Plasma esketamine and noresketamine levels and antidepressant response with oral esketamine treatment.

Cognitive behavioral therapy for insomnia (CBT-I) has been shown to improve both sleep and depressive symptoms, but predictors of depression outcome following CBT-I have not been well examined. This study investigated how chronotype (i.e., morningness-eveningness trait) and changes in sleep efficiency (SE) were related to changes in depressive symptoms among recipients of CBT-I. Included were 419 adult insomnia outpatients from a sleep disorders clinic (43.20% males, age mean ± standard deviation = 48.14 ± 14.02). All participants completed the Composite Scale of Morningness and attended at least 4 sessions of a 6-session group CBT-I. SE was extracted from sleep diary; depressive symptoms were assessed using the Beck Depression Inventory (BDI) prior to (Baseline), and at the end (End) of intervention. Multilevel structural equation modeling revealed that from Baseline to End, SE increased and BDI decreased significantly. Controlling for age, sex, BDI, and SE at Baseline, stronger evening chronotype and less improvement in SE significantly and uniquely predicted less reduction in BDI from Baseline to End. Chronotype did not predict improvement in SE. In an insomnia outpatient sample, SE and depressive symptoms improved significantly after a CBT-I group intervention. All chronotypes benefited from sleep improvement, but those with greater eveningness and/or less sleep improvement experienced less reduction in depressive symptom severity. This suggests that evening preference and insomnia symptoms may have distinct relationships with mood, raising the possibility that the effect of CBT-I on depressive symptoms could be enhanced by assessing and addressing circadian factors.

Resting-state functional connectivity of the amygdala and longitudinal changes in depression severity in adolescent depression

Instability of Depression Severity at Intake as a Moderator of Outcome in the Treatment for Major Depressive Disorder

Objective Coping trajectories are important predictors of depressive symptoms among individuals with cancer. However, less is understood about the relationship between coping and depression within the context of psychosocial interventions, especially among minoritized (i.e. “underserved”) populations. The current study addresses this gap by investigating the relationship between coping strategies and changes in depression severity among underserved cancer patients participating in the Collaborative Oncology Project to Enhance Depression Care (COPE-D), a 12-week collaborative care depression management intervention for patients with cancer. Methods The sample comprised 137 participants who completed both baseline and 12-week follow-up measures. Coping strategies were measured using a shortened version of the adapted Coping Orientation to Problems Experienced (COPE) Inventory, and depression severity was assessed using the Patient Health Questionnaire-9 (PHQ-9). Pre-intervention coping strategies were investigated as predictors of change in depression severity over the intervention, and changes in coping were investigated as moderators of the association between pre- and post-intervention depression severity. Results Participants reported significant increases in approach-oriented coping over the course of the intervention (t = 6.57, df = 140, p < 0.001). Conversely, participants exhibited a statistically significant decrease in avoidance-oriented coping (t = −2.76, df = 192, p = 0.006). Neither the degree of approach nor avoidant baseline coping strategies significantly predicted changes in depression severity over the course of the intervention. Changes in avoidance-oriented coping were associated with changes in depression severity (β = 0.2662, p = 0.0304) such that those who maintained or increased avoidant coping over time were less likely to report decreases in depressive symptoms. Conclusions Baseline coping did not predict changes in depression severity during the intervention. However, increases in avoidance-oriented coping were associated with greater increases in depression severity over time. These findings underscore the importance of considering coping strategies in depression management interventions for cancer patients.

Major depressive disorder is one of the most common psychiatric disorders, with a worldwide lifetime prevalence rate of 10%-20% in women and a slightly lower rate in men. While many patients are successfully treated using established therapeutic strategies, a significant percentage of patients fail to respond. This report describes the successful recovery of a previously treatment-resistant patient following right unilateral deep brain stimulation of Brodmann's area 25. Current therapeutic approaches to treatment-resistant patients are reviewed in the context of this case with an emphasis on the role of the right and left hemispheres in mediating disease pathogenesis and clinical recovery.

Changes in Regional Cerebral Blood Flow After Repetitive Transcranial Magnetic Stimulation of the Left Dorsolateral Prefrontal Cortex in Treatment-Resistant Depression

The authors investigated the theoretical and clinical role of depression among cocaine abusers in treatment. Eighty-nine cocaine-abusing patients underwent 2 weeks of substance abuse treatment. Posttreatment major depressive disorder, depressive symptoms before and after substance abuse treatment, and alcohol diagnoses were assessed and their relation to pretreatment substance use, cravings in high-risk situations, and 3-month follow-up status was examined. High rates of major depressive disorder were found but were unrelated to pretreatment substance use. The decrease in depressive symptoms during treatment was independent of major depressive disorder or alcohol diagnoses and predicted treatment attrition. Higher levels of depressive symptoms during treatment were associated with greater urge to use cocaine, alcohol, and other drugs in high-risk situations. Concurrent major depressive disorder and depressive symptoms did not predict cocaine use at follow-up. However, patients who had an alcohol relapse episode experienced more depressive symptoms during treatment than did those who abstained. The results highlight the relationship of depression to alcohol use among cocaine abusers and suggest a need for further studies of the association between depression and substance use disorders.

