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ABSTRACT: : Pain is a common symptom with high occurrence in somatoform syndromes and depressive disorders. Research in this area often focuses on experimental induction of pain and subsequent assessment of pain thresholds, ensuring repeatable stimuli of defined quality. Results on sensitivity to experimental pain in major depression are inconclusive, and data on pain thresholds in multiple somatoform symptoms are scarce. The goals of the present study were to differentiate between groups regarding the pressure pain thresholds, and to investigate the possible influence of physical activity on the pain thresholds in these groups. We postulate that physical fitness and physical activity influence pain thresholds in depression and persons with multiple somatoform symptoms.
: Thirty-eight persons with major depression, 26 persons with a minimum of 6 to 8 somatoform symptoms (somatoform symptom index 8, SSI-8), and 47 healthy participants participated in the study. Baseline values of pressure pain thresholds assessed at different sites of the body were compared with those after 1 week of increased and 1 week of reduced physical activity.
: We used repeated measurement design (MANCOVA) and partial correlations for data analysis. Depressed participants reported lower pain thresholds compared with controls, and persons with SSI-8 showed intermediate thresholds. After 1 week of physical activity, participants reported higher pain thresholds. Men had higher pain thresholds following activity as compared with women. Participants who reported higher general fitness also showed higher pain thresholds. Sensitivity to pressure pain is associated with depression, but not with multiple somatoform symptoms.
: Short low-graded exercise can have reducing effects on perception of pressure pain. Physical activity level is a relevant covariate when using pressure pain assessment. Reduced general fitness can partially account for lower pain thresholds in depression.
The Clinical journal of pain 06/2012; 28(9):782-9. · 3.01 Impact Factor
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ABSTRACT: Previous research suggests a dysregulation of immune-to-brain communication in the pathophysiology of somatization syndromes (multiple somatoform symptoms). We compared blood levels of the inflammatory markers tumor necrosis factor-alpha (TNF-α), interleukin-1 receptor antagonist (IL-1ra), interleukin-6 (IL-6) and neopterin between 23 patients with somatization syndromes (Somatoform Symptom Index-8, SSI-8), 23 age- and sex-matched healthy controls and 23 patients with major depression. No group differences were found for IL-1ra and IL-6. While TNF-α was increased in both clinical groups, neopterin was only increased in somatization syndromes. Correlational analyses revealed that neopterin tended to be related to somatoform pain complaints in patients with somatization syndromes. This study is the first to demonstrate increased levels of TNF-α and neopterin in patients with somatization syndromes without a diagnosis of depression, which may support a role of immune alterations in somatization syndromes. Neopterin is a reliable indicator for interferon-γ (IFN-γ) which was identified as the only cytokine that induces significant production of neopterin. Considering recent research indicating that IFN-γ can lead to increased neuronal responsiveness and body perceptions by reducing inhibitory tone in the dorsal horn, the observed association between somatization syndromes and neopterin might support the idea of central sensitization in the pathogenesis of somatoform symptoms.
Psychiatry Research 08/2011; 195(1-2):60-5. · 2.52 Impact Factor
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ABSTRACT: There is robust evidence that altered neural-immune interactions including increased levels of proinflammatory cytokines are involved in both the pathogenesis of depression and altered pain processing. Proinflammatory cytokines induce sickness behavior, a constellation of symptoms that bears a strong similarity to those of depression. A feature of sickness behavior is enhanced pain sensitivity and it has been suggested that proinflammatory cytokines interact with pain processing directly and via several neurobiological pathways. Previous research indicates that depression and pain are closely related. We investigated the association between proinflammatory cytokines and experimental pain in major depression.
Psychopathological variables, pressure pain thresholds (PPT) and concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were measured in 37 outpatients with major depression and 48 healthy controls.
Compared with controls, depressed patients exhibited significantly higher levels of TNF-α and significantly decreased PPT indicating enhanced pain sensitivity. The group differences were robust when adjusting for sex and body mass index, although sex was significantly related to PPT. No group difference was observed in IL-6. PPT correlated significantly with TNF-α in women but not in men.
Because of the cross-sectional design, causality of the relation between TNF-α and pain cannot be determined. Results should be considered preliminary given the small sample size.
