Prospective examination of anxiety and depression before and during confirmed and pseudoexacerbations in patients with multiple sclerosis.
ABSTRACT: This study was designed to determine whether pseudoexacerbations and confirmed MS exacerbations are preceded by or concurrent with increased anxiety or depressive symptoms.This was a secondary analysis of 121 patients with MS who were observed for 48 weeks during a randomized controlled trial. Participants completed monthly self-reports on depressive and anxiety symptoms. Patient-reported exacerbations were assessed through a telephone-administered symptom checklist and neurologic examination.Both pseudoexacerbations and confirmed exacerbations were associated with concurrent somatic depressive (? = .16 and ? = .33, respectively; p values < .05), affective depressive (? = .17 [p = .02] and ? = .12 [p = .06]), and anxiety symptoms (? = .24 and ? = .20, p values < .01), controlling for baseline symptoms. Preexisting somatic and affective depressive symptoms predicted amplified relationships between concurrent confirmed exacerbations and these symptoms (? = .19 and ? = .20, respectively; p values < .01). A standard deviation increase in anxiety symptoms relative to baseline predicted subsequent onset of pseudoexacerbations (odds ratio = 1.54, p = .02), whereas increased somatic depressive symptoms predicted confirmed exacerbations (odds ratio = 1.59, p = .01).Patients with MS experiencing pseudoexacerbations or confirmed exacerbations should be assessed and monitored for depressive and anxiety symptoms, and confirmed exacerbations are particularly concerning in patients with a history of depression. The psychological or psychiatric antecedents of MS exacerbations generate new hypotheses on etiologies of confirmed exacerbations and pseudoexacerbations.clinicaltrials.gov Identifier: NCT00147446.
Project description:People with multiple sclerosis (MS) are at increased risk for depression and anxiety. The symptoms of MS are often similar to the somatic or physical symptoms of depression and anxiety (fatigue, trouble concentrating). This study examined whether MS symptoms and effects biased the assessment of somatic symptoms of anxiety and depression.People with MS (n = 513) completed a survey about MS symptoms, treatments, and distress. The Patient Health Questionnaire-9 assessed depression, and the patient-report version of the Primary Care Evaluation of Mental Disorders assessed anxiety. Participants were grouped into low versus high MS symptoms based on self-reported symptoms and as high versus low disability by the Expanded Disability Status Scale (EDSS). Groups were compared using differential item functioning analysis.No bias was found on somatic symptoms of depression comparing high versus low MS symptom groups (P > .15) or comparing groups based on EDSS scores (P > .29). Two anxiety symptoms (fatigue and muscle tension) showed bias comparing high versus low MS symptom groups (P < .01) and comparing high versus low groups based on EDSS scores (P ? .01). Intraclass correlations suggested a small effect due to bias in the somatic symptoms of anxiety.Somatic symptoms of depression are unlikely to be biased by MS symptoms. However, the use of certain somatic symptoms to assess anxiety may be biased for those with high MS symptoms.
Project description:Depressive symptoms cause major impairment and may accelerate HIV progression despite the use of antiretroviral medication. The somatic symptoms criteria for HIV infection and depression partially overlap, which can make differential diagnosis challenging. Because of chronic inflammation caused by HIV infection, HIV-positive patients may develop somatic and affective-cognitive symptoms of depression. Inflammation-related depression is primarily characterized with severe somatic symptoms such as fatigue and sleep disturbance. This study sought to explore the patterns of somatic and cognitive-affective depressive symptoms that characterize HIV-positive patients. Our specific aims were (1) to identify subtypes of depressive symptoms in a sample of HIV-positive patients; and (2) to test the subtypes' difference on inflammatory and HIV disease progression biomarkers. HIV-positive men and women (N=102) with and without depressive symptoms were randomly selected from an Italian HIV clinic. Depressive symptoms (PHQ-9), viral load (VL), CD4+, Il-6, TNF-α, and monocytes were assessed. The three subtypes formed using Latent Class Analysis (LCA) identified patients with (1) severe cognitive-affective and somatic depressive symptoms; (2) severe/moderate somatic symptoms; and (3) absent or low depressive symptoms. The subtype with severe/moderate somatic symptoms was characterized with elevated levels of Il-6 and monocytes. No difference on HIV progression biomarkers was found. The subtypes of depressive symptoms might help differentiating depressive symptoms from HIV- and inflammatory-related somatic symptoms. When present, cognitive-affective and/or somatic symptoms cause significant impairment to patients' lives and thus warrant further assessment and treatment.
