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Despite effective treatment approaches within the cognitive behavioral framework general treatment effects for chronic pain are rather small to very small. Translation from efficacy trials to naturalistic settings is questionable. There is an urgent need to improve the effectiveness of well-established treatments, such as cognitive-behavior therapy (CBT) and the investigation of mechanisms of change is a promising opportunity. We performed secondary data analysis from routine data of 1,440 chronic pain patients. Patients received CBT in a multidisciplinary setting in two inpatient clinics. Effect sizes and reliable change indices were computed for pain-related disability and depression. The associations between changes in the use of different pain coping skills (cognitive restructuring, activity despite pain, relaxation techniques and mental distraction) and changes in clinical outcomes were analyzed in structural equation models. Pre–post effect sizes range from g = 0.47 (disability) to g = 0.89 (depression). Changes in the use of cognitive restructuring, relaxation and to a lesser degree mental distraction were associated with changes in disability and depression. Effects from randomized trials can be translated to naturalistic settings. The results complement experimental research on mechanisms of change in the treatment of chronic pain and indicate an important role of cognitive change and relaxation as mechanisms of change. Our findings cautiously suggest that clinicians should optimize these processes in chronic pain patients to reduce their physical and emotional disability.
Abstract
Background
Comorbidities in mental disorders are often understood by assuming a common cause. The network theory of mental disorders offers an alternative to this assumption by understanding comorbidities as mutually reinforced problems. In this study, we used network analysis to examine bridge symptoms between anxiety and depression in a large sample.
Method
Using data from a sample of patients diagnosed with both depression and an anxiety disorder before and after inpatient treatment (N = 5,614, mean age: 42.24, 63.59% female, average treatment duration: 48.12 days), network models of depression and anxiety symptoms are estimated. Topology, the centrality of nodes, stability, and changes in network structure are analyzed. Symptoms that drive comorbidity are determined by bridge node analysis. As an alternative to network communities based on categorical diagnosis, we performed a community analysis and propose empirically derived symptom subsets.
Results
The obtained network models are highly stable. Sad mood and the inability to control worry are the most central. Psychomotor agitation or retardation is the strongest bridge node between anxiety and depression, followed by concentration problems and restlessness. Changes in appetite and suicidality were unique to depression. Community analysis revealed four symptom groups.
Conclusion
The estimated network structure of depression and anxiety symptoms proves to be highly accurate. Results indicate that some symptoms are considerably more influential than others and that only a small number of predominantly physical symptoms are strong candidates for explaining comorbidity. Future studies should include physiological measures in network models to provide a more accurate understanding.