The adjuvant. In the 1980s, plasma exchange was found

The clinical features
of GBS were described by Landry in 1859.3 Eichorst in 1877 and Leyden in 1880
described the lymphocytic inflammation of nerve in some cases of peripheral neuropathy.
In 1916, Guillain, Barre´, and Strohl described the characteristic
cerebrospinal fluid (CSF) findings of increased protein concentration and
normal cell count in two French soldiers (Guillain 1916). In 1949, Haymaker and
Kernohan described the clinical and histopathological features, including
inflammatory changes of the peripheral nerve in 50 fatal cases of GBS.4 In the
mid-1950s, Waksman and Adams produced experimental allergic neuritis in animals
by injection of homologous or heterologous peripheral nerve tissue combined
with Freund adjuvant. In the 1980s, plasma exchange was found to be an

treatment,5,6 and in the 1990s, efficacy was also demonstrated for intravenous
immunoglobulin (IVIg).(1,2)

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There have been more than 30
population-based surveys of GBS from defined geographical areas of  Europe, Australia, and North and Latin
America.2,6  Most studies have reported
similar figures for  the annual incidence
of GBS. The annual incidence has months. Although substantial recovery is
common, ranged from 0.4 to 4.0 (median 1.3) cases per population of 100 000. A
recent survey involving 1752  Japanese
patients with GBS showed an annual incidence of 1.15 cases per population of
100 000 (un-published data, Japanese Research Group of  Neuroimmunological Disease.


 Age and Sex

GBS is known to occur at all ages.
Many epidemiological studies reveal a slight peak in late adolescence and young
adulthood, which may be due to an increased risk of infections by
cytomegalovirus CMV) andCampylobacterjejuni,
and in the elderly, who are possibly susceptible to autoimmune disordersbecause
of decreased immune suppressor 
mechanisms.(3).In almost al, series, men are more frequently
affected than women(1.25:1) (3) In general, autoimmune disorders
appear to be more prevalent among women; 
this preponderance of GBS among men is therefore unusaual.



The most common pathogen  is C. Jejunithat elicits GBS.Enteric
infection with C. jejuni occurs in association with an estimated 2 million
cases of diarrhoea per year in the U.S.(4) but only a very small
proportion of these are followed by development of GBS. C. Jejuni isolated from
patients with GBS and from patients with enteritis but no GBS have ganglioside
like structures on the lipopolysaccharide (LPS) of the outer membrane, but onlypatients
who developGBS have  been shown to have
elevated serum antigangliosideantibodies; those with uncomplicated diarrhoea
donot.(5) These findings indicate that patients who developGBS
respond differently to C. jejuniinfectionand
that there is a host susceptibility which is adeterminant for the occurrence of
GBS.(6) However,there is little evidence to suggest the existence of
a suspectiable immunogenetic back ground forv developing GBS. An association
between the occurrence of GBS and particular HLA type.



GBS usually develops
after a triggering event.

Infections Campylobacter jejuni, one of the most common causes of gastroenteritis worldwide,
causes 30% to 35% of GBS cases.3 Other infectious triggers include
cytomegalovirus, Mycoplasma pneumoniae,
Epstein-Barr virus, and HIV. GBS also occurs in patients with lymphoma, Hodgkin
disease, and systemic lupus erythematosus; these cases occur more frequently
than can be attributed to chance alone.(7)

Other causes

A small number of
patients develop GBS after another triggering event such as immunization,
surgery, trauma, or bone marrow transplantation. One study based on a vaccine
used in the 1970s found that the H1N1 influenza vaccine increased the risk of
developing GBS in 2 per 1 million people vaccinated.(8)



CMV causes
respiratory tract infection, mononucleosis-like syndrome or a nonspecific
flulike illnessThis virus is the most common viraltrigger of GBS, with a
prevalence ranging from 10%to 22% in several studies of GBS.(9) This
virus isespecially common in young female patients andcauses typical AIDP with
electrophysiological eviciateddence of demyelination,(9,10) in
contrast with C.jejuni-related
axonal GBS.


Haemophilus influenzae

A study in Japan
showed serological evidence of- H.
influenzae infection in 13% of 41 consecutive patients with GBS.(11)
Most of the GBS patients with H.
influenzae infection had antiganglioside anti-bodies and an
electrodiagnosis of AMAN: the feature were similar to those of patients with
associated with C. jejuniinfection.