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This study aimed to develop and test the feasibility of a primary care worker-led psychological intervention as the main feature of a collaborative stepped care for depression that is effective, affordable, culturally acceptable, tailored to patients’ clinical condition and easily integrate-able into the primary care schedule in Nigeria.

Using the Medical Research Council framework, in the first stage (modelling/theoretical development), experts reviewed and distilled evidence from literature to form the intervention components. In the second (formative) stage, local stakeholders were consulted on the practical application and feasibility of the proposed intervention. The third (piloting) stage involved testing for the clinical efficacy and acceptability of the components of the draft intervention

The final intervention components included a 2-stage screening (red-flagging and further evaluation), psychoeducation, low-intensity psychological therapy (problem-solving therapy for primary care), antidepressant prescription, proactive mobile telephony adherence support and referral to the mental health specialist if needed. At 3 months, 71.6% of depressed patients on the intervention improved. The intervention was perceived to be acceptable and useful by over 70% of health workers and clients and had high ratings (>70% score) by expert panels on intervention simplicity, facilitation strategies, and quality of delivery.

The development and feasibility testing of our integrated intervention encompassed review of current literature, expert opinions and consultation with local stakeholders and end users. Our intervention package was largely deemed acceptable, relevant, useful, and feasible. Important lessons learnt with this process will help in future intervention developments.

The purpose of the present meta-analysis was to evaluate the association between the inflammatory potential of diet, determined by the dietary inflammatory index (DII®) score, and depression.

Systematic review and meta-analysis.

A comprehensive literature search was conducted in PubMed, Web of Science and EMBASE databases up to August 2018. All observational studies that examined the association of the DII score with depression/depressive symptoms were included.

Four prospective cohorts and two cross-sectional studies enrolling a total of 49 584 subjects.

Overall, individuals in the highest DII v. the lowest DII category had a 23 % higher risk of depression (risk ratio (RR)=1·23; 95 % CI 1·12, 1·35). When stratified by study design, the pooled RR was 1·25 (95 % CI 1·12, 1·40) for the prospective cohort studies and 1·16 (95 % CI 0·96, 1·41) for the cross-sectional studies. Gender-specific analysis showed that this association was observed in women (RR=1·25; 95 % CI 1·09, 1·42) but was not statistically significant in men (RR=1·15; 95 % CI 0·83, 1·59).

The meta-analysis suggests that pro-inflammatory diet estimated by a higher DII score is independently associated with an increased risk of depression, particularly in women. However, more well-designed studies are needed to evaluate whether an anti-inflammatory diet can reduce the risk of depression.

Food insufficiency, defined by the experience of hunger, is known to be prevalent and a source of health-related harm among-street involved youth, but little is known about its relationship with depression in this population. Therefore, we sought to assess the association between food insufficiency and symptoms of depression among a cohort of street-involved youth.

Multivariable logistic regression was used to assess the relationship between food insufficiency, defined as being hungry but not having enough money to buy food, and depression as measured by the Center for Epidemiological Studies Depression (CES-D) scale.

Data from April 2006 to November 2013 were derived from the At-Risk Youth Study (ARYS), a prospective cohort of street-involved youth who use illicit drugs in Vancouver, Canada.

There were 1066 street-involved youth enrolled in the study, including 340 (31·9 %) females.

Of 1066 youth enrolled in the study, 724 (67·9 %) reported some food insufficiency and 565 (53·0 %) met criteria for depression. Compared with youth who did not report food insufficiency, those who reported often experiencing food insufficiency had a higher likelihood of reporting depression (adjusted OR=2·52; 95 % CI 1·74, 3·67), as did those who reported sometimes experiencing food insufficiency (adjusted OR=1·99; 95 % CI 1·47, 2·70).

Food insufficiency was prevalent and associated in a dose-dependent trend with symptoms of depression among street-involved youth in our setting. Findings highlight the need to address the nutritional and mental health needs of youth and identify pathways by which food insufficiency may contribute to depression among vulnerable populations.

