| 1. |
- Andreasson, Anna, et al.
(författare)
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Properties of the Sickness Questionnaire in an Australian sample with chronic medically unexplained symptoms
- 2020
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Ingår i: Brain, Behavior, & Immunity - Health. - : Elsevier BV. - 2666-3546. ; 3
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Tidskriftsartikel (refereegranskat)abstract
- Sickness behavior including malaise, fatigue and increased pain sensitivity is thought to be adaptive and facilitate recovery from disease. However, it may also reduce functioning and health if symptoms persists, which is why validated instruments for its assessment are needed. We evaluated the English translation of the Sickness Questionnaire (SicknessQ) in an Australian population of 156 participants with high level of persistent musculoskeletal pain and/or gastrointestinal symptoms without an organic explanation. The SicknessQ total score had an adequate model fit and no other models were found to fit data better. The SicknessQ correlated most strongly with fatigue, stress, anxiety and depression, which explained 62% of the variance in SicknessQ, but not with physical functioning. The mean score (8.9; 95 %CI: 8.0–9.8) was in between those previously reported in a general population sample and in primary care patients. In conclusion, the evaluation of the English version of the SicknessQ in an Australian sample with significant, chronic unexplained medical symptoms supports the use of the English version of the total SicknessQ score as an overall measure of sickness behavior.
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| 2. |
- Bachiller, S., et al.
(författare)
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Maternal separation leads to regional hippocampal microglial activation and alters the behavior in the adolescence in a sex-specific manner
- 2020
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Ingår i: Brain, Behavior, & Immunity - Health. - : Elsevier BV. - 2666-3546. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Early life adversities during childhood (such as maltreatment, abuse, neglect, or parental deprivation) may increase the vulnerability to cognitive disturbances and emotional disorders in both, adolescence and adulthood. Maternal separation (MS) is a widely used model to study stress-related changes in brain and behavior in rodents. In this study, we investigated the effect of MS (postnatal day 2–14, 3 h/day) in both, female and male adolescent mice. Specifically, we evaluated (i) the spatial working memory, anxiety and depressive-like behavior, (ii) the hippocampal synaptic gene expression, and (iii) the hippocampal neuroinflammatory response. Our results show that MS significantly increased depressive-like behavior in adolescent female mice and altered the spatial memory in adolescent male mice. In addition, MS led to decreased expression of genes related to synaptic function (5ht6r, Synaptophysin, and Cox-2) and induced an exacerbated microglial activation in dentate gyrus (DG), CA1, and CA3. However, while the levels of hippocampal inflammatory cytokines were not modified by MS, they did follow a sex-specific expression in adolescent mice. Taken together, our results suggest that MS induces long-term changes in hippocampal microglia and synaptic gene expression, alters the spatial memory, and induces depressive-like behavior in the adolescent mice, in a sex-specific manner.
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| 3. |
- Bynke, Annie, et al.
(författare)
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Autoantibodies to beta-adrenergic and muscarinic cholinergic receptors in Myalgic Encephalomyelitis (ME) patients - A validation study in plasma and cerebrospinal fluid from two Swedish cohorts
- 2020
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Ingår i: BRAIN, BEHAVIOR, & IMMUNITY - HEALTH. - : Elsevier BV. - 2666-3546. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- Myalgic encephalomyelitis (ME) also known as ME/CFS (Chronic Fatigue Syndrome) or ME/SEID (Systemic Exertion Intolerance Disorder), is a disabling and often long-lasting disease that can drastically impair quality of life and physical/social functioning of the patients. Underlying pathological mechanisms are to a large extent unknown, but the presence of autoantibodies, cytokine pattern deviations and the presentation of cognitive and autonomic nervous system related symptoms provide evidence for ME being an immunological disorder with elements of autoimmunity. Increased levels of autoantibodies binding to adrenergic and muscarinic receptors in ME-patients have been reported. It is hypothesized that these autoantibodies have pathological significance and contribute to the ME-specific symptoms, however, these observations need to be validated. This study was designed to investigate potential differences in adrenergic and muscarinic receptor autoantibody levels in plasma and cerebrospinal fluid (CSF) samples between ME patients and gender and age-matched healthy controls, and to correlate the autoantibody levels to disease severity. We collected bodyfluids and health-related questionnaires from two Swedish ME cohorts, plasma and CSF from one of the cohorts (n = 24), only plasma from the second cohort (n = 24) together with plasma samples (n = 24) and CSF (n = 6) from healthy controls. All samples were analysed for IgG autoantibodies directed against Alpha- (& alpha;1, & alpha;2) and Beta- (131-3) adrenergic receptors and Muscarinic (M) 1-5 acetylcholine receptors using an ELISA technique. The questionnaires were used as measures of disease severity. Significant increases in autoantibody levels in ME patients compared to controls were found for M3 and M4 -receptors in both cohorts and 131,132, M3 and M4-receptors in one cohort. No significant correlations were found between autoantibody levels and disease severity. No significant levels of autoantibodies were detected in the CSF samples. These findings support previous findings that there exists a general pattern of increased antibody levels to adrenergic and muscarinic receptors within the ME patient group. However, the role of increased adrenergic and muscarinic receptor autoantibodies in the pathogenesis of ME is still uncertain and further research is needed to evaluate the clinical significance of these findings.
