Guillain-Barré syndrome is a high-yield topic in clinical medicine and neurology exams. This post presents a concise, structured revision of GBS based on Kumar & Clarke’s Clinical Medicine, ideal for rapid review before exams or ward work.
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Definition
Guillain-Barré syndrome is an acute, immune-mediated inflammatory polyradiculoneuropathy characterized by rapidly progressive symmetrical weakness and loss of reflexes.
Key points to remember:
- Acute onset over days to weeks
- Immune mediated
- Affects peripheral nerves and nerve roots
Etiology and Pathogenesis
GBS is commonly post-infectious, with symptoms appearing 1 to 3 weeks after a minor infection.
Common triggers include:
- Campylobacter jejuni (most common)
- Cytomegalovirus
- Epstein-Barr virus
- Mycoplasma pneumoniae
Pathophysiology
- Molecular mimicry leads to formation of antibodies
- Antibodies cross-react with peripheral nerve gangliosides
- Results in demyelination or axonal damage
- Signal transmission from nerve to muscle becomes impaired
Clinical Features
Motor Features
- Symmetrical limb weakness
- Ascending pattern starting in the legs
- Proximal progression over days to weeks
Reflexes
- Loss of deep tendon reflexes is a hallmark feature
Sensory Features
- Mild sensory symptoms such as paresthesia
- Sensory loss is less prominent than weakness
Disease Progression
- Progressive phase lasts up to 4 weeks
- Followed by a plateau phase
- Gradual recovery phase over weeks to months
Progression beyond 8 weeks suggests an alternative diagnosis such as CIDP.
Cranial Nerve and Autonomic Involvement
- Facial nerve palsy is common
- Bulbar involvement may cause dysphagia and dysarthria
- Autonomic dysfunction may present with:
- Tachycardia or bradycardia
- Blood pressure instability
- Cardiac arrhythmias
Autonomic complications are a major cause of morbidity and mortality.
Respiratory Involvement
Up to one third of patients may develop respiratory failure.
Monitoring includes:
- Vital capacity
- Single breath count
- Use of accessory muscles
Early recognition is essential as respiratory failure can occur suddenly.
Variants of Guillain-Barré Syndrome
AIDP
- Acute inflammatory demyelinating polyneuropathy
- Most common form in Sri Lanka and Europe
AMAN
- Acute motor axonal neuropathy
- Pure motor involvement
- Often associated with Campylobacter infection
AMSAN
- Acute motor sensory axonal neuropathy
- More severe with poorer prognosis
Miller Fisher Syndrome
Classic triad:
- Ophthalmoplegia
- Ataxia
- Areflexia
Associated with anti-GQ1b antibodies.
Investigations
Cerebrospinal Fluid
- Albuminocytologic dissociation
- Raised protein with normal cell count
- CSF may be normal in the first week
Nerve Conduction Studies
- Confirms diagnosis
- Differentiates demyelinating vs axonal forms
Demyelinating pattern:
- Slowed conduction velocity
- Prolonged distal latencies
Axonal pattern:
- Reduced amplitude
Management
GBS is a medical emergency and all patients require hospital admission.
Disease-Modifying Treatment
- Intravenous immunoglobulin
- Plasma exchange
Both are equally effective.
Steroids are not beneficial.
Supportive Care
- Respiratory monitoring
- ECG monitoring
- DVT prophylaxis
- Physiotherapy
- Pain control
Prognosis
- Most patients recover fully or near fully
- Mortality is approximately 5 percent
Poor prognostic factors include:
- Older age
- Rapid progression
- Need for mechanical ventilation
- Axonal variants
One-Line Exam Summary
Guillain-Barré syndrome is an acute post-infectious immune-mediated peripheral neuropathy causing ascending weakness and areflexia, diagnosed by raised CSF protein and treated with IVIG or plasma exchange.