Fibromialgija: Razlika med redakcijama

==Patofiziologija==

 

 

Studies on the neuroendocrine system and [[HPA axis]] in fibromyalgia have been inconsistent. One study found fibromyalgia patients exhibited higher plasma [[cortisol]], more extreme peaks and troughs, and higher rates of [[dexamethasone]] non suppression. However, other studies have only found correlations between a higher [[cortisol awakening response]] and pain, and not any other abnormalities in cortisol.<ref name="bradley"/> Increased baseline [[ACTH]] and increase in response to [[stress (psychological)|stress]] have been observed, hypothesized to be a result of decreased negative feedback.<ref name="bellato"/>

 

[[Autonomic nervous system]] abnormalities have been observed in fibromyalgia, including decreased vasoconstriction response, increased drop in blood pressure and worsening of symptoms in response to [[tilt table test]], and decreased heart rate variability. Heart rate variabilities observed were different in males and females.<ref name="bradley"/>

 

Disrupted sleep, [[insomnia]], and poor-quality sleep occur frequently in FM, and may contribute to pain by decreased release of [[IGF-1]] and [[human growth hormone]], leading to decreased tissue repair. Restorative sleep was correlated with improvement in pain related symptoms.<ref name="bradley"/>

 

Neuroimaging studies have observed decreased levels of [[N-Acetylaspartic acid|''N''-acetylaspartic acid]] (NAA) in the hippocampus of people with fibromyalgia, indicating decreased neuron functionality in this region. Altered connectivity and decreased grey matter of the [[default mode network]],<ref>{{cite journal|last1=Lin|first1=Chemin|last2=Lee|first2=Shwu-Hua|last3=Weng|first3=Hsu-Huei|title=Gray Matter Atrophy within the Default Mode Network of Fibromyalgia: A Meta-Analysis of Voxel-Based Morphometry Studies|journal=BioMed Research International|date=1 January 2016|volume=2016|pages=7296125|doi=10.1155/2016/7296125|pmid=28105430|issn=2314-6141|pmc=5220433}}</ref> the [[insular cortex|insula]], and executive attention network have been found in fibromyalgia. Increased levels of [[glutamate]] and [[glutamine]] have been observed in the amygdala, parts of the [[prefrontal cortex]], the [[posterior cingulate cortex]], and the insula, correlating with pain levels in FM. Decreased GABA has been observed in the anterior insular in fibromyalgia. However, neuroimaging studies, in particular neurochemical imaging studies, are limited by methodology and interpretation.<ref name="imaging">{{cite journal|last1=Napadow|first1=Vitaly|last2=Harris|first2=Richard E|title=What has functional connectivity and chemical neuroimaging in fibromyalgia taught us about the mechanisms and management of 'centralized' pain?|journal=Arthritis Research & Therapy|date=1 January 2014|volume=16|issue=4|pages=425|doi=10.1186/s13075-014-0425-0|issn=1478-6354|pmc=4289059|pmid=25606591}}</ref> Increased cerebral blood flow in response to pain was found in one [[fMRI]] study.<ref name="ncbi.nlm.nih.gov"/> Findings of decreased blood flow in the thalamus and other regions of the [[basal ganglia]] correlating with treatment have been relatively consistent over three studies. Decreased binding of [[μ-opioid receptor]] have been observed; however, it is unknown if this is a result of increased endogenous binding in response to pain, or down regulation.<ref name="bellato"/>

 

Overlaps have been drawn between chronic fatigue syndrome and fibromyalgia. One study found increased levels of pro-inflammatory cytokines in fibromyalgia, which may increase sensitivity to pain, and contribute to mood problems.<ref name="sickness behavior">{{cite journal|last1=Dell'Osso|first1=Liliana|last2=Bazzichi|first2=Laura|last3=Baroni|first3=Stefano|last4=Falaschi|first4=Valentina|last5=Conversano|first5=Ciro|last6=Carmassi|first6=Claudia|last7=Marazziti|first7=Donatella|title=The inflammatory hypothesis of mood spectrum broadened to fibromyalgia and chronic fatigue syndrome|journal=Clinical and Experimental Rheumatology|date=1 January 2015|volume=33|issue=1 Suppl 88|pages=S109–116|issn=0392-856X|pmid=25786052}}</ref> Increased levels of IL-1RA, [[Interleukin 6]] and [[Interleukin 8]] have been found.<ref name="cytokines">{{cite journal|last1=Rodriguez-Pintó|first1=Ignasi|last2=Agmon-Levin|first2=Nancy|last3=Howard|first3=Amital|last4=Shoenfeld|first4=Yehuda|title=Fibromyalgia and cytokines|journal=Immunology Letters|date=1 October 2014|volume=161|issue=2|pages=200–203|doi=10.1016/j.imlet.2014.01.009|issn=1879-0542|pmid=24462815}}</ref> Neurogenic inflammation has been proposed as a contributing factor to fibromyalgia.<ref>{{cite journal|last1=Littlejohn|first1=Geoffrey|title=Neurogenic neuroinflammation in fibromyalgia and complex regional pain syndrome|journal=Nature Reviews. Rheumatology|date=1 November 2015|volume=11|issue=11|pages=639–648|doi=10.1038/nrrheum.2015.100|issn=1759-4804|pmid=26241184}}</ref> A systematic review found most cytokines levels were similar in patients and controls, except for IL-1 receptor antagonist, IL-6 and IL-8.<ref>{{cite journal|last1=Uçeyler|first1=Nurcan|last2=Häuser|first2=Winfried|last3=Sommer|first3=Claudia|title=Systematic review with meta-analysis: cytokines in fibromyalgia syndrome|journal=BMC Musculoskeletal Disorders|date=28 October 2011|volume=12|pages=245|doi=10.1186/1471-2474-12-245|issn=1471-2474|pmid=22034969|pmc=3234198}}</ref>