| 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 Landry's paralysis or Guillain–Barré–Strohl syndrome, is an acute polyneuropathy, a disorder affecting the peripheral nervous system. Ascending paralysis, weakness beginning in the feet and hands and migrating towards the trunk, is the most typical symptom, and some subtypes cause change in sensation or pain, as well as dysfunction of the autonomic nervous system. It can cause life-threatening complications, in particular if the respiratory muscles are affected or if the autonomic nervous system is involved. The disease is usually triggered by an infection.
The diagnosis is usually made by nerve conduction studies and with studies of the cerebrospinal fluid. With prompt treatment by intravenous immunoglobulins or plasmapheresis, together with supportive care, the majority will recover completely. Guillain–Barré syndrome is rare, at one to two cases per 100,000 people annually, but is the most common cause of acute non-trauma-related paralysis. The syndrome is named after the French physicians Georges Guillain and Jean Alexandre Barré, who described it in 1916.
Contents
- 1 Signs and symptoms
- 2 Cause
- 3 Diagnosis
- 3.1 Testing
- 3.2 Criteria
- 3.3 Classification
- 3.4 Associated problems
- 4 Treatment
- 5 Prognosis
- 6 Epidemiology
- 7 History
- 8 Notable cases
- 9 References
- 10 Literature
- 11 External links
Signs and symptoms
The disorder is characterized by symmetrical weakness that usually affects the lower limbs first, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their legs, manifesting as "rubbery legs" or legs that tend to buckle, with or without dysesthesias (numbness or tingling). As the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected. Frequently, the lower cranial nerves may be affected, leading to bulbar weakness, oropharyngeal dysphagia (drooling, or difficulty swallowing and/or maintaining an open airway) and respiratory difficulties. Most patients require hospitalization and about 30% require ventilatory assistance for treatment of type II respiratory failure.[1] Facial weakness is also common. Eye movement abnormalities are not commonly seen in ascending GBS, but are a prominent feature in the Miller-Fisher variant.
Sensory loss, if present, usually takes the form of loss of proprioception (position sense) and areflexia (complete loss of deep tendon reflexes), an important feature of GBS. Loss of pain and temperature sensation is usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain, usually in the weakened muscles, which patients compare to the pain from overexercising. These pains are self-limited and may be treated with standard analgesics. Bladder dysfunction may occur in severe cases, but is usually short-lived.
In severe cases of GBS, loss of autonomic function is common, manifesting as wide fluctuations in blood pressure, orthostatic hypotension (a fall in blood pressure on standing, leading to an increased risk of collapse), and sinus tachycardia[2] among other cardiac arrhythmias.[3]
Cause
Structure of a typical neuron
| Neuron |
Dendrite
Soma
Axon
Nucleus
Node of
Ranvier
Axon terminal
Schwann cell
Myelin sheath
|
All forms of Guillain–Barré syndrome are autoimmune diseases, due to an immune response to foreign antigens (such as infectious agents) that mistargets host nerve tissues through a mechanism known as molecular mimicry.[4] The targets of such immune attack are thought to be gangliosides, compounds naturally present in large quantities in human peripheral nerve tissues. The most well-described antecedent infection is the bacterium Campylobacter jejuni.[5][6] In addition, cytomegalovirus has a known association with GBS.[7] In many cases, identification of a specific cause is impossible. Some cases may be triggered by the influenza virus,[8] or by an immune reaction to the influenza virus.[citation needed] An increased incidence of Guillain–Barré syndrome followed influenza immunization during the 1976-1977 swine flu pandemic;[9] however, some epidemiological studies since then have demonstrated either an extremely small increased risk following immunization (under one additional case per million vaccinations) or no increased risk.[10][11]
The end result of this autoimmune process is an attack on the peripheral nerves and damage to myelin, the fatty insulating layer of the nerve, and a nerve-conduction block leading to muscle paralysis that may be accompanied by sensory or autonomic disturbances.[citation needed]
In mild cases, nerve axon (the long slender conducting portion of a nerve) function remains intact and recovery can be rapid if remyelination occurs. In severe cases, axonal damage occurs, and recovery depends on the regeneration of this important tissue. About 80% of patients have myelin loss; in the remaining 20%, the pathological hallmark is axon loss.[citation needed]
