Guillain–Barré syndrome (GBS) is a rapid-onset muscle weakness
caused by the immune system damaging the peripheral nervous system.
The initial symptoms are typically changes in sensation or pain along
with muscle weakness, beginning in the feet and hands. This often
spreads to the arms and upper body, with both sides being involved.
The symptoms develop over hours to a few weeks. During the acute
phase, the disorder can be life-threatening, with about 15% developing
weakness of the breathing muscles requiring mechanical ventilation.
Some are affected by changes in the function of the autonomic nervous
system, which can lead to dangerous abnormalities in heart rate and
The cause is unknown. The underlying mechanism involves an
autoimmune disorder in which the body's immune system mistakenly
attacks the peripheral nerves and damages their myelin insulation.
Sometimes this immune dysfunction is triggered by an infection or,
less commonly, surgery or vaccination. The diagnosis is usually
made based on the signs and symptoms, through the exclusion of
alternative causes, and supported by tests such as nerve conduction
studies and examination of the cerebrospinal fluid. There are a
number of subtypes based on the areas of weakness, results of nerve
conduction studies and the presence of certain antibodies. It is
classified as an acute polyneuropathy.
In those with severe weakness, prompt treatment with intravenous
immunoglobulins or plasmapheresis, together with supportive care, will
lead to good recovery in the majority. Recovery may take weeks to
years. About a third have some permanent weakness. Globally,
death occurs in about 7.5% of those affected. Guillain–Barré
syndrome is rare, at one or two cases per 100,000 people every
year. Both sexes and all parts of the world have similar rates
of disease. The syndrome is named after the French neurologists
Georges Guillain and Jean Alexandre Barré, who described it with
André Strohl in 1916.
1 Signs and symptoms
1.1 Respiratory failure
1.2 Autonomic dysfunction
4.1 Spinal fluid
4.3 Clinical subtypes
5.2 Respiratory failure
9 Research directions
11 Further reading
12 External links
Signs and symptoms
The first symptoms of
Guillain–Barré syndrome are numbness,
tingling, and pain, alone or in combination. This is followed by
weakness of the legs and arms that affects both sides equally and
worsens over time. The weakness can take half a day to over two
weeks to reach maximum severity, and then becomes steady. In one in
five people, the weakness continues to progress for as long as four
weeks. The muscles of the neck may also be affected, and about half
experience involvement of the cranial nerves which supply the head and
face; this may lead to weakness of the muscles of the face, swallowing
difficulties and sometimes weakness of the eye muscles. In 8%, the
weakness affects only the legs (paraplegia or paraparesis).
Involvement of the muscles that control the bladder and anus is
unusual. In total, about a third of people with Guillain–Barré
syndrome continue to be able to walk. Once the weakness has stopped
progressing, it persists at a stable level ("plateau phase") before
improvement occurs. The plateau phase can take between two days and
six months, but the most common duration is a week. Pain-related
symptoms affect more than half, and include back pain, painful
tingling, muscle pain and pain in the head and neck relating to
irritation of the lining of the brain.
Many people with
Guillain–Barré syndrome have experienced the signs
and symptoms of an infection in the 3–6 weeks prior to the onset of
the neurological symptoms. This may consist of upper respiratory tract
infection (rhinitis, sore throat) or diarrhea.
In children, particularly those younger than six years old, the
diagnosis can be difficult and the condition is often initially
mistaken (sometimes for up to two weeks) for other causes of pains and
difficulty walking, such as viral infections, or bone and joint
On neurological examination, characteristic features are the reduced
power and reduced or absent tendon reflexes (hypo- or areflexia,
respectively). However, a small proportion has normal reflexes in
affected limbs before developing areflexia, and some may have
exaggerated reflexes. In the "
Miller Fisher variant" subtype of
Guillain–Barré syndrome (see below), a triad of weakness of the eye
muscles, abnormalities in coordination, as well as absent reflexes can
be found. The level of consciousness is normally unaffected in
Guillain–Barré syndrome, but the Bickerstaff brainstem encephalitis
subtype may feature drowsiness, sleepiness, or coma.
