An 'acute paralytic polyneuropathy' that affects the peripheral nervous system
Aetiology
- Usually demyelinating or occasionally axonal, and has an immune-mediated, often post-infectious, basis
- Particularly associated with campylobacter jejuni, cytomegalovirus and Epstein-Barr virus
Pathophysiology
- Guillain-Barré is thought to occur due to a process called molecular mimicry
- The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection
- These antibodies also match proteins on the nerve cells
- They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon
Clinical presentation
- Symptoms usually start within 4 weeks of the preceding infection
- Symmetrical ascending weakness (starting at the feet and moving up the body)
- There may be peripheral loss of sensation or neuropathic pain
- It may progress to the cranial nerves and cause facial nerve weakness
Investigations
- Can be supported by:
- Nerve conduction studies
- Lumbar puncture for CSF - will show raised protein with a normal cell count and glucose
- Bedside spirometry (FVC) monitoring essential due to risk of respiratory failure
Management
- IV immunoglobulin (first line) or plasma exchange (typically used second line if IV Ig is ineffective)
- VTE prophylaxis (pulmonary embolism is a leading cause of death)
- In severe cases with respiratory failure patients may need intubation, ventilation and admission to the intensive care unit