There is increasing evidence of an association between depressive symptoms and mild cognitive impairment (MCI) in cross-sectional studies, but the longitudinal association between depressive symptoms and risk of MCI onset is less clear. The authors investigated whether baseline symptom severity of depression was predictive of time to onset of symptoms of MCI.

These analyses included 300 participants from the BIOCARD study, a cohort of individuals who were cognitively normal at baseline (mean age = 57.4 years) and followed for up to 20 years (mean follow-up = 2.5 years). Depression symptom severity was measured using the Hamilton Depression Scale (HAM-D). The authors assessed the association between dichotomous and continuous HAM-D and time to onset of MCI within 7 years versus after 7 years from baseline (reflecting the mean time from baseline to onset of clinical symptoms in the cohort) using Cox regression models adjusted for gender, age, and education.

At baseline, subjects had a mean HAM-D score of 2.2 (SD = 2.8). Higher baseline HAM-D scores were associated with an increased risk of progression from normal cognition to clinical symptom onset ≤ 7 years from baseline (p = 0.043), but not with progression > 7 years from baseline (p = 0.194). These findings remained significant after adjustment for baseline cognition.

These results suggest that low levels of depressive symptoms may be predictive of clinical symptom onset within approximately 7 years among cognitively normal individuals and may be useful in identifying persons at risk for MCI due to Alzheimer’s disease.

The goal of this study is to compare BDI-II scores obtained with two standard methods of administration in community-based older persons.

BDI-II was administered at first in the self-rated version to a sample of 60 mentally healthy older persons (age 60–87 years). Afterward, the interview-based administration was performed.

We compared the scores with nonparametric tests — Spearman’s correlation coefficient and Wilcoxon Signed Ranks test. We also computed internal consistency.

Self-rated BDI-II yielded significantly higher total score than interview (p < 0.001, P = 88%). The correlation between total scores was moderate (rs = 0.46, p < 0.001). Item analysis revealed a larger decrease (lower scores) in the somatic items in the interview-based version.

The two methods of administration result in different total score in healthy older persons. Therefore, interpretation of the scores should reflect the administration, which should be always specified in the studies.

This study investigated the characteristics of subjective memory complaints (SMCs) and their association with current and future cognitive functions.

A cohort of 209 community-dwelling individuals without dementia aged 47–90 years old was recruited for this 3-year study. Participants underwent neuropsychological and clinical assessments annually. Participants were divided into SMCs and non-memory complainers (NMCs) using a single question at baseline and a memory complaints questionnaire following baseline, to evaluate differential patterns of complaints. In addition, comprehensive assessment of memory complaints was undertaken to evaluate whether severity and consistency of complaints differentially predicted cognitive function.

SMC and NMC individuals were significantly different on various features of SMCs. Greater overall severity (but not consistency) of complaints was significantly associated with current and future cognitive functioning.

SMC individuals present distinctive features of memory complaints as compared to NMCs. Further, the severity of complaints was a significant predictor of future cognition. However, SMC did not significantly predict change over time in this sample. These findings warrant further research into the specific features of SMCs that may portend subsequent neuropathological and cognitive changes when screening individuals at increased future risk of dementia.

Previous studies on reporting bias generally examined whether trials were published in stand-alone publications. In this study, we investigated whether pooled-trials publications constitute a specific form of reporting bias. We assessed whether negative trials were more likely to be exclusively published in pooled-trials publications than positive trials and examined the research questions, individual trial results, and conclusions presented in these articles.

Data from a cohort of 105 randomized controlled trials of 16 antidepressants were extracted from earlier publications and the corresponding Food and Drug Administration (FDA) reviews. A systematic literature search was conducted to identify pooled-trials publications.

We found 107 pooled-trials publications that reported results of 23 (72%) of 32 trials not published in stand-alone publications. Only two (3.8%) of 54 positive trials were published exclusively in pooled-trials publications, compared with 21 (41.1%) of 51 negative trials (p < 0.001). Thirteen (12%) of 107 publications had as primary aim to present data on the trial's primary research question (drug efficacy compared with placebo). Only four of these publications, reporting on five (22%) trials, presented individual efficacy data for the primary research question. Additionally, only five (5%) of 107 pooled-trials publications had a negative conclusion.

