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Background and Objectives: Depression impairs working memory (WM). And, while many studies have documented impairment in WM during depression remission, those using the N-back task did not find differences between individuals with remitted depression and healthy controls. One reason for these findings may be that certain depression phenotypes, such as the childhood-onset form, which is likely to be associated with persistent WM problems, are underrepresented or unevenly represented in the studies. Because childhood-onset depression (COD) affects individuals while cognitive development is still ongoing, it is more likely to have lasting detrimental effects, as evidenced in residual memory impairment, than depression that onsets later in life. Further, it is unclear if depression episodes have cumulative effects on WM when measured via the N-back., Methods: We examined the effects of depression on WM performance (response time, accuracy, signal detection d') and subjective experience (difficulty, mental effort required) during a four-level N-back task among 112 adults with COD (42 currently depressed; 70 remitted depressed) and 80 never-depressed controls., Results: Compared to never-depressed controls, there was minimal evidence of impaired WM performance among participants with remitted or current depression; the groups also reported overall similar subjective experiences during the N-back. Notably, number of lifetime depressive episodes had a detrimental cumulative effect on response accuracy and d'., Limitations: WM was assessed only in regard to verbal memory. The sample size of currently depressed cases was smaller than that of the other groups., Conclusions: WM remains largely intact among adults with remitted COD, but increased number of depression episodes worsens WM performance., Competing Interests: Declaration of competing interest None., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: People with depression typically exhibit diminished cognitive control. Control is subjectively costly, prompting speculation that control deficits reflect reduced cognitive effort. Evidence that people with depression exert less cognitive effort is mixed, however, and motivation may depend on state affect., Methods: We used a cognitive effort discounting task to measure propensity to expend cognitive effort and fractal structure in the temporal dynamics of interbeat intervals to assess on-task effort exertion for 49 healthy control subjects, 36 people with current depression, and 67 people with remitted depression., Results: People with depression discounted more steeply, indicating that they were less willing to exert cognitive effort than people with remitted depression and never-depressed control subjects. Also, steeper discounting predicted worse functioning in daily life. Surprisingly, a sad mood induction selectively boosted motivation among participants with depression, erasing differences between them and control subjects. During task performance, depressed participants with the lowest cognitive motivation showed blunted autonomic reactivity as a function of load., Conclusions: Discounting patterns supported the hypothesis that people with current depression would be less willing to exert cognitive effort, and steeper discounting predicted lower global functioning in daily life. Heart rate fractal scaling proved to be a highly sensitive index of cognitive load, and data implied that people with lower motivation for cognitive effort had a diminished physiological capacity to respond to rising cognitive demands. State affect appeared to influence motivation among people with current depression given that they were more willing to exert cognitive effort following a sad mood induction., (Copyright © 2022 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Background: Ecological momentary assessment (EMA) is a high-frequency ambulatory data collection approach that has come to be widely used in emotion research. It therefore is timely to examine two features of EMA needed for a successful study: compliance with survey prompts and high affective yield (survey prompts that capture affect experience). We posit that compliance may be subject to temporal variation (time-of-day, days in study) and individual differences (depression history), and that affective yield may also differ by social context., Methods: We examined these issues in a sample of 318 young adults (Mage = 24.7 years, SD = 2.7), including those with current depression (n = 28), remitted depression (n = 168) and never-depressed controls (n = 122) who participated in a 7-day EMA protocol of negative and positive affect (NA and PA, respectively)., Results: The overall compliance rate was 91% and remained stable across the survey week. However, subjects were significantly less likely to respond to the first daily prompt compared to those that followed. The likelihood of capturing NA and PA decreased with each EMA protocol day, and affective yield across social contexts differed by participants' depression status., Limitations: The sample was largely comprised of White young adults. Relative to the remitted and control groups, the sample size for the currently depressed was unbalanced., Conclusion: Researchers can optimize compliance and affective yield within EMA by considering depression, time-of-day, study duration, and social context. Clinicians using EMA to monitor affect may benefit from considering these parameters., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Offspring of parents with depression histories are at increased risk of developing depression and also report maladaptive ways of self-regulating sadness. Maladaptive regulation of sadness tends to be more prevalent among females than males and has been proposed as one explanation of sex differences in depression rates that emerge around mid-adolescence. However, there is scant information about the age at which the sex differences in maladaptive regulatory responses become evident and whether such age-related sex differences vary depending on depression risk. The present study examined two samples aged 8-18 years: 86 offspring of emotionally healthy parents and 98 offspring of parents with depression histories. Subjects were clinically assessed and provided self-reports of maladaptive responses to sadness. In the combined samples, sex differences in maladaptive responses were significant at age 12.5 years and older ages (i.e., chronologically earlier than the documented emergence of sex differences in depression). While in the high-risk group, sex differences in maladaptive regulatory responses were significant at 12.11 years of age and older, in the low-risk group there was no age at which sex differences were significant. Our findings support the possible mechanistic role of maladaptive emotion regulation in the emergence of sex disparities in depression rates and have implications for prevention., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Youths at high risk for depression have been shown to have problems in repairing their own sad mood. Given that sympathetic arousal has been implicated both in the experience and regulation of affect, an atypical pattern of arousal may be one of the factors that contribute to mood repair problems. In the current study, we measured sympathetic arousal of never-depressed youths at high (n = 56) and low (n = 67) familial risk for depression during sad mood induction and instructed mood repair. Sympathetic arousal was indexed by skin conductance level (SCL) and cardiac pre-ejection period (PEP); mood repair outcome was indexed by self-rated affect. High-risk youths demonstrated increased SCL during sadness induction, which persisted during mood repair; low-risk youths evidenced increased SCL only during mood repair. Shortened PEP was evident only among high-risk youths and only during mood repair. Furthermore, shortened PEP during mood induction predicted less successful mood repair in the low-risk but not in the high-risk group. The findings suggest that: (a) depression-prone youths differ from control peers in patterns of sympathetic responses to emotional stimuli, which may impair their ability to relieve sadness, and (b) activation patterns differ across subsystems (SCL vs. PEP) of sympathetic activity, in conjunction with depression risk status., (© 2020 Society for Psychophysiological Research.)

The aim of the present study was to examine whether offspring at high and low familial risk for depression differ in the immediate and more lasting behavioural and physiological effects of hedonically-based mood repair. Participants (9- to 22-year olds) included never-depressed offspring at high familial depression risk (high-risk, n  = 64), offspring with similar familial background and personal depression histories (high-risk/DEP, n  = 25), and never-depressed offspring at low familial risk (controls, n  = 62). Offspring provided affect ratings at baseline, after sad mood induction, immediately following hedonically-based mood repair, and at subsequent, post-repair epochs. Physiological reactivity, indexed via respiratory sinus arrhythmia (RSA), was assessed during the protocol. Following mood induction and mood repair, high- and low-risk (control) offspring reported comparable changes in levels of sadness and RSA. However, sadness increased among high-risk offspring following the post-repair epoch, whereas low-risk offspring maintained mood repair benefits. High-risk/DEP offspring also reported higher levels of sadness following the post-repair epoch than did low-risk offspring. Change in RSA did not differ across the three offspring groups. Self-ratings confirm that one source of difficulty associated with depression risk is diminished ability to maintain hedonically-based mood repair gains, which were not apparent at the physiological level.

