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.