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| ==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 involves an auto-immune mechanism in which the antibodies formed against the lipopolysaccharides of bacteria or certain vaccines cross reacts with the [[gangliosides]] present in myelin of peripheral nerves. As a result of which, myelin degeneration occurs leading to conduction defects that manifests as [[flaccid paralysis]].
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| ==Pathophysiology== | | ==Pathophysiology== |
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| * GBS is often associated with an antecedent infection with agents such as [[Campylobacter jejuni]] or exposure to some vaccines (influenza vaccine).
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| * These causative agents have certain [[lipopolysaccharides]] [[antigens]] in their capsules that are similar to [[gangliosides]] and [[glycolipids]], such as GM1 and GD1b found in [[myelin]] tissues of the [[peripheral nerve]].
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| * The immune responses directed against these bacterial capsular lipopolysaccharides also targets the similar GM1 ganglioside which are complex glycosphingolipids present in large quantities on human nerve tissues, especially in the [[nodes of Ranvier]]. An example is the GM1 ganglioside, which can be affected in as many as 20-50% of cases, especially in those preceded by ''[[Campylobacter jejuni]]'' infections. Another example is the GQ1b ganglioside, which is the target in the [[Miller Fisher syndrome]] variant.
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| * Cellular and humoral immune mechanisms play an important role in the development of disease. Pathologic findings in GBS include lymphocytic infiltration of peripheral nerves, followed by macrophage-mediated, multifocal attack of myelin.
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| * These type of immune response that are primarily for foreign antigens (such as infectious agents or vaccines) but are mis-targeted to host nerve tissues instead are called [[antigenic mimicry]] or [[molecular mimicry]].
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| * The end result of such [[autoimmune]] attack on the peripheral nerves is inflammation of [[myelin]], defects in the propagation of electrical nerve impulses and conduction block, leading to a muscle [[paralysis]] that may be accompanied by sensory or [[autonomic]] disturbances.
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| * However, in mild cases, axonal function remains intact and recovery can be rapid if remyelination occurs.
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| * In severe cases, such as in the AMAN or AMSAN variants, axonal degeneration occurs, and recovery depends on axonal regeneration. Recovery becomes much slower, and there is a greater degree of residual damage.
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| * Recent studies on the disease have demonstrated that approximately 80% of the patients have [[myelin]] loss, whereas, in the remaining 20%, the pathologic hallmark of the disease is indeed [[axon]] loss.
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| {{#ev:youtube|i_jsTpiR8rw&feature}}
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| === Physiology === | | === Physiology === |
| The normal physiology of [name of process] can be understood as follows:
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| === Pathogenesis === | | === Pathogenesis === |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.
Overview
Pathophysiology
Physiology
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
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