Neck-shoulder pain and depressive symptoms: a cohort study with a 7-year follow-up.
ABSTRACT The presence of neck-shoulder pain as a predictor of depression is not widely studied.
To analyse the association of neck-shoulder pain at baseline with depressive symptomatology after a 7-year follow-up.
A total of 604 subjects who had not had depressive symptomatology at baseline participated in 7-year follow-up survey. The number of subjects with depressive symptomatology (Beck Depression Score10) after 7-year follow-up were measured in three groups - subjects without neck-shoulder pain, with infrequent neck-shoulder pain and with daily neck-shoulder pain at baseline.
A total of 77 (13%) participants had developed depressive symptomatology by the follow-up. Prevalence of depressive symptomatology in follow-up in subjects without neck-shoulder pain, with infrequent neck-shoulder pain and with daily neck-shoulder pain at baseline pain was 9.5%, 11.2% and 28.4%. In multivariate logistic regression analysis odds for having depressive symptomatology in daily neck-shoulder pain subjects was almost three fold higher (OR, 2.64, 95% CI, 1.27-5.48) compared to those without neck-shoulder pain.
Frequent neck-shoulder pain is a preceding symptom for the depressive symptomatology in adults.
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ABSTRACT: To ascertain the dimensions of the Beck Depression Inventory-II (BDI-II; Beck, Steer, & Brown, 1996) in clinically depressed outpatients, exploratory factor analyses were performed with the BDI-II responses of 210 adult (> or =18 years) outpatients who were diagnosed with DSM-IV depressive disorders. Two factors representing Somatic-Affective and Cognitive dimensions were found whose compositions were comparable to those previously reported by Beck, Steer, and Brown (1996) for psychiatric outpatients in general. A subsequent confirmatory factor analysis supported a model in which the BDI-II reflected one underlying second-order dimension of self-reported depression composed of two first-order factors representing cognitive and noncognitive symptoms. The clinical utility of using subscales based on these two latter first-order symptom dimensions was discussed.Journal of Clinical Psychology 02/1999; 55(1):117-28. · 2.12 Impact Factor
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ABSTRACT: Basic and clinical studies provide convincing evidence that altered stress hormone regulation frequently observed in depression and anxiety are caused by elevated secretion of the hypothalamic neuropeptides corticotrophin releasing hormone (CRH) and vasopressin. CRH predominantly acts through CRH(1) receptors to produce a number of anxiety- and depression-like symptoms, which resulted in extensive validation of CRH(1) receptors as potential drug target. A number of orally available nonpeptidergic small molecules capable to pass the blood-brain barrier have been discovered; only some of these compounds entered clinical development. Here, we summarize results from clinical studies of two CRH(1) receptor antagonists. In the first study originally designed as a safety and tolerability trial in major depression, it was observed that the CRH(1) receptor antagonist NBI-30775/R121919 has a clinical profile comparable to the antidepressant paroxetine. In a second study the effect of another CRH(1) receptor antagonist, NBI-34041, upon stress hormone secretion in response to a psychosocial stressor was investigated. Administration of this compound reduced the stress-elicited secretion of cortisol. Both compounds, however, did not impair the CRH-induced release of ACTH and cortisol rejecting the possibility that the peripheral stress hormone system is impaired by CRH(1) receptor antagonists. From these studies we conclude that both CRH(1) receptor antagonists have psychotropic effects unrelated to their neuroendocrine action, which is in line with behavioral data obtained from transgenic mice. The results of the clinical studies underscore that CRH(1) receptor antagonists represent promising novel therapeutics in the psychopharmacology of depression and anxiety.European Journal of Pharmacology 05/2008; 583(2-3):350-7. · 2.59 Impact Factor
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ABSTRACT: To determined the association between spinal pain, headache, health, demographic and socio-economic characteristics, and development of depressive symptomatology. A population-based, random sample of adults was surveyed and followed at 6 and 12 months. Individuals at risk of depression at baseline are the subjects of this article (n=845). We used Cox proportional hazards models to measure the time-varying effects of demographic, socio-economic, and health status; comorbid medical conditions; spinal pain; and headaches on the development of depression. After adjusting for baseline depressive symptoms and factors associated with nonresponse to follow-up, we found that spinal pain severity, younger age, marital status (separated/divorced/widowed), self-perceived poor health status, and comorbid neurologic and gastro-intestinal disease were associated with onset of a new episode of depression. Important predictors of depressive symptomatology include demographic characteristics, health problems, and pain problems.Journal of Clinical Epidemiology 08/2003; 56(7):651-8. · 5.33 Impact Factor