Background: As the rates of suicidal behaviors continue to rise, research is needed that can facilitate prevention. The present study therefore examined whether a modifiable process, dysfunctional regulation of sadness (maladaptive mood repair), predicts a range of suicidal behaviors and if its impact is affected by risk and protective factors., Methods: Young adults with histories of childhood-onset mood disorder (COMD) (n = 173) or no histories of major psychiatric illness (controls, n = 96) were followed for approximately 3 years. Self-rated questionnaires and psychiatric evaluations were administered at study entry (T1) and across the follow-up (T2) and clinicians assessed the DSM-range of non-fatal suicidal behaviors. We hypothesized that the impact of depression on suicidal behaviors was mediated by dysfunctional regulation of sadness., Results: At T1, 90% of the COMD group had histories of various suicidal behaviors; 63% had past suicide attempts. During follow-up, 40% exhibited suicidal behaviors; 7% reported suicide attempts. Controlling for prior suicidal behaviors, T1 maladaptive mood repair predicted suicidal behavior during the follow-up and differentiated recurrent thoughts of death from other forms of suicidality. Protective and risk factors lost their predictive power in the presence of maladaptive mood repair., Limitations: Few control cases exhibited suicidal behavior during the follow-up and the high inter-correlations among several key variables constrained the models that could be fitted., Conclusions: Programs to prevent suicidal behavior among high-risk individuals should include maladaptive mood repair as an intervention target. Further research is needed on whether recurrent thoughts of death constitute a valid index of suicidality., Competing Interests: Declaration of Competing Interest The authors have no conflicts to declare., (Copyright © 2019. Published by Elsevier B.V.)

Adverse life events have been causally linked to depression among youth at high risk for depression. But given that not all high-risk youth develop depression following adversity, individual differences in various processes, including physiological reactivity to stress, are likely to be at play. This longitudinal prospective study tested the hypothesis that, among high-risk youth exposed to adversities, extent of physiological reactivity to laboratory stress (indexed as respiratory sinus arrhythmia; RSA) would predict subsequent depressive symptoms. Subjects were youth at high (n = 80) and low (n = 74) familial risk for depression. At Time 1 (T1), RSA was assessed during a cognitive stress task. At Time 2 (T2) about 2 years later, parents reported on adversities experienced by their offspring during the interim. At T1 and T2, youth received a diagnostic evaluation, which included assessment of their depressive symptoms. The three-way interaction of group-X-adversities-X-RSA predicted T2 depressive symptoms (controlling for T1 depressive symptoms). This interaction was mostly driven by the moderating effect of RSA among high-risk youth, such that adversities predicted higher depressive symptoms for those who displayed greater RSA reactivity to stress. Among low-risk youth, an inverse marginal moderating effect of RSA was found, such that adversities tended to predict depressive symptoms for those who displayed blunted RSA reactivity to stress. Thus, high physiological stress reactivity appears to be an additional risk factor for depressive symptoms only among youth at elevated risk for such outcomes, and should be taken into consideration in efforts to prevent depression in these populations.

Affect dysregulation in response to rewarding stimuli has been proposed as a vulnerability factor for major depressive disorder (MDD). However, it remains unclear how affective behavioral dynamics may be altered among individuals who are at high risk for depression but not currently depressed. We examined the dynamics of affective facial behavior during hedonic probes among 3 groups of adolescents: remitted probands who had histories of childhood-onset MDD (n = 187), never-depressed siblings of probands (high familial risk; n = 207), and healthy controls (n = 166). Participants' happy and sad facial expressions were coded during 3 hedonic laboratory tasks: receiving a preferred prize, describing a positive autobiographical memory, and watching a humorous film. Happy and sad behavioral dynamics were indexed by mean level- and time-dependent reactivity, variability (mean of the squared successive differences), and inertia (autocorrelation). Relative to controls, probands and siblings exhibited a more rapid decrease in happy behaviors, and probands exhibited higher inertia of sad behaviors during hedonic probes. Both probands and siblings exhibited lower inertia of sad behaviors while receiving a desired prize, which highlights the importance of context variation in testing hypotheses. Overall, our study provides new evidence that hedonic behavioral dysregulation, as reflected in dynamic facial behavior, may highlight depression vulnerability. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Objectives: Impaired positive autobiographical memory (AM) is closely linked to emotional disorders. AM impairments are often found in depressed adults and may be related to the difficulties such persons have in regulating their dysphoric mood. By contrast, less is known about AM disturbances among adolescents, or about the functional relationship of AM disturbances to early-onset depression., Design: A high-risk family design served to compare four groups of youth who differed in depression histories and familial depression risk., Methods: Thirty-one currently depressed probands, 185 remitted probands, 204 never-depressed siblings of probands, and 180 healthy control youth were induced into a negative mood prior to recalling positive AMs via a novel memory elicitation procedure. Several positive AM characteristics were assessed., Results: Relative to control youth, unaffected siblings and probands exhibited consistently impaired positive AMs. Moreover, we also found some evidence that probands were more impaired than siblings, who were in turn more impaired than controls, consistent with a gradient effect., Conclusions: Positive AM disturbances may not only precede the onset of depression in vulnerable youth, but also continue to persist after remission of a depressive episode. Clinical and basic research implications of the findings are discussed., Practitioner Points: Positive AM impairments may be trait-like, persist in the euthymic phase of depression, and may serve as a risk marker for early-onset depression among vulnerable adolescents. Disturbances in positive AM may negatively impact the mood-regulatory functions of positive memory recall and contribute to persistent sadness and anhedonia, which are core features of depression. Our sample of currently depressed youth was relatively small, tempering our conclusions. Although we collected data on some important covariates (e.g., socioeconomic status), we lacked information on other relevant variables such as youths' executive functioning or IQ., (© 2017 The British Psychological Society.)

We examined whether the combined indices of respiratory sinus arrhythmia at rest (resting RSA) and in response to a sad film (RSA reactivity) predict effective and ineffective responses to reduce sadness (adaptive vs. maladaptive mood repair) in women with histories of juvenile-onset depression (n=74) and no history of major mental disorders (n=75). Structural equation models were used to estimate latent resting RSA, depression, and adaptive and maladaptive mood repair and to test the study hypotheses. Results indicated that combinations of resting RSA+RSA reactivity (RSA patterns) predicted maladaptive mood repair, which in turn, mediated the effects of RSA pattern on depression. Further, RSA patterns moderated the depressogenic effects of maladaptive mood repair. RSA patterns were unrelated to adaptive mood repair. Our findings suggest that mood repair is one mechanism through which physiological vulnerabilities adversely affect mental health., (Copyright © 2013 Elsevier B.V. All rights reserved.)

