Inflammatory polyneuropathy: Difference between revisions
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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. Guillain-Barre syndrome is the best-known acute form, while chronic inflammatory demyelinating polyradiculoneuropathy is the classic chronic variant. <ref name=eMed-CIDP>{{citation | ||
| author = Lewis RA | |||
| title = Chronic Inflammatory Demyelinating Polyradiculoneuropathy | |||
| date = 15 January 2009 | |||
| journal = eMedicine | |||
| url = http://emedicine.medscape.com/article/1172965-overview}}</ref> | |||
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 | 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 | ||
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| author = D. Maimone, P. Annunziata, I. Simone, P. Livrea, G. Guazzi | | author = D. Maimone, P. Annunziata, I. Simone, P. Livrea, G. Guazzi | ||
}}</ref> | }}</ref> | ||
==Chronic | ==Chronic== | ||
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the best-known variant of this uncommon disease. It has several variants: | |||
*predominantly sensory symptoms | |||
*distal symmetric disorder (DADS) | |||
*multifocal sensorimotor neuropathy or sensorimotor mononeuropathy multiplex with prominent conduction block (also known as Lewis-Sumner neuropathy) | |||
*CIDP with associated CNS demyelination or with other systemic disorders | |||
It is differentiated from: | |||
*demyelinating neuropathies associated with immunoglobulin M (IgM) paraproteins, including those with anti–myelin-associated glycoprotein (MAG) antibodies | |||
*POEMS syndrome of polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes | |||
*[[multifocal motor neuropathy]] | |||
A slowly progressive autoimmune demyelinating disease of peripheral nerves and nerve roots. Clinical manifestations include weakness and sensory loss in the extremities and enlargement of peripheral nerves. The course may be relapsing-remitting or demonstrate a step-wise progression. Protein is usually elevated in the spinal fluid and cranial nerves are typically spared. [[#Guillain-Barre syndrome|Guillain-Barre syndrome]] features a relatively rapid progression of disease which distinguishes it from this condition. <ref>Adams et al., Principles of Neurology, 6th ed, p. 1337</ref> | A slowly progressive autoimmune demyelinating disease of peripheral nerves and nerve roots. Clinical manifestations include weakness and sensory loss in the extremities and enlargement of peripheral nerves. The course may be relapsing-remitting or demonstrate a step-wise progression. Protein is usually elevated in the spinal fluid and cranial nerves are typically spared. [[#Guillain-Barre syndrome|Guillain-Barre syndrome]] features a relatively rapid progression of disease which distinguishes it from this condition. <ref>Adams et al., Principles of Neurology, 6th ed, p. 1337</ref> | ||
[[Intravenous immune globulin]] has been reported to improve quality of life. <ref>{{citation | [[Intravenous immune globulin]] (IVIG) has been reported to improve quality of life. <ref>{{citation | ||
| title = Immune Globulin Helpful in Polyradiculoneuropathy | |||
| author = Merkies ISJ, ''Neurology'' 2009 Apr 14; 72:1337 | |||
| url = http://www.medscape.com/viewarticle/702178}}</ref> Patient response to IVIG, however, is influenced by a single nucleotide polymorphism in the transient axonal glycoprotein 1 gene (TAG-1)<ref>{{citation | |||
| title = Immune Globulin Helpful in Polyradiculoneuropathy | | title = Immune Globulin Helpful in Polyradiculoneuropathy | ||
| author = | | author = Sobue G ''et al.'', ''Neurology'' 2009;73:1348-1352,1344-1345 | ||
| url = http://www.medscape.com/viewarticle/ | | url = http://www.medscape.com/viewarticle/712043}}</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== | ==References== | ||
{{reflist}} | {{reflist|2}} | ||
Revision as of 15:54, 31 January 2010
Inflammatory polyneuropathy covers a range of syndromes, both acute and chronic. Guillain-Barre syndrome is the best-known acute form, while chronic inflammatory demyelinating polyradiculoneuropathy is the classic chronic variant. [1]
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. [2]
Chronic
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the best-known variant of this uncommon disease. It has several variants:
- predominantly sensory symptoms
- distal symmetric disorder (DADS)
- multifocal sensorimotor neuropathy or sensorimotor mononeuropathy multiplex with prominent conduction block (also known as Lewis-Sumner neuropathy)
- CIDP with associated CNS demyelination or with other systemic disorders
It is differentiated from:
- demyelinating neuropathies associated with immunoglobulin M (IgM) paraproteins, including those with anti–myelin-associated glycoprotein (MAG) antibodies
- POEMS syndrome of polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes
- multifocal motor neuropathy
A slowly progressive autoimmune demyelinating disease of peripheral nerves and nerve roots. Clinical manifestations include weakness and sensory loss in the extremities and enlargement of peripheral nerves. The course may be relapsing-remitting or demonstrate a step-wise progression. Protein is usually elevated in the spinal fluid and cranial nerves are typically spared. Guillain-Barre syndrome features a relatively rapid progression of disease which distinguishes it from this condition. [3]
Intravenous immune globulin (IVIG) has been reported to improve quality of life. [4] Patient response to IVIG, however, is influenced by a single nucleotide polymorphism in the transient axonal glycoprotein 1 gene (TAG-1)[5]
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
- ↑ Lewis RA (15 January 2009), "Chronic Inflammatory Demyelinating Polyradiculoneuropathy", eMedicine
- ↑ 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): 55-61
- ↑ Adams et al., Principles of Neurology, 6th ed, p. 1337
- ↑ Merkies ISJ, Neurology 2009 Apr 14; 72:1337, Immune Globulin Helpful in Polyradiculoneuropathy
- ↑ Sobue G et al., Neurology 2009;73:1348-1352,1344-1345, Immune Globulin Helpful in Polyradiculoneuropathy