The adaptation of a Danish version of the Pain Self-Efficacy Questionnaire: reliability and construct validity in a population of patients with fibromyalgia in Denmark.
The aim of this study was to translate, culturally adapt and evaluate the psychometric properties of the Pain Self-Efficacy Questionnaire (PSEQ) in a population of patients with fibromyalgia in Denmark. The study sample included 102 patients diagnosed with fibromyalgia referred to a specialist clinic. The PSEQ was translated and adapted to a Danish setting using a standard stepwise forward-backward translation procedure, followed by initial testing and focus group interview. Reliability was examined by analysing internal consistency and test-retest agreement. Construct validity was examined by investigating dimensionality, targeting, local independence, category functioning and differential item functioning (DIF). Reliability was high: Cronbach's alpha 0.88, test-retest correlation 0.93, intraclass correlation coefficient (ICC) 0.89 and item-total correlations 0.44-0.70. Factor analyses and item response (IRT) models indicated unidimensionality, and the PSEQ-DK was well targeted to the sample. High interitem correlation was observed between two items, indicating local dependence, and item misfit and DIF were observed for a few items. However, the overall fit of the scale to a single-factor model and IRT models supported acceptable construct validity. The PSEQ-DK showed acceptable psychometric properties and can therefore represent a reliable and valid measure for evaluating self-efficacy in patients with fibromyalgia in Denmark.
Elevated levels of chemokines have been reported in plasma and brain tissue of individuals with Autism Spectrum Disorders (ASD). The aim of this study was to examine chemokine levels in amniotic fluid (AF) samples of individuals diagnosed with ASD and their controls.
A Danish Historic Birth Cohort (HBC) kept at Statens Serum Institute, Copenhagen was utilized. Using data from Danish nation-wide health registers, a case-control study design of 414 cases and 820 controls was adopted. Levels of MCP-1, MIP-1a and RANTES were analyzed using Luminex xMAP technology. Case-control differences were assessed as dichotomized at below the 10th percentile or above the 90th percentile cut-off points derived from the control biomarker distributions (logistic regression) or continuous measures (tobit regression).
AF volume for 331 cases and 698 controls was sufficient for Luminex analysis. Including all individuals in the cohort yielded no significant differences in chemokine levels in cases versus controls. Logistic regression analyses, performed on individuals diagnosed using ICD-10 only, showed increased risk for ASD with elevated MCP-1 (elevated 90th percentile adjusted OR: 2.32 [95% CI: 1.17-4.61]) compared to controls. An increased risk for infantile autism with elevated MCP-1 was also found (adjusted OR: 2.28 [95% CI: 1.16-4.48]). Elevated levels of MCP-1 may decipher an etiologic immunologic dysfunction or play rather an indirect role in the pathophysiology of ASD. Further studies to confirm its role and to identify the potential pathways through which MCP-1 may contribute to the development of ASD are necessary.
The aim of the study was to analyze cytokine profiles in amniotic fluid (AF) samples of children developing autism spectrum disorders (ASD) and controls, adjusting for maternal autoimmune disorders and maternal infections during pregnancy.
AF samples of 331 ASD cases and 698 controls were analyzed for inflammatory cytokines using Luminex xMAP technology utilizing a historic birth cohort. Clinical data were retrieved from nationwide registers, and case-control differences in AF cytokine levels were assessed using chi-square tests, logistic and tobit regression models.
Overall, individuals with ASD had significantly elevated AF levels of TNF-a and TNF-ß compared to controls. Analyzing individuals diagnosed only with ICD-10 codes yielded significantly elevated levels of IL-4, IL-10, TNF-a and TNF-ß in ASD patients. Restricting analysis to infantile autism cases showed significantly elevated levels of IL-4, TNF-a and TNF-ß compared to controls with no psychiatric comorbidities. Elevated levels of IL-6 and IL-5 were found in individuals with other childhood psychiatric disorders (OCPD) when compared to controls with no psychiatric comorbidities.
AF samples of individuals with ASD or OCPD showed differential cytokine profiles compared to frequency-matched controls. Further studies to examine the specificity of the reported cytokine profiles in ASD and OCPD are required.