This study examined whether frontal alpha electroencephalographic (EEG) asymmetry moderates the association between stressful life events and depressive symptoms in children at familial risk for depression. Participants included 135 children ages 6 to 13, whose mothers had either a history of depression or no history of major psychiatric conditions. Frontal EEG was recorded while participants watched emotion-eliciting films. Symptoms and stressful life events were obtained via the Child Behavior Check List and a clinical interview, respectively. High-risk children displayed greater relative right lateral frontal activation (F7/F8) than their low-risk peers during the films. For high-risk children, greater relative left lateral frontal activation moderated the association between stressful life events and internalizing symptoms. Specifically, greater relative left lateral frontal activation mitigated the effects of stress in at-risk children., (Copyright © 2012 Society for Psychophysiological Research.)

We examined respiratory sinus arrhythmia (RSA), emotion regulation (ER), and prospective depressive symptoms in children at risk for depression and controls. Of the 65 children (35 boys; 5-13 years) in the sample, 39 had a parent with childhood-onset mood disorder and 26 had a parent with no history of major psychiatric disorder. RSA during pre- and post-film baselines and RSA reactivity to sad film clip were measured. Later, children's ER responses (focusing on sad/distressing affect) were assessed using a parent-reported questionnaire, and depressive symptoms were measured via clinical ratings. Results indicated that, compared to the initial baseline, a greater decrease in RSA (i.e., more vagal withdrawal) in response to the sad film clip predicted more adaptive ER responses and lower levels of clinician-rated depressive symptoms. However, tests for ER as a mediator of the association between RSA reactivity and depressive symptoms were precluded because maladaptive, but not adaptive, ER was associated with depressive symptoms. Overall, results suggest that cardiac vagal withdrawal (a greater decrease in RSA) in response to an emotional stimulus reflects more adaptive parasympathetic activity, which could facilitate children's ability to effectively manage their sadness and distress and predict lower risk of depressive symptoms over time.

Background: Psychiatric assessments of children typically involve two informants, the child and the parent. Understanding discordance in their reports has been of interest to clinicians and researchers. We examine differences between mothers' and children's report of children's depressive symptom severity, and factors that may influence their reports and level of agreement. We hypothesized that agreement between mother and child would improve if (1) the mother is depressed, due to improved recall of mood congruent symptoms, (2) the child is older, due to better social-cognitive and communication skills, and (3) the child is a female., Methods: Subjects were 354 children (158 girls; mean age 11.69 years, SD: 2.05 years) with Major Depressive Disorder. Depressive symptoms were evaluated by a semi-structured interview separately with the mother and the child. Agreement on symptom severity was based on concordance of the presence and extent of symptoms., Results: Maternal reports were significantly higher than their son's but not daughters'. Girls, particularly with increasing age, reported higher levels of symptoms; however mothers' reports were not affected by child sex or age. Maternal depression predicted more severe symptom reports for both children and mothers. Agreement between the mother and the child increased as children got older., Limitations: The same clinician interviewed the mother and the child, which might inflate rates of agreement. However, this method mirrors clinical evaluation., Conclusion: During a clinical interview one must consider the age and sex of the child and the depressive state of the mother in assimilating information about the child.

Objective: To pilot test the acceptability and efficacy of contextual emotion-regulation therapy (CERT), a new, developmentally appropriate intervention for childhood depression, which focuses on the self-regulation of dysphoria., Method: Two samples of convenience (n = 29, n = 2) served to verify some CERT constructs; it was then operationalized in a treatment manual. To pilot test CERT, 20 children (ages 7-12; 35% girls) with DSM dysthymic disorder (mean duration 24.4 months) entered an open, 30-session, 10-month, 4-phase trial, with 6- and 12-month follow-up. Assessments included independent clinical evaluations and self-rated questionnaires., Results: Fifteen children completed theraphy, four were administratively terminated and one dropped out. Completers did not clinically differ from the rest, but they were more likely to have better educated and less depressed mothers and intact families. At the end of treatment, 53% of the completers had full and 13% partial remission of dysthymia (remission from superimposed major depression was 80%). By 6- and 12-month follow-up, 79% and 92% had full remission of dysthymia (p < 0.0001). Self-reported depressive and anxiety symptoms significantly declined by the end of treatment (p < .001) and remained so throughout follow-up., Conclusions: CERT enables clinicians to "match" the intervention to children's emotion regulatory needs and symptoms and was readily accepted by families. The promising results suggest the need for a randomized trial.

Background: Despite findings that parent depression increases children's risk for internalizing and externalizing problems, little is known about other factors that combine with parent depression to contribute to behavior problems., Methods: As part of a longitudinal, interdisciplinary study on childhood-onset depression (COD), we examined the association of mother history of COD, child frontal electroencephalogram asymmetry, and affective behavior with children's concurrent behavior problems., Results: Children in the COD group had higher anxious/depressed and aggressive problems than did children in the control group, but this was qualified by a COD-by-asymmetry interaction effect. For COD but not control children, left frontal asymmetry was associated with both anxious/depressed and aggressive child problems. Children with left frontal asymmetry and low affect regulation behavior had higher anxious/depressed problems than did those with high affect regulation behavior. Boys with left frontal asymmetry had higher aggressive problems than did those with right frontal asymmetry., Conclusions: In children of mothers with COD, physiological and behavioral indices of affect regulation may constitute risks for behavior problems.

Clinicians who treat depressed children and adolescents are faced with substantial challenges. Although to date the results of controlled psychotherapy trials with depressed youths offer limited guidance regarding choice of treatment, some general guidelines can be culled from the available data. Interventions or elements of therapies that are structured and directed towards cognitive behavioral or relationship issues show promise for the treatment of juvenile depression. Group interventions seem to be as effective as the more traditional individual therapy. Parental participation in empiric treatment trials of pediatric depression has been limited to either separate parent groups as an adjunct or to family therapy,but for various practical and clinical reasons it may be wise to involve parents directly. Parents may be critical to the success of interventions with depressed children and should be regarded as potentially important agents of change.

