Guillain-Barré syndrome pathophysiology: Difference between revisions
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** Cytpmegalo virus | ** Cytpmegalo virus | ||
** Hemphilus influanza | ** Hemphilus influanza | ||
* It is believed that the main underlying etiology of GBS is an autoimmune reaction. | |||
* The main theory explaining the relation between these infections and GBS is molecular mimicry. | * The main theory explaining the relation between these infections and GBS is molecular mimicry. | ||
* There are many antigens on the surface of these pathogens which are similar to myelin sheath or axonal proteins. | * There are many antigens on the surface of these pathogens which are similar to myelin sheath or axonal proteins. | ||
Line 32: | Line 33: | ||
* In the serum of GBS patients with CMV as the antecedent infection, we may see antibodies against GM2. | * In the serum of GBS patients with CMV as the antecedent infection, we may see antibodies against GM2. | ||
* Haemophilus influenzae have GM1 like structure on its surface and in the serum of patients with haemophilus influenzae related GBS we may see antibodies against GM1. | * Haemophilus influenzae have GM1 like structure on its surface and in the serum of patients with haemophilus influenzae related GBS we may see antibodies against GM1. | ||
* although antibody formation and humoral immunity said to be the underlying pathophysiology mechanism, sometimes pathologic findings underscore the importance of circulating antibodies in the pathogenesis of GBS. | |||
* there are 4 types of GBS with different pathological sequences of events: | |||
** AIDP: | |||
*** Lymphocytes will infiltrate in peripheral nerves and nerves root of spinal cord. | |||
*** Complement components will deposit in the outer surface of schwann cell membrane and starts the process of myelin disruption. | |||
*** Macrophages will infiltrate and complete the demyelination. | |||
** AMAN: | |||
*** IgG and activated complement attack to the axolemma of motor fibers in ranvier nodes. | |||
*** Macrophages will migrate to these nodes and separate the axon from overlying shcwann cells and destroy the axolemma. | |||
** AMSAN: | |||
*** Very little lymphocyte infiltration | |||
*** direct attack to the axon of motor and sensory neurons. | |||
** Miller Fisher: | |||
*** IgG antibody against GQ1b ganglioside which is present in the ocolomotor nerve, cerebellar neurons and dorsal root ganglion cells. | |||
*** | |||
== Genetics == | == Genetics == | ||
[Disease name] is transmitted in [mode of genetic transmission] pattern. | [Disease name] is transmitted in [mode of genetic transmission] pattern. |
Revision as of 16:29, 19 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
Pathophysiology
Physiology
- Soma is the neuronal cell body which is a closed area with cell membrane.
- Dendrites are branched processes which lead the impulse into the neuronal cell body.
- Axons in a single process which lead the impulse away from the neuronal cell body.
- Myelin sheath is the oligodendrocyte membrane which wraps around the axons.
- Myelin sheath is insulated against electrical impulses and is separated by nodes of ranvier which can transfer the electrical impulse.
- This structure leads to fast traveling of electrical impulses.[1]
Pathogenesis
- The exact pathogenesis of Guillain Barre syndrome is not completely understood but in 2/3 of cases there is a history of an infectious disease in the past month.
- The most common pathogens responsible for these antecedent infections are:
- Campylobacter jejuni
- Cytpmegalo virus
- Hemphilus influanza
- It is believed that the main underlying etiology of GBS is an autoimmune reaction.
- The main theory explaining the relation between these infections and GBS is molecular mimicry.
- There are many antigens on the surface of these pathogens which are similar to myelin sheath or axonal proteins.
- Campylobacter jejuni LPS contains antigens resembling GM1 and GQ1b.
- In the serum of GBS patients with campylobacter jejuni as the antecedent infection, we may see antibodies against GM1 and GQ1b which can cause AMAN and Miller Fisher respectively.
- In the serum of GBS patients with CMV as the antecedent infection, we may see antibodies against GM2.
- Haemophilus influenzae have GM1 like structure on its surface and in the serum of patients with haemophilus influenzae related GBS we may see antibodies against GM1.
- although antibody formation and humoral immunity said to be the underlying pathophysiology mechanism, sometimes pathologic findings underscore the importance of circulating antibodies in the pathogenesis of GBS.
- there are 4 types of GBS with different pathological sequences of events:
- AIDP:
- Lymphocytes will infiltrate in peripheral nerves and nerves root of spinal cord.
- Complement components will deposit in the outer surface of schwann cell membrane and starts the process of myelin disruption.
- Macrophages will infiltrate and complete the demyelination.
- AMAN:
- IgG and activated complement attack to the axolemma of motor fibers in ranvier nodes.
- Macrophages will migrate to these nodes and separate the axon from overlying shcwann cells and destroy the axolemma.
- AMSAN:
- Very little lymphocyte infiltration
- direct attack to the axon of motor and sensory neurons.
- Miller Fisher:
- IgG antibody against GQ1b ganglioside which is present in the ocolomotor nerve, cerebellar neurons and dorsal root ganglion cells.
- AIDP:
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
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
- ↑ Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.