Project description:Hypothalamic-pituitary-adrenal (HPA)-axis hyperactivity and inflammation are thought to be prominent in the aetiology of depression. Although meta-analyses have confirmed this relationship, there is considerable variability in the effect sizes across studies. This could be attributed to a differential role of such biological systems in somatic versus cognitive-affective depressive symptoms which remains largely unexplored. Furthermore, most longitudinal research to date has focused on transient rather than persistent depressive symptoms. In the current study, we investigated the associations of hair cortisol and plasma C-reactive protein (CRP) with the longitudinal persistence and dimensions (cognitive-affective versus somatic) of depressive symptoms over a 14-year period using Trait-State-Occasion (TSO) structural equation modelling. The data came from a large sample of older adults from the English Longitudinal Study of Ageing. Depressive symptoms were assessed from wave 1 (2002-03) to wave 8 (2016-17). Hair cortisol (N?=?4761) and plasma CRP (N?=?5784) were measured in wave 6 (2012-13). Covariates included demographic, socioeconomic, lifestyle, chronic disease, and medication data. Our results revealed that higher cortisol and CRP levels were significantly associated with persistent depressive symptoms across the study period. Notably, both biomarkers exhibited stronger relationships with somatic than with cognitive-affective symptoms. The associations with somatic symptoms were also independent of relevant confounding factors. In contrast, their associations with cognitive-affective symptoms were weak after adjustment for all covariates. These distinct associations reveal the importance of considering symptom-specific effects in future studies on pathophysiological mechanisms. Ultimately, this will have the potential to advance the search for biomarkers of depression and facilitate more targeted treatments.
Project description:Psychologic factors affect how patients with COPD respond to attempts to improve their self-management skills. Learned helplessness may be one such factor, but there is no validated measure of helplessness in COPD.We administered a new COPD Helplessness Index (CHI) to 1,202 patients with COPD. Concurrent validity was assessed through association of the CHI with established psychosocial measures and COPD severity. The association of helplessness with incident COPD exacerbations was then examined by following subjects over a median 2.1 years, defining COPD exacerbations as COPD-related hospitalizations or ED visits.The CHI demonstrated internal consistency (Cronbach alpha = 0.75); factor analysis was consistent with the CHI representing a single construct. Greater CHI-measured helplessness correlated with greater COPD severity assessed by the BODE (Body-mass, Obstruction, Dyspnea, Exercise) Index (r = 0.34; P < .001). Higher CHI scores were associated with worse generic (Short Form-12, Physical Component Summary Score) and respiratory-specific (Airways Questionnaire 20) health-related quality of life, greater depressive symptoms, and higher anxiety (all P < .001). Controlling for sociodemographics and smoking status, helplessness was prospectively associated with incident COPD exacerbations (hazard ratio = 1.31; P < .001). After also controlling for the BODE Index, helplessness remained predictive of COPD exacerbations among subjects with BODE Index </= median (hazard ratio = 1.35; P = .01), but not among subjects with higher BODE Index values (hazard ratio = 0.93; P = .34).The CHI is an internally consistent and valid measure, concurrently associated with health status and predictively associated with COPD exacerbations. The CHI may prove a useful tool in analyzing differential clinical responses mediated by patient-centered attributes.
