| Guillain–Barré syndrome |
|
A handheld spirometry device, which can be used to anticipate breathing complications of Guillain-Barré syndrome
|
| Classification and external resources |
| ICD-10 |
G61.0 |
| ICD-9 |
357.0 |
| OMIM |
139393 |
| DiseasesDB |
5465 |
| MedlinePlus |
000684 |
| eMedicine |
emerg/222 neuro/7 pmr/48 neuro/598 |
| Patient UK |
Guillain–Barré syndrome |
| MeSH |
D020275 |
Guillain–Barré syndrome (GBS) (French pronunciation: [ɡiˈlɛ̃ baˈʁe], English pronunciation: //), sometimes Guillain–Barré–Strohl syndrome or Landry's paralysis, is a rapid-onset weakness of the limbs as a result of an acute polyneuropathy, a disorder affecting the peripheral nervous system. The disease is usually triggered by an infection, which provokes immune-mediated nerve dysfunction. Many experience changes in sensation or develop pain, followed by muscle weakness beginning in the feet and hands that develops rapidly (between half a day and two weeks). Guillain-Barre syndrome damages the myelin sheaths covering the nerves in the peripheral nervous system, which disrupts the nerve impulses, similar to multiple sclerosis and other demyelinating diseases. During the acute phase, the disorder can be life-threatening with about a quarter requiring admission to intensive care unit for mechanical ventilation. Some are affected by fluctuations in the function of the autonomic nervous system, which can lead to dangerous abnormalities in heart rate and blood pressure.
The diagnosis is usually made on clinical grounds, through the exclusion of alternative causes, and supported by tests such as nerve conduction studies and examination of the cerebrospinal fluid. Various classifications exist, depending on the areas of weakness, results of nerve conduction studies, and presence of antiganglioside antibodies. In those with severe weakness, prompt treatment with intravenous immunoglobulins or plasmapheresis, together with supportive care, will lead to good recovery in the majority, although some may experience ongoing difficulty with walking, painful symptoms, and sometimes require breathing support. Guillain–Barré syndrome is rare, at one to two cases per 100,000 people annually. The syndrome is named after the French physicians Georges Guillain and Jean Alexandre Barré, who described it with André Strohl in 1916.
Contents
- 1 Signs and symptoms
- 1.1 Respiratory failure
- 1.2 Autonomic dysfunction
- 2 Causes
- 3 Mechanism
- 4 Diagnosis
- 4.1 Spinal fluid
- 4.2 Neurophysiology
- 4.3 Clinical subtypes
- 5 Treatment
- 5.1 Immunotherapy
- 5.2 Pain
- 5.3 Rehabilitation
- 6 Prognosis
- 7 Epidemiology
- 8 History
- 9 Research directions
- 10 See also
- 11 References
- 12 Further reading
- 13 External links
Signs and symptoms
The first symptoms of Guillain-Barré syndrome are numbness and tingling, weakness, and pain, alone or in combination. This is followed by weakness of the legs and arms that is symmetrical and worsening in time.[1] The weakness can take half a day to over two weeks to reach maximum severity, and then becomes steady.[1] In one in five people the weakness continues to progress for as long as four weeks.[2] 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.[2] In 8% the weakness affects only the legs (paraplegia or paraparesis).[2] Involvement of the muscles that control the bladder and anus is unusual.[1] In total, about a third of people with Guillain-Barré syndrome continue to be able to walk.[2] Once the weakness has stopped progressing, it persists at a stable level ("plateau phase") before improvement can be noticed. The plateau phase can take between two days and six months, but the median duration is a week.[2] 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 brain's lining.[2]
Many people with Guillain-Barré 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.[1]
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,[2] or bone and joint problems.[3]
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 delevoping areflexia, and some may even have exaggerated reflexes.[2] In the "Miller Fisher variant" subtype of Guillain-Barré syndrome (see below), weakness of the eye muscles (ophthalmoplegia) is more pronounced and may occur together with abnormalities in coordination (ataxia).[1] The level of consciousness is normally unaffected in Guillain-Barré syndrome, but the "Bickerstaff brainstem encephalitis" subtype may feature drowsiness, sleepiness (hypersomnolence) or coma.[4][5]
Respiratory failure
25% of 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.[1][2][6] This may require intubation of the windpipe 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 respiratory failure.[7] 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.[1]
Autonomic dysfunction
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.[2] 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.[1] Other associated problems are abnormalities in perspiration and changes in the pupillary response.[4] Autonomic nervous system involvement can affect even those who do not have severe muscle weakness.[4]
Causes
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.[2] Approximately 30% of cases are provoked by Campylobacter jejuni, which causes diarrhea. A further 10% cases 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).[1] 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.[2]
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.[1] The tropical viral infection dengue fever has been associated with episodes of GBS.[8] Previous hepatitis E virus infection has been found to be more common in people with Guillain-Barré syndrome.[2][9]
