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Published by: Kim Gonzales on Aug 24, 2010
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GuillainGuillain-Barré Syndrome

³Ascending Paralysis ³ AI-Destruction-Nodes of Ranvier AI-Destruction-

GuillainGuillain-Barré Syndrome
Acute inflammatory demyelinating polyneuropathy (AIDP) caused by an autoimmune disorder affecting the peripheral nervous system, usually triggered by an acute infectious process characterized by ascending paralysis.

Demyelination of Nerve Fibers
Negative conduction abnormalities slowed axonal conduction, variable conduction blocks occur in the presence of high- but not -low frequency volleys of impulse. Positive conduction abnormalities generations of ectopic impulses, spontaneous and abnormal ³crosstalk´ between demyelinated axons



Acute autoimmune disorder There is involvement of T and B lymphocytes ±
cytokines and cytokine receptors in serum (IL 2, soluble IL 2 receptor) and CSF (IL 6, TNF , interferon)

Brain is unable to send messages Legs and arms are commonly affected

75% of cases are preceded by an acute infectious process usually GI or Respiratory in origin 2020-35% of cases are preceded by a Campylobacter jejuni, jejuni, HV, EBV infection. Recent: swine influenza vaccine Destruction most often occurs in segments between the Nodes of Ranvier

Immune response to foreign antigens that are mistargeted at host nerve tissues instead.

Source: Harrison Internal medicine pp 2509

Why Nodes of Ranvier are the target of attack?
Neural targets are likely to be gangliosides Gangliosides are complex glycosphingolipids that contain one or more sialic acid residue Gangliosides are present in large quantities in human nervous tissues and in key sites: NODES OF RANVIER

Pathophysiology of GBS

Etiology  Autoimmue  Campylobacter jejuni  Virus EBV HV SIV

Antigens enter into the body by multifenestrated cells Innate immune response results in the uptake of the pathogens by immature APC Production of antibodies and Phagocytosis of the bacteria B cells are activated by newly activated Th2 cells. This produces a cell-mediated and humoral response against the pathogen.

Migration to lymph nodes , a mature, differentiated APC activate CD4 T cells that recognize antigen from the infectious pathogen Molecular mimicry Immune responses directed against the capsular components, produce antibodies that cross-react with myelin. Lymphocytes and macrophages circulate in the blood and eventually find myelin.

Lymphocytic infiltration of spinal roots and peripheral nerves, followed by macrophage-mediated, multifocal stripping of myelin causing axonal damage

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