Evidence suggests that some developmental disorders, such as autism spectrum disorders (ASDs), are caused by errors in brain plasticity. Given the important role of matrix metalloproteinases (MMPs) and neurotrophins (NTs) in neuroplasticity, amniotic fluid samples for 331 ASD cases and 698 frequency-matched controls were analyzed for levels of MMP-9, brain-derived neurotrophic factor, NT-4 and transforming growth factor-ß utilizing a Danish historic birth cohort and Danish nationwide health registers. Laboratory measurements were performed using an in-house multiplex sandwich immunoassay Luminex xMAP method, and measurements were analyzed using tobit and logistic regression. Results showed elevated levels of MMP-9 in ASD cases compared with controls (crude and adjusted tobit regression P-values: 0.01 and 0.06). Our results highlight the importance of exploring the biologic impact of MMP-9 and potential therapeutic roles of its inhibitors in ASD and may indicate that neuroplastic impairments in ASD may present during pregnancy.
This randomized prospective study examines durability of improvement in general symptomatology, psychosocial functioning and interpersonal problems, and compares the long-term efficacy of analytic and systemic group psychotherapy in women 1 year after completion of treatment for childhood sexual abuse.
Women (n = 106) randomly assigned to analytic or systemic psychotherapy completed the Symptom Checklist-90-R, Global Assessment of Functioning, Global Life Quality, Registration Chart Questionnaire, and Flashback Registration at pre-treatment, post-treatment, and at a 1-year follow-up.
Post-treatment gains were significant for both treatment modalities on all measures, but significantly larger after systemic therapy. Significant treatment response was maintained 1-year post-treatment, but different trajectories were observed: 1 year after treatment completion, improvements for analytic therapy were maintained, whereas they decreased after systemic therapy, resulting in no statistically significant difference in gains between the groups at the 1-year follow-up. Despite maintaining significant gains, more than half of the patients remained above cut-off for caseness concerning general symptomatology at post-treatment and at 1-year follow-up.
The findings stress the importance of long-term follow-up data in effect studies. Different trajectories were associated with the two treatments, but improvement in the two treatment groups did not differ significantly at the 1-year follow-up. Implications of the difference in trajectories for treatment planning are discussed.
Both analytic and systemic group therapy proved efficient in improving general symptomatology, psychosocial functioning, and interpersonal problems in women with a history of CSA and gains were maintained at a 1-year follow-up. Despite maintaining statistically significant gains at the 1-year follow-up, 54% of the patients remained above the cut-off for caseness with respect to general symptomatology, which may indicate a need for further treatment. Different pre-post follow-up treatment trajectories were observed between the two treatment modalities. Thus, while systemic group therapy showed a significantly better outcome immediately after termination, gains in the systemic treatment group decreased during follow-up, while gains were maintained during follow-up in analytic group therapy.
Numerous studies have been trying to disentangle the complex pathophysiology of autism spectrum disorders (ASD). In our study, we explored the potential role of maternal serum (MS) alpha-fetoprotein (AFP) in the prediction and the pathophysiology of ASD.
A total of 112 patients with ASD and 243 control subjects were included in a case-control study, using a historic birth cohort maintained at Statens Serum Institute. Measurements of MS-AFP were obtained from a multicentre screening program, whereas clinical data were obtained from nationwide registers. Association between MS-AFP and ASD status was analyzed using logistic regression models and nonparametric tests.
Crude, but not adjusted, estimates showed that MS-AFP levels were slightly, but significantly, higher in mothers of children with ASD, compared with their control subject counterparts. People with ASD had an odds ratio of 2.33, with 95% confidence intervals of 1.00 to 5.39, to have MS-AFP above 2.5 multiple of median. Excluding subjects with congenital malformation comorbidities did not alter the direction of our estimates (OR 2.60; 95% CI 1.04 to 6.51, P = 0.04).
Biologic plausibility of its role in the pathophysiology of ASD makes AFP a good candidate for further larger-scale studies to confirm such an association and to determine whether this pattern is unique to ASD or related to other psychiatric disorders as well.
Center of Inflammation and Metabolism, Department of Infectious Diseases, Faculty of Health Sciences, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. karen.krabbe@dadlnet.dk
To test the hypothesis that low circulating brain-derived neurotrophic factor (BDNF), a secretory member of the neurotrophin family that has a protective role in neurodegeneration and stress responses and a regulatory role in metabolism, predicts risk of all-cause mortality in 85-year-old men and women.