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.[10] The 2009 flu pandemic vaccine (against pandemic swine flu virus H1N1/PDM09) did not cause a significant increase in cases.[1] The benefits from vaccination to prevent influenza outweigh the small risks of GBS after vaccination.[11] Even those who have previously experienced Guillain-Barré syndrome are considered safe to receive the vaccine in the future.[2] Other vaccines, such as those against poliomyelitis, tetanus or measles, have not been associated with a risk of GBS.[3]
Mechanism
Structure of a typical neuron
| Neuron |
Dendrite
Soma
Axon
Nucleus
Node of
Ranvier
Axon terminal
Schwann cell
Myelin sheath
|
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.[1] 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 directly against the cell membrane covering the axon without lymphocyte involvement.[1]
In the axonal form of Guillain-Barré syndrome (but not the demyelinating variant), various antibodies directed at nerve cells have been reported. These 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.[1] 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 epitopes occurring naturally in the body.[1][12] 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 know how this process escapes central tolerance to gangliosides, which is meant to suppress the production of antibodies against the body's own substances.[13] 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 ofter strains of bacteria in the bowel.[13]
Diagnosis
The diagnosis of Guillain-Barré syndrome depends on findings such as rapid development of muscle paralysis, absent reflexes, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and nerve conduction studies are supportive investigations commonly performed in the diagnosis of GBS.[1][2][9] Testing for antiganglioside antibodies is often performed, but their contribution to diagnosis is usually limited.[2] Blood tests are generally performed to exclude the possibility of another cause for weakness, such as a low level of potassium in the blood.[1] 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.[14]
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.[1][2] If an MRI scan shows enhancement of the nerve roots, this may be indicative of GBS.[2]
Spinal fluid
Cerebrospinal fluid (CSF) envelops the brain and the spine, and lumbar puncture is the removal of a small amount of fluid using a needle inserted between the lumbar vertebrae. A characteristic finding in Guillain-Barré syndrome is an elevated protein level with low numbers of white blood cells ("albuminocytological dissociation"); this distinguishes it from a number of other conditions (such as lymphoma and poliomyelitis) where both the protein and the cell count are elevated. Despite this, the CSF is unremarkable in 50% of people with Guillain-Barré syndrome in the first few days of symptoms, and 80% after the first week; therefore, normal results do not exclude the condition.[2]
Repeating the lumbar puncture during the disease course is not recommended. The protein levels may rise after treatment has been administered.[2]
Neurophysiology
|
This section requires expansion. (December 2014) |
Electrodiagnostic medicine studies such as needle electromyography (EMG) and nerve conduction studies may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound muscle action potential in demyelinating cases.[15] F waves and H-reflexes may be prolonged or absent. Needle EMG is frequently normal in acute cases. Reduced, neuropathic recruitment in weak muscles can be seen. Fibrillations will be seen on needle EMG if some axonal injury occurs after three to four weeks. In primary axonal damage, the findings include reduced amplitude of the action potentials without conduction slowing.[citation needed]
Clinical subtypes
A number of key subtypes of Guillain–Barré syndrome are currently recognized.[2][15] Despite this, many people have overlapping symptoms that can make the classification difficult.[4][16] 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.[16]
| Type[2] |
Symptoms |
Population affected |
Nerve conduction studies |
Antiganglioside antibodies |
| 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 |
Demyelinating polyneuropathy |
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 paralytic syndrome" |
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 |
GM1, GD1a |
| Pharyngeo-cervico-brachial variant |
Weakness particularly of the throat muscles, face, neck and shoulder muscles |
- |
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.[17] |
Generally normal, sometimes discrete changes in sensory conduction or H-reflex detected |
GQ1b, GT1a |
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, as well as a related condition labelled "acute ataxic hypersomnolence" where coordination and drowsiness are present but no muscle weakness can be detected.[16] BBE is characterized by the acute 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.[16] The course of the disease can be monophasic or remitting-relapsing. Large, irregular hyperintense lesions located mainly in the brainstem, especially in the pons, midbrain and medulla, are described. Despite severe initial presentation, BBE usually has a good prognosis. Magnetic resonance imaging plays a critical role in the diagnosis of BBE. Many BBE patients have associated axonal Guillain–Barré syndrome suggesting that these two disorders are closely related.[citation needed]
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 symptoms.[11]
Treatment
Immunotherapy
Subsequent treatment consists of attempting to reduce the body's attack on the nervous system, either by plasmapheresis, filtering antibodies out of the bloodstream, or by administering intravenous immunoglobulins (IVIg), to neutralize harmful antibodies and inflammation causing disease. These two treatments are equally effective and a combination of the two is not significantly better than either alone.[18] Plasmapheresis hastens recovery when used within four weeks of the onset of symptoms.[19] IVIg has equivalent efficacy to plasmapheresis when started within two weeks of the onset of symptoms, and has fewer complications.[19] IVIg is usually used first because of its ease of administration and safety profile. Its use is not without risk; occasionally it causes liver inflammation, or in rare cases, kidney failure.[20] Glucocorticoids alone have not been found to be effective in hastening recovery, and could potentially delay it.[21]