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| 4. |
- Gupta, Sunjai, et al.
(författare)
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The role of inflammation in the relationship of self-rated health with mortality and implications for public health : Data from the English Longitudinal Study of Aging (ELSA)
- 2020
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Ingår i: Brain, Behavior, & Immunity. - Amsterdam, the Netherlands : Elsevier. - 0889-1591 .- 1090-2139 .- 2666-3546. ; 8, s. 100139-100139
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Tidskriftsartikel (refereegranskat)abstract
- Self-rated health (SRH) predicts mortality after adjustment for potential confounders, including measures of health status. Prodromal disease might lead to worsened SRH and higher mortality. But no study of SRH and mortality has focussed on inflammation. The objective of this study is to investigate the influence of inflammation upon the association between SRH and mortality in a British cohort. The English Longitudinal Study of Ageing (ELSA) involves interviewing participants aged over 50 every two years. We analysed data for 3405 men and 4139 women. Mortality for consenting members was detected by linkage with UK National Health Care registry up to March 2012. Demographic, clinical, and health behaviours at wave 2 were treated as confounders, as well as inflammation-related disease and C-reactive protein (CRP). A five-step hierarchical multivariable logistic regression was estimated. An association was observed between SRH and mortality after adjusting for all variables. In men, compared to those with excellent health, CRP only, and CRP and inflammation-related disease combined, could explain 7.03% and 24.35% of increased risk of dying associated with poor health, respectively. For women, the corresponding figures were 8.95% and 24.28%, respectively. Inflammation is associated with increased risk of death, and may help to explain approximately a quarter of the association between SRH and mortality. Individuals with relatively poor SRH may be aware of underlying inflammation that increases the risk of illness and death, and this may lead to increased use of services, for example. Identifying the cause and treating inflammation in those without a diagnosis may help to increase survival and life quality among those who perceive their health to be relatively poor.
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| 5. |
- Handke, Analena, et al.
(författare)
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Acute inflammation and psychomotor slowing : Experimental assessment using lipopolysaccharide administration in healthy humans
- 2020
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Ingår i: Brain, Behavior, and Immunity - Health. - : Elsevier BV. - 2666-3546. ; 8
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Tidskriftsartikel (refereegranskat)abstract
- Data from clinical and cross-sectional studies suggest that inflammation contributes to psychomotor slowing and attentional deficits found in depressive disorder. However, experimental evidence is still lacking. The aim of this study was to clarify the effect of inflammation on psychomotor slowing using an experimental and acute model of inflammation, in which twenty-two healthy volunteers received an intravenous injection of lipopolysaccharide (LPS, dose: 0.8 ng/kg body weight) and of placebo, in a randomized order following a double-blind within-subject crossover design. A reaction time test and a go/no-go test were conducted 3 h after the LPS/placebo injection and interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were assessed. No effect of experimental inflammation on reaction times or errors for either test was found. However, inflammation was related to worse self-rated performance and lower effort put in the tasks. Exploratory analyses indicated that reaction time fluctuated more over time during acute inflammation. These data indicate that acute inflammation has only modest effects on psychomotor speed and attention in healthy subjects objectively, but alters the subjective evaluation of test performance. Increased variability in reaction time might be the first objective sign of altered psychomotor ability and would merit further investigation.
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| 6. |
- Jonsjö, Martin A., et al.