IntroductionAmong randomised controlled trials for depressed adolescents, the extent of variation in how depressive symptom outcomes are defined is unknown. The variability in which potential predictors of these outcomes are...

Standard clinical trial methodology in depression does not allow for careful examination of early changes in symptom intensity. The purpose of this study was to use daily "Mental Health Telemetry" (MHT) to prospectively record change in depressive and anxiety symptoms for depressed patients receiving augmentation treatment, and determine the extent and predictive capacity of early changes. We report results of a 6-week, open-label study of the addition of quetiapine XR (range, 50-300 mg) for adult patients (n = 26) with major depressive disorder who were nonresponsive to antidepressant treatment. In addition to regular study visits, all participants completed daily, wirelessly transmitted self-report ratings of symptoms on a Smartphone. Daily and 3-day moving average mean scores were calculated, and associations between early symptom change and eventual response to treatment were determined. Improvement in depressive and anxiety symptoms was identified as early as day 1 of treatment. Of the total decline in depression severity over 6 weeks, 9% was present at day 1, 28% at day 2, 39% at days 3 and 4, 65% at day 7, and 80% at day 10. Self-report rating of early improvement (≥20%) in depressive symptoms at day 7 significantly predicted responder status at week 6 (P = 0.03). Clinician-rated depressive and anxiety symptoms only became significantly associated with responder status at day 14. In conclusion, very early changes in depressive symptoms were identified using MHT, early changes accounted for most of total change, and MHT-recorded improvement as early as day 7 significantly predicted response to treatment at study end point.

Suicide risk is high in patients with major depressive disorder (MDD), bipolar disorder (BD) and borderline personality disorder (BPD). Whether risk levels of and risk factors for suicidal ideation (SI) and suicide attempts (SA) are similar or different in these disorders remains unclear, as few directly comparative studies exist. The relationship of short-term changes in depression severity and SI is underinvestigated, and might differ across groups, for example, between BPD and non-BPD patients. We followed, for 6 months, a cohort of treatment-seeking, major depressive episode (MDE) patients in psychiatric care (original n = 124), stratified into MDE/MDD, MDE/BD and MDE/BPD subcohorts. We examined risks of suicide-related outcomes and their risk factors prospectively. We examined the covariation of SI and depression over time with biweekly online modified Patient Health Questionnaire 9 surveys and analysed this relationship through multi-level modelling. Risk of SA in BPD (22.2%) was higher than non-BPD (4.23%) patients. In regression models, BPD severity was correlated with risk of SA and clinically significant SI. During follow-up, mean depression severity and changes in depression symptoms were associated with SI risk regardless of diagnosis. Concurrent BPD in depression seems predictive for high risk of SA. Severity of BPD features is relevant for assessing risk of SA and SI in MDE. Changes in depressive symptoms indicate concurrent changes in risk of SI. BPD status at intake can index risk for future SA, whereas depressive symptoms appear a useful continuously monitored risk index.

The objectives of this study were to determine the ability of the 30-, 15- and 8-item versions of the GDS for screening and assessing change in severity of depression in nursing home patients. The GDS and the MADRS were administered to 350 elderly NH-patients by trained interviewers. The presence of major (MaD) or minor depression (MinD) was evaluated with the Schedules for Clinical Assessment in Neuropsychiatry. Receiver Operator Characteristic (ROC) curves of the GDS-versions were performed to measure the ability to screen on depression. The ability to measure change in severity of depression was measured by differences in mean GDS-scores and mean MADRS-scores between patients with MaD, MinD and no depression, and expressed in terms of effect sizes. It was found that in ROC-curves all three GDS-versions performed well. The MADRS showed larger effect sizes for the differences between MaD, MinD and no depression than the GDS-versions. The effect sizes of the three GDS versions were comparable. We conclude that all three versions of the GDS can be used for screening on depression among NH-patients. The MADRS is superior to the GDS for assessment of (changes in) severity of depression, but the GDS also appears to be an acceptable instrument for this purpose and is less time-consuming.