Pain
Pain is common in people with Guillain–Barré syndrome, but studies comparing different types of pain medication have been of insufficient quality to make a specific recommendation as to which should be used.[22]
Rehabilitation
Following the acute phase, treatment often consists of rehabilitation with the help of a multidisciplinary team to focus on improving activities of daily living (ADLs). Occupational therapists may offer equipment (such as wheelchair and special cutlery) to help the patient achieve ADL independence. Physiotherapists assist to correct functional movement, avoiding harmful compensations that might have a negative effect in the long run. Also, some evidence supports physiotherapy in helping patients with Guillain–Barré syndrome to regain strength, endurance, and gait quality,[23] as well as helping them prevent contractures, bedsores, and cardiopulmonary difficulties.[24] Speech and language therapists help regain speaking and swallowing abilities, especially if the patient was intubated for mechanical ventilation or received a tracheostomy.[citation needed] Neither amantadine nor ascorbic acid have evidence to support an effect on fatigue.[25]
Prognosis
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.[1]
In most patients the symptoms increase in the first one to three weeks.[1] Recovery usually starts after the fourth week from the onset of the disorder,[citation needed] but there is a variation in the rate and extent of recovery.[1] About 80% of patients have a complete recovery within a few months to a year, although minor findings may persist, such as areflexia. About 5–10% recover with severe disability, with most of such cases involving severe proximal motor and sensory axonal damage with inability of axonal regeneration. About 5–10% of patients have one or more late relapses, in which case they are then classified as having chronic inflammatory demyelinating polyneuropathy.[citation needed]
In research studies, the outcome from an episode of Guillain–Barré syndrome is recorded on a scale from 0-6, 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 death.[26]
The prognosis of 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 in the prodrome have a worse prognosis.[6] On the nerve conduction study, the presence of conduction block predicts poorer outcome at 6 months.[6] In those who have received intravenous immunoglobulins, a small 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.[6]
Epidemiology
In Western countries, the incidence (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.[27] Men are more likely to develop Guillain-Barré syndrome than women; the relative risk for men is 1.78 compared to women.[1][27]
The distribution of subtypes varies significantly 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.[2] Miller Fisher variant is thought to be more common in Southeast Asia.[1][5]
History
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 1925.
[28]
French physician Jean-Baptiste Octave Landry first described the disorder in 1859.[29] In 1916, Georges Guillain, Jean Alexandre Barré, and 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.[4][9]
Canadian neurologist C. Miller Fisher described the variant that bears his name in 1956.[5][30] British neurologist Edwin Bickerstaff, based in Birmingham, described the brainstem encephalitis type in 1951 with Philip Cloake, and made further contributions with a further paper in 1957.[5][31][32] Guillain had reported on some of these features prior to their full description in 1938.[5] Further subtypes have been described since then, such as the form featuring pure ataxia and the type causing pharyngeal-cervical-brachial weakness.[5] The axonal subtype was first described in the 1990s.[12]
Diagnostic criteria were developed in the late 1970s after the series of cases associated with swine flu vaccination. These were refined in 1990.[2][33] The case definition was revised by the Brighton Collaboration for vaccine safety in 2009,[34] but is mainly intended for research.[2] Plasma exchange was first used in 1978 and its benefit confirmed in larger studies in 1985.[35] Intravenous immunoglobulins were introduced in 1988, and its non-inferiority compared to plasma exchange was demonstrated in studies in the early 1990s.[35]
Research directions
The understanding of the disease mechanism of Guillain-Barré syndrome has evolved in recent years.[11] Development of new treatments has been limited since immunotherapy was introduced in the 1980s and 1990s.[11][35] Current research is aimed at demonstrating whether some patients 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.[6][35] 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.[35]
An animal model (experimental autoimmune neuritis in rats) is often used for studies, and some agents have shown promise: glatiramer acetate, quinpramine, fausadil (an inhibitor of the Rho-kinase enzyme),[11] and the heart drug flecainide.[35] An antibody targeted against the anti-GD3 antiganglioside antibody has shown benefit in laboratory research.[11] Given the role of the complement system in GBS, it has been suggested that complement inhibitors (such as the drug eculizumab) may be effective.[35]
See also
- List of people with Guillain–Barré syndrome
References
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- ^ Goetz, C. G. (1 May 1998). "Georges Guillain's neurologic exploration of America". Neurology 50 (5): 1451–1455. doi:10.1212/WNL.50.5.1451. PMID 9596004.
