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 Journal of Neurology Neurosurgery and Psychiatry 2003;74:ii9
© 2003


Robert D M Hadden1 and Richard A C Hughes2

1 West London Neurosciences Centre, Charing Cross Hospital, London, UK
2  Guy’s, King’s and St Thomas’ School of Medicine, London, UK

Inflammatory neuropathies are uncommon but important to diagnosebecause they are treatable. This review summarises the clinicalapproach 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 cerebro spinal 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.




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 criteria 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 () 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). 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 cases in Europe and North America. Reflexes are sometimes preserved in AMAN. Rarer variants of GBS are thepharyngo-cervico-brachial pattern, acute oropharyngeal palsy(not to be confused with diphtheria), involvement of the lower but not upper limbs, and a pure motor and a pure sensory form. Acute pan dysautonomia and acute sensory neuronopathy may also be related.

Box 1 Differential diagnosis of acute flaccid paralysis (after Cornblath)

  1. Acute anterior poliomyelitis

caused by poliovirus or  other neurotropic viruses

  1. Acute myelopathy

space occupying lesions or acute transverse myelitis

  1. Peripheral neuropathy (all except GBS usually have axonal neurophysiology)

Guillain-Barré syndromes

– post-rabies vaccineneuropathy

– diphtheritic neuropathy

– heavy metals,biological toxins or drug intoxication

– acute intermittentporphyria (usually pure motor neuropathy)

– vasculitic neuropathy, critical illness neuropathy

– lymphomatous neuropathy

– infections (HIV, Borrelia, heptatic- C)

  1. Disordersof neuromuscular transmission

– myasthenia gravis

biological or industrial toxins—for example, botulism

Disordersof muscle

– hypokalaemia

– hypophosphataemia

inflammatory myopathy

– acute rhabdomyolysis


– periodic paralyses

  1. Functional/non-organic

Cerebrospinal fluid examination is needed largely to excludealternative diagnoses, such as infectious (for example, Borreliaor poliomyelitis) or lymphomatous polyradiculitis. The CSF proteinis classically elevated as a result of albumin leakage from the blood, but may be normal within the first week. The CSF leucocyte count is usually normal but the diagnostic criteria allow up to 50 cells/µl. Pleocytosis is more likely incoexistent HIV infection.

GBS is preceded in two thirds of cases by an infection such as Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus or Mycoplasma pneumoniae. The infection is usually cleared before development of neurological symptoms. Identification of serum IgM antibodies to one of these agents demonstrates recent infection but is not clinically useful. Stool culture occasionally isolates C jejuni, but antibiotics probably do not influence outcome (level 4 evidence; box 2 . The risk of developing GBS after C jejuni enteritis is less than 1 in 2500.



Nerve conduction studies may help in diagnosis, classification and (to a limited extent) predicting prognosis. Neurophysiology helps to exclude alternative diagnoses such as myositis and myasthenia. Neurophysiological abnormalities are often very mild or occasionally normal in early GBS, and do not correlate well with clinical disability. The earliest consequence of acute demyelination is focal axonal conduction block, and it takes several days before slowing of conduction develops. Unfortunately for the purposes of diagnosis, conduction block is most common in the proximal nerve roots at sites that are awkward to test, at distal sites that mimic axonopathy, and at sites of compression, so it is often difficult or impossible to distinguish between axonal and demyelinating GBS in the early stages. Axonal degeneration may occur as a consequence of primary autoimmune attack on the axon or as a bystander phenomenon secondary to a primary attack on the myelin. It becomes evident after a few weeks as muscle wasting and electromyographic features of denervation, which signify a poor outcome. In the early stages, axonal neurophysiology may represent reversible axonal dysfunction rather than degeneration.



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