Guillain-Barré syndrome classification: Difference between revisions

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(/* Acute motor axonal neuropathy (AMAN) {{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 |jour...)
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{{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.
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==
Six different subtypes of Guillain–Barré syndrome exist:
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>
===Acute inflammatory demyelinating polyneuropathy===
* 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.
* [[Campylobacter jejuni]] is the commonest causative agent (positive in approximately 2 out of 5 patients).
* Peripheral nerve demyelination is present. Symptoms generally resolve with remyelination.
===Miller Fisher syndrome===
* Accounts for approximately 5% of GBS cases
* Unlike '''Acute inflammatory demyelinating polyneuropathy'''it manifests as a descending [[paralysis]]
* It usually affects the [[human eye|eye]] muscles first and presents with the triad of [[ophthalmoplegia]], [[ataxia]], and [[areflexia]].
* The ataxia predominantly affects the gait and trunk, with the limbs relatively spared.
* [[Anti-ganglioside antibodies#Anti-GQ1b|Anti-GQ1b]] antibodies are present in 90% of cases.
===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>===
* Also known as '''Chinese paralytic syndrome'''
* Prevalent in [[China]] and [[Mexico]].
* The disease may have seasonal variations.
* Recovery can be rapid.
* Due to auto-immune response directed against the [[axoplasm]] and [[nodes of Ranvier]] of [[peripheral nervous system|peripheral nerves]].
* 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.


===Acute motor sensory axonal neuropathy''' (AMSAN)===
{|
* It is similar to [[AMAN]] however unlike AMAN it also affects sensory nerves.
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Subtypes
* It is probably due to an auto-immune response directed against the [[axoplasm]] of peripheral nerves.
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Explanation
* 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>
|-
* '''Acute panautonomic neuropathy''' is the most rare variant of GBS, sometimes accompanied by [[encephalopathy]]. It is associated with a high mortality rate, owing to cardiovascular involvement, and associated [[cardiac arrhythmia|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 (Suarez et al. 1994). [[Parasympathetic]] impairment (abdominal pain, vomiting, constipation, ileus, urinary retention, dilated unreactive pupils, loss of accommodation) may also be observed.
! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN)
* '''Bickerstaff's brainstem encephalitis''' (BBE) is a further variant of Guillain–Barré syndrome. It is characterized by acute onset of ophthalmoplegia, ataxia, disturbance of consciousness, hyperreflexia or [[Plantar reflex|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.  BBE despite severe initial presentation usually has a good prognosis. [[Magnetic resonance imaging]] (MRI) 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.
| style="background: #F5F5F5;" |
* 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 [[Lymphocyte|lymphocytic]] infiltration of peripheral nerves and [[macrophage]] invasion of [[myelin sheath]] and [[Schwann cell|schwann cells]].
|-
! style="background: #DCDCDC; text-align: center;" |Acute Motor Axonal Neuropathy (AMAN)
| style="background: #F5F5F5;" |
* It’s common among Chinese and Japanese people.
* It can be triggered by C. jejuni.
* It is associated with anti[[ganglioside]] [[antibodies]].
* [[Autoimmunity|Autoimmune]] disorder.
* Target is [[Axon|axonal]] membrane.
* Causes [[Axon|axonal]] degeneration in [[Motor neuron|motor neurons]].
* In electrodiagnostic study we can see reduction of compound muscle [[action potential]].
|-
! style="background: #DCDCDC; text-align: center;" |Acute motor and sensory axonal neuropathy
| style="background: #F5F5F5;" |
* The incidence rate is under 10%.
* Causes [[Axon|axonal]] [[degeneration]].
* It is similar with [[Acute motor axonal neuropathy|AMAN]] but involves both motor and sensory [[Axon|axons]].
|-
! style="background: #DCDCDC; text-align: center;" |Miller Fisher syndrome
| style="background: #F5F5F5;" |
* Causes a clinical triad: [[ophthalmoplegia]], [[ataxia]] and [[areflexia]].
* Associated with [[ganglioside]] GQ1b [[antibody]].
|}


==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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