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Complex regional pain syndrome (CRPS type 1 and type 2), sometimes referred to by the hyponyms reflex sympathetic dystrophy (RSD) or reflex neurovascular dystrophy (RND), is a rare and severe form of neuroinflammatory and dysautonomic disorder causing chronic pain, neurovascular, and neuropathic symptoms.
Complex regional pain syndrome is characterized by pain that is distributed regionally, usually starts in an extremity distally, occurs after a trauma, and is disproportionate in severity or duration compared to the expected course of the trauma — the sites affected by complex regional pain syndrome experience autonomic and inflammatory changes.
Chronic systemic inflammation (SI) is the result of release of pro-inflammatory cytokines from immune-related cells and the chronic activation of the innate immune system.It can contribute to the development or progression of certain conditions such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease, autoimmune and neurodegenerative ...
Here are links to possibly useful sources of information about Complex regional pain syndrome. PubMed provides review articles from the past five years (limit to free review articles ) The TRIP database provides clinical publications about evidence-based medicine .
Chronic pain has many pathophysiological and environmental causes and can occur in cases such as neuropathy of the central nervous system, after cerebral hemorrhage, tissue damage such as extensive burns, inflammation, autoimmune disorders such as rheumatoid arthritis, psychological stress such as headache, migraine or abdominal pain (caused by ...
Chronic inflammatory demyelinating polyneuropathy disrupts self-tolerance and activates autoreactive T and B cells, which are normally suppressed immune cells. This leads to the organ-specific damage typical of autoimmune disease. [19] Molecular mimicry may be particularly relevant to the tolerance breakdown linked to autoimmune neuropathies.
It can double every 8 hours and reaches its peak at 36 to 50 hours following injury or inflammation. CRP between 100 and 500 mg/L is considered highly predictive of inflammation due to bacterial infection. Once inflammation subsides, CRP level falls quickly because of its relatively short half-life. [13]
Their mutations induce increased and/or prolonged secretion of IL-1β, a pro-inflammatory and pyrogenic cytokine. [4] Patients with AIDs often suffer from non-infectious fever and systemic and/or disease-specific organ inflammation. The over-secretion of pro-inflammatory cytokines and chemokines leads to organ damage and can be life-threatening.