(författare)
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Patients with ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) and chronic pain report similar level of sickness behavior as individuals injected with bacterial endotoxin at peak inflammation
- 2020
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Ingår i: Brain, Behavior, & Immunity - Health. - : Elsevier BV. - 2666-3546. ; 2
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Tidskriftsartikel (refereegranskat)abstract
- Background: Chronic sickness behavior is implicated in ME/CFS (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) and chronic pain but the level of subjective sickness behavior in these conditions has not been investigated or compared to other clinical and non-clinical samples, or to the level in experimental inflammation. Furthermore, the relationship between sickness behavior and self-rated health and functioning is not known in patients with ME/CFS and chronic pain. The aim of the present study was to investigate how sickness behavior in patients with chronic conditions differs from that in individuals with experimental acute sickness, primary care patients, the general population and healthy subjects. In addition, we wanted to explore how sickness behavior is related to self-rated health and health-related functioning.Methods: Sickness behavior was quantified using the sickness questionnaire (SicknessQ). Self-ratings were collected at one time-point in 6 different samples. Levels of sickness behavior in patients with ME/CFS (n = 38) and patients with chronic pain (n = 190) were compared to healthy subjects with lipopolysaccharide(LPS)-induced inflammation (n = 29), primary care patients (n = 163), individuals from the general population (n = 155) and healthy subjects (n = 48), using linear regression. Correlations and moderated regression analyses were used to investigate associations between sickness behavior and self-rated health and health-related functioning in ME/CFS, chronic pain and the general population.Results: LPS-injected individuals (M = 16.3), patients with ME/CFS (M = 16.1), chronic pain (M = 16.1) and primary care patients (M = 10.7) reported significantly higher SicknessQ scores than individuals from the general population (M = 5.4) and healthy subjects (M = 3.6) all p’s < 0.001). In turn, LPS-injected individuals, patients with ME/CFS and chronic pain reported significantly higher SicknessQ scores than primary care patients (p’s < 0.01). Higher levels of sickness behavior were associated with poorer self-rated health and health-related functioning (p’s < 0.01), but less so in patients with ME/CFS and chronic pain than in individuals from the general population.Conclusions: Patients with ME/CFS and chronic pain report similar high levels of sickness behavior; higher than primary care patients, and comparable to levels in experimental inflammation. Further study of sickness behavior in ME/CFS and chronic pain populations is warranted as immune-to-brain interactions and sickness behavior may be of importance for functioning as well as in core pathophysiological processes in subsets of patients.
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| 7. |
- Nicoll, Rachel
(författare)
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Sickness behavior may follow fracture as well as infection
- 2020
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Ingår i: Brain, Behavior, and Immunity - Health. - : Elsevier BV. - 2666-3546. ; 1
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Tidskriftsartikel (refereegranskat)abstract
- Sickness behavior, induced by pro-inflammatory cytokines in the early stages of an infection, is well known. A case report of three fracture patients, who were not taking analgesic medication, suggests that the initial symptoms experienced, particularly fatigue and mood changes, mirror those of the sickness behavior of infection. A mini-review only found studies investigating one physical, mental or emotional symptom in fracture patients and none drew a parallel with sickness behavior, suggesting that this is a hitherto unrecognised phenomenon which would benefit from further investigation.
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| 8. |
- Santoft, Fredrik, et al.
(författare)
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Inflammatory cytokines in patients with common mental disorders treated with cognitive behavior therapy
- 2020
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Ingår i: Brain, Behavior, & Immunity - Health. - : Elsevier BV. - 2666-3546. ; 3
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Tidskriftsartikel (refereegranskat)abstract
- Peripheral inflammation has been found associated with psychiatric disorders. However, results are inconclusive as to its role in common mental disorders (CMDs), i.e., depression, anxiety, insomnia and stress-related disorders. Further, some research suggests that cognitive behavior therapy (CBT) could reduce inflammatory markers in CMDs. In the present study, we measured pro-inflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-6 [IL-6] and IL-8) pre- and post-treatment in two clinical trials (N = 367) investigating CBT for patients with CMDs in primary care. We hypothesized that higher levels of these cytokines would be associated with more severe psychiatric symptoms (i.e., symptoms of depression, stress and anxiety). We also hypothesized that level of cytokines would decrease after CBT and that the reduced levels would correlate with a reduction in symptoms. Results showed that in men, higher levels of TNF-α were associated with more severe psychiatric symptoms. Further, age moderated the association between TNF-α, as well as IL-6, and stress, and exploratory stratified analyses revealed significant associations in subgroups. No other significant associations between cytokines and psychiatric symptoms were found. None of the cytokines were reduced following CBT, and the marked improvements in psychiatric symptoms after treatment were not associated with changes in cytokines. In conclusion, although inflammation might be of relevance in subgroups, it seems to be of limited importance for clinical improvements across mild to moderate CMDs.
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