Compared with positive trials, negative trials of antidepressants for depression were much more likely to be reported exclusively in pooled-trials publications. Pooled-trials publications flood the evidence base with often-redundant articles that, instead of addressing the original primary research question, present (positive) results on secondary questions. Therefore, pooled-trials publications distort the apparent risk–benefit profile of antidepressants.

Depression in palliative advanced cancer patients is common, but often goes unrecognized. One of the first steps toward improving detection is the development of tools that are valid in the specific language and setting in which they are to be used. The Brief Edinburgh Depression Scale (BEDS) is a sensitive case-finding tool for depression in advanced cancer patients that was developed in the United Kingdom. There are no validated instruments to identify depression in Mexican palliative patients. Our aim was to validate the Spanish-language version of the BEDS in Mexican population with advanced cancer.

We conducted a cross-sectional study with outpatients from the palliative care unit at the Instituto Nacional de Cancerología in Mexico City. The Mexican BEDS was validated against a semistructured psychiatric clinical interview according to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, classification criteria for major depressive disorder. The interviewer was blind to the BEDS score at the time of the assessment.

Seventy subjects completed the scale and interview. Women represented 71.4% of the sample and median age of subjects was 56.5 years (range, 20–85 years). The prevalence of major depressive disorder according to the psychiatric interview was 20%. The most valid cutoff for defining a case of depression was a score ≥5 of 18 on the Mexican BEDS, which gave a sensitivity of 85.7% and specificity of 62.5%. The scale's Cronbach's alpha was 0.71.

Major depressive disorder is frequent in Mexican palliative patients. The Spanish-language Mexican version of the BEDS is the first valid case-finding tool in advanced cancer patients in this setting.

Electroconvulsive therapy (ECT), an effective antidepressive treatment, is frequently accompanied by cognitive impairment (predominantly memory), usually transient and self-limited. The hippocampus is a key region involved in memory and emotion processing, and in particular, the anterior-posterior hippocampal subregions has been shown to be associated with emotion and memory. However, less is known about the relationship between hippocampal-subregion alterations following ECT and antidepressant effects or cognitive impairments.

Resting-state functional connectivity (RSFC) based on the seeds of hippocampal subregions were investigated in 45 pre- and post-ECT depressed patients. Structural connectivity between hippocampal subregions and corresponding functionally abnormal regions was also conducted using probabilistic tractography. Antidepressant effects and cognitive impairments were measured by the Hamilton Depressive Rating Scale (HDRS) and the Category Verbal Fluency Test (CVFT), respectively. Their relationships with hippocampal-subregions alterations were examined.

After ECT, patients showed increased RSFC in the hippocampal emotional subregion (HIPe) with the left middle occipital gyrus (LMOG) and right medial temporal gyrus (RMTG). Decreased HDRS was associated with increased HIPe-RMTG RSFC (r = −0.316, p = 0.035) significantly and increased HIPe-LMOG RSFC at trend level (r = −0.283, p = 0.060). In contrast, the hippocampal cognitive subregion showed decreased RSFC with the bilateral angular gyrus, and was correlated with decreased CVFT (r = 0.418, p = 0.015 for left; r = 0.356, p = 0.042 for right). No significant changes were found in structural connectivity.

The hippocampal-subregions functional alterations may be specially associated with the antidepressant and cognitive effects of ECT.

Trauma exposure is associated with development of depression and anxiety; yet, some individuals are resilient to these trauma-associated effects. Differentiating mechanisms underlying development of negative affect and resilience following trauma is critical for developing effective interventions. One pathway through which trauma could exert its effects on negative affect is reward-learning networks. In this study, we examined relationships among lifetime trauma, reward-learning network function, and emotional states in young adults.