Guillain–Barré, unlike disorders such as multiple sclerosis (MS) and Lou Gehrig's disease (ALS), is a purely peripheral nerve disorder and does not in general cause nerve damage to the brain or spinal cord.[citation needed]
Diagnosis
The diagnosis of GBS depends on findings such as rapid development of muscle paralysis, areflexia, absence of fever, and a likely inciting event. Cerebrospinal fluid analysis (through a lumbar spinal puncture) and electrodiagnostic tests of nerves and muscles (such as nerve conduction studies) are common tests ordered in the diagnosis of GBS.[citation needed]
Testing
In cerebrospinal fluid (CSF), characteristic findings include albumino-cytological dissociation. As opposed to infectious causes, this is an elevated protein level (100–1000 mg/dl), without an accompanying increased cell count (absence of pleocytosis). A sustained increased white blood cell count may indicate an alternative diagnosis such as infection.[citation needed]
Electromyography (EMG) and nerve conduction studies may show prolonged distal latencies, conduction slowing, conduction block, and temporal dispersion of compound action potential in demyelinating cases. 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]
Criteria
Features required for diagnosis are progressive weakness in legs and often arms, and areflexia (the absence of deep tendon reflexes).[12][13]
Features that strongly support diagnosis are progression of symptoms over days to four weeks, relative symmetry of symptoms, mild sensory symptoms or signs, cranial nerve involvement (especially bilateral weakness of facial muscles), autonomic dysfunction, pain (often present), high concentration of protein in CSF, and typical electrodiagnostic features.[12][13]
Features that should raise doubt about the diagnosis include severe pulmonary dysfunction with limited limb weakness at onset, severe sensory signs with limited weakness at onset, bladder or bowel dysfunction at onset, fever at onset, sharp sensory level, slow progression with limited weakness without respiratory involvement (subacute inflammatory demyelinating polyneuropathy or CIDP is more likely), marked persistent asymmetry of weakness, persistent bladder or bowel dysfunction, increased number of mononuclear cells in CSF (>50×106/L), and polymorphonuclear cells in CSF.[12][13]
Classification
Six different subtypes of Guillain–Barré syndrome exist:[citation needed]
- Acute inflammatory demyelinating polyneuropathy (AIDP) is the most common form of GBS, and the term is often used synonymously with GBS. It is caused by an autoimmune response directed against Schwann cell membranes.
- Miller Fisher syndrome (MFS) is a rare variant of GBS. Accounting for about 5% of GBS cases, it manifests as a descending paralysis, proceeding in the reverse order of the more common form of GBS.[14] It usually affects the eye muscles first and presents with the triad of ophthalmoplegia, ataxia, and areflexia.[15] The ataxia predominantly affects the gait and trunk, with the limbs relatively spared. Anti-GQ1b antibodies are present in 90% of cases.
- Acute motor axonal neuropathy (AMAN),[16] also known as Chinese paralytic syndrome, attacks motor nodes of Ranvier and is prevalent in China and Mexico. It is probably due to an auto-immune response directed against the axoplasm of peripheral nerves. The disease may be seasonal and recovery can be rapid. Anti-GD1a antibodies[17] are present. Anti-GD3 antibodies are found more frequently in AMAN.
- Acute motor sensory axonal neuropathy (AMSAN) is similar to AMAN, but also affects sensory nerves with severe axonal damage. Like AMAN, it is probably due to an autoimmune response directed against the axoplasm of peripheral nerves. Recovery is slow and often incomplete.[18]
- Acute panautonomic neuropathy is the rarest variant of GBS, sometimes accompanied by encephalopathy. It is associated with a high mortality rate, owing to cardiovascular involvement, and associated dysrhythmias. Frequently occurring symptoms include impaired sweating, lack of tear formation, photophobia, dryness of nasal and oral mucosa, itching and peeling of skin, nausea, dysphagia, and constipation unrelieved by laxatives or alternating with diarrhea. Initial nonspecific symptoms of lethargy, fatigue, headache, and decreased initiative are followed by autonomic symptoms including orthostatic lightheadedness, blurring of vision, abdominal pain, diarrhea, dryness of eyes, and disturbed micturition. The most common symptoms at onset are related to orthostatic intolerance, as well as gastrointestinal and sudomotor dysfunction.[19][full citation needed] Parasympathetic impairment (abdominal pain, vomiting, constipation, ileus, urinary retention, dilated unreactive pupils; loss of accommodation) may also be observed.