Project description:This study describes the relationship of irritable mood (IRR) with affective disorders in youths with attention deficit hyperactivity disorder (ADHD).Five hundred ADHD subjects were assessed with the childhood version of the Schedule for Affective Disorder & Schizophrenia. Subjects were in a genetic ADHD protocol and limited to those of Caucasian/European descent.The most prevalent concurrent diagnoses were oppositional defiant disorder (ODD) (43.6%), minor depression/dysthymic disorder (MDDD) (18.8%), and generalized anxiety (13.2%)/overanxious disorder (12.4%). IRR subjects (21.0%) compared to the non-IRR (NIRR) group had higher rates of all affective disorders (76.2% vs. 9.6%) and ODD (83.8% vs. 32.9%) but lower rates of hyperactive ADHD (1.9% vs. 8.9%). Among those without comorbidities, 98.3% were NIRR. Logistic regression found IRR mood significantly associated with major depressive disorder (odds ratio [OR]: 33.4), MDDD (OR: 11.2), ODD (OR: 11.6), and combined ADHD (OR: 1.7) but not with anxiety disorders. Among symptoms, it associated IRR mood with a pattern of dysthymic and ODD symptoms but with fewer separation anxiety symptoms. Diagnostic and symptomatic parameters were unaffected by demographic variables.Potential confounders influencing these results include patient recruitment from only one clinical service; a cohort specific sample effect because some presumed affective disorders and non-Caucasians were excluded; and the young mean age (10.2 years) limiting comorbid patterns.The prominence of an MDDD pattern suggests this IRR group is appropriate in the DSM V's proposed chronic depressive disorder, possibly with or without temper dysregulation. A new diagnosis of disruptive mood dysregulation disorder may be unwarranted.
Project description:AIMS:The objective of this study is to investigate whether type of depressive symptoms (i.e. cognitive-affective or somatic) is related to a patient-perceived need for professional psychological care in individuals with diabetes. METHODS:In total 2266 participants were recruited as part of the screening procedure for a multi-center randomized controlled trial on the treatment of depressive symptoms among individuals with diabetes. Individuals were invited to complete Beck Depression Inventory-II (BDI-II). Patients with elevated depressive symptoms (BDI-II ?14) were interviewed about their psychological care need. Based on their care needs patients were categorized into: unmet need, no need, met need and unclear need. These groups were compared on type of depressive symptoms, as categorized into cognitive-affective symptoms and somatic symptoms. RESULTS:568 eligible individuals had elevated depressive symptoms, of whom 519 were reached. Among these depressed individuals, 19.7% (102 of 519) had an unmet need for psychological care. Participants with an unmet need were younger (p<0.001) and had higher total depression scores compared to the group with no need (p<0.001). They also scored higher on cognitive-affective symptoms (p<0.001), whereas somatic symptoms did not significantly differ (p = 0.232). Logistic regression revealed that cognitive-affective symptoms predicted an unmet need (p = 0.001). However, overall predictive capacity of type of depressive symptoms on care needs was weak. CONCLUSIONS:Cognitive-affective symptoms of depression-but not somatic symptoms-were associated with an unmet need for psychological care among depressed individuals with diabetes. Future research is needed to reveal better predictors explaining the discrepancy between distress and low care needs in order to optimize screening procedures.
Project description:Depression is an independent predictor of adverse outcomes in patients with heart failure (HF). However, the effect of changes in cognitive-affective and somatic symptoms on mortality of HF patients is not known. The purpose of this study was to examine whether changes in cognitive-affective and somatic depressive symptoms over time were associated with mortality in HF.In this secondary analysis of data from the Rural Education to Improve Outcomes in Heart Failure clinical trial, we analyzed data from 457 HF patients (39% female, mean [standard deviation] age = 65.6 [12.8] years) who survived at least 1 year and repeated the Patient Health Questionnaire at 1 year. Cognitive-affective and somatic depression scores were calculated, respectively, based on published Patient Health Questionnaire factor models. Using Cox proportional hazards regression analyses, we evaluated the effect of changes in cognitive-affective and somatic symptoms from baseline to 1 year on cardiac and all-cause deaths.Controlling for baseline depression scores and other patient characteristics, the change in somatic symptoms was associated with increased risk of cardiac death during the subsequent 1-year period (hazard ratio = 1.24, 95% confidence interval = 1.07-1.44, p = .005), but the change in cognitive-affective symptoms was not (hazard ratio = 0.94, 95% confidence interval = 0.81-1.08, p = .38). Similar results were found for all-cause mortality.Worsening somatic depressive symptoms, not cognitive-affective symptoms, are independently associated with increased mortality of HF patients. The findings suggest that routine and ongoing assessment of somatic depressive symptoms in HF patients may help clinicians identify patients at increased risk for adverse outcomes.ClinicalTrials.gov NCT00415545.
