Guillain-Barré syndrome classification: Difference between revisions

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__NOTOC__
{{Guillain-Barré syndrome}}
{{Guillain-Barré syndrome}}


{{CMG}}; '''Associate Editors-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh@perfuse.org]
{{CMG}}; {{AE}} {{Fs}}


==Overview==
==Overview==
'''Guillain-Barré syndrome''' ('''GBS''') is an acute, autoimmune, [[neuropathy|polyradiculoneuropathy]] affecting the [[peripheral nervous system]], usually triggered by an acute infectious process. It is included in the wider group of [[peripheral neuropathy|peripheral neuropathies]]. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, acute inflammatory demyelinating polyneuropathy (AIDP). It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. The other less common variants involve [[Miller Fisher syndrome]], [[Acute motor axonal neuropathy]] (AMAN), [[Acute motor sensory axonal neuropathy]](AMSAN), [[Acute panautonomic neuropathy]], and [[Bickerstaff's brainstem encephalitis]] (BBE)
Guillain Barre syndrome may be classified according to the underlying pathophysiology into four groups: [[Acute motor axonal neuropathy]] (AMAN), acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy and [[Miller Fisher syndrome]].


==Classification==
==Classification==
===Acute inflammatory demyelinating polyneuropathy===
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>
* Commonest form of GBS, and the term is often used synonymously with GBS.
 
