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Neurology›Condition·Updated Jul 11, 2026·v1

Guillain-Barre Syndrome

Guillain-Barré syndrome is an acute immune-mediated polyradiculoneuropathy presenting with rapidly progressive symmetric limb weakness, areflexia, and a monophasic course. Diagnosis is clinical, supported by CSF albuminocytologic dissociation and nerve conduction studies. First-line immunotherapy with IVIG (0.4 g/kg/day × 5 days) or plasma exchange (5 sessions) is equally effective. Corticosteroids are ineffective and should be avoided. Prognosis is generally good, but 20-30% require mechanical ventilation and 20% have residual disability at 6 months. Early recognition, respiratory monitoring, and prompt immunotherapy are critical to reducing mortality and long-term disability.

High Evidence210 references·10,190 words·41 min read·v1
Guillain-Barre syndromeacute flaccid paralysisimmune-mediated polyneuropathyIVIGplasma exchangeMiller Fisher syndromeCampylobacter jejunialbuminocytologic dissociationmEGOSEGRIS

Quick Reference

RxDrug of choiceIVIG 0.4 g/kg/day × 5 days (total 2 g/kg) OR plasma exchange (5 sessions, 1-1.5 plasma volumes each)
AltAlternativesNone proven; immunoadsorption or efgartigimod in refractory cases (limited evidence); complement inhibitors (eculizumab, ANX005) not recommended outside clinical trials
⊘AvoidCorticosteroids (monotherapy), ineffective and may worsen outcomes; routine combination of IVIG + PE, no benefit, increased cost; second IVIG course in poor-prognosis patients, no benefit, increased adverse events
DxTest of choiceCSF analysis for albuminocytologic dissociation (elevated protein, normal WBC <50/μL); nerve conduction studies (NCS/EMG) for subtype classification and prognostication
ScKey scoremEGOS (day 7) for 6-month outcome; EGRIS (admission) for respiratory failure risk; Brighton criteria for diagnostic certainty
→When to referICU if bulbar weakness, FVC <20 mL/kg, or autonomic instability; neurology for diagnosis and treatment; rehabilitation after acute phase for functional recovery; pulmonology for prolonged mechanical ventilation
Acute progressive symmetric weakness + areflexia = GBS until proven otherwise; treat with IVIG or PE immediately; avoid steroids; monitor FVC closely; use mEGOS/EGRIS for prognostication; no role for long-term immunotherapy.
Guillain-Barré syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy and the most common cause of acute flaccid paralysis worldwide. The hallmark is rapidly progressive, symmetric limb weakness with areflexia, reaching nadir within 4 weeks in 97% of patients. Diagnosis is clinical, supported by CSF albuminocytologic dissociation and nerve conduction studies. First-line immunotherapy with IVIG or plasma exchange is equally effective and should be initiated promptly. Corticosteroids are ineffective and harmful. With modern treatment, mortality is 3-10%, but 20% of patients require mechanical ventilation and 20% have persistent disability. Early recognition, respiratory monitoring, and multidisciplinary care are critical to optimizing outcomes.

Overview and Recommendations

Background

  • •Guillain-Barré syndrome (GBS) is an acute, monophasic, immune-mediated polyradiculoneuropathy that causes rapidly progressive bilateral limb weakness and areflexia, with an annual incidence of 1-2 per 100,000 population. It is the most common cause of acute flaccid paralysis globally, affecting all ages with a slight male predominance and a median age of 57 years.
  • •The central pathophysiology is molecular mimicry: antecedent infections, most commonly Campylobacter jejuni (30% of cases), cytomegalovirus, Epstein-Barr virus, Zika virus, and SARS-CoV-2, trigger cross-reactive IgG autoantibodies against gangliosides expressed at the nodes of Ranvier. Antibody binding activates complement, disrupting voltage-gated sodium channel clusters and leading to conduction block and axonal degeneration.
  • •GBS encompasses several subtypes. Acute inflammatory demyelinating polyneuropathy (AIDP) is the most common in Europe and the Americas, characterized by demyelination on nerve conduction studies. Acute motor axonal neuropathy (AMAN) is more frequent in Asia and associated with anti-GM1 and anti-GD1a antibodies. Miller Fisher syndrome (MFS) presents with ophthalmoplegia, ataxia, and areflexia and is highly specific for anti-GQ1b IgG.
  • •Without treatment, mortality historically exceeded 15%. With modern immunotherapy (IVIG or plasma exchange), case-fatality is 3-10%, and approximately 20% of survivors remain unable to walk independently at 6 months. Respiratory failure requiring mechanical ventilation occurs in 20-30% of patients, and autonomic dysfunction in up to 70%.
  • •The Brighton criteria provide a standardized framework for diagnostic certainty, requiring bilateral limb weakness, areflexia, a monophasic course, CSF albuminocytologic dissociation, and electrophysiologic evidence of neuropathy. The modified Erasmus GBS Outcome Score (mEGOS) and Erasmus GBS Respiratory Insufficiency Score (EGRIS) are validated tools for early prognostication.

