЯ ОСТРАЯ, ПОЛИРАДИКУЛОНЕВРОПАТИЯ ВОСПАЛИТЕЛЬНАЯ ОСТРАЯ, ПОЛИРАДИКУЛОНЕВРОПАТИЯ ДЕМИЕЛИНИЗИРУЮЩАЯ ВОСПАЛИТЕЛЬНАЯ ОСТРАЯ
Korean 길랑-바레 증후군
Polish Polineuropatia zapalna, Neuropatia autoimmunologiczna ostra, Zespół Landry-Guillaina-Barrego, GBS, Zespół Guillaina-Barrego
Hungarian Felszálló bénulás, Guillain-Barré-syndroma, Guillain-Barré-tünetegyüttes, Guillain-Barré syndroma, Acut fertőző polyneuritis, Acut gyulladásos demyelinisatiós polyradiculo-neuropathia
Norwegian Guillain-Barré syndrom, Guillain-Barrés syndrom, Akutt inflammatorisk demyeliniserende polyradikulonevropati, AIDP
Derived from the NIH UMLS (Unified Medical Language System)

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