- ^ {{cite journal| last1=Landry | first=Jean-Baptiste | title=Note sur la paralysie ascendante aiguë | journal=Gazette Hebdomadaire de Médecine et de Chirurgie | date=1859 | volume=6 | pages=472–474, 486–488} | Link}
- ^ Fisher M (1956). "An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmolplegia, ataxia and areflexia)". N. Engl. J. Med. 255 (2): 57–65. doi:10.1056/NEJM195607122550201. PMID 13334797.
- ^ Bickerstaff, E.R.; Cloake, P.C. (14 July 1951). "Mesencephalitis and rhombencephalitis.". British Medical Journal 2 (4723): 77–81. doi:10.1136/bmj.2.4723.77. PMC 2069534. PMID 14848512.
- ^ Bickerstaff, E.R. (15 June 1957). "Brain-stem encephalitis; further observations on a grave syndrome with benign prognosis.". British Medical Journal 1 (5032): 1384–7. doi:10.1136/bmj.1.5032.1384. PMC 1973653. PMID 13436795.
- ^ Asbury, Arthur K.; Cornblath, David R. (1990). "Assessment of current diagnostic criteria for Guillain-Barré syndrome.". Annals of Neurology. 27 Suppl: S21–4. doi:10.1002/ana.410270707. PMID 2194422.
- ^ Sejvar, James J.; Kohl, Katrin S.; Gidudu, Jane; Amato, Anthony; Bakshi, Nandini; Baxter, Roger; Burwen, Dale R.; Cornblath, David R.; Cleerbout, Jan; Edwards, Kathryn M.; Heininger, Ulrich; Hughes, Richard; Khuri-Bulos, Najwa; Korinthenberg, Rudolf; Law, Barbara J.; Munro, Ursula; Maltezou, Helena C.; Nell, Patricia; Oleske, James; Sparks, Robert; Velentgas, Priscilla; Vermeer, Patricia; Wiznitzer, Max (January 2011). "Guillain–Barré syndrome and Fisher syndrome: Case definitions and guidelines for collection, analysis, and presentation of immunization safety data". Vaccine 29 (3): 599–612. doi:10.1016/j.vaccine.2010.06.003. PMID 20600491.
- ^ a b c d e f g Walgaard, Christa; Jacobs, Bart C; van Doorn, Pieter A (March 2011). "Emerging drugs for Guillain-Barré syndrome". Expert Opinion on Emerging Drugs 16 (1): 105–120. doi:10.1517/14728214.2011.531699. PMID 21352072.
Further reading
- Steinberg, Gareth J. Parry, Joel S. (2006). Guillain-Barré syndrome: from diagnosis to recovery (American Academy of Neurology). New York, N.Y.: Pub Group West. ISBN 978-1932603569.