- Bickerstaff's brainstem encephalitis (BBE), a further variant of Guillain–Barré syndrome, is characterized by acute onset of ophthalmoplegia, ataxia, disturbance of consciousness, hyperreflexia or Babinski's sign. 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 in the literature. Despite severe initial presentation, BBE usually has a good prognosis. Magnetic resonance imaging plays a critical role in the diagnosis of BBE. A considerable number of BBE patients have associated axonal Guillain–Barré syndrome, indicative that the two disorders are closely related and form a continuous spectrum.
Associated problems
Hyponatremia (abnormally low levels of sodium in the blood) is commonly encountered in Guillain–Barré syndrome. This is probably related to the inappropriate secretion of antidiuretic hormone.[citation needed]
Treatment
Supportive care is the cornerstone of successful management in the acute patient. Of greatest concern is respiratory failure due to paralysis of the diaphragm, the muscle most important for breathing. Intubation may be needed when evidence of impending failure of the muscles of breathing is present – when the vital capacity (VC) is less than 20 ml/kg, the negative inspiratory force (NIF) is less negative (i.e., closer to zero) than −25 cmH2O, more than 30% decrease in either VC or NIF within 24 hours, rapid progression of disorder, or autonomic instability.
Subsequent treatment consists of attempting to reduce the body's attack on the nervous system, either by plasmapheresis, filtering antibodies out of the blood stream, 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. Glucocorticoids have not been found to be effective in GBS.[20][21] Treatment is usually begun as soon as the diagnosis is made. Plasmapheresis hastens recovery when used within four weeks of the onset of symptoms.[21] IVIg has equivalent efficacy to plasmapheresis when started within two weeks of the onset of symptoms, and has fewer complications.[21] IVIg is usually used first because of its ease of administration and safety profile. Its use is not without risk; occasionally it causes hepatitis, or in rare cases, renal failure if used for longer than five days.
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,[22] as well as helping them prevent contractures, bedsores, and cardiopulmonary difficulties.[23] Speech and language therapists help regain speaking and swallowing abilities, especially if the patient was intubated or received a tracheostomy.
Prognosis
Recovery usually starts after the fourth week from the onset of the disorder. 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. Despite all improvements in treatment and supportive care, the death rate is still about 2–3%, even in the best intensive care units. Worldwide, the death rate runs slightly higher (4%), mostly from a lack of availability of life-support equipment during the lengthy plateau lasting four to six weeks, and in some cases up to one year, when a ventilator is needed in the worst cases. About 5–10% of patients have one or more late relapses, in which case they are then classified as having chronic inflammatory demyelinating polyneuropathy.
Poor prognostic factors include age over 40 years, duration of active disease, history of preceding diarrheal illness, disability, electrophysiological signs of axonopathy, requiring ventilator support, high anti-GM1 titre, and poor upper-limb muscle strength. The main treatments did not affect the chance of recovery[24]
Epidemiology
Worldwide, the annual incidence is about 0.6–4.0 occurrences per 100,000 people. Men are one and a half times more likely to be affected than women. The incidence increases with age; about one case per 100,000 occurs in people aged below 30 years and about four cases per 100,000 in those older than 75 years.[25]
The incidence of GBS during pregnancy is 1.7 cases per 100,000 of the population.[26] Congenital and neonatal Guillain–Barré syndrome have also been reported.[27]
History
French physician Jean Landry first described the disorder in 1859. In 1916, Georges Guillain, Jean Alexandre Barré, and André Strohl diagnosed two soldiers with the illness and described the key diagnostic abnormality of increased spinal-fluid protein production, but normal cell count.[28]
GBS is also known as acute idiopathic polyradiculoneuritis, acute idiopathic polyneuritis, French polio, Landry's ascending paralysis and Landry–Guillain–Barré syndrome.[citation needed]
Canadian neurologist C. Miller Fisher described the variant that bears his name in 1956.[29]
Notable cases
American actor Andy Griffith developed Guillain-Barré syndrome in 1983. Griffith is seen here receiving an award at the White House in 2005.