Evaluation

  • •Suspect GBS in any patient presenting with rapidly progressive, bilateral, symmetric limb weakness that evolves over days to 4 weeks, accompanied by decreased or absent deep tendon reflexes in affected limbs. Ask about antecedent infectious illness (diarrheal or respiratory) within the prior 6 weeks, as 75% of cases have a preceding trigger.
  • •Examine for ascending motor weakness, starting in the lower extremities and progressing to the arms, trunk, and cranial nerves. Document the Medical Research Council (MRC) sum score (0-60) to quantify severity. Assess for bilateral facial weakness (most common cranial nerve deficit, in 50% of cases), bulbar weakness (dysphagia, dysarthria, stridor), and ocular motor abnormalities (suggesting MFS).
  • •Evaluate respiratory status immediately: measure forced vital capacity (FVC) every 4-6 hours. An FVC < 20 mL/kg or a >30% decline from baseline indicates impending respiratory failure; a decline to < 15 mL/kg is a red flag for intubation. Check for paradoxical abdominal breathing and inability to count in one breath.
  • •Order CSF analysis (lumbar puncture). Albuminocytologic dissociation, elevated protein (>0.45 g/L) with a normal white cell count (<50 cells/μL), is the hallmark, present in 70% of patients overall but only 57% within the first 4 days of symptom onset. Normal CSF protein early does not exclude GBS. A pleocytosis >50 cells/μL should prompt a search for alternative diagnoses such as infectious myelitis or HIV polyradiculoneuropathy.
  • •Perform nerve conduction studies (NCS) and electromyography (EMG) within the first week to confirm peripheral nerve involvement and classify the electrophysiologic subtype. Demyelinating findings (prolonged distal motor latencies, slowed conduction velocities, conduction block) suggest AIDP; reduced compound muscle action potential amplitudes with preserved conduction velocities suggest axonal subtypes (AMAN, AMSAN).
  • •Apply the Brighton criteria for diagnostic certainty. Level 1 (highest certainty) requires bilateral limb weakness, areflexia, monophasic course, time from onset to nadir between 12 hours and 28 days, CSF protein elevation, and NCS abnormalities. Level 4 is used when clinical features are present but ancillary studies are unavailable or normal.
  • •Consider selective antibody testing in atypical presentations. Anti-GQ1b IgG is highly specific for Miller Fisher syndrome (sensitivity >90%) and Bickerstaff brainstem encephalitis. Anti-GM1 IgG is associated with AMAN and preceding C. jejuni infection. Anti-pan-neurofascin antibodies should be tested in patients >60 years with severe, progressive GBS or prolonged mechanical ventilation, as they define autoimmune nodopathy requiring rituximab therapy.
  • •Use the Erasmus GBS Respiratory Insufficiency Score (EGRIS) at admission to predict the need for mechanical ventilation. EGRIS incorporates days between weakness onset and admission, MRC sum score, and facial/bulbar weakness. A score ≥4 confers a 30-91% risk of respiratory failure within the first week and should prompt ICU admission.
  • •Use the modified Erasmus GBS Outcome Score (mEGOS) at day 7 to predict inability to walk unaided at 6 months. The score uses age, preceding diarrhea, and MRC sum score at day 7. A mEGOS ≥6 identifies poor prognosis and was the entry criterion for the negative SID-GBS trial of a second IVIG course.
  • •Consider differential diagnoses: transverse myelitis (sensory level, sphincter dysfunction, hyperreflexia), acute-onset CIDP (progression >8 weeks or ≥3 treatment-related fluctuations), myasthenia gravis (fatigability, ocular/bulbar predominance, no sensory loss), botulism (descending paralysis, fixed dilated pupils, outbreak setting), tick paralysis (ascending flaccid paralysis, tick on body, no CSF abnormalities), and vasculitic neuropathy (asymmetric mononeuritis multiplex, eosinophilia, ANCA).