Respiratory sinus arrhythmia (RSA) is an index of parasympathetic nervous system activity reflecting respiratory influences on heart rate. This influence is typically measured as high frequency heart rate variability (HF‐HRV) or root mean square of successive differences (RMSSD) of adjacent inter‐beat intervals. Examining the long‐term stability of its measurement is important as levels of resting RSA have been conceptualized as a marker of individual differences; in particular, of an individual's autonomic regulation and affect‐related processes, including emotion regulation. At present, it is not known if resting RSA levels reflect stable differences over a long‐term period (i.e., >1 year). Even less is known about how RSA stability differs as a function of depression history and whether it relates to depression risk trajectories. In the present study, we examined the 1.5‐year test–retest reliability of resting RSA using the intraclass correlation coefficient (ICC) in 82 adults: n = 41 with a history of depression (ever‐depressed); n = 41 controls with no depression history (never‐depressed). HF‐HRV was fairly stable in both groups (ever‐depressed ICC = 0.55, never‐depressed ICC = 0.54). RMSSD was also fairly stable in ever‐depressed adults (ICC = 0.57) and never‐depressed controls (ICC = 0.40). ICC values for both indices did not differ between groups per overlapping 95% confidence intervals. Therefore, RSA stability as assessed by both frequency (HF‐HRV) and time domain (RMSSD) measures was not attenuated by a depression history. Implications and the need for future research are discussed. Researchers commonly utilize resting levels of parasympathetically‐mediated heart rate variability (e.g., HF‐HRV, RMSSD) to assess emotion regulation in healthy and clinical samples, particularly depression. However, little is known about its long‐term stability, and even less so in the presence of psychopathology. Our findings indicate that resting HF‐HRV and RMMSD are fairly stable indices of RSA over a period of 1.5 years, on average, among adults with and without a history of depression. [ABSTRACT FROM AUTHOR]

Depression has been associated with high blood pressure (BP). However, the mechanisms of the relation between depression and high BP are unclear. We therefore examined whether impaired cardiac vagal control, indexed as low levels of resting respiratory sinus arrhythmia (RSA), serves as a route from depression to high BP. The sample included 125 subjects with histories of depression (probands), 123 never depressed siblings of probands (high‐risk siblings), and 156 controls. Resting RSA was assessed at Time 1 (T1) along with BP when subjects were adolescents (Mage = 16.3 years); systolic and diastolic BP (SBP and DBP) were measured again at Time 2 (T2) when subjects were young adults (Mage = 22.3 years). Linear mixed‐effects models were used to examine the group differences in resting RSA and T2 BP outcomes and to test for RSA mediation of the relation between depression (history or being at high risk) and BP. Resting RSA was lower among probands than controls but was similar among high‐risk siblings and controls, while the subject groups did not differ in T2 SBP or DBP. Controlling for T1 BP, depression history indirectly affected T2 DBP (but not SBP) through resting RSA. The findings suggest that, although the direct detrimental effects of depression on BP are not yet evident in young adulthood, among those with depression histories, impaired cardiac vagal control appears to serve as a mechanism of elevated DBP. Depression is associated with hypertension but the mechanism of the association is unclear. Our study is the first to report that impaired cardiac vagal control is a pathway from depression history to hypertension. Therefore, screening for low respiratory sinus arrythmia may facilitate early identification of individuals at high risk for hypertension. [ABSTRACT FROM AUTHOR]

Experimental induction of sad mood states is a mainstay of laboratory research on affect and cognition, mood regulation, and mood disorders. Typically, the success of such mood manipulations is reported as a statistically significant pre- to post-induction change in the self-rated intensity of the target affect. The present commentary was motivated by an unexpected finding in one of our studies concerning the response rate to a well-validated sad mood induction. Using the customary statistical approach, we found a significant mean increase in self-rated sadness intensity with a moderate effect size, verifying the “success” of the mood induction. However, that “success” masked that, between one-fifth and about one-third of our samples (adolescents who had histories of childhood-onset major depressive disorder and healthy controls) reported absolutely no sadness in response to the mood induction procedure. We consider implications of our experience for emotion research by (1) commenting upon the typically overlooked phenomenon of nonresponse, (2) suggesting changes in reporting practices regarding mood induction success, and (3) outlining future directions to help scientists determine why some subjects do not respond to experimental mood induction. [ABSTRACT FROM AUTHOR]

The internalizing spectrum of psychiatric disorders-depression and anxiety-are common, highly comorbid, and challenging to treat. Individuals with childhood onset depression have a particularly poor prognosis. There is compelling evidence that individuals with depression display reduced resting-state EEG activity at sensors overlying the left prefrontal cortex, even during periods of remission, but it remains unknown whether this asymmetry is evident among individuals with a comorbid anxiety disorder. Here, we demonstrate that women with a history of childhood onset depression and no anxiety disorder ( n = 37) show reduced left lateral frontal activity compared to psychiatrically healthy controls ( n = 69). In contrast, women with a history of childhood onset depression and pathological levels of anxious apprehension ( n = 18)-as indexed by a current generalized anxiety disorder, obsessive compulsive disorder, or separation anxiety disorder diagnosis-were statistically indistinguishable from healthy controls. Collectively, these observations suggest that anxious apprehension can mask the relationship between prefrontal EEG asymmetry and depression. These findings have implications for understanding (a) prefrontal EEG asymmetry as a neurophysiological marker of depression, (b) the comorbidity of depression and anxiety, and (c) failures to replicate the relationship between prefrontal EEG asymmetry and depression. More broadly, they set the stage for developing refined interventions for internalizing psychopathology. [ABSTRACT FROM AUTHOR]

Background Adversity during early development has been shown to have enduring negative physiological consequences. In turn, atypical physiological functioning has been associated with maladaptive processing of negative affect, including its regulation. The present study therefore explored whether exposure to adverse life events in childhood predicted maladaptive (less flexible) parasympathetic nervous system functioning during the processing of negative affect among adolescents with depression histories. Methods An initially clinic-referred, pediatric sample ( N = 189) was assessed at two time points. At Time 1, when subjects were 10.17 years old ( SD = 1.42), on average, and were depressed, parents reported on adverse life events the offspring experienced up to that point. At Time 2, when subjects were 17.18 years old ( SD = 1.28), and were remitted from depression, parents again reported on adverse life events in their offspring's lives for the interim period. At time 2, subjects' parasympathetic nervous system functioning (quantified as respiratory sinus arrhythmia) also was assessed at rest, during sad mood induction, and during instructed mood repair. Results Extent of adverse life events experienced by T1 (but not events occurring between T1 and T2) predicted less flexible RSA functioning 7 years later during the processing of negative affect. Adolescents with more extensive early life adversities exhibited less vagal withdrawal following negative mood induction and tended to show less physiological recovery following mood repair. Conclusions Early adversities appear to be associated with less flexible physiological regulatory control during negative affect experience, when measured later in development. Stress-related autonomic dysfunction in vulnerable youths may contribute to the unfavorable clinical prognosis associated with juvenile-onset depression. [ABSTRACT FROM AUTHOR]