The present findings suggest that increased pain sensitivity in depression may be linked to increased TNF-α concentration. The absence of this association in men is discussed in terms of pain-related psychobiological sex differences.
Journal of affective disorders 12/2010; 131(1-3):143-9. · 3.76 Impact Factor
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ABSTRACT: Comorbidity studies have shown that depression and somatization (multiple somatoform symptoms) often overlap. Therefore it has been suggested to classify at least some patients with somatization syndromes under the category of depressive disorders. We wanted to investigate whether psychobiological investigations confirm the lumping of somatization and depression, or whether psychobiological pathways favor distinguishing these disorders.
An overview is presented summarizing psychobiological studies including patients with depression and/or somatization-associated syndromes. We focus on the following topics: heritability, polymorphisms in special candidate genes, immune activation, hypothalamic-pituitary-adrenal (HPA) axis reactivity, serotonergic pathways, monoamino acids, and fatty acid concentrations.
Immunological activation seems to be associated with specific features of somatoform disorders, namely, sickness behavior and pain thresholds. Genetic factors can also contribute to somatic complaints, e.g., via serotonergic pathways, HPA-axis response, immune activation, and other biological systems that contribute to the self-description of not being healthy. Some results indicate that psychobiological aspects of depression and somatization overlap in part (e.g., the relevance of serotonergic pathways), but there is clearly more evidence for discrepancies of psychobiological pathways in depression and somatization (e.g., the relevance of proinflammatory immune processes; HPA-axis activity; monoamino acid availability; omega-3-concentration; the role of triallelic subtypes of 5-HTTLPR).
Many psychobiological pathways act differently in depression and somatization. These differences in psychobiology favor the distinction of these syndromes in classification approaches.
Journal of psychosomatic research 05/2010; 68(5):495-502. · 2.91 Impact Factor
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ABSTRACT: Symptoms of somatoform and affective disorders are thought to be connected to serotonergic neurotransmission because serotonin is known to regulate the functions relevant in these disorders, such as pain and mood. Previous studies have reported associations of these disorders with a functional polymorphism in the promoter region of the serotonin transporter gene, a limiting factor of the serotonergic neuronal system, as its alleles have been associated with differences in levels of synthesized transporter and therefore differences in reuptake efficiency.
Ninety-one patients with at least 2 unexplained physical symptoms were clinically evaluated and genotyped for the triallelic genotypes of the serotonin transporter gene polymorphism; patients were recruited from 2001 until 2004. DSM-IV diagnoses were assessed using the International Checklists for ICD-10 and DSM-IV. Somatic complaints were quantified with an interview version of the Screening for Somatoform Symptoms, persistent symptoms in the last 2 years (SOMS-2) and the SOMS-7 (current symptoms in the last 7 days). Depressive symptoms were quantified with the Beck Depression Inventory (BDI).
Subjects with higher-expressing allele variants of the serotonin transporter gene (L'L' and L'S') had significantly more somatic symptoms in the last 2 years (trait) than those with lower-expressing variants (S'S') (P < .01). No differences could be found in regard to short-term somatic symptoms (ie, in the last 7 days). Neither depressive symptoms nor a comorbid diagnosis of major depression was associated with allelic variants.
Somatoform symptoms may be associated with a functional polymorphism in the promoter region of the serotonin transporter gene.
The Journal of Clinical Psychiatry 06/2009; 70(11):1536-9. · 5.80 Impact Factor
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ABSTRACT: Overweight and obesity are prevalent in our society, and obese people are often stigmatized. The present study addressed effects of an intervention to reduce prejudice against obese people. 602 students at the mean age of 15.68 +/- 3.86 years watched a video of 20 minutes length that showed interviews with obese adolescents. In the interviews, the adolescents talked about their problems with being discriminated for weight and about reasons for being overweight. The intervention was performed in order to enhance understanding for obese people's problems and to improve attitudes towards them. Changes in attitudes were measured with a questionnaire presented before and three months after the video intervention. Although there was an increased understanding of the problems of obese people, students also showed stronger prejudice against them. Differential effects were obeserved for age, sex, and body mass index. Older and female participants showed a more positive attitude after the intervention.
PPmP - Psychotherapie · Psychosomatik · Medizinische Psychologie 57(9-10):359-63. · 1.02 Impact Factor
