With the eradication of polio, GBS is now the commonest cause of acute flaccid paralysis. GBS is an acute immune mediated polyradiculoneuropathy with an incidence of 1–1.5 per 100000 per year. It occurs in all age groups, with peaks in young adulthood and in late life where a gradual increase in incidence is seen with advancing age (Kennedy et al., 1978; Hankey, 1987; Rees et al., 1998).
Criteria for diagnosis
GBS is an acute, monophasic, predominantly motor polyneuropathy. The currently accepted criteria for the diagnosis of Guillain–Barré syndrome (Asbury et al., 1978) include the following.
Features required for diagnosis
• Progressive motor weakness of more than one limb
• Areflexia which is usually universal but distal areflexia with more proximal hyporeflexia is adequate if other features are consistent
Features strongly supportive of the diagnosis
• Rapid progression of weakness which has ceased by 4 Weeks
• Relative symmetry of involvement
• Mild sensory involvement, cranial nerve involvement, autonomic involvement
• Recovery usually beginning 2 to 4 weeks after progression Stops
Features that rule out the diagnosis
• A diagnosis of botulism, toxic neuropathy or poliomyelitis.
• Abnormal porphyrin metabolism
• Recent diphtheric infection
This immune-mediated polyradiculoneuropathy often follows an acute infective illness. One-half to two-thirds of GBS patients report symptoms of a respiratory tract or gastrointestinal infection within the month preceding neurological symptoms (Winer et al., 1988a; Jacobs et al., 1998). The most commonly identified organism is Campylobacter jejuni; recent infection being detected by bacteriologic or serologic techniques in 26–40% of patients (Kaldor & Speed 1984; Rees et al., 1995). Other identified antecedent infections include Cytomegalovirus (CMV), Epstein–Barr virus, Mycoplasma pneumoniae and Haemophilus influenza (Winer et al., 1988a; Jacobs et al., 1998; Mori et al., 2000). GBS may be an early manifestation of HIV infection, presenting at the time of seroconversion or in the immunocompetent phase of the disease. A small proportion of GBS cases follow surgery by an interval of 1 to 4 weeks, in the absence of identifiable infection.
An increased incidence of GBS was reported with the no longer used rabies vaccines containing neural tissue (Arnason & Soliven 1993), with swine influenza vaccination in the United States in 1976 (Schonberger et al., 1979) and with oral poliovirus vaccine (Kinnunen et al., 1989).