Project description:To investigate vilazodone, currently approved for major depressive disorder in adults, for generalized anxiety disorder (GAD).Three randomized, double-blind, placebo-controlled studies showing positive results for vilazodone (2,040 mg/d) in adult patients with GAD (DSM-IV-TR) were pooled for analyses; data were collected from June 2012 to March 2014. Post hoc outcomes in the pooled intent-to-treat population (n = 1,462) included mean change from baseline to week 8 in Hamilton Anxiety Rating Scale (HARS) total score, psychic and somatic anxiety subscale scores, and individual item scores; HARS response (? 50% total score improvement) and remission (total score ? 7) at week 8; and category shifts, defined as HARS item score ? 2 at baseline (moderate to very severe symptoms) and score of 0 at week 8 (no symptoms).The least squares mean difference was statistically significant for vilazodone versus placebo in change from baseline to week 8 in HARS total score (-1.83, P < .0001) and in psychic anxiety (-1.21, P < .0001) and somatic anxiety (-0.63, P < .01) subscale scores; differences from placebo were significant on 11 of 14 HARS items (P < .05). Response rates were higher with vilazodone than placebo (48% vs 39%, P < .001), as were remission rates (27% vs 21%, P < .01). The percentage of patients who shifted to no symptoms was significant for vilazodone on several items: anxious mood, tension, intellectual, depressed mood, somatic-muscular, somatic-sensory, cardiovascular, respiratory, and autonomic symptoms (P < .05).Treatment with vilazodone versus placebo was effective in adult GAD patients, with significant differences between treatment groups found on both psychic and somatic HARS items.ClinicalTrials.gov identifiers: NCT01629966, NCT01766401, NCT01844115.
Project description:This study evaluated the distinctive clinical and biological manifestations of depressive symptom subtypes (i.e., cognitive-affective and somatic) in Veterans with hepatitis C viral infection (HCV) before and during interferon-alpha (IFN) based antiviral therapy.Thirty-two Veterans with HCV and no prior history of IFN therapy were followed prospectively during the first 16weeks of therapy to evaluate depressive symptoms and to determine if baseline cytokine and serotonin levels predicted subsequent changes in depressive scores.IFN therapy resulted in a significant increase in total depressive symptoms from baseline (week 0) to week 16, with neurovegetative and somatic symptoms of depression including loss of appetite, fatigue and irritability increasing within the first two weeks of therapy and continuing to increase throughout IFN therapy. When depressive symptoms were evaluated using a two-factor (i.e., Cognitive-Affective and Somatic) model, the Cognitive-Affective factor score did not change significantly following IFN therapy initiation, while the Somatic factor score showed a significant increase from week 0 to week 16. Veterans with the largest increases in somatic symptoms from week 0 to week 2 had significantly higher levels of tumor necrosis factor-alpha (TNF-?) and lower levels of serotonin at baseline, as compared to Veterans with minimal or no increase in somatic symptoms.Somatic symptoms of depression can be significantly exacerbated during IFN therapy and may be predicted by higher TNF-? levels and lower serotonin levels at baseline.
Project description:Genetic susceptibility to depression has been established using polygenic scores, but the underlying mechanisms and the potentially differential effects of polygenic scores on specific types of depressive symptoms remain unknown. This study examined whether systemic low-grade inflammation mediated the association between polygenic scores for depressive symptomatology (DS-PGS) and subsequent somatic versus cognitive-affective depressive symptoms. The sample consisted of 3510 men and women (aged 50+) recruited from the English Longitudinal Study of Ageing. DS-PGS were derived using the results of a recent genome-wide association study. Plasma C-reactive protein (CRP) was measured at wave 6 (2012/13). Depressive symptoms were assessed at wave 8 (2016/17), using the eight-item version of the Centre for Epidemiological Studies Depression Scale. Covariates (wave 2, 2004/05) included age, sex and ten principal components (PCs) to control for population stratification. Confirmatory factor analysis was performed to corroborate a previously identified two-factor structure of the CES-D, distinguishing between cognitive-affective and somatic symptoms. Longitudinal structural equation modelling was used to investigate the mediating role of CRP in the relationship between DS-PGS and cognitive-affective versus somatic symptoms. Our results showed that participants with a higher polygenic susceptibility to DS were significantly more likely to report cognitive-affective and somatic symptoms at follow-up. Mediation analyses revealed that CRP mediated the relationship between DS-PGS and somatic symptoms, but not the association between DS-PGS and cognitive-affective symptoms. These differential effects highlight the importance of considering individual differences in depression profiles in future studies. Ultimately, this will inform healthcare professionals to design more targeted treatments.