Guillain--Barré syndrome and Campylobacter jejuni infection.

1. SUMMARY Guillain±Barre  syndrome (GBS) is the most common cause of acute neuromuscular paralysis, usually due to acute in¯ammatory demyelinating polyradiculoneuropathy. The presence of activated T lymphocytes and antibodies against peripheral nerve myelin suggests an autoimmune patho-genesis, although there is wide heterogeneity. Gangliosides are sialylated glycolipids widely distributed in nervous system membranes. GBS is usually preceded by an infection, most frequently Campylobacter jejuni enteritis, but also cytomegalovirus, Mycoplasma pneumoniae or Ep-stein±Barr virus. Patients with GBS and C. jejuni infection are more likely to have neurophysiological features of axonal neuropathy, antibodies to ganglioside GM1, pure motor GBS, a less elevated CSF protein concentration and a worse outcome than other GBS patients. Although molecular mimicry between peripheral nerve gangliosides and epitopes present on C. jejuni lipopolysaccharide could explain some of these associations, this hypothesis is inadequate to account for many aspects of the pathogenesis of GBS. 2. INTRODUCTION Guillain±Barre  syndrome (GBS) is characterized by temporary paralysis due to acute autoimmune in¯ammatory polyradiculoneuropathy. It is usually preceded by an infection, the commonest of which is Campylobacter jejuni enteritis. Patients with C. jejuni-associated GBS are more likely to have antibodies to ganglioside GM1, neurophysi-ology suggesting axonal neuropathy and a worse outcome than GBS preceded by other infections. 3. GUILLAIN±BARRE  SYNDROME 3.1. Clinical features Guillain±Barre  syndrome is de®ned clinically by progressive weakness of two or more limbs due to neuropathy, reduced or absent tendon re¯exes, < 50 mononuclear leucocytes per ll cerebrospinal ¯uid (CSF), and absence of other known causes of acute neuropathy (Asbury and Cornblath 1990). The duration of worsening of disease was later arbitrarily de®ned as less than 4 weeks to distinguish GBS