Guillain-Barré syndrome pathophysiology: Difference between revisions

	Guillain-Barré syndrome Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Guillain-Barré syndrome from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural history, Complications, and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Guillain-Barré syndrome pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Guillain-Barré syndrome pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Guillain-Barré syndrome pathophysiology
CDC on Guillain-Barré syndrome pathophysiology
Guillain-Barré syndrome pathophysiology in the news
Blogs on Guillain-Barré syndrome pathophysiology
Directions to Hospitals Treating Guillain-Barré syndrome
Risk calculators and risk factors for Guillain-Barré syndrome pathophysiology

VisualWikitext

Revision as of 15:24, 19 December 2018

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
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.

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.

Template:WH Template:WS

[:0-1] Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.

[1]

@@ Line 21: / Line 21: @@
 === Pathogenesis ===
-* The exact pathogenesis of [disease name] is not completely understood.
+* 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.
-OR
+* The most common pathogens responsible for these antecedent infections are:
-* 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].
+** Campylobacter jejuni
-* [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
+** Cytpmegalo virus
-* Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
+** Hemphilus influanza
-* [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
+* The main theory explaining the relation between these infections and GBS is molecular mimicry.
-* The progression to [disease name] usually involves the [molecular pathway].
+* There are many antigens on the surface of these pathogens which are similar to myelin sheath or axonal proteins.
-* The pathophysiology of [disease/malignancy] depends on the histological subtype.
+* 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.
 == Genetics ==