* Caused by an auto-immune response directed against [[Schwann cell]] membranes.
{|
* Commonly preceded by a bacterial or viral infection.
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Subtypes
* [[Campylobacter jejuni]] is the commonest causative agent (positive in approximately 2 out of 5 patients).
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Explanation
* Peripheral nerve demyelination is present. Symptoms generally resolve with remyelination.
|-
===Acute motor axonal neuropathy (AMAN) <ref name="McKhann1991">{{Cite journal|author=McKhann GM, Cornblath DR, Ho T, ''et al'' |year=1991 |month= |title=Clinical and electrophysiological aspects of acute paralytic disease of children and young adults in northern China |journal=Lancet |volume=338 |issue=8767 |pages=593–7 |pmid=1679153 |url= |accessdate= |quote= |doi=10.1016/0140-6736(91)90606-P }}</ref>===
! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN)
* Also known as '''Chinese paralytic syndrome'''
| style="background: #F5F5F5;" |
* Prevalent in [[China]] and [[Mexico]].
* The most common type (85-90%).
* The disease may have seasonal variations.
* Prior infection can trigger it.
* Recovery can be rapid.
* [[Autoimmune disorder]].
* Due to auto-immune response directed against the [[axoplasm]] and [[nodes of Ranvier]] of [[peripheral nervous system|peripheral nerves]].
* The target is [[schwann cell]] surface membrane or the [[myelin]].
* Anti-GD1a antibodies<ref name="Ho1995">{{Cite journal|author=Ho TW, Mishu B, Li CY, ''et al'' |title=Guillain-Barré syndrome in northern China. Relationship to Campylobacter jejuni infection and anti-glycolipid antibodies |journal=Brain |volume=118 ( Pt 3) |issue= 3|pages=597–605 |year=1995 |pmid=7600081 |doi= 10.1093/brain/118.3.597}}</ref> are present. [[Anti-ganglioside antibodies#Anti-GD3|Anti-GD3]] antibodies are commonly found associated with it.
* Causes [[demyelination]].
===Acute motor sensory axonal neuropathy''' (AMSAN)===
* In electrodiagnostic tests we can see slowing of nerve conduction.
* It is similar to [[AMAN]] however unlike AMAN it also affects sensory nerves <ref name="pmid12391383">{{cite journal |author=Winer JB |title=Treatment of Guillain-Barré syndrome |journal=[[QJM : Monthly Journal of the Association of Physicians]] |volume=95 |issue=11 |pages=717–21 |year=2002 |month=November |pmid=12391383 |doi= |url=http://qjmed.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=12391383 |accessdate=2012-02-19}}</ref>.
* In pathology we can see [[Lymphocyte|lymphocytic]] infiltration of peripheral nerves and [[macrophage]] invasion of [[myelin sheath]] and [[Schwann cell|schwann cells]].
* It is probably due to an auto-immune response directed against the [[axoplasm]] of peripheral nerves.
|-
* Recovery is slow and often incomplete.<ref name="Griffin1995">{{Cite journal|author=Griffin JW, Li CY, Ho TW, ''et al'' |title=Guillain–Barré syndrome in northern China. The spectrum of neuropathological changes in clinically defined cases |journal=Brain |volume=118 ( Pt 3) |issue= 3|pages=577–95 |year=1995 |pmid=7600080 |doi= 10.1093/brain/118.3.577}}</ref>
! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN)
===Miller Fisher syndrome===
| style="background: #F5F5F5;" |
* Accounts for approximately 5% of GBS cases
* It’s common among Chinese and Japanese people.
* Unlike '''Acute inflammatory demyelinating polyneuropathy'''it manifests as a descending [[paralysis]]
* It can be triggered by C. jejuni.
* It usually affects the [[human eye|eye]] muscles first and presents with the triad of [[ophthalmoplegia]] (external) <ref name="pmid17130419">{{cite journal |author=Kimoto K, Koga M, Odaka M, Hirata K, Takahashi M, Li J, Gilbert M, Yuki N |title=Relationship of bacterial strains to clinical syndromes of Campylobacter-associated neuropathies |journal=[[Neurology]] |volume=67 |issue=10 |pages=1837–43 |year=2006 |month=November |pmid=17130419 |doi=10.1212/01.wnl.0000244468.22377.6b |url=http://www.neurology.org/cgi/pmidlookup?view=long&pmid=17130419 |accessdate=2012-02-19}}</ref>, [[ataxia]], and [[areflexia]] <ref name="pmid13334797">{{cite journal |author=FISHER M |title=An unusual variant of acute idiopathic polyneuritis (syndrome of ophthalmoplegia, ataxia and areflexia) |journal=[[The New England Journal of Medicine]] |volume=255 |issue=2 |pages=57–65 |year=1956 |month=July |pmid=13334797 |doi=10.1056/NEJM195607122550201 |url=http://www.nejm.org/doi/abs/10.1056/NEJM195607122550201?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed |accessdate=2012-02-19}}</ref>.
* It is associated with anti[[ganglioside]] [[antibodies]].
* The ataxia predominantly affects the gait and trunk, with the limbs relatively spared.
* [[Autoimmunity|Autoimmune]] disorder.
* [[Anti-ganglioside antibodies#Anti-GQ1b|Anti-GQ1b]] antibodies are present in 90% of cases <ref name="pmid8413947">{{cite journal |author=Chiba A, Kusunoki S, Obata H, Machinami R, Kanazawa I |title=Serum anti-GQ1b IgG antibody is associated with ophthalmoplegia in Miller Fisher syndrome and Guillain-Barré syndrome: clinical and immunohistochemical studies |journal=[[Neurology]] |volume=43 |issue=10 |pages=1911–7 |year=1993 |month=October |pmid=8413947 |doi= |url= |accessdate=2012-02-19}}</ref>.
* Target is [[Axon|axonal]] membrane.
===Acute panautonomic neuropathy===
* Causes [[Axon|axonal]] degeneration in [[Motor neuron|motor neurons]].
* Most rare variant of GBS
* In electrodiagnostic study we can see reduction of compound muscle [[action potential]].
* Prognosis may be poor because of its association with [[encephalopathy]] and cardiovascular involvement, and associated [[cardiac arrhythmia|dysrhythmias]].
|-
* Initial symptoms of lethargy, fatigue, headache can be present.
! style="background: #DCDCDC; text-align: center;" |Acute motor and sensory axonal neuropathy
* Common symptoms include impaired sweating, lack of tear formation, [[photophobia]], dryness of nasal and oral mucosa, itching and peeling of skin, [[nausea]], [[dysphagia]], and constipation or alternating with diarrhea.  
| style="background: #F5F5F5;" |
* Autonomic symptoms like orthostatic hypotension, lightheadedness, blurring of vision, abdominal pain, diarrhea, dryness of eyes, and disturbed [[micturition]] can be seen.
* The incidence rate is under 10%.
* [[Parasympathetic]] impairment (abdominal pain, vomiting, constipation, ileus, urinary retention, dilated unreactive pupils, loss of accommodation) may also be observed.
* Causes [[Axon|axonal]] [[degeneration]].
===Bickerstaff's brainstem encephalitis (BBE)===
* It is similar with [[Acute motor axonal neuropathy|AMAN]] but involves both motor and sensory [[Axon|axons]].
* Another rare variant of GBS
|-
* Associated with acute onset ophthalmoplegia, ataxia, disturbance of consciousness, hyperreflexia or [[Plantar reflex|Babinski's sign]]. * It can have monophasic or remitting-relapsing progression.
! style="background: #DCDCDC; text-align: center;" |Miller Fisher syndrome
* Neuroimaging with [[Magnetic resonance imaging]] (MRI)  plays a critical role in the diagnosis.
| style="background: #F5F5F5;" |
* Large, irregular hyperintense lesions located mainly in the brainstem, especially in the [[pons]], [[midbrain]] and [[medulla]] can be seen.  
* Causes a clinical triad: [[ophthalmoplegia]], [[ataxia]] and [[areflexia]].
* Prognosis is good despite the initial severe presentation
* Associated with [[ganglioside]] GQ1b [[antibody]].
* It is commonly found associated with axonal Guillain–Barré syndrome suggesting some linking between the two disorders
|}


==References==
==References==
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Latest revision as of 15:49, 27 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

Guillain Barre syndrome may be classified according to the underlying pathophysiology into four groups: Acute motor axonal neuropathy (AMAN), acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy and Miller Fisher syndrome.

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)
Acute Motor Axonal Neuropathy (AMAN)
Acute motor and sensory axonal neuropathy
Miller Fisher syndrome

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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