A quarter of all people with
Guillain–Barré syndrome develop
weakness of the breathing muscles leading to respiratory failure, the
inability to breathe adequately to maintain healthy levels of oxygen
and/or carbon dioxide in the blood. This life-threatening
scenario is complicated by other medical problems such as pneumonia,
severe infections, blood clots in the lungs and bleeding in the
digestive tract in 60% of those who require artificial ventilation.
The autonomic or involuntary nervous system, which is involved in the
control of body functions such as heart rate and blood pressure, is
affected in two thirds of people with Guillain–Barré syndrome, but
the impact is variable. Twenty percent may experience severe
blood-pressure fluctuations and irregularities in the heart beat,
sometimes to the point that the heart beat stops and requiring
pacemaker-based treatment. Other associated problems are
abnormalities in perspiration and changes in the reactivity of the
Autonomic nervous system
Autonomic nervous system involvement can affect even those
who do not have severe muscle weakness.
A scanning electron microscope-derived image of Campylobacter jejuni,
which triggers about 30% of cases of Guillain–Barré syndrome
Two thirds of people with
Guillain–Barré syndrome have experienced
an infection before the onset of the condition. Most commonly these
are episodes of gastroenteritis or a respiratory tract infection. In
many cases, the exact nature of the infection can be confirmed.
Approximately 30% of cases are provoked by Campylobacter jejuni
bacteria, which cause diarrhea. A further 10% are attributable to
cytomegalovirus (CMV, HHV-5). Despite this, only very few people with
Campylobacter or CMV infections develop Guillain–Barré syndrome
(0.25–0.65 per 1000 and 0.6–2.2 per 1000 episodes,
respectively). The strain of Campylobacter involved may determine
the risk of GBS; different forms of the bacteria have different
lipopolysaccharides on their surface, and some may induce illness (see
below) while others will not.
Links between other infections and GBS are less certain. Two other
herpesviruses (Epstein–Barr virus/HHV-4 and varicella zoster
virus/HHV-3) and the bacterium
Mycoplasma pneumoniae have been
associated with GBS. The tropical viral infection dengue fever and
Zika virus have also been associated with episodes of GBS.
Previous hepatitis E virus infection has been found to be more common
in people with Guillain–Barré syndrome.
Some cases may be triggered by the influenza virus and potentially
influenza vaccine. An increased incidence of Guillain–Barré
syndrome followed influenza immunization that followed the 1976 swine
flu outbreak (H1N1 A/NJ/76); 8.8 cases per million recipients
developed the complication. Since then, close monitoring of cases
attributable to vaccination has demonstrated that influenza itself can
induce GBS. Small increases in incidence have been observed in
subsequent vaccination campaigns, but not to the same extent. The
2009 flu pandemic vaccine
2009 flu pandemic vaccine (against pandemic swine flu virus
H1N1/PDM09) did not cause a significant increase in cases. It is
considered that the benefits of vaccination in preventing influenza
outweigh the small risks of GBS after vaccination. Even those who
have previously experienced
Guillain–Barré syndrome are considered
safe to receive the vaccine in the future. Other vaccines, such as
those against poliomyelitis, tetanus or measles, have not been
associated with a risk of GBS.
Structure of a typical neuron
Guillain–Barré syndrome – nerve damage
The nerve dysfunction in
Guillain–Barré syndrome is caused by an
immune attack on the nerve cells of the peripheral nervous system and
their support structures. The nerve cells have their body (the soma)
in the spinal cord and a long projection (the axon) that carries
electrical nerve impulses to the neuromuscular junction where the
impulse is transferred to the muscle. Axons are wrapped in a sheath of
Schwann cells that contain myelin. Between Schwann cells are gaps
(nodes of Ranvier) where the axon is exposed. Different types of
Guillain–Barré syndrome feature different types of immune attack.
