An acquired immune-mediated condition known as chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) affects the peripheral nervous system. The traditional presentation comprises symmetrical proximal & distal motor and sensory involvement, despite the fact that it has a variety of clinical manifestations.
The 8-week duration of CIDP can be relapsed, monophasic, and progressive. CIDP can be distinguished from Guillain-Barre syndrome (GBS) and other AIDP (acute inflammatory demyelinated polyneuropathy) by its period course of eight weeks and the length of time it takes to reach its nadir. Eichhorst Burns wrote about the first instance in 1890. Acute GBS is found in around 16 percent of cases.
Epidemiology
The crude incidence rate was 0.33 for every 100 000 people, according to a recent meta-analysis. The prevalence ranges from 0.8 to 8.9 for every 100,000 people overall, rises with age, and peaks between the ages of 40 and 60.
The prevalence and incidence statistics also fluctuate because different clinical manifestations and screening standards are utilized in different parts of the world. Males are impacted by CIDP 2:1 more frequently than females.
Anatomy
Pathophysiology
T cells play a major role in the CIDP pathway. However, the reaction to plasmapheresis raises the possibility that immunological responses mediated by B cells may be involved. The forms of CIDP are related to antibodies directed against proteins or myelin found at the Ranvier node, while the conventional form is idiopathic.
Neuronal dysfunction and injury are caused by inflammation that is mediated by both B and T cells. In order to encourage demyelination, the T cells & macrophages serve as antigen-presenting cells and adhere directly to the targeted sites.
While several antibodies, including GD1a, GM1, GQ1b, and GD1b, are connected to GBS, CIDP is not connected to any specific antibody. Only a small number of autoantibodies, including perinodal antigens like neurofascin 186, 140, and 155, have been found to be associated with CIDP variations thus far.
Contactin and gliomedin are additionally targeted. In terms of early therapy with IVIG (injectable immunoglobulins) and corticosteroids, along with the cellular response, the subtypes linked to the contactin-1 and NF155 antibodies differ from conventional CIDP.
Etiology
Humoral immunological mechanisms and T cell-activated immune processes are both involved in the autoimmune condition CIDP, which targets myelin elements in the peripheral nerve system. Idiopathic CIDP is the standard form.
However, it has variations linked to neoplastic phenomena (e.g., Waldenstrom macroglobulinaemia, osteosclerotic myeloma, monoclonal gammopathy, and lymphoma of unknown significance), Human immunodeficiency infections, and persistent history of type II diabetes. With GBS/AIDP, anteceding disorders are frequently recorded; with CIDP, they are less common.
Genetics
Prognostic Factors
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
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Imaging Studies
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Histologic Findings
Staging
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References
https://www.ncbi.nlm.nih.gov/books/NBK563249/
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An acquired immune-mediated condition known as chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) affects the peripheral nervous system. The traditional presentation comprises symmetrical proximal & distal motor and sensory involvement, despite the fact that it has a variety of clinical manifestations.
The 8-week duration of CIDP can be relapsed, monophasic, and progressive. CIDP can be distinguished from Guillain-Barre syndrome (GBS) and other AIDP (acute inflammatory demyelinated polyneuropathy) by its period course of eight weeks and the length of time it takes to reach its nadir. Eichhorst Burns wrote about the first instance in 1890. Acute GBS is found in around 16 percent of cases.
The crude incidence rate was 0.33 for every 100 000 people, according to a recent meta-analysis. The prevalence ranges from 0.8 to 8.9 for every 100,000 people overall, rises with age, and peaks between the ages of 40 and 60.
The prevalence and incidence statistics also fluctuate because different clinical manifestations and screening standards are utilized in different parts of the world. Males are impacted by CIDP 2:1 more frequently than females.
T cells play a major role in the CIDP pathway. However, the reaction to plasmapheresis raises the possibility that immunological responses mediated by B cells may be involved. The forms of CIDP are related to antibodies directed against proteins or myelin found at the Ranvier node, while the conventional form is idiopathic.