Background Impaired emotion regulation is increasingly recognized as a core feature of depressive disorders. Indeed, currently and previously depressed adults both report greater problems in attenuating sadness (mood repair) in daily life than healthy controls. In contrast, studies of various strategies to attenuate sad affect have mostly found that currently or previously depressed adults and controls were similarly successful at mood repair in the laboratory. But few studies have examined mood repair among depression-prone youths or the effects of trait characteristics on mood repair outcomes in the laboratory. Methods Adolescents, whose first episode of major depressive disorder ( MDD) had onset at age 9, on average (probands), and were either in remission or depressed, and control peers, watched a sad film clip. Then, they were instructed to engage in refocusing attention (distraction) or recalling happy memories. Using affect ratings provided by the youths, we tested two developmentally informed hypotheses about whether the subject groups would be similarly able to attenuate sadness via the two mood repair strategies. We also explored if self-reported habitual (trait) mood repair influenced laboratory performance. Results Contrary to expectations, attention refocusing and recall of happy memories led to comparable mood benefits across subjects. Control adolescents reported significantly greater reductions in sadness than did depressed (Cohen's d = .48) or remitted (Cohen's d = .32) probands, regardless of mood repair strategy, while currently depressed probands remained the saddest after mood repair. Habitual mood repair styles moderated the effects of instructed (state) mood repair in the laboratory. Conclusions Whether depressed or in remission, adolescents with MDD histories are not as efficient at mood repair in the laboratory as controls. But proband-control group differences in mood repair outcomes were modest in scope, suggesting that the abilities that subserve affect regulation have been preserved in probands to some degree. Further information about the nature of mood repair problems among youths with depression histories would help to better understand the clinical course of MDD and to design personalized interventions for depression. [ABSTRACT FROM AUTHOR]

Background: By emphasizing the importance of emotions, the 'affect revolution' in how human behavior is conceptualized has inspired a new generation of studies on dysphoric experience and its regulation in clinical depression, and novel efforts to characterize the precursors of affective disorders in juveniles at familial risk for depression. Method: We review clinical, behavioral, and functional neuroimaging studies of dysphoric experience and its regulation in depressed children and adolescents, and in juvenile offspring of parents with histories of clinical depression. We discuss the implication of the literature in the context of maternal depression. Results: Findings confirm the high rate of clinically significant dysphoria in depressed children and adolescents and reveal notable affective lability in daily life as a function of context and activity. Findings also show that depressed youngsters have problems in attenuating dysphoria. Similarly, never-depressed offspring at familial risk for depression display problems in mood repair and impaired mood repair mechanisms. Brain neuroimaging findings indicate that, overall, depressed, and high-risk youngsters differ from never depressed controls in neural functioning (activation, connectivity) both at rest and in response to emotion triggers. Conclusion: The evaluation of depressed youngsters should include questions about reactivity of dysphoric mood to the changing contexts of daily life and about how they manage (respond to) their own sadness and distress. The resultant information may help the clinician to restructure a young patient's day for the better and identify helpful mood repair responses. Evidence of impaired mood repair mechanisms in youngsters at high-risk for depression suggests the need for early intervention. But interventions must consider that many depressed and high-risk children have depressed mothers, who may be constrained in their ability to help offspring's emotion regulation efforts. To optimize treatment response of offspring, mothers of depressed children should therefore be routinely screened for depression and treated, as warranted. [ABSTRACT FROM AUTHOR]

Background: Offspring of depressed parents are at greatly increased risk for mood disorders. Among potential mechanisms of risk, recent studies have focused on information processing anomalies, such as attention and memory biases, in the offspring of depressed parents. In this study we examined another information processing domain, perceptual sensitivity to emotion cues in facial expressions, as a potential mechanism of risk that characterizes the offspring of depressed parents. Methods: The study included 64 children at familial-risk for depression and 40 low-risk peers between the ages 7 and 13(Mage = 9.51; SD = 2.27). Participants were presented with pictures of facial expressions that varied in emotional intensity from neutral to full-intensity sadness or anger (i.e., emotion recognition), or pictures of faces morphing from anger to sadness (emotion discrimination). After each picture was presented, children indicated whether the face showed a specific emotion (i.e., sadness, anger) or no emotion at all (neutral) using a forced choice paradigm. We examined group differences in the intensity of emotion that suggested greater sensitivity to specific emotions. Results: In the emotion recognition task, boys (but not girls) at familial-risk for depression identified sadness at significantly lower levels of emotional intensity than did their low-risk peers. The high and low-risk groups did not differ with regard to identification of anger. In the emotion discrimination task, both groups displayed over-identification of sadness in ambiguous mixed faces but high-risk youth were less likely to show this labeling bias than their peers. Conclusion: Our findings are consistent with the hypothesis that enhanced perceptual sensitivity to subtle traces of sadness in facial expressions may be a potential mechanism of risk among boys at familial-risk for depression. This enhanced perceptual sensitivity does not appear to be due to biases in the labeling of ambiguous faces. [ABSTRACT FROM AUTHOR]

Compromised respiratory sinus arrhythmia (RSA, i.e., low cardiac vagal control) frequently characterizes clinically depressed adults and also has been detected in infants of depressed mothers; however, its existence has not been established in older at-risk offspring. We investigated developmental patterns of RSA in a sample of 163 5- to 14-year-old children, who were either at high risk for depression (due to having a parent with a childhood-onset mood disorder) or low-risk for depression. We hypothesized that high-risk children have lower resting RSA than do low-risk children, which could reflect atypical developmental trajectories. Children's RSA was assessed during resting baseline periods on multiple occasions, typically 1-year apart. Linear growth modeling indicated a group by age interaction. Low-risk children (but not the high-risk children) exhibited a significantly increasing trajectory in resting RSA with age. Mood disorders in offspring did not account for the Group X Age interaction effect. Our study provides new evidence that children at high risk for depression have an atypical developmental trajectory of RSA across late childhood. © 2011 Wiley Periodicals,Inc. Dev Psychobiol 54: 556-567, 2012. [ABSTRACT FROM AUTHOR]

