Guillain-Barré Syndrome (GBS) is an acute, autoimmune, inflammatory demyelinating polyneuropathy that affects the peripheral nervous system.
It causes rapidly progressive muscle weakness and areflexia, often beginning in the lower limbs and ascending upwards.
Etiology / Causes
The exact cause is unknown, but it usually follows an infection or immune trigger.
Common triggers:
Viral or bacterial infections:
Campylobacter jejuni (most common)
Cytomegalovirus (CMV)
Epstein–Barr virus (EBV)
Influenza
Post-vaccination (rare)
Surgery or trauma
Pathophysiology
The immune system mistakenly attacks the myelin sheath of peripheral nerves.
This causes inflammation and demyelination, leading to slowed or blocked nerve conduction.
In severe cases, axon damage can occur.
The condition typically progresses symmetrically from distal to proximal muscles (“ascending paralysis”).
Types of GBS
AIDP (Acute Inflammatory Demyelinating Polyneuropathy) – Most common; affects myelin.
AMAN (Acute Motor Axonal Neuropathy) – Pure motor involvement; affects axons.
AMSAN (Acute Motor and Sensory Axonal Neuropathy) – Motor + sensory axon damage.
Miller Fisher Syndrome (MFS) – Triad: Ophthalmoplegia, Ataxia, Areflexia.
Clinical Features / Symptoms
Typical progression:
Initial phase:
Tingling, numbness in hands and feet
Muscle weakness (legs → arms → face → respiratory muscles)
Peak weakness (1–3 weeks):
Symmetrical flaccid paralysis
Absent reflexes (areflexia)
Facial nerve involvement → facial weakness
Respiratory muscle weakness → breathing difficulty
Autonomic dysfunction → BP fluctuations, arrhythmias, sweating abnormalities
Sensory symptoms are usually mild compared to motor weakness.
Complications
Respiratory failure (needs ventilatory support)
Deep vein thrombosis (DVT)
Pressure sores
Joint contractures
Chronic pain or fatigue
Investigations
Nerve conduction studies: Slowed conduction velocity
Lumbar puncture (CSF analysis):
Albumin cytologic dissociation (↑ protein, normal cell count)
Pulmonary function tests: To monitor respiratory status
Medical Management
Hospitalization (often ICU) for monitoring respiration and autonomic function
Immunotherapy:
Intravenous immunoglobulin (IVIG)
Plasmapheresis (plasma exchange)
Supportive care:
Respiratory support (if vital capacity < 15 mL/kg)
DVT prophylaxis
Nutritional and psychological support
Physiotherapy Management
- Acute Stage (Flaccid Paralysis Phase) Goals: Prevent complications, maintain joint integrity, support respiration. Positioning: To prevent pressure sores and nerve compression Passive ROM exercises: To prevent contractures Chest physiotherapy: Breathing exercises, postural drainage if needed Splinting: Foot drop prevention (ankle-foot orthosis) Pain management: Gentle handling, relaxation techniques
- Recovery Stage (Reinnervation Phase) Goals: Facilitate muscle strength and function recovery. Active-assisted to active exercises: Gradual progression Resistive exercises: Only when fatigue-free Postural training and balance exercises Gait training: Start with parallel bars → walker → independent walking Coordination and fine motor exercises Energy conservation techniques Avoid fatigue — overexertion can delay recovery.
- Functional Rehabilitation Occupational therapy: ADL training, hand function improvement Home exercise program: Continuation of strengthening and mobility Psychological support: Coping with anxiety and fatigue Prognosis Good prognosis in most cases — recovery begins within weeks to months. 80–90% recover completely or with minimal deficits. Poorer outcomes with: older age, severe axonal damage, respiratory failure. Summary Table Feature Description Affected system Peripheral nervous system Type Autoimmune, demyelinating neuropathy Key sign Ascending symmetrical weakness with areflexia CSF finding High protein, normal cells Treatment IVIG, Plasmapheresis, Supportive care PT focus Prevent complications, restore mobility, avoid fatigue
Written by : Dayana Onkarappa Senior Physiotherapist at Advanced Physiotherapy Clinic and Homecare
https://physioji.com/
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