- Ryūtarō Arimura, vocalist for Japanese rock band Plastic Tree: His case was detected and treated early, and Arimura was able to return to touring within three months.[30]
- Markus Babbel, former international footballer, contracted GBS in 2001, following a period suffering from the Epstein–Barr virus. He lost almost an entire year of his footballing career between the two illnesses.[31]
- Tony Benn, British politician[32]
- Rachel Chagall, actress, contracted GBS in 1982. In 1987, she portrayed Gabriela Brimmer, a notable disabilities activist.[33]
- Alastair Clarkson, Coach of Hawthorn Football Club[34]
- Tom Edlefsen, American tennis player, made the fourth round of Wimbledon in 1968, a year after he developed GBS.[35]
- Mike Egener, Canadian hockey player[36]
- Samuel Goldstein, American athlete and Paralympian[37]
- Andy Griffith, an American actor best known for The Andy Griffith Show and Matlock, developed GBS in 1983.[38]
- Joseph Heller, author, contracted GBS in 1981. This episode in his life is recounted in the autobiographical No Laughing Matter.[39]
- Luci Baines Johnson, daughter of President Lyndon Johnson and Lady Bird Johnson, was diagnosed and under treatment for GBS in April 2010.[40]
- Hugh McElhenny, former professional American football player with the San Francisco 49ers[41]
- Scott McKenzie (born Philip Wallach Blondheim), an American singer and songwriter most notable for his hit single and hippie anthem "San Francisco (Be Sure to Wear Flowers in Your Hair)", died August 18, 2012, at the age of 73 from GBS.[42]
- Sabine Moussier, Mexican actress[43]
- Lucky Oceans, Grammy Award-winning musician with Asleep at the Wheel, was diagnosed with GBS in 2008.[44]
- Len Pasquarelli, sports writer and analyst for ESPN and resident of the Pro Football Writers of America, was diagnosed in 2008.[45]
- Serge Payer, Canadian-born professional hockey player, after battling and overcoming the syndrome, set up the Serge Payer Foundation, which is dedicated to raising money for research into new treatments and cures for GBS.[46]
- William “The Refrigerator” Perry, former professional American football player with the Chicago Bears, was diagnosed with GBS in 2008.[47]
- Toni Rüttimann, bridge builder in developing countries, in Cambodia (2002); he used the rehabilitation time in Thailand to develop software to support bridge-building works.[48]
- Norton Simon, American industrialist and philanthropist[49]
- Kay Smith (artist), current Illinois Artist Laureate, was diagnosed with Guillain-Barre syndrome at the age of 73, after extensive rehabilitation at the Rehabilitation Institute of Chicago she was able to continue painting and teaching[50]
- Kelly-Marie Stewart, British actress[51]
- Hans Vonk, Dutch conductor.[52]
- Morten Wieghorst, Danish former footballer and football coach[53]
- Danny Wuerffel, 1996 Heisman Trophy winner from the University of Florida[54]
- Rich Ceisler, American standup comedian, became sick while performing on a cruise ship. He was flown to a hospital in the Dominican Republic where diagnosis of Guillain–Barré syndrome was made. Ceisler passed away soon after, on 4 August 2014.[55]
References
- ^ Burt CC, Arrowsmith JE (1 November 2009). "Respiratory failure". Surgery (Oxford) 27 (11): 475–479. doi:10.1016/j.mpsur.2009.09.007.
- ^ Flachenecker P, Toyka KV, Reiners K (Aug 2001). "[Cardiac arrhythmias in Guillain-Barre syndrome. An overview of the diagnosis of a rare but potentially life-threatening complication].". Der Nervenarzt 72 (8): 610–7. PMID 11519201.