Randomized controlled clinical trials that have investigated minocycline as an adjunctive treatment for major depressive disorder have proved promising. Data from two studies were pooled to evaluate more definitively whether the addition of minocycline to standard treatment for major depressive disorder leads to an improvement of depressive symptoms when compared with placebo. Both studies were multi-site, double-blinded, placebo-controlled trials of minocycline 200 mg/day added to treatment as usual during a 12-week period. The primary outcome measure was change in depressive symptoms (Montgomery-Asberg Depression Rating Scale in Dean et al. and Hamilton Depression Rating Scale in Husain et al.). Secondary outcomes were change in depression severity (Montgomery-Asberg Depression Rating Scale for Dean et al. and 9-item Patient Health Questionnaire in Husain et al.), anxiety severity (Hamilton Anxiety Rating Scale in Dean et al. and Generalized Anxiety Disorder 7-item scale in Husain et al.) and functional status, which were also evaluated as potential mediators on the primary outcome. A total of 112 participants were included in the pooled data (Dean et al., n = 71; Husain et al., n = 41). A significant change from baseline to week 12 was noted in depressive symptoms - differential change (Placebo vs Minocycline): 9.0, 95% confidence interval = [4.2, 13.9], Cohen's D (95% confidence interval): 0.71 [0.29, 1.14], p < 0.001 - anxiety severity - differential change (Placebo vs Minocycline): 0.38, confidence interval = [0.00, 0.75], Cohen's D (95% confidence interval): 0.41 [0.00, 0.82], p = 0.050) and functional status - differential change (Placebo vs Minocycline): 1.0, 95% confidence interval = [0.4, 1.5], Cohen's D (95% confidence interval): 0.76 [0.34, 1.19], p = 0.001). Duration of illness, current use of benzodiazepine and pain medication were identified as moderators, whereas functional status as a mediator/predictor. The improvement of depressive symptoms, anxiety severity and functional status is promising and suggests that minocycline has potential as an adjunctive treatment for major depressive disorder. However, further studies are warranted to confirm therapeutic effects of minocycline in major depressive disorder. NCT02263872, registered October 2014, and ACTRN12612000283875, registered March 2012.

Depression Screening of Perinatal Women: An Evaluation of the Healthy Start Depression Initiative

Background: While preliminary evidence suggests that sensors may be employed to detect presence of low mood it is still unclear whether they can be leveraged for measuring depression symptom severity. This study evaluates the feasibility and performance of assessing depressive symptom severity by using behavioral and physiological features obtained from wristband and smartphone sensors.Method: Participants were thirty-one individuals with Major Depressive Disorder (MDD). The protocol included 8 weeks of behavioral and physiological monitoring through smartphone and wristband sensors and six in-person clinical interviews during which depression was assessed with the 17-item Hamilton Depression Rating Scale (HDRS-17).Results: Participants wore the right and left wrist sensors 92 and 94% of the time respectively. Three machine-learning models estimating depressive symptom severity were developed–one combining features from smartphone and wearable sensors, one including only features from the smartphones, and one including features from wrist sensors–and evaluated in two different scenarios. Correlations between the models' estimate of HDRS scores and clinician-rated HDRS ranged from moderate to high (0.46 [CI: 0.42, 0.74] to 0.7 [CI: 0.66, 0.74]) and had moderate accuracy with Mean Absolute Error ranging between 3.88 ± 0.18 and 4.74 ± 1.24. The time-split scenario of the model including only features from the smartphones performed the best. The ten most predictive features in the model combining physiological and mobile features were related to mobile phone engagement, activity level, skin conductance, and heart rate variability.Conclusion: Monitoring of MDD patients through smartphones and wrist sensors following a clinician-rated HDRS assessment is feasible and may provide an estimate of changes in depressive symptom severity. Future studies should further examine the best features to estimate depressive symptoms and strategies to further enhance accuracy.

See related article, pages 16–21 A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between depression and many neurological illnesses, and that mood disorders can affect the course of the diseases.1 Depression commonly occurs after a stroke, with an estimated prevalence as high as 30% in the first year after the event.2 It is well known that poststroke depression affects quality of life, functional recovery, cognitive function and health care use in stroke survivors.3 Inversely, does any association exist between a history of a previous affective disorder and future risk of cardiovascular events? Recent prospective studies have shown an association between depression and incidence of hypertension,4,5 coronary heart disease,6,7 and cardiovascular mortality.8–11 In the Multiple Risk Factor Intervention Trial, 12 866 men were followed for 18 years; those with greater depressive symptoms, as measured by the Center for Epidemiologic Studies Depression Scale (CES-D), were associated with a significant higher risk of cardiovascular mortality (hazard ratio=1.21; 95% CI, 1.03 to 1.41; P <0.05) and stroke mortality (hazard ratio= 2.03; 95% CI, 1.20 to 3.44; P <0.01).12 The NHANES I Epidemiologic Study13 showed that individuals reporting 5 or more symptoms of depression at baseline were 50% more likely to die of a stroke-related cause during a 29-year follow-up. The Baltimore Epidemiologic Catchment Area Study showed that individuals with a history of depressive disorder, measured with the diagnostic interview schedule, were 2.6 times more likely to report stroke.14 Depressive symptoms, measured by the Zung Self-rating Depression Scale, were also associated with an increased incidence of ischemic stroke in a Japanese 10-year follow study.15 Self-reported depression scores significantly predicted stroke in an Australian cohort of people …