Guillain-Barré Syndrome (GBS) – Symptoms, Clinical Features, Diagnosis & Treatment

Guillain-Barré Syndrome (GBS) is an acute, immune-mediated polyneuropathy that affects the peripheral nervous system (PNS). It is characterized by rapidly progressive muscle weakness, often starting in the lower limbs and ascending upwards, sometimes leading to paralysis.

GBS is the most common cause of acute flaccid paralysis worldwide since the eradication of poliomyelitis. The condition is usually triggered by an antecedent infection (commonly gastrointestinal or respiratory), leading to an autoimmune response in which the body’s immune system attacks peripheral nerves.

Pathophysiology

1. The immune system mistakenly targets myelin sheaths or axons of peripheral nerves.

2. This is often due to molecular mimicry, where antigens of infectious agents resemble components of peripheral nerves.

3. Common triggers include:

• Campylobacter jejuni infection (most frequent)
• Cytomegalovirus (CMV)
• Epstein-Barr virus (EBV)
• Influenza virus
• Mycoplasma pneumoniae
• Vaccinations (rare)

Symptoms and Clinical Features

The provided image highlights important clinical features of Guillain-Barré Syndrome.

Key Symptoms/Clinical Features

1. Antecedent Diarrhea

• Often linked to Campylobacter jejuni infection.
• Diarrheal illness occurs 1–3 weeks before neurological symptoms.

2. Mild Disability Without Treatment

• Some cases are self-limiting, but most require treatment.
• If untreated, progression can cause respiratory failure.

3. Hand Weakness

• Early weakness usually begins in the legs but can involve hands and arms.
• Weakness is typically symmetric and ascending.

4. Partially Preserved Deep Tendon Reflexes (DTRs)

• Classically, GBS shows areflexia (loss of reflexes).
• However, some patients may retain partial reflexes.

5. Normal Protein Level in CSF (early stage)

• In the first week, cerebrospinal fluid (CSF) protein levels may be normal.
• Later, albuminocytologic dissociation (high protein, normal WBC count) develops.

6. Positive Anti-Ganglioside Antibodies

• Anti-GM1

• Many patients have autoantibodies against nerve components, e.g.:

• Anti-GD1a

• Anti-GQ1b (in Miller Fisher variant)

7. Axonal or RCF (Reversible Conduction Failure) Pattern

Electrophysiological studies reveal:

• Demyelinating form (most common in Western countries).
• Axonal form (more severe, common in Asia/Latin America).
• Reversible conduction failure in some cases.

Other Common Clinical Manifestations

1. Sensory symptoms: Tingling, numbness, paresthesias.

2. Autonomic dysfunction: Tachycardia, arrhythmias, BP fluctuations, urinary retention.

3. Cranial nerve involvement: Facial weakness, bulbar palsy.

4. Respiratory failure: Requires ventilatory support in severe cases.

Variants of Guillain-Barré Syndrome

1. Acute Inflammatory Demyelinating Polyneuropathy (AIDP) – Most common in Europe/USA.

2. Acute Motor Axonal Neuropathy (AMAN) – Common in Asia, often post-Campylobacter infection.

3. Acute Motor-Sensory Axonal Neuropathy (AMSAN) – Severe form affecting motor and sensory nerves.

4. Miller Fisher Syndrome (MFS): Triad of ophthalmoplegia, ataxia, and areflexia.

Diagnosis

Diagnosis is clinical, supported by laboratory and electrophysiological findings.

1. Clinical Evaluation

• Symmetric ascending weakness.
• Areflexia or hyporeflexia.
• Recent infection.

2. Cerebrospinal Fluid (CSF) Analysis

• Albuminocytologic dissociation: High protein (>45 mg/dL) with normal WBC count.
• Early stages may show normal protein levels (as noted in the image).

3. Nerve Conduction Studies (NCS) / Electromyography (EMG)

• Slowed conduction velocities in demyelinating GBS.
• Reduced amplitude in axonal forms.

4. Antibody Testing

• Anti-ganglioside antibodies (GM1, GD1a, GQ1b).

5. Other Tests

• Exclude mimics: Myasthenia gravis, poliomyelitis, botulism, tick paralysis.

Management

Early recognition and treatment are critical.

1. Supportive Care

• Admit to hospital for monitoring.
• Monitor for respiratory failure (spirometry, blood gases).
• Manage autonomic instability (ECG monitoring).
• Physiotherapy to prevent complications.

2. Specific Therapies

• IV Immunoglobulin (IVIG): First-line therapy.
• Plasmapheresis (Plasma Exchange): Removes autoantibodies.
• Both are equally effective if started early (within 2 weeks of onset).

3. Respiratory Support

• Mechanical ventilation if vital capacity <15 mL/kg.

4. Steroids

• Not effective in GBS and not recommended.

Prognosis

1. Most patients recover within 6–12 months, though some may have residual weakness.

2. Mortality rate: 3–7%, often due to respiratory or autonomic complications.

3. Poor prognostic factors:

• Older age
• Rapid progression
• Severe weakness at onset
• Ventilator dependence
• Axonal subtype

Tabular Overview – Guillain-Barré Syndrome

Feature	Details
Definition	Acute immune-mediated polyneuropathy
Trigger	Campylobacter jejuni, CMV, EBV, vaccines (rare)
Key Symptoms	Ascending weakness, sensory symptoms, autonomic dysfunction
CSF Findings	Albuminocytologic dissociation
NCS/EMG	Demyelinating or axonal pattern
Treatment	IVIG, Plasmapheresis, supportive care
Prognosis	Recovery in most cases, 3–7% mortality

Frequently Asked Questions (FAQs)

Q1: What usually triggers Guillain-Barré Syndrome?

It is most often triggered by infections, especially Campylobacter jejuni, but also by CMV, EBV, influenza, and rarely vaccinations.

Q2: How is GBS different from Myasthenia Gravis?

GBS causes ascending paralysis with areflexia, while myasthenia gravis presents with fluctuating weakness, worsens with activity, and preserved reflexes.

Q3: Can Guillain-Barré Syndrome cause death?

Yes, mortality is 3–7%, mainly due to respiratory failure or autonomic instability. Early ICU care reduces risk.

Q4: What is the role of steroids in GBS?

Steroids are not effective in GBS and should not be used.

Q5: Can GBS recur?

Yes, in about 3–5% of patients, GBS may recur after recovery.