Editorial comment on Karlsson et al. “Cognitive behavior therapy in women with fibromyalgia. A randomized clinical trial”

Abstract

In this edition of Scandinavian Journal of Pain, Karlsson et al. test he effect of a manual based cognitive behavioral intervention for emale patients with fibromyalgia [1]. The randomized, controlled tudy focuses on maladaptive cognitions and behavior thought to aintain and exacerbate pain conditions. The bio-psycho-social odel of pain, a definition of stress presented by Lazarus and Folkan [2], as well as the fear-avoidance model by Vlayen and Linton 3] provide the overarching theoretical framework. The authors se a dimension of the West Haven-Yale Multidimensional Pain nventory as a primary outcome, hypothesizing that a cognitive ehavioral therapy (CBT) developed for pain and stress would nfluence perceived life control. They also hypothesized secondary ffects on interference from pain, emotional distress and social suport, as well as stress, depression and pain severity. Their results howed a significant increase in life control, reduction in affective istress and depression, as well as a reduction of stress. The study ells a story about CBT changing the perception of pain in particpants, giving a higher quality of life, even though they actually eport more pain during the follow-up period. Their results on stress reduction through CBT are enticing onsidering the different lines of research indicating the maintainng and exacerbating role of stress in chronic widespread pain [4]. ome even claim that poor stress management alongside cognitivemotional sensitization, central sensitization and sustained arousal rovides us with a causal model for such idiopathic conditions [5,6]. Hypotheses on how the stress construct can affect pain condiions stem in part from studies on childhood traumatic experiences. ne study detailed how increased sensitivity to glucocorticoids in he hypothalamic–pituitary–adrenal (HPA)-axis and/or up reguated corticotrophin-releasing factor came as a result of early-life hanges in the HPA-axis [7]. Sustained or increased glucocortioid exposure can have adverse effects on the hippocampus, which auses decreases of synapses and decreased production of new neuons. This damage might progressively reduce the control of the PA axis and lead to increased stress responses [6]. This would