Longitudinal study with 50- to 58-month follow-up.
The 1914 cohort, a population-based cohort established in 1964 by the Research Center for Prevention and Health at Glostrup Hospital.
One hundred eighty-eight unselected 85-year-old Danes.
BDNF was measured in plasma and serum. The Danish National Register of Patients was used to collect data on morbidity. The primary outcome in Cox regression analyses was all-cause mortality.
Women with low plasma BDNF (lowest tertile) had greater all-cause mortality risk than women with high plasma BDNF (highest tertile) (hazard ratio=2.2, 95% confidence interval=1.1-4.7). Low plasma BDNF predicted mortality independently of activities of daily living; education; and a history of central nervous system disease, cerebrovascular accidents, cardiovascular disease, cancer, respiratory disease, and low-grade inflammation. No association was found between plasma BDNF and mortality in men, and serum BDNF did not influence mortality in either sex.
Low plasma BDNF is a novel, independent, and robust biomarker of mortality risk in old women. BDNF may be a central factor in the network of multimorbidity in old populations.
While recent studies have reported an inverse relation between childhood intelligence test scores and all-cause mortality in later life, the link with disease-specific outcomes has been rarely examined. Furthermore, the potential confounding effect of birthweight and childhood social circumstances is unknown. We investigated the relation of childhood intelligence with coronary heart disease (CHD) and stroke risk in a cohort of 6910 men born in 1953 in the Copenhagen area of Denmark. Events were ascertained from 1978 to 2000 using a cause-of-death register and hospital discharge records. There were 150 CHD (19 fatal; 131 non-fatal) and 93 stroke (4 fatal; 89 non-fatal) events during follow-up into mid-life. Childhood intelligence was inversely related to CHD with the highest rate apparent in adults with low childhood test scores (HR(lowest vs. highest quartile), 2.70; 95% confidence interval: 1.60, 4.57; P(trend) = 0.0001). After adjustment for paternal social class and birthweight, this association was attenuated only marginally. There was little evidence of a IQ-stroke relationship. The cognitive characteristics captured by IQ testing in the present study, such as communication and problem solving ability, appear to be associated with risk of CHD. Health promotion specialists and clinical practitioners may wish to consider these skills in their interactions with the general public. Replication of these results using studies which hold data on intelligence and socio-economic position across the life course is required.
Studies examining the relationship between early-life IQ and the risk of subsequent psychiatric disorder in adulthood are scarce. In the present investigation, the childhood IQ scores of 7022 singleton-born Danish males were linked to psychiatric hospital discharge records in adulthood. IQ scores were inversely related to the risk of total psychiatric illness, with the highest levels apparent in the lowest scoring IQ group (HRlowest quintile v. highest=1.70, 95% CI 1.34-2.14). Adjusting for paternal occupational social class and birth weight had only a small attenuating effect. Low childhood IQ may have an aetiological role in the development of adult total psychiatric disorder.
The authors examined whether motor coordination difficulties assessed in childhood predict later adult schizophrenia spectrum outcomes.
A standardized childhood neurological examination was administered to a sample of 265 Danish children in 1972, when participants were 10-13 years old. Adult diagnostic information was available for 244 members of the sample. Participants fell into three groups: children whose mothers or fathers had a psychiatric hospital diagnosis of schizophrenia (N=94); children who had at least one parent with a psychiatric record of hospitalization for a nonpsychotic disorder (N=84); and children with no parental records of psychiatric hospitalization (N=66). Psychiatric outcomes of the offspring were assessed through psychiatric interviews in 1992 when participants were 31-33 years of age, as well as through a scan of national psychiatric registers completed in May 2007.
Children who later developed a schizophrenia spectrum disorder (N=32) displayed significantly higher scores on a scale of coordination deficits compared with those who did not develop a mental illness in this category (N=133).
Results from this study provide further support for the neurodevelopmental hypothesis of schizophrenia and underscore the potential role of cerebellar and/or basal ganglia abnormalities in the etiology and pathophysiology of schizophrenia.