One hundred eleven young adults self-reported trauma and emotional states and underwent functional magnetic resonance imaging during a monetary reward task. Trauma-associated neural activation and functional connectivity were analyzed during reward prediction error (RPE). Relationships between trauma-associated neural functioning and affective and anxiety symptoms were examined.

Number of traumatic events was associated with greater ventral anterior cingulate cortex (vACC) activation, and lower vACC connectivity with the right insula, frontopolar, inferior parietal, and temporoparietal regions, during RPE. Lower trauma-associated vACC connectivity with frontoparietal regions implicated in regulatory and decision-making processes was associated with heightened affective and anxiety symptoms; lower vACC connectivity with insular regions implicated in interoception was associated with lower affective and anxiety symptoms.

In a young adult sample, two pathways linked the impact of trauma on reward-learning networks with higher v. lower negative affective and anxiety symptoms. The disconnection between vACC and regions implicated in decision-making and self-referential processes may reflect aberrant regulatory but appropriate self-focused mechanisms, respectively, conferring risk for v. resilience against negative affective and anxiety symptoms.

To evaluate brexpiprazole adjunctive to antidepressant therapies (ADTs) as maintenance treatment in patients with major depressive disorder with inadequate response to ADT, utilising a novel study design.

The study comprised an 8-week prospective treatment period with open-label ADT with double-blind placebo treatment and a 24-week randomised treatment period. Investigators and patients were blinded to treatment periods, randomisation criteria, and timing of randomisation. Patients with early response to open-label ADT were withdrawn at Week 6. Patients fulfilling criteria for inadequate response were randomised to ADT+brexpiprazole 1–3 mg/day, or ADT+placebo. The primary endpoint was full remission: Montgomery–Åsberg Depression Rating Scale (MADRS) total score ≤10 and ≥50% decrease from randomisation (i.e. baseline) in MADRS total score for at least 8 consecutive weeks.

The primary efficacy analysis failed to show a statistically significant difference between the proportions of patients on ADT+brexpiprazole (21.4%) and ADT+placebo (24.9%) achieving full remission; odds ratio: 0.83; p=0.2641. The secondary endpoint of change from baseline to Week 6 in MADRS total score showed no difference between ADT+brexpiprazole and ADT+placebo (−0.4; p=0.3259). The most frequent treatment-emergent adverse event (TEAE) in patients receiving ADT+brexpiprazole was weight increased (9.5% vs. 5.0% in ADT+placebo). The incidence of TEAEs leading to withdrawal in the randomised treatment period was 6.3% in the ADT+brexpiprazole group and 3.4% in the ADT+placebo group.

Adjunctive brexpiprazole did not differentiate from ADT+placebo on the primary endpoint of full remission. A number of design elements in this previously untried study design may have contributed to the study result. Brexpiprazole was well tolerated.

In an effort to optimize patient outcomes, considerable attention is being devoted to identifying patient characteristics associated with major depressive disorder (MDD) and its responsiveness to treatment. In the current study, we extend this work by evaluating whether early change in these sensitivities is associated with response to antidepressant treatment for MDD.

Participants included 210 patients with MDD who were treated with 8 weeks of escitalopram and 112 healthy comparison participants. Of the original 210 patients, 90 non-responders received adjunctive aripiprazole for an additional 8 weeks. Symptoms of depression and anhedonia were assessed at the beginning of treatment and 8 weeks later in both samples. Reward and punishment sensitivity were assessed using the BIS/BAS scales measured at the initiation of treatment and 2 weeks later.

Individuals with MDD exhibited higher punishment sensitivity and lower reward sensitivity compared with healthy comparison participants. Change in reward sensitivity during the first 2 weeks of treatment was associated with improved depressive symptoms and anhedonia following 8 weeks of treatment with escitalopram. Similarly, improvement in reward responsiveness during the first 2 weeks of adjunctive therapy with aripiprazole was associated with fewer symptoms of depression at post-treatment.

Findings highlight the predictive utility of early change in reward sensitivity during antidepressant treatment for major depression. In a clinical setting, a lack of change in early reward processing may signal a need to modify a patient's treatment plan with alternative or augmented treatment approaches.