The demyelinating variant (AIDP, see below) features damage to the
myelin sheath by white blood cells (T lymphocytes and macrophages);
this process is preceded by activation of a group of blood proteins
known as complement. In contrast, the axonal variant is mediated by
IgG antibodies and complement against the cell membrane covering the
axon without direct lymphocyte involvement.
Various antibodies directed at nerve cells have been reported in
Guillain–Barré syndrome. In the axonal subtype, these antibodies
have been shown to bind to gangliosides, a group of substances found
in peripheral nerves. A ganglioside is a molecule consisting of
ceramide bound to a small group of hexose-type sugars and containing
various numbers of N-acetylneuraminic acid groups. The key four
gangliosides against which antibodies have been described are GM1,
GD1a, GT1a, and GQ1b, with different anti-ganglioside antibodies being
associated with particular features; for instance, GQ1b antibodies
have been linked with
Miller Fisher variant GBS and related forms
including Bickerstaff encephalitis. The production of these
antibodies after an infection is probably the result of molecular
mimicry, where the immune system is reacting to microbial substances
but the resultant antibodies also react with substances occurring
naturally in the body. After a Campylobacter infection, the
body produces antibodies of the IgA class; only a small proportion of
people also produce IgG antibodies against bacterial substance cell
wall substances (e.g. lipooligosaccharides) that crossreact with human
nerve cell gangliosides. It is not currently known how this process
escapes central tolerance to gangliosides, which is meant to suppress
the production of antibodies against the body's own substances.
Not all antiganglioside antibodies cause disease, and it has recently
been suggested that some antibodies bind to more than one type of
epitope simultaneously (heterodimeric binding) and that this
determines the response. Furthermore, the development of pathogenic
antibodies may depend on the presence of other strains of bacteria in
The diagnosis of
Guillain–Barré syndrome depends on findings such
as rapid development of muscle paralysis, absent reflexes, absence of
fever, and a likely cause.
Cerebrospinal fluid analysis (through a
lumbar spinal puncture) and nerve conduction studies are supportive
investigations commonly performed in the diagnosis of GBS.
Testing for antiganglioside antibodies is often performed, but their
contribution to diagnosis is usually limited. Blood tests are
generally performed to exclude the possibility of another cause for
weakness, such as a low level of potassium in the blood. An
abnormally low level of sodium in the blood is often encountered in
Guillain–Barré syndrome. This has been attributed to the
inappropriate secretion of antidiuretic hormone, leading to relative
retention of water.
In many cases, magnetic resonance imaging of the spinal cord is
performed to distinguish between
Guillain–Barré syndrome and other
conditions causing limb weakness, such as spinal cord
compression. If an MRI scan shows enhancement of the nerve
roots, this may be indicative of GBS. In children, this feature is
present in 95% of scans, but it is not specific to Guillain–Barré
syndrome, so other confirmation is also needed.
Cerebrospinal fluid envelops the brain and the spine, and lumbar
puncture or spinal tap is the removal of a small amount of fluid using
a needle inserted between the lumbar vertebrae. Characteristic
Guillain–Barré syndrome are an elevated protein level,
usually greater than 0.55 g/L, and fewer than 10 white blood
cells per cubic millimeter of fluid ("albuminocytological
dissociation"). This combination distinguishes Guillain–Barré
syndrome from other conditions (such as lymphoma and poliomyelitis) in
which both the protein and the cell count are elevated. Elevated CSF
protein levels are found in approximately 50% of patients in the first
3 days after onset of weakness, which increases to 80% after the first
Repeating the lumbar puncture during the disease course is not
recommended. The protein levels may rise after treatment has been
Directly assessing nerve conduction of electrical impulses can exclude
other causes of acute muscle weakness, as well as distinguish the
different types of Guillain–Barré syndrome. Needle electromyography
(EMG) and nerve conduction studies may be performed. In the first two
weeks, these investigations may not show any abnormality.
