Synopsis
Identify chronic or relapsing immune demyelinating neuropathy, require electroclinical concordance before long-term treatment, and monitor objective response to IVIg, corticosteroids or plasma exchange.
- Typical CIDP causes progressive or relapsing symmetrical proximal and distal weakness, sensory loss and reduced or absent reflexes over at least 8 weeks.
- The time course distinguishes it from monophasic GBS, although acute-onset CIDP can initially reach severe weakness quickly and declare itself through later progression or relapses.
- Nerve-conduction evidence of acquired demyelination across multiple nerves is central: conduction block, temporal dispersion, prolonged distal latencies and slowed velocities must meet validated criteria.
Key red flags
An apparent GBS episode that continues progressing beyond 8 weeks or has repeated treatment-related deteriorations may evolve into a chronic immune neuropathy.
Investigation priorities
Demonstrate acquired demyelination across sufficient nerves and quantify secondary axonal loss.
Management branches
Chronic or relapsing areflexic weakness raises possible CIDP.
- Document more-than-8-week tempo, proximal and distal power, sensory modalities, reflexes, gait and alternative central or motor-neurone signs.
- Obtain expert nerve conduction using validated demyelination criteria and repeat or expand testing when the first study is technically limited.
Probable or definite CIDP causes meaningful progression or disability.
Key medicines
Intravenous human immunoglobulinA common induction totals 2 g/kg over 2–5 days; maintenance dose and interval are individualised under NHS England commissioning and objective response criteria.
Corticosteroid therapyUse a specialist daily oral or pulsed regimen with planned taper, response measurement and bone, gastric and infection protection appropriate to exposure.