Background: Given the long-term morbidity of juvenile-onset major depressive disorder (MDD), it is timely to consider whether more effort should be dedicated to its primary and secondary prevention. Methods: We reviewed studies of prodromal symptoms that may herald a first episode pediatric MDD and considered whether that literature has made an impact on secondary prevention (efforts to prevent progression from symptoms to full disorder). We also reviewed studies of children at familial risk for MDD that addressed atypical affectivity and the regulation of sad, dysphoric affect (mood repair) and related physiological systems, and considered whether research in those areas has made an impact on primary prevention of pediatric MDD (efforts to prevent the disorder). Results: A compelling body of literature indicates that depressive symptoms in youngsters predict subsequent MDD across the juvenile (and early adult) years and that any combination of several symptoms for at least one week is informative in that regard. These findings are echoed in the case selection criteria used by many secondary prevention programs. Convergent findings also indicate that (compared to typical peers) young offspring at familial risk for depression manifest low positive affectivity and compromised mood repair, along with signs of dysfunction in three intertwined physiological systems that contribute to affectivity and mood repair (the hypothalamic–pituitary–adrenal (HPA) axis, cerebral hemispheric asymmetry, and cardiac vagal control). While all these affect-related parameters are suitable for case selection and as intervention targets, they have not yet made an impact on primary prevention programs. Conclusions: According to recent meta-analyses, attempts to prevent pediatric depression have not lived up to expectations. Based on our review, possible reasons for this include: (a) the use of case selection criteria that yield samples heterogeneous with regard to whether the symptoms are truly prodromal to an episode of MDD or are trait-like (which could affect response to the intervention), (b) failure to fully capitalize on the broad-ranging literature on vulnerability to pediatric MDD, as evidenced by the infrequent use of family history of depression (a robust index of vulnerability) or combined indices of vulnerability for case selection, and (c) lack of synchrony between dimensions of vulnerability and the content of the prevention program, as indicated by the overwhelming use of cognitive-behavioral interventions, irrespective of subjects’ age, developmental readiness, and whether or not they evidenced the relevant cognitive vulnerability. Prevention trials of pediatric MDD could benefit from new approaches to case selection that combine various indices of vulnerability, more effective use of existing findings, and new or modified interventions that are developmentally sensitive. [ABSTRACT FROM AUTHOR]

Studies in both animals and humans advocate a role for the vasopressin (AVP) system in the aetiology of depressive symptoms. Attention has particularly focused on the role of AVP in the overactivation of the hypothalamic-pituitary-adrenal (HPA)-axis in mood disorders. Elevated AVP plasma levels have been found in mood disorder patients, which are often positively correlated with the severity of symptoms. We recently reported an association between childhood-onset mood disorders (COMD) and polymorphisms in the receptor responsible for the AVP-mediated activation of the HPA-axis ( AVPR1B). As genetic variation in the vasopressinergic system could provide a mechanism to explain the endocrine alterations observed in mood disorders, we investigated other genes in this system. The gene encoding AVP is the strongest candidate, particularly as genetic variation in this gene in rodents is associated with anxiety-related behaviours. Six single-nucleotide polymorphisms (SNPs) were genotyped across the AVP gene in a sample comprised of 586 Hungarian nuclear families ascertained through affected probands with a diagnosis of COMD. In addition, AVP coding and putative regulatory regions were screened for mutations using denaturing high-performance liquid chromatography. One SNP, 3′ to the AVP, gene reached significance ( P = 0.03), as did the overtransmission of a five-marker haplotype with a frequency of 22% ( P = 0.0001). The subsequent mutation screen failed to identify any putative functional polymorphisms. The outcome of this study, combined with our previous association between COMD and AVPR1B, implicates genetic variation in vasopressinergic genes in mediating vulnerability to COMD. [ABSTRACT FROM AUTHOR]

Summary: Research findings on the hypothalamic–pituitary–adrenal (HPA) axis and pediatric depression reflect a variety of methodological approaches that tap different facets of HPA-axis functions. Partly owing to the methodological heterogeneity of studies, descriptive reviews of this area have produced inconsistent conclusions. Therefore, we conducted formal meta-analyses of pertinent studies in order to advance our understanding of HPA-axis dysregulation in pediatric depression. We examined: (a) 17 published studies of HPA-axis response to the dexamethasone suppression test (DST) in depressed youth (DST; N =926) and (b) 17 studies of basal HPA-axis functioning (N =1332). We also examined descriptively studies that used corticotropin-releasing hormone (CRH) infusion, and those that used psychological probes of the HPA-axis. The global standardized mean effect size difference in HPA-axis response to the DST between depressed and non-depressed youth was 0.57, z =4.18, p <0.01. The global standardized mean difference effect size in basal HPA-axis functioning was 0.20, z =4.53, p <0.01. Age, sex, timing of sampling, dexamethasone dosage, or type of control group was not a significant source of variability for the DST or basal studies. In addition, when compared to non-depressed peers, depressed youth have a normative response to CRH infusion but an overactive response to psychological stressors. In conclusion, the HPA-axis system tends to be dysregulated in depressed youth, as evidenced by atypical responses to the DST, higher baseline cortisol values, and an overactive response to psychological stressors. This pattern of dysregulation suggests anomalies within the axis''s negative feedback system and CRH production, but intact pituitary and adrenal sensitivity. [Copyright &y& Elsevier]

Clinical depression is a significant mental health problem that is associated with personal suffering and impaired functioning. These effects underscore the continuing need for new approaches that can inform researchers and clinicians when designing interventions. The present article proposes that individual differences in the self-regulation of sadness and distress provide an important link between stress, depressed mood, and the onset of depressive disorder, and that a better understanding of the ways children successfully manage dysphoric emotions will lead to improved prevention and treatment of pediatric depression. After examining the normative development of responses that children use to attenuate sadness, aspects of the neurobiological infrastructure that both enable and constrain such self-regulatory efforts, and affect regulation of children at familial risk for depressive disorders, this article concludes by calling for integrated, developmental, multidisciplinary studies of sadness self-regulation. [ABSTRACT FROM AUTHOR]

We investigated the relationship of the gene for the X-linked orphan G protein-coupled receptor (GPR50) to childhood-onset mood disorders in a sample of 384 families with 468 affected children and adolescents collected in Hungary. Our choice of this gene for study was based on a previous report of an association of GPR50 with bipolar disorder and major depressive disorder. A significant association with the deletion allele of an insertion/deletion polymorphism (Δ502-505) located in exon 2 had been reported in a sample of 226 patients with major depressive disorder and 264 patients with bipolar disorder. The association was more significant in females compared with males in those samples. We used for this study a polymorphism in complete linkage disequilibrium with the Δ502-505 polymorphism, Thr532Ala (rs561077), and two additional polymorphisms, Val606Ile (rs13440581) and an intronic polymorphism (rs2072621). We found no evidence for an association for the markers analyzed individually, nor for haplotypes of these markers. Further, we found no evidence of association when the results were analyzed in girls only (n=215). We, therefore, failed to replicate the previous association of this gene with mood disorders. [ABSTRACT FROM AUTHOR]