Management

  • •Admit all patients with rapid progression, bulbar weakness, or autonomic signs to an intensive care unit (ICU) or step-down unit for continuous cardiorespiratory monitoring. Measure FVC every 4-6 hours; elective intubation is indicated when FVC < 15 mL/kg, maximal inspiratory pressure < 20 cm H₂O, or the patient cannot clear secretions.
  • •Initiate disease-modifying therapy as soon as the diagnosis is established, ideally within the first week of symptom onset. Do not delay treatment while awaiting confirmatory NCS or CSF results if the clinical picture is highly suggestive.
  • •First-line immunotherapy: Intravenous immunoglobulin (IVIG) 0.4 g/kg/day infused over 5 consecutive days (total dose 2 g/kg). Alternatively, plasma exchange (PE): 5 sessions of 1-1.5 plasma volumes over 1-2 weeks, exchanging with 5% albumin. Both are equally effective (Level A evidence).
  • •Choose IVIG in patients with hemodynamic instability, difficult venous access, coagulopathy, or active infection. Choose PE in patients with IgA deficiency (risk of anaphylaxis with IVIG) or hyperviscosity syndromes. Do not routinely combine IVIG and PE; sequential therapy does not improve outcomes and increases cost.
  • •Monitor for treatment-related fluctuation (TRF): clinical worsening within 8 weeks after initial improvement or stabilization, occurring in 5-10% of patients. If TRF occurs, re-treat with the same modality (IVIG or PE) at the same dose. More than 2 fluctuations or deterioration after 8 weeks suggests acute-onset CIDP, not GBS.
  • •Do NOT use corticosteroids as monotherapy, they are ineffective and may worsen outcomes (Level A evidence against). A 2004 trial of methylprednisolone added to IVIG showed a borderline benefit only after adjusted analysis, but this is not considered practice-changing.
  • •For patients with poor prognosis (mEGOS ≥6), a second IVIG course (2 g/kg) is not recommended. The SID-GBS trial found no benefit and increased serious adverse events (35% vs 16%), including thromboembolic events and death.
  • •Provide DVT/PE prophylaxis: subcutaneous enoxaparin 40 mg once daily (or unfractionated heparin 5000 units three times daily) plus graduated compression stockings, started on admission unless contraindicated.
  • •Manage neuropathic pain: first-line gabapentin (starting 300 mg three times daily, titrate to 900-3600 mg/day) or pregabalin (75-150 mg twice daily). Amitriptyline 10-50 mg at bedtime is an alternative for burning pain with sleep disturbance. Avoid opioids for routine pain to reduce risk of respiratory depression and ileus.
  • •Begin early rehabilitation as soon as medically stable: respiratory muscle training, range-of-motion exercises, strengthening, balance and gait training. Occupational therapy addresses fine motor skills; speech therapy manages dysphagia. Sessions of 45-60 minutes, 3-4 times per week for at least 12 weeks are associated with best outcomes.
  • •Monitor for autonomic dysfunction: labile blood pressure, cardiac arrhythmias, ileus, urinary retention. Use short-acting agents (e.g., labetalol for hypertension, phenylephrine for hypotension). Treat bradyarrhythmias with atropine or temporary pacing. Ileus may require nasogastric decompression and prokinetic agents.
  • •Monitor for SIADH: check serum sodium daily. Hyponatremia occurs in 48% of patients and is associated with bulbar weakness and need for ventilatory support. Fluid restrict if symptomatic; avoid hypotonic IV fluids.
  • •Refer to neurology for diagnosis and management; respiratory therapy and speech therapy for bulbar weakness; physical and occupational therapy for functional recovery; and a rehabilitation specialist for long-term planning. The acute immunotherapy phase is a single course; no maintenance immunosuppression is indicated.
  • •Discharge criteria: stable respiratory status (FVC > 20 mL/kg, no oxygen requirement), ability to manage oral secretions, controlled pain, and a clear rehabilitation plan. Patients with residual disability should be transitioned to an inpatient rehabilitation facility or home health services.

Board Review — High Yield

  • •Albuminocytologic dissociation, elevated CSF protein with normal WBC (<50/μL) is the hallmark of GBS, but sensitivity is only 57% within the first 4 days; normal CSF does not exclude GBS.
  • •Anti-GQ1b antibody, highly specific for Miller Fisher syndrome (ophthalmoplegia, ataxia, areflexia); present in >90% of MFS cases.
  • •Brighton criteria Level 1, requires bilateral limb weakness, areflexia, monophasic course, CSF protein elevation, and NCS abnormalities; used for research and vaccine safety surveillance.
  • •mEGOS (day 7), uses age, preceding diarrhea, and MRC sum score to predict inability to walk unaided at 6 months; AUC 0.87 at day 7; score ≥6 defines poor prognosis.
  • •EGRIS, predicts need for mechanical ventilation within first week; score ≥4 indicates high risk (30-91%) and should prompt ICU admission.
  • •IVIG vs PE, equivalent efficacy for severe GBS; choice based on contraindications; combination not beneficial (1997 trial, N=383).
  • •Corticosteroids, contraindicated as monotherapy; worsen outcomes (1978 trial: steroids worse than placebo; 2004 trial: methylprednisolone+IVIG borderline benefit only after adjustment).
  • •Treatment-related fluctuation (TRF), worsening within 8 weeks after initial improvement; occurs in 5-10%; re-treat with same modality; >2 TRFs or deterioration after 8 weeks suggests acute-onset CIDP.
  • •Axonal variant (AMAN), more common in Asia; associated with anti-GM1 antibodies; can have preserved or brisk reflexes; may recover rapidly if conduction block is reversible.
  • •Respiratory failure threshold, FVC <20 mL/kg triggers ICU admission; FVC <15 mL/kg or inability to clear secretions indicates intubation; elective intubation is safer than emergency.

Deep Dive — Evidence Details

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