- ^ Zochodne DW (Oct 1994). "Autonomic involvement in Guillain-Barré syndrome: a review.". Muscle & nerve 17 (10): 1145–55. doi:10.1002/mus.880171004. PMID 7935521.
- ^ Ang CW, Jacobs BC, Laman JD (2004). "The Guillain-Barré syndrome: a true case of molecular mimicry". Trends Immunol. 25 (2): 61–6. doi:10.1016/j.it.2003.12.004. PMID 15102364.
- ^ Yuki N (June 2008). "[Campylobacter genes responsible for the development and determinant of clinical features of Guillain-Barré syndrome]". Nippon Rinsho. Japanese Journal of Clinical Medicine (in Japanese) 66 (6): 1205–10. PMID 18540372.
- ^ Kuwabara S, Ogawara K, Misawa S, Koga M, Mori M, Hiraga A, Kanesaka T, Hattori T, Yuki N (2004-08-10). "Does Campylobacter jejuni infection elicit "demyelinating" Guillain-Barré syndrome?". Neurology (Lippincott Williams & Wilkins) 63 (3): 529–33. doi:10.1212/01.WNL.0000133205.05169.04. PMID 15304587.
- ^ Orlikowski D, Porcher R, Sivadon-Tardy V, Quincampoix JC, Raphaël JC, Durand MC, Sharshar T, Roussi J, Caudie C, Annane D, Rozenberg F, Leruez-Ville M, Gaillard JL, Gault E (April 2011). "Guillain–Barré Syndrome following Primary Cytomegalovirus Infection: A Prospective Cohort Study". Clin Infect Dis. 52 (7): 837–844. doi:10.1093/cid/cir074. PMID 21427390.
- ^ Sivadon-Tardy V, Orlikowski D, Porcher R, Sharshar T, Durand MC, Enouf V, Rozenberg F, Caudie C, Annane D, van der Werf S, Lebon P, Raphaël JC, Gaillard JL, Gault E (Jan 1, 2009). "Guillain-Barré syndrome and influenza virus infection". Clinical Infectious Diseases (The University of Chicago Press) 48 (1): 48–56. doi:10.1086/594124. PMID 19025491.
- ^ Haber P, DeStefano F, Angulo FJ, Iskander J, Shadomy SV, Weintraub E, Chen RT (Nov 24, 2004). "Guillain-Barré syndrome following influenza vaccination". JAMA 292 (20): 2478–81. doi:10.1001/jama.292.20.2478. PMID 15562126.
- ^ Lehmann HC, Hartung HP, Kieseier BC, Hughes RA (Sep 2010). "Guillain-Barré syndrome following influenza vaccination". Lancet Infect Dis 10 (9): 643–51. doi:10.1016/S1473-3099(10)70140-7. PMID 20797646.
- ^ Liang XF, Li L, Liu DW, Li KL, Wu WD, Zhu BP, Wang HQ, Luo HM, Cao LS, Zheng JS, Yin DP, Cao L, Wu BB, Bao HH, Xu DS, Yang WZ, Wang Y (February 2011). "Safety of Influenza A (H1N1) Vaccine in Postmarketing Surveillance in China". New England Journal of Medicine 364 (7): 638–647. doi:10.1056/NEJMoa1008553. PMID 21288090.
- ^ a b c van Doorn PA, Ruts L, Jacobs BC (October 2008). "Clinical features, pathogenesis, and treatment of Guillain-Barré syndrome". Lancet Neurol 7 (10): 939–50. doi:10.1016/S1474-4422(08)70215-1. PMID 18848313.
- ^ a b c Lerner AJ. Diagnostic Criteria in Neurology (Current Clinical Neurology). Totowa, NJ: Humana Press. p. 186. ISBN 1-61737-594-2.
- ^ Davids, H. "Guillain-Barre Syndrome". Medscape Reference. Retrieved 3 Jan 2012.
- ^ Mori M, Kuwabara S, Fukutake T, Hattori T (2002). "Plasmapheresis and Miller Fisher syndrome: analysis of 50 consecutive cases". Journal of neurology, neurosurgery, and psychiatry 72 (5): 680. doi:10.1136/jnnp.72.5.680. PMC 1737859. PMID 11971070.
