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==Classification==
==Classification==
Guillain barre syndrome may be classified according to the underlying pathophysiology into four groups:<ref name="pmid9818934">{{cite journal |vauthors=Hadden RD, Cornblath DR, Hughes RA, Zielasek J, Hartung HP, Toyka KV, Swan AV |title=Electrophysiological classification of Guillain-Barré syndrome: clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group |journal=Ann. Neurol. |volume=44 |issue=5 |pages=780–8 |date=November 1998 |pmid=9818934 |doi=10.1002/ana.410440512 |url=}}</ref><ref name="pmid5059983">{{cite journal |vauthors=Prineas JW |title=Acute idiopathic polyneuritis. An electron microscope study |journal=Lab. Invest. |volume=26 |issue=2 |pages=133–47 |date=February 1972 |pmid=5059983 |doi= |url=}}</ref><ref name="pmid7600081">{{cite journal |vauthors=Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM |title=Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies |journal=Brain |volume=118 ( Pt 3) |issue= |pages=597–605 |date=June 1995 |pmid=7600081 |doi= |url=}}</ref><ref name="pmid7224616">{{cite journal |vauthors=Prineas JW |title=Pathology of the Guillain-Barré syndrome |journal=Ann. Neurol. |volume=9 Suppl |issue= |pages=6–19 |date=1981 |pmid=7224616 |doi= |url=}}</ref><ref name="pmid9708542">{{cite journal |vauthors=Kuwabara S, Yuki N, Koga M, Hattori T, Matsuura D, Miyake M, Noda M |title=IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome |journal=Ann. Neurol. |volume=44 |issue=2 |pages=202–8 |date=August 1998 |pmid=9708542 |doi=10.1002/ana.410440210 |url=}}</ref><ref name="pmid11026446">{{cite journal |vauthors=Ogawara K, Kuwabara S, Mori M, Hattori T, Koga M, Yuki N |title=Axonal Guillain-Barré syndrome: relation to anti-ganglioside antibodies and Campylobacter jejuni infection in Japan |journal=Ann. Neurol. |volume=48 |issue=4 |pages=624–31 |date=October 2000 |pmid=11026446 |doi= |url=}}</ref><ref name="pmid8572662">{{cite journal |vauthors=Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Cornblath DR, Macko C, McKhann GM, Asbury AK |title=Pathology of the motor-sensory axonal Guillain-Barré syndrome |journal=Ann. Neurol. |volume=39 |issue=1 |pages=17–28 |date=January 1996 |pmid=8572662 |doi=10.1002/ana.410390105 |url=}}</ref><ref name="pmid13334797">{{cite journal |vauthors=FISHER M |title=An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmoplegia, ataxia and areflexia) |journal=N. Engl. J. Med. |volume=255 |issue=2 |pages=57–65 |date=July 1956 |pmid=13334797 |doi=10.1056/NEJM195607122550201 |url=}}</ref><ref name="pmid8228822">{{cite journal |vauthors=Yuki N, Taki T, Inagaki F, Kasama T, Takahashi M, Saito K, Handa S, Miyatake T |title=A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure |journal=J. Exp. Med. |volume=178 |issue=5 |pages=1771–5 |date=November 1993 |pmid=8228822 |pmc=2191246 |doi= |url=}}</ref>
Guillain Barre syndrome may be classified according to the underlying pathophysiology into four groups:<ref name="pmid9818934">{{cite journal |vauthors=Hadden RD, Cornblath DR, Hughes RA, Zielasek J, Hartung HP, Toyka KV, Swan AV |title=Electrophysiological classification of Guillain-Barré syndrome: clinical associations and outcome. Plasma Exchange/Sandoglobulin Guillain-Barré Syndrome Trial Group |journal=Ann. Neurol. |volume=44 |issue=5 |pages=780–8 |date=November 1998 |pmid=9818934 |doi=10.1002/ana.410440512 |url=}}</ref><ref name="pmid5059983">{{cite journal |vauthors=Prineas JW |title=Acute idiopathic polyneuritis. An electron microscope study |journal=Lab. Invest. |volume=26 |issue=2 |pages=133–47 |date=February 1972 |pmid=5059983 |doi= |url=}}</ref><ref name="pmid7600081">{{cite journal |vauthors=Ho TW, Mishu B, Li CY, Gao CY, Cornblath DR, Griffin JW, Asbury AK, Blaser MJ, McKhann GM |title=Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies |journal=Brain |volume=118 ( Pt 3) |issue= |pages=597–605 |date=June 1995 |pmid=7600081 |doi= |url=}}</ref><ref name="pmid7224616">{{cite journal |vauthors=Prineas JW |title=Pathology of the Guillain-Barré syndrome |journal=Ann. Neurol. |volume=9 Suppl |issue= |pages=6–19 |date=1981 |pmid=7224616 |doi= |url=}}</ref><ref name="pmid9708542">{{cite journal |vauthors=Kuwabara S, Yuki N, Koga M, Hattori T, Matsuura D, Miyake M, Noda M |title=IgG anti-GM1 antibody is associated with reversible conduction failure and axonal degeneration in Guillain-Barré syndrome |journal=Ann. Neurol. |volume=44 |issue=2 |pages=202–8 |date=August 1998 |pmid=9708542 |doi=10.1002/ana.410440210 |url=}}</ref><ref name="pmid11026446">{{cite journal |vauthors=Ogawara K, Kuwabara S, Mori M, Hattori T, Koga M, Yuki N |title=Axonal Guillain-Barré syndrome: relation to anti-ganglioside antibodies and Campylobacter jejuni infection in Japan |journal=Ann. Neurol. |volume=48 |issue=4 |pages=624–31 |date=October 2000 |pmid=11026446 |doi= |url=}}</ref><ref name="pmid8572662">{{cite journal |vauthors=Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Cornblath DR, Macko C, McKhann GM, Asbury AK |title=Pathology of the motor-sensory axonal Guillain-Barré syndrome |journal=Ann. Neurol. |volume=39 |issue=1 |pages=17–28 |date=January 1996 |pmid=8572662 |doi=10.1002/ana.410390105 |url=}}</ref><ref name="pmid13334797">{{cite journal |vauthors=FISHER M |title=An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmoplegia, ataxia and areflexia) |journal=N. Engl. J. Med. |volume=255 |issue=2 |pages=57–65 |date=July 1956 |pmid=13334797 |doi=10.1056/NEJM195607122550201 |url=}}</ref><ref name="pmid8228822">{{cite journal |vauthors=Yuki N, Taki T, Inagaki F, Kasama T, Takahashi M, Saito K, Handa S, Miyatake T |title=A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure |journal=J. Exp. Med. |volume=178 |issue=5 |pages=1771–5 |date=November 1993 |pmid=8228822 |pmc=2191246 |doi= |url=}}</ref>