Background: Although it is well documented that teenage girls are at increased risk for depression, little is known about the importance of sex and development subsequent to onset of depression. In this article, we therefore report on sex differences in the developmental phenomenology of depression in a clinical sample.Methods: Longitudinal analyses were used to examine changes in the risk of depression, patterns of comorbid diagnoses, and depressive symptoms from ages 8-13 years up to young adulthood (age 21) among 87 patients.Results: Girls and boys were at similar risk for recurrent depression during follow-up. As girls got older, they had higher rates of comorbid eating disorders and lower rates of externalizing and substance use disorders than did boys; high risk periods for comorbid conditions also differed by sex. Comorbid disorders were usually contemporaneous with depression among girls but not among boys, and comorbidity patterns were influenced by age at depression onset. Girls with earlier (compared to later) onset depression were at lower risk for nonaffective disorders; boys evidenced the opposite pattern and were at particularly high risk for substance use disorders. There also were sex differences in developmental symptom patterns.Limitations: Results based on this initially clinically referred sample may not generalize to youths in other settings.Conclusions: Among depressed youths, sex-associated developmental trajectories in comorbid disorders and depressive symptoms have implications for intervention. Such information may help identify optimal timing of efforts to reduce the risk of or to treat comorbid disorders, and help select developmentally appropriate target symptoms for girls versus boys. [ABSTRACT FROM AUTHOR]

To convey an impressionistic landscape of depressive disorders in childhood, studies of clinically referred and diagnosed patients as well us community samples, and data from experimental investigations are used to consider five questions: Are depressive syndromes morbid slates in childhood? Should we be concerned a should depression in childhood? How do very early-onset depressions arise? What happens lo depressed children as they grow up and how can we help youngsters who suffer from depression? The information is discussed with respect to this implications for the management of clinically depressed children, as well as the prevention of very early-onset depressive disorders. [ABSTRACT FROM AUTHOR]

Suicidal thoughts and behaviors (STBs) have been associated with emotion dysregulation and atypical responses to affective and stressful stimuli. To investigate the psychophysiology involved, we measured changes in respiratory sinus arrhythmia (RSA) and cardiac pre‐ejection period (PEP; indexing parasympathetic and sympathetic functioning, respectively) in response to stressful‐ and sadness‐eliciting laboratory probes. Our sample included adolescents with a history of depression and STBs (n = 177), adolescents with a history of depression but no history of STBs (n = 47), and healthy controls (n = 175). The outcome of interest was the most severe form of clinician‐rated STBs across the subject's lifetime. In partial support of our hypotheses, during the stressful task, adolescents with a history of depression and STBs did not evidence the RSA decrease that was exhibited by controls and displayed greater PEP shortening compared to ever‐depressed adolescents with no lifetime STBs. No group differences were found in either RSA or PEP reactivity to the sadness‐eliciting stimulus. As expected, severity of STBs was positively correlated with the extent of PEP shortening during the stressful task. The results suggest that adolescents with a history of depression and STBs experience blunted parasympathetic responses to stress along with compensatory efforts. Our findings contribute to a better understanding of STBs among youths and underscore that future studies should examine physiological risk factors for these psychopathological outcomes. We investigated autonomic correlates of lifetime suicidal thoughts and behaviors (STBs) and addressed the spectrum of STBs (including the forms of STBs that have been generally ignored by researchers in this area). This study contributes to the relatively scant literature on physiological markers of STBs and is the first to report that sympathetic activity indexes severity of lifetime STBs. Our findings may help strengthen efforts at early identification and possible prevention of STBs. [ABSTRACT FROM AUTHOR]

Major depressive disorder is often associated with worsened reward learning, with blunted reward response persisting after remission. In this study, we developed a probabilistic learning task with social rewards as a learning signal. We examined the impacts of depression on social rewards (facial affect displays) as an implicit learning signal. Fifty-seven participants without a history of depression and sixty-two participants with a history of depression (current or remitted) completed a structured clinical interview and an implicit learning task with social reward. Participants underwent an open-ended interview to evaluate whether they knew the rule consciously. Linear mixed effects models revealed that participants without a history of depression learned faster and showed a stronger preference towards the positive than the negative stimulus when compared to the participants with a history of depression. In contrast, those with a history depression learned slower on average and displayed greater variability in stimulus preference. We did not detect any differences in learning between those with current and remitted depression. The results indicate that on a probabilistic social reward task, people with a history of depression exhibit slower reward learning and greater variability in their learning behavior. Improving our understanding of alterations in social reward learning and their associations with depression and anhedonia may help to develop translatable psychotherapeutic approaches for modification of maladaptive emotion regulation. Depression is often associated with social and emotional impairments, such as feeling disconnected from others and social withdrawal. In this study, we examine if history of depression is associated with the ability to learn from socially rewarding stimuli – a phenomena that may, in part, explain the underlying causes of social and emotional impairments in depression. [ABSTRACT FROM AUTHOR]

Depression is associated with protracted despondent mood, blunted emotional reactivity, and dysregu-lated parasympathetic nervous system (PNS) activity. PNS activity is commonly indexed via cardiac output, using indictors of its level (resting respiratory sinus arrhythmia [RSA]) or fluctuations (RSA reactivity). RSA reactivity can reflect increased or decreased PNS cardiac output (RSA augmentation and RSA withdrawal, respectively). Because a single index of a dynamic physiological system may be inadequate to characterize interindividual differences, we investigated whether the interaction of RSA reactivity and resting RSA is a better predictor of depression. Adult probands with childhood-onset depressive disorder histories (n = 113) and controls with no history of major mental disorders (n = 93) completed a psychophysiology protocol involving assessment of RSA at multiple rest periods and while watching a sad film. When examined independently, resting RSA and RSA reactivity were unrelated to depression, but their interaction predicted latent depression levels and proband status. In the context of high resting RSA, RSA withdrawal from the sad film predicted the lowest levels of depressive symptoms (irrespective of depression histories) and the greatest likelihood of having had no history of major mental disorder (irrespective of current distress). Our findings highlight the utility of combining indices of physiological responses in studying depression; combinations of RSA indices should be given future consideration as reflecting depression endophenotypes. [ABSTRACT FROM AUTHOR]

Abstract: Background: There is limited information on the characteristics of stressful life events in depressed pediatric clinical populations and the extent to which sex, age, and their interactions may influence the relations of life events and depression. Using a very large clinical sample of children and adolescents with major depressive disorder (MDD), we therefore examined life events in various ways, as well as their relations to age and sex. Methods: The study included a clinic-based sample of 434 children (ages 7–14) with a DSM-IV diagnosis of MDD and their mothers, and a school-based comparison sample of 724 children and their mothers. Life event information was obtained from the mothers. Results: Children with MDD had twice the number of lifetime stressful events than did the comparison group, with very high levels of stressors by the age of 7–9 that stabilized across adolescence. In contrast, the comparison sample experienced a gradual increase in stressful life events as a function of age up to mid-adolescence. Parental health events, death of close relatives, and intrafamilial events were significantly associated with MDD diagnosis. There were significantly stronger associations between parental health- as well as death-event clusters and MDD diagnosis among younger children than adolescents. Limitations: Geographical differences between the clinical and comparison samples, as well as possible parental reporting biases may affect the generalizability of these findings. Conclusion: The association between some stressful life events and MDD seems to be moderated by age, underscoring the need to examine specific events, as well as clusters of events. Better understanding of such interactions may facilitate early identification of possible risk factors for pediatric MDD. [Copyright &y& Elsevier]

