Eva Kosek's research group
Mechanisms of pain and treatment
Typically, there is a discrepancy between the degree of peripheral pathology and pain intensity, for example the degree of radiological abnormalities or inflammation in an arthritic joint and the joint pain. Furthermore, severe, generalized pain can exist also in patients without any known peripheral pathology, as for example in fibromyalgia. The importance of central nervous system (CNS) mechanisms, i.e., central sensitisation (deranged bottom-up regulation) or dysfunction of endogenous pain inhibitory mechanisms (deranged top-down regulation) for pain perception in chronic pain patients has previously been reported by our research group as well as others.
Recently we could show that individual differences in the function of endogenous pain regulatory mechanisms in healthy subjects are, to a large part, genetically mediated. Several ongoing projects deal with teasing out the importance of genetic factors for pain and treatment outcome in various patient groups. Animal data show that immunocompetent gliacells in the CNS become activated during chronic pain and these activated glia release inflammatory and algogenic substances giving rise to central inflammation.
We have shown that central inflammation is present in patients with fibromyalgia and rheumatoid arthritis, respectively. Currently ongoing studies in our laboratory deal with the assessments of glia cell activation and central inflammation and how these mechanisms affect clinical symptoms in patients with musculoskeletal pain.
In addition we have ongoing studies assessing the treatment effects of drugs or non-pharmacological treatments such as physical therapy or surgery on pain and endogenous pain regulation in different long-term pain conditions.
- The effect of genetic factors on pain regulation and treatment outcome in patients with long-term muskuloskeletal pain
- The importance of peripheral and central inflammation on pain and pain regulation in patients with long-term muskuloskeletal pain
- The effect of physical training or relaxation exercise on pain mechanisms and clinical symptoms in fibromyalgia patients
- Treatment effects of drugs, exercise and surgery on pain and pain regulation in patients with long-term muskuloskeletal pain
- The development of quantitative sensory testing (QST) to become a diagnostic tool useful to detect and classify dysfunctions of endogenous pain modulation
The translocator protein gene is associated with symptom severity and cerebral pain processing in fibromyalgia.
Kosek E, Martinsen S, Gerdle B, Mannerkorpi K, Löfgren M, Bileviciute-Ljungar I, et al
Brain Behav. Immun. 2016 Nov;58():218-227
Do we need a third mechanistic descriptor for chronic pain states?
Kosek E, Cohen M, Baron R, Gebhart GF, Mico JA, Rice AS, et al
Pain 2016 07;157(7):1382-6
Evidence of different mediators of central inflammation in dysfunctional and inflammatory pain--interleukin-8 in fibromyalgia and interleukin-1 β in rheumatoid arthritis.
Kosek E, Altawil R, Kadetoff D, Finn A, Westman M, Le Maître E, et al
J. Neuroimmunol. 2015 Mar;280():49-55
Segregating the cerebral mechanisms of antidepressants and placebo in fibromyalgia.
Jensen KB, Petzke F, Carville S, Choy E, Fransson P, Gracely RH, et al
J Pain 2014 Dec;15(12):1328-37
Overlapping structural and functional brain changes in patients with long-term exposure to fibromyalgia pain.
Jensen KB, Srinivasan P, Spaeth R, Tan Y, Kosek E, Petzke F, et al
Arthritis Rheum. 2013 Dec;65(12):3293-303