{| class="wikitable"
{|
! style="background: #4479BA; text-align: center;" |Subtypes
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Subtypes
! style="background: #4479BA; text-align: center;" |explanation
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Explanation
|-
|-
! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN)
! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN)
Line 17: Line 17:
* The most common type (85-90%).
* The most common type (85-90%).
* 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.

Revision as of 19:49, 21 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)
  • The most common type (85-90%).
  • Prior infection can trigger it.
  • Autoimmune disorder.
  • The target is schwann cell surface membrane or the myelin.
  • Causes demyelination.
  • 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.
Acute Motor Axonal Neuropathy (AMAN)
  • It’s common among Chinese and Japanese people.
  • It can be triggered by C. jejuni.
  • It is associated with antiganglioside antibodies.
  • Autoimmune disorder.
  • Target is axonal membrane.
  • Causes axonal degeneration in motor neurons.
  • In electrodiagnostic study we can see reduction of compound muscle action potential.
Acute motor and sensory axonal neuropathy
  • The incidence rate is under 10%.
  • Causes axonal degeneration.
  • It is similar with AMAN but involves both motor and sensory axons.
Miller Fisher syndrome
  • Causes a clinical triad: ophthalmoplegia, ataxia and areflexia.
  • Associated with ganglioside GQ1b antibody.

References

  1. ↑ 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.
  2. ↑ Prineas JW (February 1972). "Acute idiopathic polyneuritis. An electron microscope study". Lab. Invest. 26 (2): 133–47. PMID 5059983.
  3. ↑ 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.
  4. ↑ Prineas JW (1981). "Pathology of the Guillain-Barré syndrome". Ann. Neurol. 9 Suppl: 6–19. PMID 7224616.
  5. ↑ 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.
  6. ↑ 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.

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