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MANAGEMENT OF INFLAMMATORY NEUROPATHIES
  1. Robert D M Hadden1,
  2. Richard A C Hughes2
  1. 1West London Neurosciences Centre, Charing Cross Hospital, London, UK
  2. 2Department of Neuroimmunology, Guy’s, King’s and St Thomas’ School of Medicine, London, UK
  1. Correspondence to:
 Dr Robert Hadden, West London Neurosciences Centre, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UK; 
 rob.hadden{at}doctors.org.uk

https://doi.org/10.1136/jnnp.74.suppl_2.ii9

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    Inflammatory neuropathies are uncommon but important to diagnose because they are treatable. This review summarises the clinical approach to diagnosis and treatment of Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and related neuropathies which are thought to be caused by direct autoimmune attack on peripheral nerves. Features that suggest that a neuropathy is likely to be inflammatory include loss of reflexes without muscle wasting, elevated cerebrospinal fluid (CSF) protein, positive sensory symptoms such as pain or tingling, asymmetry, and proximal weakness. Nerve conduction studies show features of demyelination, especially motor nerve conduction block and temporal dispersion. Inflammatory neuropathy has been arbitrarily classified according to the time from symptom onset until maximal severity, where “acute” is less than four weeks and “chronic” is more than eight weeks, with a rare intermediate “subacute” group. Assessing the efficacy of potential treatments is difficult because the natural history is variable and may include spontaneous improvement. However, some progress has been made in conducting the randomised trials and systematic reviews as a basis for management decisions.

    GUILLAIN-BARRé SYNDROME (GBS)

    Definition

    GBS is a clinically defined syndrome with several underlying pathologies. It affects 1–4 per 100 000 per year, men slightly more often than women. Diagnostic criteria1 include progressive weakness of two or more limbs reaching a maximum within four weeks, reduced or absent tendon reflexes in the weak limbs, and exclusion of alternative causes (box 1).2 Some cases may be so mild that medical attention is never sought. Most cases are caused by acute inflammatory demyelinating polyradiculoneuropathy (AIDP), but some are caused by acute motor axonal neuropathy (AMAN) or acute motor and sensory axonal neuropathy (AMSAN).3 Primary axonal GBS is thought to be caused by an autoimmune attack on axonal antigens, and is common in Asia, but is responsible for less than 5% of GBS …

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    Footnotes

    • Competing interests: RACH’s department has received research grants during the past five years from Novartis, AMRAD, and Serono International, and has received consultancy payments from Biogen (USA) and Bayer. RACH has personally received honoraria from attending meetings or speaking at symposia from LFB (France), ZLB Bioplasma AG, Kedrion (Italy), Biogen (USA), and Bayer.