Neurophysiology studies are not required for the diagnosis.
Formal criteria exist for each of the main subtypes of
Guillain–Barré syndrome (AIDP and AMAN/AMSAN, see below), but these
may misclassify some cases (particularly where there is reversible
conduction failure) and therefore changes to these criteria have been
proposed. Sometimes, repeated testing may be helpful.
A number of subtypes of
Guillain–Barré syndrome are
recognized. Despite this, many people have overlapping symptoms
that can make the classification difficult in individual cases.
All types have partial forms. For instance, some people experience
only isolated eye-movement or coordination problems; these are thought
to be a subtype of
Miller Fisher syndrome and have similar
antiganglioside antibody patterns.
Nerve conduction studies
Acute inflammatory demyelinating polyneuropathy (AIDP)
Sensory symptoms and muscle weakness, often with cranial nerve
weakness and autonomic involvement
Most common in Europe and North America
No clear association
Acute motor axonal neuropathy (AMAN)
Isolated muscle weakness without sensory symptoms in less than 10%;
cranial nerve involvement uncommon
Rare in Europe and North America, substantial proportion (30-65%) in
Asia and Central and South America; sometimes called "Chinese
Axonal polyneuropathy, normal sensory action potential
GM1a/b, GD1a & GalNac-GD1a
Acute motor and sensory axonal neuropathy (AMSAN)
Severe muscle weakness similar to AMAN but with sensory loss
Axonal polyneuropathy, reduced or absent sensory action potential
Weakness particularly of the throat muscles, and face, neck, and
Generally normal, sometimes axonal neuropathy in arms
Mostly GT1a, occasionally GQ1b, rarely GD1a
Miller Fisher syndrome
Ataxia, eye muscle weakness, areflexia but usually no limb weakness
This variant occurs more commonly in men than in women (2:1 ratio).
Cases typically occur in the spring and the average age of occurrence
is 43 years old.
Generally normal, sometimes discrete changes in sensory conduction or
Other diagnostic entities are often included in the spectrum of
Guillain–Barré syndrome. Bickerstaff's brainstem encephalitis, for
instance, is part of the group of conditions now regarded as forms of
Miller Fisher syndrome (anti-GQ1b antibody syndrome), as well as a
related condition labelled "acute ataxic hypersomnolence" where
coordination problems and drowsiness are present but no muscle
weakness can be detected. BBE is characterized by the rapid onset
of ophthalmoplegia, ataxia, and disturbance of consciousness, and may
be associated with absent or decreased tendon reflexes and as well as
Babinski's sign. The course of the disease is usually monophasic,
but recurrent episodes have been reported. MRI abnormalities in the
brainstem have been reported in 11%.
Whether isolated acute sensory loss can be regarded as a form of
Guillain–Barré syndrome is a matter of dispute; this is a rare
occurrence compared to GBS with muscle weakness but no sensory
Plasmapheresis and intravenous immunoglobulins (IVIG) are the two main
immunotherapy treatments for GBS.
Plasmapheresis attempts to reduce
the body's attack on the nervous system by filtering antibodies out of
the bloodstream. Similarly, administration of IVIG neutralizes harmful
antibodies and inflammation. These two treatments are equally
effective, but a combination of the two is not significantly better
than either alone.
Plasmapheresis speeds recovery when used within
four weeks of the onset of symptoms. IVIG works as well as
plasmapheresis when started within two weeks of the onset of symptoms,
and has fewer complications. IVIG is usually used first because of
its ease of administration and safety. Its use is not without risk;
occasionally it causes liver inflammation, or in rare cases, kidney
Glucocorticoids alone have not been found to be effective
in speeding recovery and could potentially delay recovery.
