Inflammatory polyneuropathy: Difference between revisions
imported>Howard C. Berkowitz (New page: '''Inflammatory polyneuropathy''' covers a range of syndromes, both acute and chronic. ==Guillain-Barre syndrome== An acute inflammatory autoimmune neuritis caused by T cell- mediated cel...) |
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'''Inflammatory polyneuropathy''' covers a range of syndromes, both acute and chronic. | '''Inflammatory polyneuropathy''' covers a range of syndromes, both acute and chronic. | ||
Clinical and experimental findings suggest that humoral factors, such as anti-peripheral nerve antibodies and cytokines, may be implicated in the immunopathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Interleukin-6 (IL-6) is a multifunctional cytokine that promotes immunoglobulin synthesis by B lymphocytes. Inflammatory substances generated include [[interleukin]]-6; increased IL-6 release is associated with autoantibody production in a number of immune-mediated and neoplastic disorders. <ref>{{citation | |||
| title = Interleukin-6 levels in the cerebrospinal fluid and serum of patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy | |||
| journal = Journal of Neuroimmunology | |||
| volume=47 | issue = 1 | Pages 55-61 | |||
| author = D. Maimone, P. Annunziata, I. Simone, P. Livrea, G. Guazzi | |||
}}</ref> | |||
==Guillain-Barre syndrome== | ==Guillain-Barre syndrome== | ||
An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. | An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. | ||
==References== | |||
{{reflist}} | |||
Revision as of 15:20, 31 January 2010
Inflammatory polyneuropathy covers a range of syndromes, both acute and chronic.
Clinical and experimental findings suggest that humoral factors, such as anti-peripheral nerve antibodies and cytokines, may be implicated in the immunopathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Interleukin-6 (IL-6) is a multifunctional cytokine that promotes immunoglobulin synthesis by B lymphocytes. Inflammatory substances generated include interleukin-6; increased IL-6 release is associated with autoantibody production in a number of immune-mediated and neoplastic disorders. [1]
Guillain-Barre syndrome
An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur.
References
- ↑ D. Maimone, P. Annunziata, I. Simone, P. Livrea, G. Guazzi, "Interleukin-6 levels in the cerebrospinal fluid and serum of patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy", Journal of Neuroimmunology 47 (1)