External links
- Guillain–Barré syndrome at DMOZ
- GBS/CIDP Foundation International
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Nervous system pathology, PNS, somatic (G50–G64, 350–357)
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|
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Nerve, nerve root, plexus
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|
Cranial nerve
disease |
- V Trigeminal neuralgia
- Anesthesia dolorosa
- VII Facial nerve paralysis
- Bell's palsy
- Melkersson–Rosenthal syndrome
- Parry–Romberg syndrome
- Central seven
- XI Accessory nerve disorder
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|
Radiculopathy,
plexopathy |
- brachial plexus Brachial plexus lesion
- Thoracic outlet syndrome
- Phantom limb
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|
Mono-
neuropathy |
| Upper limb |
| median nerve: |
- Carpal tunnel syndrome
- Ape hand deformity
|
|
| ulnar nerve: |
- Ulnar nerve entrapment
- Froment's sign
- Guyon's canal syndrome
- Ulnar claw
|
|
| radial nerve: |
- Radial neuropathy
- Wrist drop
- Cheiralgia paresthetica
|
|
| long thoracic nerve: |
- Winged scapula
- Backpack palsy
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|
|
| Lower limb |
| lateral cutaneous nerve of thigh: |
|
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| tibial nerve: |
|
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| plantar nerve: |
|
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| superior gluteal nerve: |
|
|
| sciatic nerve: |
|
|
|
| General |
- Causalgia
- Mononeuritis multiplex
- Neuropathy Neuralgia/Neuritis
- Nerve compression syndrome
|
|
|
|
|
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Polyneuropathies/Polyradiculoneuropathy
|
|
| HMSN |
- Charcot–Marie–Tooth disease
- Dejerine–Sottas disease
- Refsum's disease
- Hereditary spastic paraplegia
- Hereditary neuropathy with liability to pressure palsy
- Familial amyloid neuropathy
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|
| Autoimmune/demyelinating |
- Guillain–Barré syndrome
- Chronic inflammatory demyelinating polyneuropathy
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| Other |
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|
|
Index of the peripheral nervous system
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|
| Description |
- Anatomy
- Nerves
- cranial
- trigeminal
- cervical
- brachial
- lumbosacral plexus
- somatosensory
- spinal
- autonomic
- Physiology
- reflexes
- proteins
- neurotransmitters
- transporters
- Development
|
|
| Disease |
- Autonomic
- Congenital
- Injury
- Neoplasms and cancer
- Other
- Symptoms and signs
|
|
| Treatment |
- Procedures
- Local anesthetics
|
|
|
|
Hypersensitivity and autoimmune diseases (279.5–6)
|
|
Type I/allergy/atopy
(IgE) |
| Foreign |
- Atopic eczema
- Allergic urticaria
- Allergic rhinitis (Hay fever)
- Allergic asthma
- Anaphylaxis
- Food allergy
- Milk
- Egg
- Peanut
- Tree nut
- Seafood
- Soy
- Wheat
- Penicillin allergy
|
|
| Autoimmune |
|
|
|
Type II/ADCC
|
| Foreign |
- Hemolytic disease of the newborn
|
|
| Autoimmune |
| Cytotoxic |
- Autoimmune hemolytic anemia
- Idiopathic thrombocytopenic purpura
- Bullous pemphigoid
- Pemphigus vulgaris
- Rheumatic fever
- Goodpasture's syndrome
- Guillain–Barré syndrome
|
|
| "Type V"/receptor |
- Graves' disease
- Myasthenia gravis
- Pernicious anemia
|
|
|
|
Type III
(Immune complex) |
| Foreign |
- Henoch–Schönlein purpura
- Hypersensitivity vasculitis
- Reactive arthritis
- Farmer's lung
- Post-streptococcal glomerulonephritis
- Serum sickness
- Arthus reaction
|
|
| Autoimmune |
- Systemic lupus erythematosus
- Subacute bacterial endocarditis
- Rheumatoid arthritis
|
|
|
Type IV/cell-mediated
(T cells) |
| Foreign |
- Allergic contact dermatitis
- Mantoux test
|
|
| Autoimmune |
- Diabetes mellitus type 1
- Hashimoto's thyroiditis
- Multiple sclerosis
- Coeliac disease
- Giant-cell arteritis
|
|
| GVHD |
- Transfusion-associated graft versus host disease
|
|
|
Unknown/
multiple |
| Foreign |
- Hypersensitivity pneumonitis
- Allergic bronchopulmonary aspergillosis
- Transplant rejection
- Latex allergy (I+IV)
|
|
| Autoimmune |
- Sjögren's syndrome
- Autoimmune hepatitis
- Autoimmune polyendocrine syndrome
- Autoimmune adrenalitis
- Systemic autoimmune disease
|
|
|
|
Index of the immune system
|
|
| Description |
- Physiology
- cells
- autoantigens
- autoantibodies
- complement
- surface antigens
- IG receptors
|
|
| Disease |
- Allergies
- Immunodeficiency
- Immunoproliferative immunoglobulin disorders
- Hypersensitivity and autoimmune disorders
- Neoplasms and cancer
|
|
| Treatment |
- Procedures
- Drugs
- antihistamines
- immunostimulants
- immunosuppressants
- monoclonal antibodies
|
|
|