Neuronal dysfunction and injury are caused by inflammation that is mediated by both B and T cells. In order to encourage demyelination, the T cells & macrophages serve as antigen-presenting cells and adhere directly to the targeted sites.
While several antibodies, including GD1a, GM1, GQ1b, and GD1b, are connected to GBS, CIDP is not connected to any specific antibody. Only a small number of autoantibodies, including perinodal antigens like neurofascin 186, 140, and 155, have been found to be associated with CIDP variations thus far.
Contactin and gliomedin are additionally targeted. In terms of early therapy with IVIG (injectable immunoglobulins) and corticosteroids, along with the cellular response, the subtypes linked to the contactin-1 and NF155 antibodies differ from conventional CIDP.
Humoral immunological mechanisms and T cell-activated immune processes are both involved in the autoimmune condition CIDP, which targets myelin elements in the peripheral nerve system. Idiopathic CIDP is the standard form.
However, it has variations linked to neoplastic phenomena (e.g., Waldenstrom macroglobulinaemia, osteosclerotic myeloma, monoclonal gammopathy, and lymphoma of unknown significance), Human immunodeficiency infections, and persistent history of type II diabetes. With GBS/AIDP, anteceding disorders are frequently recorded; with CIDP, they are less common.
An acquired immune-mediated condition known as chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) affects the peripheral nervous system. The traditional presentation comprises symmetrical proximal & distal motor and sensory involvement, despite the fact that it has a variety of clinical manifestations.
The 8-week duration of CIDP can be relapsed, monophasic, and progressive. CIDP can be distinguished from Guillain-Barre syndrome (GBS) and other AIDP (acute inflammatory demyelinated polyneuropathy) by its period course of eight weeks and the length of time it takes to reach its nadir. Eichhorst Burns wrote about the first instance in 1890. Acute GBS is found in around 16 percent of cases.
The crude incidence rate was 0.33 for every 100 000 people, according to a recent meta-analysis. The prevalence ranges from 0.8 to 8.9 for every 100,000 people overall, rises with age, and peaks between the ages of 40 and 60.
The prevalence and incidence statistics also fluctuate because different clinical manifestations and screening standards are utilized in different parts of the world. Males are impacted by CIDP 2:1 more frequently than females.
T cells play a major role in the CIDP pathway. However, the reaction to plasmapheresis raises the possibility that immunological responses mediated by B cells may be involved. The forms of CIDP are related to antibodies directed against proteins or myelin found at the Ranvier node, while the conventional form is idiopathic.
Neuronal dysfunction and injury are caused by inflammation that is mediated by both B and T cells. In order to encourage demyelination, the T cells & macrophages serve as antigen-presenting cells and adhere directly to the targeted sites.
While several antibodies, including GD1a, GM1, GQ1b, and GD1b, are connected to GBS, CIDP is not connected to any specific antibody. Only a small number of autoantibodies, including perinodal antigens like neurofascin 186, 140, and 155, have been found to be associated with CIDP variations thus far.
Contactin and gliomedin are additionally targeted. In terms of early therapy with IVIG (injectable immunoglobulins) and corticosteroids, along with the cellular response, the subtypes linked to the contactin-1 and NF155 antibodies differ from conventional CIDP.
Humoral immunological mechanisms and T cell-activated immune processes are both involved in the autoimmune condition CIDP, which targets myelin elements in the peripheral nerve system. Idiopathic CIDP is the standard form.
However, it has variations linked to neoplastic phenomena (e.g., Waldenstrom macroglobulinaemia, osteosclerotic myeloma, monoclonal gammopathy, and lymphoma of unknown significance), Human immunodeficiency infections, and persistent history of type II diabetes. With GBS/AIDP, anteceding disorders are frequently recorded; with CIDP, they are less common.
https://www.ncbi.nlm.nih.gov/books/NBK563249/
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