Guillain-Barré syndrome

Guillain-Barré syndrome
ICD-10	G61.0
ICD-9	357.0
DiseasesDB	5465
MeSH	D020275

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 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 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
CDC on Guillain-Barré syndrome
Guillain-Barré syndrome in the news
Blogs on Guillain-Barré syndrome
Directions to Hospitals Treating Guillain-Barré syndrome
Risk calculators and risk factors for Guillain-Barré syndrome

For patient information click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Priyamvada Singh, MBBS [2]

Pathophysiology

All forms of Guillain-Barré syndrome are due to an immune response to foreign antigens (such as infectious agents or vaccines) but mistargeted to host nerve tissues instead (a form of antigenic mimicry). The targets of such immune attack are thought to be gangliosides, 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 (see below).

The end result of such autoimmune attack on the peripheral nerves is inflammation of myelin and conduction block, leading to a muscle paralysis that may be accompanied by sensory or autonomic disturbances.

However, in mild cases, axonal function remains intact and recovery can be rapid if remyelination occurs. In severe cases, such as in the AMAN or AMSAN variants (see below), axonal degeneration occurs, and recovery depends on axonal regeneration. Recovery becomes much slower, and there is a greater degree of residual damage. 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.