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Guillain-Barré Syndrome

Acute Immune-Mediated Polyradiculoneuropathy with Ascending Paralysis Requiring Urgent Treatment

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

References (5)

This content is for informational purposes only and does not constitute medical advice. You can book an appointment at our Nöroloji department. Book Appointment →

What is Guillain-Barré Syndrome?

Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy and the most common cause of acute flaccid paralysis worldwide; annual incidence 1–2 per 100,000.

Pathophysiology: post-infectious autoimmune attack on peripheral nerves; molecular mimicry between microbial antigens (Campylobacter jejuni, CMV, EBV, Mycoplasma, Zika virus) and gangliosides on peripheral nerve myelin or axon; T-cell and antibody-mediated demyelination.

Subtypes: AIDP (acute inflammatory demyelinating polyradiculoneuropathy, 85–90% in Europe/North America), AMAN (acute motor axonal neuropathy, more common in Asia and pediatric population), AMSAN (acute motor and sensory axonal neuropathy), Miller Fisher syndrome (ophthalmoplegia, ataxia, areflexia).

Clinical presentation: ascending symmetric weakness peaking in 2–4 weeks, areflexia, sensory symptoms, autonomic instability, respiratory failure (20–30% require mechanical ventilation).

Symptoms

Ascending symmetric weakness starting in lower extremities, progressing proximally over days to weeks
Reduced or absent deep tendon reflexes (areflexia) — hallmark feature
Sensory symptoms: paresthesias, numbness, often distal and symmetric
Cranial nerve involvement: facial weakness (50%, often bilateral), bulbar weakness with dysphagia and dysarthria, ophthalmoplegia
Respiratory failure: weak inspiratory effort, decreased vital capacity, paradoxical breathing, requires mechanical ventilation in 20–30%
Autonomic dysfunction: blood pressure fluctuations, arrhythmias, urinary retention, ileus
Pain: severe back, neck or limb pain (50–80%), often early symptom
Miller Fisher variant: ophthalmoplegia, ataxia, areflexia (without significant weakness)
Disease nadir: typically 2–4 weeks after onset; recovery over weeks to months

Risk Factors

Recent infection (60–70%): respiratory or gastrointestinal illness 1–6 weeks before onset
Campylobacter jejuni (most common, 30%, associated with AMAN and severe disease)
Cytomegalovirus, Epstein-Barr virus, Mycoplasma pneumoniae
Influenza, Zika virus (epidemic regions), HIV
COVID-19 association (case reports)
Vaccination (rare, weak association with influenza, swine flu vaccines historically)
Surgery and trauma (postoperative GBS)
Bone marrow transplantation, malignancy
Older age (incidence increases with age)
Male sex (slight male predominance)

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Rapidly progressive weakness, especially with ascending pattern
  • New onset weakness with areflexia
  • Sensory symptoms accompanied by weakness
  • Cranial nerve dysfunction: facial weakness, dysphagia, dysarthria
  • Respiratory difficulty, shortness of breath (urgent)
  • Autonomic symptoms: severe blood pressure swings, arrhythmias
  • Severe back or limb pain with neurological symptoms
  • Acute neurological symptoms following recent infection or vaccination

Treatment Methods

01
Diagnostic workup: detailed neurological examination, deep tendon reflexes, sensory testing, motor testing, cranial nerves, autonomic assessment
02
Lumbar puncture: characteristic albuminocytologic dissociation (elevated protein with normal cell count, typically after first week); useful but not always present at presentation
03
Electrodiagnostic studies (EMG/NCS): demonstrates demyelination (AIDP) or axonal involvement (AMAN/AMSAN); may be normal in first week
04
Antibody testing: anti-GQ1b for Miller Fisher syndrome, anti-GM1 for AMAN; not always required but supportive
05
Pulmonary function monitoring: forced vital capacity, negative inspiratory force, ABG; intubation if FVC <20 mL/kg or NIF <-30 cmH2O
06
Cardiac monitoring: continuous ECG for arrhythmias, hourly blood pressure for autonomic instability
07
Plasmapheresis: 5 sessions over 1–2 weeks, 50 mL/kg per session; effective if started within 4 weeks of onset; first-line therapy
08
Intravenous immunoglobulin (IVIg): 0.4 g/kg/day for 5 days (total 2 g/kg); effective if started within 2–4 weeks of onset; equivalent efficacy to plasmapheresis but easier administration
09
Combination therapy (plasmapheresis followed by IVIg): no additional benefit; not recommended routinely
10
Mechanical ventilation: indicated for FVC <15 mL/kg, severe bulbar dysfunction, hypercapnia; tracheostomy for prolonged ventilation
11
Pain management: gabapentin (300–1200 mg/day), carbamazepine, opioids for severe pain; tricyclic antidepressants for neuropathic pain
12
DVT prophylaxis: low-molecular-weight heparin, mechanical prophylaxis (intermittent pneumatic compression)
13
Autonomic dysfunction management: cautious treatment of hypertension and bradycardia; avoid excessive fluid loading; arrhythmia monitoring and treatment
14
Nutritional support: enteral feeding for prolonged dysphagia or mechanical ventilation
15
Physical therapy and rehabilitation: early passive range of motion, progressive strength training, gait training; intensive rehabilitation in chronic phase
16
Long-term outcomes: 70–80% good functional recovery within 12 months; 20–30% have residual deficits (weakness, fatigue, sensory symptoms); 5% mortality (older patients, respiratory failure, autonomic dysfunction)
17
Recurrent and chronic forms: chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a distinct chronic form (different treatment approach)
18
Family education: signs of recurrence, recovery time course, return to work and daily activities
19
Multidisciplinary follow-up: neurology, intensive care, pulmonology, physical medicine and rehabilitation, occupational therapy, psychology

Which Department to Visit?

You can visit our Nöroloji department for these complaints. Our specialist physicians will create the most suitable treatment plan for you.

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Health Disclaimer: The information on this page is prepared for general informational purposes only. It does not replace medical diagnosis and treatment. Please consult your physician for your complaints. Saygı Hospital does not accept responsibility for actions taken based on the information on this page.