- ^ McKhann GM, Cornblath DR, Ho T, Li CY, Bai AY, Wu HS, Yei QF, Zhang WC, Zhaori Z, Jiang Z (1991). "Clinical and electrophysiological aspects of acute paralytic disease of children and young adults in northern China". Lancet 338 (8767): 593–7. doi:10.1016/0140-6736(91)90606-P. PMID 1679153.
- ^ Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM (1995). "Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies". Brain 118 (3): 597–605. doi:10.1093/brain/118.3.597. PMID 7600081.
- ^ Griffin JW, Li CY, Ho TW, Xue P, Macko C, Gao CY, Yang C, Tian M, Mishu B, Cornblath DR (1995). "Guillain–Barré syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases". Brain 118 (3): 577–95. doi:10.1093/brain/118.3.577. PMID 7600080.
- ^ Suarez et al. 1994
- ^ Merck Manual [Online]. Peripheral Neuropathy, Treatment. Retrieved 8-22-2009.
- ^ a b c Hughes RA, Wijdicks EF, Barohn R, Benson E, Cornblath DR, Hahn AF, Meythaler JM, Miller RG, Sladky JT, Stevens JC (September 2003). "Practice parameter: immunotherapy for Guillain-Barré syndrome: report of the Quality Standards Subcommittee of the American Academy of Neurology". Neurology 61 (6): 736–40. doi:10.1212/WNL.61.6.736. PMID 14504313.
- ^ Davidson I, Wilson C, Walton T, Brissenden S (2009). "Physiotherapy and Guillain–Barré syndrome: Results of a national survey". Physiotherapy 95 (3): 157–163. doi:10.1016/j.physio.2009.04.001. PMID 19635334.
- ^ Karavatas SG (2005). "The role of neurodevelopmental sequencing in the physical therapy management of a geriatric patient with Guillain–Barre syndrome.". Topics in Geriatric Rehabilitation 21 (2): 133–135. doi:10.1097/00013614-200504000-00008.
- ^ The prognosis and main prognostic indicators of Guillain-Barré syndrome. A multicentre prospective study of 297 patients The Italian Guillain-Barre Study Group. Brain, 1996 119: 2053-61
- ^ Pithadia AB, Kakadia N (March–April 2010). "Guillain-Barré syndrome (GBS)". Pharmacol Rep 62 (2): 220–32. doi:10.1016/s1734-1140(10)70261-9. PMID 20508277.
- ^ Brooks H, Christian AS, May AE (2000). "Pregnancy, anaesthesia and Guillain-Barré syndrome". Anaesthesia 55 (9): 894–8. doi:10.1046/j.1365-2044.2000.01367.x. PMID 10947755.
- ^ Iannello, S (2004). Guillain–Barré syndrome: Pathological, clinical and therapeutical aspects. Nova Publishers. ISBN 1-59454-170-1.
- ^ Guillain-Barré-Strohl syndrome and Miller Fisher's syndrome at Who Named It?
- ^ 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.
- ^ "Plastic Tree’s vocalist, Arimura Ryutaro recovers from "Guillain-Barre syndrome"". Tokyohive.com. 2011-01-20. Retrieved 2012-10-20.
- ^ Wallace, Sam (2002-08-10). "Grateful Babbel a tower of strength again". London: Telegraph. Retrieved 2009-11-23.
- ^ Lea, Robert (2002-10-17). "Relative Values: Tony and Josh Benn". London: The Times. Retrieved 2009-01-15.
- ^ http://tcm.tv/this-month/article.html?isPreview=&id=499692%7C218343&name=Gaby-A-True-Story
- ^ http://www.afl.com.au/news/2014-05-27/clarksons-health-crisis
- ^ Los Angeles Times, "Tom Edlefsen Beats Virus", 30 June 1968
- ^ http://www.coventryblaze.co.uk/index.php/news/latest-news/631-egener-illness-forces-contract-cancellation
- ^ The case of Sam Goldstein and the swine flu vaccine, jta.org, May 5, 2009
- ^ "Andy in Guideposts Magazine".