Respiratory failure may require intubation of the trachea and
breathing support through mechanical ventilation, generally on an
intensive care unit. The need for ventilatory support can be
anticipated by measurement of two spirometry-based breathing tests:
the forced vital capacity (FVC) and the negative inspiratory force
(NIF). An FVC of less than 15 ml per kilogram body weight or an
NIF of less than 60 cmH2O are considered markers of severe
While pain is common in people with Guillain–Barré syndrome,
studies comparing different types of pain medication are insufficient
to make a recommendation as to which should be used.
Following the acute phase, around 40% of people require intensive
rehabilitation with the help of a multidisciplinary team to focus on
improving activities of daily living (ADLs). Studies into the
subject have been limited, but it is likely that intensive
rehabilitation improves long-term symptoms. Teams may include
physical therapists, occupational therapists, speech language
pathologists, social workers, psychologists, other allied health
professionals and nurses. The team usually works under the supervision
of a neurologist or rehabilitation physician directing treatment
Physiotherapy interventions include strength, endurance and gait
training with graduated increases in mobility, maintenance of posture
and alignment as well as joint function.
Occupational therapy aims to
improve everyday function with domestic and community tasks as well as
driving and work. Home modifications, gait aids, orthotics and splints
may be provided.
Speech-language pathology input may be required
in those with speech and swallowing problems, as well as to support
communication in those who require ongoing breathing support (often
through a tracheostomy). Nutritional support may be provided by the
team and by dietitians. Psychologists may provide counseling and
support. Psychological interventions may also be required for anxiety,
fear and depression.
Guillain–Barré syndrome can lead to death as a result of a number
of complications: severe infections, blood clots, and cardiac arrest
likely due to autonomic neuropathy. Despite optimum care this occurs
in about 5% of cases.
There is a variation in the rate and extent of recovery. The
Guillain–Barré syndrome is determined mainly by age
(those over 40 may have a poorer outcome), and by the severity of
symptoms after two weeks. Furthermore, those who experienced diarrhea
before the onset of disease have a worse prognosis. On the nerve
conduction study, the presence of conduction block predicts poorer
outcome at 6 months. In those who have received intravenous
immunoglobulins, a smaller increase in IgG in the blood two weeks
after administration is associated with poorer mobility outcomes at
six months than those whose IgG level increased substantially. If
the disease continues to progress beyond four weeks, or there are
multiple fluctuations in the severity (more than two in eight weeks),
the diagnosis may be chronic inflammatory demyelinating
polyneuropathy, which is treated differently.
In research studies, the outcome from an episode of Guillain–Barré
syndrome is recorded on a scale from 0 to 6, where 0 denotes
completely healthy, 1 very minor symptoms but able to run, 2 able to
walk but not to run, 3 requiring a stick or other support, 4 confined
to bed or chair, 5 requiring long-term respiratory support, 6
The health-related quality of life (HRQL) after an attack of
Guillain–Barré syndrome can be significantly impaired. About a
fifth are unable to walk unaided after six months, and many experience
chronic pain, fatigue and difficulty with work, education, hobbies and
social activities. HRQL improves significantly in the first
See also: List of people with Guillain–Barré syndrome
In Western countries, the number of new episodes per year has been
estimated to be between 0.89 and 1.89 cases per 100,000 people.
Children and young adults are less likely to be affected than the
elderly: the risk increases by 20% for every decade of life. Men
are more likely to develop
Guillain–Barré syndrome than women; the
relative risk for men is 1.78 compared to women.
The distribution of subtypes varies between countries. In Europe and
the United States, 60–80% of people with Guillain–Barré syndrome
have the demyelinating subtype (AIDP), and AMAN affects only a small
number (6–7%). In Asia and Central and South America, that
proportion is significantly higher (30–65%). This may be related to
the exposure to different kinds of infection, but also the genetic
characteristics of that population.
Miller Fisher variant is
thought to be more common in Southeast Asia.
