Factors explaining variance in perceived pain in women with fibromyalgia

BACKGROUND: We hypothesized that a substantial proportion of the subjectively experienced variance in pain in fibromyalgia patients would be explained by psychological factors alone, but that a combined model, including neuroendocrine and autonomic factors, would give the most parsimonious explanation of variance in pain. METHODS: Psychometric assessment included McGill Pain Questionnaire, General Health Questionnaire, Hospital Anxiety and Depression Rating Scale, Eysenck personality Inventory, Neuroticism and Lie subscales, Toronto Alexithymia Scale, and Multidimensional Health Locus of Control Scale and was performed in 42 female patients with fibromyalgia and 48 female age matched random sample population controls. A subgroup of the original sample (22 fibromyalgia patients and 13 controls) underwent a pharmacological challenge test with buspirone to assess autonomic and adrenocortical reactivity to serotonergic challenge. RESULTS: Although fibromyalgia patients scored high on neuroticism, anxiety, depression and general distress, only a minor part of variance in pain was explained by psychological factors alone. High pain score was associated with high neuroticism, low baseline cortisol level and small drop in systolic blood pressure after buspirone challenge test. This model explained 41.5% of total pain in fibromyalgia patients. In population controls, psychological factors alone were significant predictors for variance in pain. CONCLUSION: Fibromyalgia patients may have reduced reactivity in the central sympathetic system or perturbations in the sympathetic-parasympathetic balance. This study shows that a biopsychosocial model, including psychological factors as well as factors related to perturbations of the autonomic nervous system and hypothalamic-pituitary-adrenal axis, is needed to explain perceived pain in fibromyalgia patients

Effects of selective serotonin reuptake inhibitor treatment on plasma oxytocin and cortisol in major depressive disorder

Background: Oxytocin is known for its capacity to facilitate social bonding, reduce anxiety and for its actions on the stress hypothalamopituitary adrenal (HPA) axis. Since oxytocin can physiologically suppress activity of the HPA axis, clinical applications of this neuropeptide have been proposed in conditions where the function of the HPA axis is dysregulated. One such condition is major depressive disorder (MDD). Dysregulation of the HPA system is the most prominent endocrine change seen with MDD, and normalizing the HPA axis is one of the major targets of recent treatments. The potential clinical application of oxytocin in MDD requires improved understanding of its relationship to the symptoms and underlying pathophysiology of MDD. Previous research has investigated potential correlations between oxytocin and symptoms of MDD, including a link between oxytocin and treatment related symptom reduction. The outcomes of studies investigating whether antidepressive treatment (pharmacological and non-pharmacological) influences oxytocin concentrations in MDD, have produced conflicting outcomes. These outcomes suggest the need for an investigation of the influence of a single treatment class on oxytocin concentrations, to determine whether there is a relationship between oxytocin, the HPA axis (e.g., oxytocin and cortisol) and MDD. Our objective was to measure oxytocin and cortisol in patients with MDD before and following treatment with selective serotonin reuptake inhibitors, SSRI. Method: We sampled blood from arterial plasma. Patients with MDD were studied at the same time twice; pre- and post- 12 weeks treatment, in an unblinded sequential design (clinicaltrials.govNCT00168493). Results: Results did not reveal differences in oxytocin or cortisol concentrations before relative to following SSRI treatment, and there were no significant relationships between oxytocin and cortisol, or these two physiological variables and psychological symptom scores, before or after treatment. Conclusions: These outcomes demonstrate that symptoms of MDD were reduced following effective treatment with an SSRI, and further, stress physiology was unlikely to be a key factor in this outcome. Further research is required to discriminate potential differences in underlying stress physiology for individuals with MDD who respond to antidepressant treatment, relative to those who experience treatment resistance.Charlotte Keating, Tye Dawood, David A Barton, Gavin W Lambert and Alan J Tilbroo

Stress biomarkers' associations to pain in the neck, shoulder and back in healthy media workers: 12-month prospective follow-up

Physiological and psychological mechanisms have been proposed to link stress and musculoskeletal pain (MSP), and a number of stress biomarkers in patients with chronic pain have shown to be associated with stress-related disorders as well as health and recovery. The aim was to study if similar results might be found in a working population, in stress and computer intensive occupations with mild/moderate pain in neck, shoulder and back. The questions were if there are: (1) associations between self rated neck, shoulder and back pain (VAS) on one hand and stress-related (catabolic), recovery related (anabolic) variables, cardiovascular/lifestyle factors and immune markers on the other hand. (2) associations between long term changes in pain and stress marker values (6 month period). (3) predictive values in stress biomarkers for pain (12 month period) A study group with 121 media workers, 67 males (average 45 years) and 53 females (average 43 years), at three news departments of a media company was recruited. Pain occurrence and pain level in neck, shoulder, upper and low back were self-rated at three times with a 6-month interval towards the last month. Stress biomarker sampling was performed, at the same intervals. An additional similar questionnaire with momentary ratings focusing on “at present” i.e. within the same hour as stress biomarker sampling was performed. There were no changes in medicine intake or computer working hours during the 12 month study period. The total pain level and prevalence of pain decreased between baseline and 12 months´ follow-up. The rate of participation was 95%. Cross-sectional analyses on differences in stress biomarkers in groups of “no pain” and “pain” showed less beneficial stress biomarker levels (P < 0.05) in the “pain” group after age and gender adjustments in: S-DHEA-S and P-endothelin, S-insulin and P-fibrinogen. Analyses of each gender separately, adjusted for age, revealed in males differences in S-insulin, saliva cortisol 3, and P-endothelin. Furthermore, tendencies were seen in BMI, P-fibrinogen, and S-testosterone. In the female “pain” group a less beneficial P-BNP level was found. Longitudinal analysis of changes in pain levels and stress biomarkers within an interval of 6 months showed beneficial changes in the following stress markers: P-NPY, S-albumin, S-growth hormone and S-HDL when pain decreased, and vice versa when pain increased. Linear regression analyses showed statistically significant predicting values at the initial test instance for pain 12 months later in lower S-DHEA-S and S-albumin and higher B-HbA1c and P-fibrinogen. In stepwise regression and after age and gender adjustments, the associations with S-DHEA-S remained statistically significant. The present study shows that individuals in working life with a high level of regenerative/anabolic activity have less pain than other subjects, and that decreased regenerative/anabolic activity is associated with increasing pain. The levels of NPY, albumin, GH and HDL increased when pain decreased and vice versa. Low DHEA-S predicted pain 12 months later. These findings might contribute to increased knowledge about strategies to prevent further progression of neck/shoulder/back pain in persons who are “not yet in chronic pain”