Guillain-Barré syndrome: Difference between revisions
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− | == |
+ | ==Background== |
+ | === Types === |
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− | * Causes either acute inflammatory demyelinating polyneuropathy, or acute motor axonal neuropathy, or acute motor and sensory axonal neuropathy |
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+ | |||
+ | *Guillain-Barré syndrome |
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+ | **Acute inflammatory demyelinating polyneuropathy (AIDP) |
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+ | **Acute motor axonal neuropathy |
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+ | ***Acute motor-sensory axonal neuropathy |
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+ | ***Acute motor-conduction-block neuropathy |
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+ | ***Pharyngeal-cervical-branchial weakness |
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+ | *Miller Fisher syndrome |
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+ | **Incomplete MFS |
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+ | ***Acute motor-ophthalmoparesis, without ataxia |
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+ | ***Acute ataxic neyropathy, without ophthalmoparesis |
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+ | **Bickerstaff's brainstem encephalitis |
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===Etiology=== |
===Etiology=== |
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*Non-infectious causes, including immunization, surgery, trauma, and hematopoietic stem cell transplantation |
*Non-infectious causes, including immunization, surgery, trauma, and hematopoietic stem cell transplantation |
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− | === |
+ | === Pathophysiology === |
+ | |||
+ | * Immune crossreactivity causes autoimmune destruction of either the myelin sheath (AIDP) or the axon itself |
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+ | * Most common ADAM antibodies are anti-GM1 or anti-GD1a IgG, which recognize gangliosides |
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+ | * Most common MFS antibody is anti-GQ1b IgG (in 90%) |
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+ | |||
+ | ===Epidemiology=== |
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− | * |
+ | *About 1 case per 100,000 people per year in Western countries |
− | == |
+ | ==Clinical Manifestations== |
− | * |
+ | *Ascending paralysis ± sensory involvement |
− | * |
+ | *Usually occurs 1 to 2 weeks after an immune-stimulating even such as illness or vaccination |
− | ** |
+ | **Preceding illness usually a gastrointestinal or respiratory infection |
− | ** |
+ | **[[Campylobacter jejuni]] is the most common causative organism identified |
− | ** |
+ | **Rare following influenza vaccination; most notable was the 1976 H1N1 vaccine, with about 1 in 100,000 vaccine recipients developing GBS |
− | == |
+ | ==Further Reading== |
− | * |
+ | *Guillain-Barré syndrome. ''Lancet''. 2016;388:717-727. doi: [https://doi.org/10.1016/S0140-6736(16)00339-1 10.1016/S0140-6736(16)00339-1] |
[[Category:Neurology]] |
[[Category:Neurology]] |
Revision as of 15:56, 14 July 2020
Background
Types
- Guillain-Barré syndrome
- Acute inflammatory demyelinating polyneuropathy (AIDP)
- Acute motor axonal neuropathy
- Acute motor-sensory axonal neuropathy
- Acute motor-conduction-block neuropathy
- Pharyngeal-cervical-branchial weakness
- Miller Fisher syndrome
- Incomplete MFS
- Acute motor-ophthalmoparesis, without ataxia
- Acute ataxic neyropathy, without ophthalmoparesis
- Bickerstaff's brainstem encephalitis
- Incomplete MFS
Etiology
- Campylobacter jejuni
- Cytomegalovirus
- Epstein-Barr virus
- Zika virus
- HIV
- Non-infectious causes, including immunization, surgery, trauma, and hematopoietic stem cell transplantation
Pathophysiology
- Immune crossreactivity causes autoimmune destruction of either the myelin sheath (AIDP) or the axon itself
- Most common ADAM antibodies are anti-GM1 or anti-GD1a IgG, which recognize gangliosides
- Most common MFS antibody is anti-GQ1b IgG (in 90%)
Epidemiology
- About 1 case per 100,000 people per year in Western countries
Clinical Manifestations
- Ascending paralysis ± sensory involvement
- Usually occurs 1 to 2 weeks after an immune-stimulating even such as illness or vaccination
- Preceding illness usually a gastrointestinal or respiratory infection
- Campylobacter jejuni is the most common causative organism identified
- Rare following influenza vaccination; most notable was the 1976 H1N1 vaccine, with about 1 in 100,000 vaccine recipients developing GBS
Further Reading
- Guillain-Barré syndrome. Lancet. 2016;388:717-727. doi: 10.1016/S0140-6736(16)00339-1