Depressive disorders that onset in the juvenile years have been linked to far-reaching adverse consequences, making it imperative to elucidate key mechanisms and contributory factors. Excessive use of regulatory responses that exacerbate sadness (maladaptive mood repair) or insufficient use of regulatory responses that reduce it (adaptive mood repair) may reflect behavioral mechanisms of depression risk. Cardiac vagal control, indexed by patterns of respiratory sinus arrhythmia (RSA), has received attention as a putative physiological risk factor for depression. Although mood repair and RSA are related, the nature of this relationship is not well characterized in the context of depression risk. Therefore, we tested alternative models of the relationships between RSA patterns (at rest and in response to a sad film), trait mood repair, and the effectiveness of a mood repair response in the laboratory (state mood repair) among adolescents with depression histories (n = 210) and emotionally healthy peers (n = 161). In our data, a mediation model best explained the association between the key constructs: Adolescents with normative RSA patterns exhibited lower levels of depression and trait maladaptive mood repair, and benefited more from instructed (state) mood repair in the laboratory. By contrast, adolescents with atypical RSA patterns exhibited higher levels of depression and dispositional maladaptive mood repair, which, in turn, mediated the relations of RSA patterns and depression symptoms. Atypical RSA patterns also predicted reduced benefits from laboratory mood repair. [ABSTRACT FROM AUTHOR]

Abstract: We investigated the test–retest stability of resting EEG asymmetry and power in the alpha frequency range across a 0.6- to 3-year interval in 125 children (57 girls and 68 boys) for two age groups, 87 preschool children (3 to 5 year-olds) and 38 school-age children (6 to 9 year-olds). Children were from families with a parent''s history of unipolar or bipolar depression (36 girls and 43 boys) or control families with no parent history of depression nor any other psychiatric disorder (21 girls and 25 boys). Frontal EEG asymmetry stability was low to moderate; intraclass correlations ranged from zero to 0.48 in the eyes-open condition, and from 0.19 to 0.45 in the eyes-closed condition. Also, parietal EEG asymmetry was low to moderate; intraclass correlations ranged from 0.21 to 0.52 in the eyes-open condition and from 0.27 to 0.72 in the eyes-closed condition. Stability of EEG asymmetry was not related to age, sex of the child, or parent''s history of mood disorder. Frontal and parietal EEG power appeared moderately to highly stable. Intraclass correlations were between 0.65 and 0.86 in the eyes-open condition and between 0.52 and 0.90 in the eyes-closed condition. Although stability of EEG power was not statistical significantly different between preschool and school-age children, it consistently showed higher stability values in school-age children than in preschool children. Stability in school-age children approached values as has been reported for adults. The findings provide partial support to the concept of frontal EEG asymmetry as a trait marker in childhood. [Copyright &y& Elsevier]

Abstract: Objective: We investigate the relations of early atypical characteristics (perinatal problems, developmental delay, and difficult temperament) and onset-age (as well as severity of) first major depressive disorder (MDD) and first internalizing disorder in a clinical sample of depressed children in Hungary. Method: Participants were 371 children (ages 7–14) with MDD, and their biological mothers, recruited through multiple clinical sites. Diagnoses (via DSM-IV criteria) and onset dates of disorders were finalized “best estimate” psychiatrists, and based on multiple information sources. Mothers provided developmental data in a structured interview. Results: Difficult temperament predicted earlier onset of MDD and first internalizing disorder, but its effect was ameliorated if the family was intact during early childhood. Further, the importance of difficult temperament decreased as a function of time. Perinatal problems and developmental delay did not impact onset ages of disorders, and none of the early childhood characteristics associated with MDD episode severity. Conclusions: Children with MDD may have added disadvantage of earlier onset if they had a difficult temperament in infancy. Because early temperament mirrors physiological reactivity and regulatory capacity, it can affect various areas of functioning related to psychopathology. Early caregiver stability may attenuate some adverse effects of difficult infant temperament. [Copyright &y& Elsevier]

Abstract: Psychophysiological responses during affect regulation were examined in 57 children ages 3–9 years, 41 of whom had a parent history of childhood-onset depression (COD). During a structured laboratory task, children were given first a disappointing toy and then a desired toy. Frontal electroencephalogram (EEG) asymmetry, respiratory sinus arrhythmia (RSA), heart period, and heart period variability were measured during resting and task conditions. Affective and self-regulatory behaviors were coded from videotape. In 3–5-year olds, greater relative right frontal activity was associated with withdrawal behavior. High heart period was associated with approach behavior. Compared with children of psychiatrically healthy parents, children of parents with COD exhibited poor heart period recovery after disappointment. For children of parents with COD, greater relative left frontal activity was related to concurrent internalizing and externalizing problems, and low resting RSA was related to internalizing problems. Physiological responses associated with affect regulation may help identify children at risk for depression. [Copyright &y& Elsevier]

Abstract: We investigated the stability in resting EEG across a 1- to 3-year interval in 49 adults (33 female and 16 male) with a history of unipolar depression (first onset prior to the age of 14) and 50 controls (33 female and 17 male) with no history of major psychopathology. Current depressive symptoms were quantified by self-report at both assessments. For the entire sample, EEG asymmetry in the alpha range was moderately stable (intraclass correlations between 0.39 and 0.61). Sex, history of depression, depressive symptom severity at Time 2, and change in symptom severity between Time 1 and Time 2 were unrelated to stability of EEG asymmetry. These findings support the view that resting frontal EEG asymmetry reflects a moderately stable individual difference in adults, irrespective of sex and history of depression. [Copyright &y& Elsevier]

Abstract: To study affect regulation in adults with unipolar (n=38) and bipolar (n=38) forms of childhood-onset depression (COD), as compared with adults with no history of psychiatric illness (n=60), we examined affective modulation of the startle eyeblink reflex. Participants were subjected to binaural bursts of white noise while viewing pictures designed to elicit pleasant, neutral, or unpleasant affective states. The blink response was recorded from surface electrodes over the orbicularis oculi muscle during and following pictures. Participants rated the valence and arousal of their responses. Unlike control or bipolar groups, the unipolar group displayed a greater startle during the neutral condition than during the pleasant condition, and failed to display an increase in startle during the unpleasant condition. The bipolar group, unlike the unipolar and control groups, displayed a similar startle response after pleasant and unpleasant pictures. Participants with a high number of lifetime depressive episodes displayed a blunted startle response across affective conditions. Groups reported similar subjective responses to affective stimuli. Current affective symptoms and comorbid diagnoses did not influence startle modulation. In unipolar and bipolar forms of COD, unusual affective modulation or maintenance of the startle response, respectively, may reflect underlying deficits in affect regulation. [Copyright &y& Elsevier]