Georges Guillain, together with Barré and Strohl, described two cases
of self-limiting acute paralysis with peculiar changes in the
cerebrospinal fluid. He succeeded his teacher
Pierre Marie as
professor of neurology at the Salpêtrière hospital in Paris in
French physician Jean-Baptiste Octave Landry first described the
disorder in 1859. In 1916, Georges Guillain, Jean Alexandre
André Strohl diagnosed two soldiers with the illness and
described the key diagnostic abnormality—albuminocytological
dissociation—of increased spinal fluid protein concentration but a
normal cell count. 
Canadian neurologist C.
Miller Fisher described the variant that bears
his name in 1956. British neurologist Edwin Bickerstaff, based
in Birmingham, described the brainstem encephalitis type in 1951 with
Philip Cloake, and made further contributions with another paper in
1957. Guillain had reported on some of these features
prior to their full description in 1938. Further subtypes have
been described since then, such as the form featuring pure ataxia and
the type causing pharyngeal-cervical-brachial weakness. The axonal
subtype was first described in the 1990s.
Diagnostic criteria were developed in the late 1970s after the series
of cases associated with swine flu vaccination. These were refined in
1990. The case definition was revised by the Brighton
Collaboration for vaccine safety in 2009, but is mainly intended
for research. Plasma exchange was first used in 1978 and its
benefit confirmed in larger studies in 1985. Intravenous
immunoglobulins were introduced in 1988, and its non-inferiority
compared to plasma exchange was demonstrated in studies in the early
The understanding of the disease mechanism of Guillain–Barré
syndrome has evolved in recent years. Development of new
treatments has been limited since immunotherapy was introduced in the
1980s and 1990s. Current research is aimed at demonstrating
whether some people who have received IVIg might benefit from a second
course if the antibody levels measured in blood after treatment have
only shown a small increase. Studies of the immunosuppressive
drug mycophenolate mofetil, brain-derived neurotrophic factor and
interferon beta (IFN-β) have not demonstrated benefit to support
their widespread use.
An animal model (experimental autoimmune neuritis in rats) is often
used for studies, and some agents have shown promise: glatiramer
acetate, quinpramine, fasudil (an inhibitor of the Rho-kinase
enzyme), and the heart drug flecainide. An antibody targeted
against the anti-GD3 antiganglioside antibody has shown benefit in
laboratory research. Given the role of the complement system in
GBS, it has been suggested that complement inhibitors (such as the
drug eculizumab) may be effective.
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V · T · D
eMedicine: emerg/222 neuro/7 pmr/48 neuro/598
Patient UK: Guillain–Barré syndrome
Guillain–Barré syndrome at Curlie (based on DMOZ)
GBS/CIDP Foundation International
Nervous system pathology, PNS, somatic (G50–G64, 350–357)
Nerve, nerve root, plexus
V Trigeminal neuralgia
Facial nerve paralysis
Accessory nerve disorder
Brachial plexus lesion
Thoracic outlet syndrome
Carpal tunnel syndrome
Ape hand deformity
Ulnar nerve entrapment
Guyon's canal syndrome
long thoracic nerve:
lateral cutaneous nerve of thigh:
Tarsal tunnel syndrome
superior gluteal nerve:
Nerve compression syndrome
Hereditary spastic paraplegia
Hereditary neuropathy with liability to pressure palsy
Familial amyloid neuropathy
Chronic inflammatory demyelinating polyneuropathy
Hypersensitivity and autoimmune diseases (279.5–6)
Allergic rhinitis (Hay fever)
common allergies include: Milk
Hemolytic disease of the newborn
Autoimmune hemolytic anemia
Immune thrombocytopenic purpura
Systemic lupus erythematosus
Subacute bacterial endocarditis
Allergic contact dermatitis
Diabetes mellitus type 1
Postorgasmic illness syndrome
Transfusion-associated graft versus host disease
Allergic bronchopulmonary aspergillosis
Latex allergy (I+IV)
Autoimmune polyendocrine syndrome