Eva Kosek´s research group

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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.

Research projects

  •     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

Selected publications

Evidence of central inflammation in fibromyalgia-increased cerebrospinal fluid interleukin-8 levels.
Kadetoff D, Lampa J, Westman M, Andersson M, Kosek E
J. Neuroimmunol. 2012 Jan;242(1-2):33-8

Conditioned pain modulation is associated with common polymorphisms in the serotonin transporter gene.
Lindstedt F, Berrebi J, Greayer E, Lonsdorf T, Schalling M, Ingvar M, et al
PLoS ONE 2011 Mar;6(3):e18252

Anxiety and depressive symptoms in fibromyalgia are related to poor perception of health but not to pain sensitivity or cerebral processing of pain.
Jensen K, Petzke F, Carville S, Fransson P, Marcus H, Williams S, et al
Arthritis Rheum. 2010 Nov;62(11):3488-95

Dysfunction of endogenous pain inhibition during exercise with painful muscles in patients with shoulder myalgia and fibromyalgia.
Lannersten L, Kosek E
Pain 2010 Oct;151(1):77-86

Genetic variation in the serotonin transporter gene (5-HTTLPR, rs25531) influences the analgesic response to the short acting opioid Remifentanil in humans.
Kosek E, Jensen K, Lonsdorf T, Schalling M, Ingvar M
Mol Pain 2009 Jul;5():37

Group members

Aisha Siddiqah AhmedAssociated
Svante BergAssociated, Postdoc
Karin JensenAssistant professor
Diana KadetoffAssociated
Eva KosekResearch team leader, Professor/senior physician
Sofia MartinsenAssociated
Anton RaschAssociated
Annelie RosénPhD student, Graduate Student
Angelica SandströmResearch assistant
Jeanette TourTeaching assistant