Inflammatory neuropathy (Guillain-Barré) (534)

Tests in package

Contactin-1 IgG antibodies (CNTN1), Contactin-1 IgG antibodies (CNTN1) – IgG4 subclass determination, Ganglioside antibodies – IgG and IgM, Myelin associated glycoprotein (MAG) antibodies, Neurofascin-155 (NF155) antibodies - IgG4 subclass determination, Neurofascin-155 IgG and IgM antibodies (NF155), Sulfatide IgM

Indication

Polyneuropathy where the cause is unknown or is suspected to be autoimmune.

Clinic

Gangliosides are a group of sialic acid-containing glycolipids, as occurs in the nervous system. They are integrated into cell membranes, where a ceramide anchor the lipid layer and an extracellular oligosaccharide is accessible to antibodies. Many gangliosides are known, but it is mainly GM1, GM2, GM3, GQ1b, GD1a, GD1b, GT1b that are available for diagnostic testing related to peripheral nerve diseases. Antibodies against the gangliosid antigens, which are often cross-react, are considered to be pathogenetic.

The autoantibodies against gangliosides are known to occur naturally at very low titers in healthy individuals and various infections are considered to trigger an increase in the expression of these autoantibodies. Campylobacter jejuni is thought to be the most common infectious cause of the alteration to a pathogenic expression of anti-ganglioside antibodies. The antibody reactivity is considered to be due to the high level of molecular mimicry between bacterial membrane components and the ganglioside structures.

IgM antibodies against GM1 are detected in high frequency in multifocal motor neuropathy (MMN) and are an important differential diagnosis of ALS. IgG antibodies against GM1 and IgG antibodies against GD1a are found in patients with Guillain-Barré syndrome, primarily in the motor axonal form (AMAN).

Miller Fisher syndrome, with varying degrees of ophthalmoplegia and ataxia, is a variant of Guillain-Barre syndrome associated with a very high frequency of IgG antibody to ganglioside GQ1b. IgM antibodies to GQ1b is often detected at a particular form of sensory polyneuropathy with an M component of IgM class (CANOMAD). GD1b IgM antibodies have been observed at MMN and at CANOMAD.

Antibodies to myelin-associated glycoprotein (MAG) cross-react with the carbohydrate portion of the myelin protein P0 and SPGP. High titers of IgM antibodies to MAG is often combined with a sensory polyneuropathy. Anti-MAG antibodies are detected in approximately half of the patients with an M component of the IgM class.

Recent research reported that autoantibodies in peripheral neuropathies in many occasions bind to complexes between one or more antigens. Methods for analyzing antibodies against these complexes are not yet commercially available.

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