- ^ Vogel, Speed; Heller, Joseph (2004). No Laughing Matter. New York: Simon & Schuster. ISBN 0-7432-4717-5.
- ^ "Luci Baines Johnson hospitalized with nervous system disorder".
- ^ Raley, Dan (2004-09-02). "The untold story of Hugh McElhenny, the King of Montlake". Seattle PI. Retrieved 2010-01-07.
- ^ "Scott McKenzie Dead". Celebritydiagnosis.com. 2012-08-21. Retrieved 2012-10-20.
- ^ "People en español".
- ^ "Lucky Oceans in hospital". The Australian. 2008-10-13. Retrieved 2008-10-28.
- ^ "Chris Mortensen on Len Pasquarelli's comeback". ESPN.com. 2009-01-26. Retrieved 2009-01-26.
- ^ Serge Payer Foundation, Serge Payer Foundation Mission.
- ^ . YumaSun.com. 2008-09-08 http://www.yumasun.com/sports/tatum_44249___article.html/perry_night.html. Retrieved 2008-10-28.
- ^ Gallanti, Fabrizio (30 November 2006). "The bridge builder". Domus. Italy.
- ^ "Norton Simon Biography". Retrieved 13 October 2009.
- ^ Artist Discovers That A Still Life Can Be Moving http://articles.chicagotribune.com/1997-05-18/news/9705180077_1_guillain-barre-syndrome-paint-tahiti
- ^ Sutton, Jessica. "Kelly-Marie Stewart: disability and motherhood". Retrieved 3 January 2013.
- ^ Kozinn, Allan (2004-08-31). "Hans Vonk, 63, Conductor Of the St. Louis Symphony". The New York Times. Retrieved 2009-08-26.
- ^ "Recovering Wieghorst is now talking". BBC News. 2000-11-01.
- ^ Dooley, Pat. "Wuerffel hospitalized to treat nervous system disorder". Gatorsports.com. Retrieved 16 June 2011.
- ^ Procida, Billy. "Comedian Rich Ceisler dies from rare Guillain-Barré syndrome". Laughspin.com. Retrieved 5 August 2014.
Literature
- Pithadia AB, Kakadia N (March–April 2010). "Guillain-Barré syndrome (GBS)". Pharmacol Rep 62 (2): 220–32. doi:10.1016/s1734-1140(10)70261-9. PMID 20508277.
- Newswanger DL, Warren CR (May 2004). "Guillain-Barré syndrome". Am Fam Physician 69 (10): 2405–10. PMID 15168961.
External links
- Guillain–Barré syndrome at DMOZ
- GBS/CIDP Foundation International
|
Nervous system pathology, PNS, somatic (G50–G64, 350–357)
|
|
|
Nerve, nerve root, plexus
|
|
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
|
|
Radiculopathy,
plexopathy |
- brachial plexus Brachial plexus lesion
- Thoracic outlet syndrome
- Phantom limb
|
|
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: |
|
|
|
| Lower limb |
| lateral cutaneous nerve of thigh: |
|
|
| tibial nerve: |
|
|
| plantar nerve: |
|
|
| superior gluteal nerve: |
|
|
| sciatic nerve: |
|
|
|
| General |
- Causalgia
- Mononeuritis multiplex
- Neuropathy Neuralgia/Neuritis
- Nerve compression syndrome
|
|
|
|
|
|
Polyneuropathies/Polyradiculoneuropathy
|
|
| HMSN |
- Charcot–Marie–Tooth disease
- Dejerine–Sottas disease
- Refsum's disease
- Hereditary spastic paraplegia
|
|
| Autoimmune/demyelinating |
- Guillain–Barré syndrome
- Chronic inflammatory demyelinating polyneuropathy
|
|
| Other |
|
|
|
|
|
|
anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp
|
noco/auto/cong/tumr, sysi/epon, injr
|
|
|
|
|
|
Immune disorders: 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
|
|
| "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
- Guillain–Barré syndrome
- 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
|
|
|
|
|
cell/phys/auag/auab/comp, igrc
|
|
|
|
|
|
