Eva Kosek's research group
Our research investigates the interaction of the nervous- and the immune systems with regard to the development of chronic pain. The goal is to contribute knowledge that forms the basis for preventing the emergence of pain due to a dysfunctional pain regulation (nociplastic pain) and to enable new treatment strategies.
Chronic pain – symptom or disease?
Chronic pain affects 10-20% of the general population and is globally a major cause of disability, leading to much human suffering and staggering economical costs for society. Generally, chronic pain is regarded as a symptom either of tissue injury or inflammation (nociceptive pain) or of a disease/lesion in the nervous system (neuropathic pain). However, certain kinds of chronic pain are best understood in terms of altered nociception, meaning dysfunctional pain regulation (nociplastic pain), where the pain is considered as a disease, not a symptom. Many patients who initially suffer from nociceptive pain such as osteoarthritis or rheumatoid arthritis gradually develop a nociplastic pain condition. Once nociplastic pain has developed, treatments targeting the peripheral pathology become less effective and the pain is challenging to treat, stressing the need to develop new, efficient treatment strategies. The overarching aim of our current research is to investigate how the nervous- and the immune systems interact in the development of chronic pain, with particular reference to nociplastic pain mechanisms. The development of new efficient treatment strategies for intractable chronic pain is the ultimate goal.
Chronic pain patients and healthy controls are recruited to our clinical pain research projects. The symptoms are characterized using validated questionnaires. We use quantitative sensory testing to assess pain sensitivity and the function of endogenous pain regulatory mechanisms, such as descending pain inhibition. Functional magnetic resonance imaging (fMRI) is used to investigate cerebral pain related activation during rest, during evoked pain (painful stimulation) and the interactions between different brain networks are analyzed in the context of pain perception. To analyze neuroinflammation with particular focus on the periphery-to-brain neuroimmune cross-talk, samples of peripheral tissues, blood and cerebrospinal fluid are analyzed regarding pro-inflammatory substances, including antibodies and related to symptoms and pain processing. The activation of glia, the immunocompetent cells of the nervous system, is investigated with positron emission tomography (PET) and magnetic resonance spectroscopy (MRS), the latter is also used to assess cerebral concentrations of various transmitter substances. Finally, we combine genotyping, quantitative pain testing and imaging (MRS, fMRI) to explore cerebral pain related mechanisms.
- The neuroimmune cross-talk between peripheral tissues and brain in patients suffering from knee osteoarthritis, degenerative disc disease (nociceptive pain) and lumbar disc herniations (predominantly neuropathic pain) and the associations between neuroinflammation and symptom severity.
- Are autoreactive IgG antibodies associated with symptom severity, peripheral nerve pathology and/or abberrations in cerebral pain processing or brain metabolism in fibromyalgia patients?
- Cerebral pain processing and brain network interactions in patients suffering from rheumatoid arthritis, disc degenerative disease or fibromyalgia, similarities and differences between nociceptive and nociplastic pain.
- The effect of genetic factors on pain regulation in patients suffering from disc degenerative disease or fibromyalgia. Possible genetic predictors for treatment outcome following surgery (fusion/disc implants) in disc degenerative disease.
Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system.
Kosek E, Clauw D, Nijs J, Baron R, Gilron I, Harris RE, Mico JA, Rice AS, Sterling M.Pain. 2021 May 7. doi: 10.1097/j.pain.0000000000002324. Online ahead of print.
Elevated inflammatory proteins in cerebrospinal fluid from patients with painful knee osteoarthritis are associated with reduced symptom severity.
Palada V, Ahmed AS, Freyhult E, Hugo A, Kultima K, Svensson CI, Kosek E.J Neuroimmunol. 2020 Dec 15;349:577391. doi: 10.1016/j.jneuroim.2020.577391. Epub 2020 Sep 12.PMID: 32987275 Free article.
Neural correlates of conditioned pain responses in fibromyalgia subjects indicate preferential formation of new pain associations rather than extinction of irrelevant ones. Sandström A, Ellerbrock I, Tour J, Kadetoff D, Jensen KB, Kosek E.Pain. 2020 Sep 1;161(9):2079-2088. doi: 10.1097/j.pain.0000000000001907.PMID: 32379218 Free PMC article.
Brain glial activation in fibromyalgia - A multi-site positron emission tomography investigation.
Albrecht DS, Forsberg A, Sandström A, Bergan C, Kadetoff D, Protsenko E, Lampa J, Lee YC, Höglund CO, Catana C, Cervenka S, Akeju O, Lekander M, Cohen G, Halldin C, Taylor N, Kim M, Hooker JM, Edwards RR, Napadow V, Kosek E, Loggia ML.Brain Behav Immun. 2019 Jan;75:72-83. doi: 10.1016/j.bbi.2018.09.018. Epub 2018 Sep 14.PMID: 30223011 Free PMC article.
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, Fransson P, Schalling M, Ingvar M, Ernberg M, Jensen KB.Brain Behav Immun. 2016 Nov;58:218-227. doi: 10.1016/j.bbi.2016.07.150. Epub 2016 Jul 20.PMID: 27448744 Free article. Clinical Trial.