Guillain-Barré syndrome classification: Difference between revisions
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* Prior infection can trigger it. | * Prior infection can trigger it. | ||
* [[Autoimmune disorder]]. | * [[Autoimmune disorder]]. | ||
* The target is [[schwann cell]] surface membrane or the myelin. | * The target is [[schwann cell]] surface membrane or the [[myelin]]. | ||
* Causes demyelination. | * Causes [[demyelination]]. | ||
* In electrodiagnostic tests we can see slowing of nerve conduction. | * In electrodiagnostic tests we can see slowing of nerve conduction. | ||
* In pathology we can see lymphocytic infiltration of peripheral nerves and macrophage invasion of myelin sheath and schwann cells. | * In pathology we can see [[Lymphocyte|lymphocytic]] infiltration of peripheral nerves and [[macrophage]] invasion of [[myelin sheath]] and [[Schwann cell|schwann cells]]. | ||
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! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN) | ! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN) | ||
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* It’s common among Chinese and Japanese people. | * It’s common among Chinese and Japanese people. | ||
* It can be triggered by C. jejuni. | * It can be triggered by C. jejuni. | ||
* It is associated with | * It is associated with anti[[ganglioside]] [[antibodies]]. | ||
* Autoimmune disorder. | * [[Autoimmunity|Autoimmune]] disorder. | ||
* Target is axonal membrane. | * Target is [[Axon|axonal]] membrane. | ||
* Causes axonal degeneration in motor neurons. | * Causes [[Axon|axonal]] degeneration in [[Motor neuron|motor neurons]]. | ||
* In electrodiagnostic study we can see reduction of compound muscle action potential. | * In electrodiagnostic study we can see reduction of compound muscle [[action potential]]. | ||
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! style="background: #DCDCDC; text-align: center;" |Acute motor and sensory axonal neuropathy | ! style="background: #DCDCDC; text-align: center;" |Acute motor and sensory axonal neuropathy | ||
| style="background: #F5F5F5;" | | | style="background: #F5F5F5;" | | ||
* The incidence rate is under 10%. | * The incidence rate is under 10%. | ||
* Causes axonal degeneration. | * Causes [[Axon|axonal]] [[degeneration]]. | ||
* It is similar with AMAN but involves both motor and sensory axons. | * It is similar with [[Acute motor axonal neuropathy|AMAN]] but involves both motor and sensory [[Axon|axons]]. | ||
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! style="background: #DCDCDC; text-align: center;" |Miller Fisher syndrome | ! style="background: #DCDCDC; text-align: center;" |Miller Fisher syndrome | ||
| style="background: #F5F5F5;" | | | style="background: #F5F5F5;" | | ||
* Causes a clinical triad: ophthalmoplegia, ataxia and areflexia. | * Causes a clinical triad: [[ophthalmoplegia]], [[ataxia]] and [[areflexia]]. | ||
* Associated with ganglioside GQ1b antibody. | * Associated with [[ganglioside]] GQ1b [[antibody]]. | ||
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Revision as of 23:57, 26 December 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.
Overview
Classification
Guillain Barre syndrome may be classified according to the underlying pathophysiology into four groups:[1][2][3][4][5][6][7][8][9]
| Subtypes | Explanation |
|---|---|
| Acute Motor Axonal Neuropathy (AMAN) |
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| Acute Motor Axonal Neuropathy (AMAN) |
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| Acute motor and sensory axonal neuropathy |
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| Miller Fisher syndrome |
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References
- ↑ Hadden RD, Cornblath DR, Hughes RA, Zielasek J, Hartung HP, Toyka KV, Swan AV (November 1998). "Electrophysiological classification of Guillain-Barré syndrome: clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group". Ann. Neurol. 44 (5): 780–8. doi:10.1002/ana.410440512. PMID 9818934.
- ↑ Prineas JW (February 1972). "Acute idiopathic polyneuritis. An electron microscope study". Lab. Invest. 26 (2): 133–47. PMID 5059983.
- ↑ Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM (June 1995). "Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies". Brain. 118 ( Pt 3): 597–605. PMID 7600081.
- ↑ Prineas JW (1981). "Pathology of the Guillain-Barré syndrome". Ann. Neurol. 9 Suppl: 6–19. PMID 7224616.
- ↑ Kuwabara S, Yuki N, Koga M, Hattori T, Matsuura D, Miyake M, Noda M (August 1998). "IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome". Ann. Neurol. 44 (2): 202–8. doi:10.1002/ana.410440210. PMID 9708542.
- ↑ Ogawara K, Kuwabara S, Mori M, Hattori T, Koga M, Yuki N (October 2000). "Axonal Guillain-Barré syndrome: relation to anti-ganglioside antibodies and Campylobacter jejuni infection in Japan". Ann. Neurol. 48 (4): 624–31. PMID 11026446.
- ↑ Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Cornblath DR, Macko C, McKhann GM, Asbury AK (January 1996). "Pathology of the motor-sensory axonal Guillain-Barré syndrome". Ann. Neurol. 39 (1): 17–28. doi:10.1002/ana.410390105. PMID 8572662.
- ↑ FISHER M (July 1956). "An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmoplegia, ataxia and areflexia)". N. Engl. J. Med. 255 (2): 57–65. doi:10.1056/NEJM195607122550201. PMID 13334797.
- ↑ Yuki N, Taki T, Inagaki F, Kasama T, Takahashi M, Saito K, Handa S, Miyatake T (November 1993). "A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure". J. Exp. Med. 178 (5): 1771–5. PMC 2191246. PMID 8228822.