Katie L. Burkhouse

Pupillary reactivity to emotional stimuli in children of depressed and anxious mothers

BACKGROUND The primary aim of this study was to examine differences in physiological reactivity (measured via pupillometry) to emotional stimuli between children of depressed versus nondepressed mothers. A second goal was to examine differences in pupil dilation to emotional stimuli between children of anxious versus nonanxious mothers. METHOD Participants included 117 mother-child pairs drawn from the community. Children were between the ages of 8 and 14. Pupil dilation was assessed using an eye-tracker while participants viewed angry, happy, or sad faces. RESULTS Children of mothers with a history of major depression (MDD) exhibited increased pupil dilation to sad, but not happy or angry, faces compared with children of nondepressed mothers. Second, we found that children of anxious mothers exhibited increased pupil dilation to angry, but not happy or sad, faces compared to youth of nonanxious mothers. CONCLUSIONS The current findings add to the growing body of research suggesting that differences in physiological reactivity to depression- and anxiety-relevant cues may represent an important mechanism in the intergenerational transmission of MDD and anxiety.

Expressed Emotion-Criticism and Risk of Depression Onset in Children

The primary goal of the current study was to examine the impact of maternal criticism (expressed emotion-criticism; EE-Crit) on the prospective development of depressive episodes in children. In addition to examining baseline levels of EE-Crit, we also sought to determine whether distinct subgroups (latent classes) of mothers could be identified based on the levels of EE-Crit they exhibited over a multiwave assessment and whether that latent class membership would predict depression onset in children. Finally, we examined whether EE-Crit and maternal depression would independently predict childrens depression risk or whether EE-Crit would moderate the link between maternal depression and childrens depression onset. Children of mothers with or without a history of major depression (N = 100) were assessed 5 times over 20 months. Children completed the Childrens Depression Inventory and mothers completed the Five Minute Speech Sample and the Beck Depression Inventory at the baseline assessment, and at 2-, 4-, and 6-month follow-up assessments. Children and mothers completed diagnostic interviews assessing childrens onsets of depressive episodes at the 20-month follow-up. Latent class analysis of the 4 waves of EE-Crit assessments revealed two distinct groups, exhibiting relatively lower versus higher levels of EE-Crit across the first 6 months of follow-up. EE-Crit latent class membership predicted childrens depression onset over the subsequent 14 months. This finding was maintained after controlling for mothers and childrens depressive symptoms during the initial 6 months of follow-up. Finally, maternal depression did not moderate the link between EE-Crit and childhood depression onset. Continued exposure to maternal criticism appears to be an important risk factor for depression in children, risk that is at least partially independent of the risk conveyed by maternal depression. These results highlight the importance of a modifiable risk factor for depression—repeated exposure to maternal criticism.

Serotonin Transporter Genotype Moderates the Link Between Children’s Reports of Overprotective Parenting and Their Behavioral Inhibition

The goal of the current study was to examine environmental and genetic correlates of children’s levels of behavioral inhibition (BI). Participants were 100 mother child pairs drawn from the community who were part of a larger study of the intergenerational transmission of depression. Results indicated that higher levels of maternal overprotection, as reported by the child, were associated with elevations in BI among children carrying two copies of the lower expressing 5-HTTLPR alleles (S or LG), but not among those carrying only one copy or those homozygous for the LA allele. In addition, this interaction was specific for the social component of BI, not the nonsocial component. This relation was maintained even after statistically controlling for children’s and mother’s psychopathology. Together, these findings add to emerging research demonstrating that G × E interactions predict variation in BI during childhood.

Brooding rumination and cardiovascular reactivity to a laboratory-based interpersonal stressor.

There is a well-known link between stress and depression, but diathesis-stress models suggest that not all individuals are equally susceptible to stress. The current study examined if brooding rumination, a known risk factor for depression, influences cardiovascular reactivity to a laboratory-based interpersonal stressor. Sixty-five women watched a baseline video and were exposed to an interpersonal stressor while high frequency heart rate variability (HRV) was collected. We found that women who endorsed higher levels of brooding rumination exhibited greater HRV withdrawal from baseline to stressor, an effect that was maintained when we controlled for levels of depression. This physiological vulnerability, when combined with high levels of stress, may be one mechanism underlying how brooding rumination increases depression risk.

NEURAL REACTIVITY TO REWARD AS A PREDICTOR OF COGNITIVE BEHAVIORAL THERAPY RESPONSE IN ANXIETY AND DEPRESSION

Cognitive behavioral therapy (CBT) is a well‐established treatment for anxiety and depression; however, response to CBT is heterogeneous across patients and many remain symptomatic after therapy, raising the need to identify prospective predictors for treatment planning. Altered neural processing of reward has been implicated in both depression and anxiety, and improving hedonic capacity is a goal of CBT. However, little is known about how neural response to reward relates to CBT outcomes in depression and anxiety. The current study used the reward positivity (RewP) event‐related potential (ERP) component to examine whether neural reactivity to reward would predict CBT response in a sample of patients with anxiety without depression (n = 30) and comorbid anxiety and depression (CAD, n = 22).

Aberrant resting-state functional connectivity in limbic and cognitive control networks relates to depressive rumination and mindfulness: A pilot study among adolescents with a history of depression

BACKGROUND Resting state functional connectivity (RSFC) research among adults indicates abnormalities within and between neural networks during acute depressive episodes, some of which are likely to remain into remission. The examination of RSFC among adolescents within the remitted state of MDD may implicate markers of illness course during a critical developmental window wherein secondary prevention can be implemented. METHODS RSFC data were collected on a 3.0T GE scanner from adolescents (12-18, M=15.61, SD=1.90; 57% female) in full or partial remission from MDD (rMDD; n=23) and age- and gender-matched healthy controls (HC; n=10). RSFC data were examined using seed-based connectivity of the left amygdala, left dorsolateral prefrontal cortex (dlPFC), and left posterior cingulate cortex (PCC). These seeds were chosen to probe the emotional salience, cognitive control, and default mode networks, respectively. RESULTS rMDD adolescents demonstrated relative hyperconnectivity from the left amygdala to the right PCC, as well as from the left dlPFC to the right middle frontal and left inferior frontal gyri (MFG, IFG). Amygdala to PCC connectivity was correlated with greater rumination, dlPFC to MFG connectivity was positively associated with depression severity, and dlPFC to IFG connectivity was inversely associated with mindfulness. CONCLUSIONS Aberrant functional connectivity within and between neural networks responsible for salience attribution, introspective thought, and executive control can be observed among adolescents in the remitted phase of MDD and is associated with residual clinical symptoms. These patterns may confer risk for future relapse or alternatively, support wellness.

Eye tracking indices of attentional bias in children of depressed mothers: Polygenic influences help to clarify previous mixed findings

Information-processing biases may contribute to the intergenerational transmission of depression. There is growing evidence that children of depressed mothers exhibit attentional biases for sad faces. However, findings are mixed as to whether this bias reflects preferential attention toward, versus attentional avoidance of, sad faces, suggesting the presence of unmeasured moderators. To address these mixed findings, we focused on the potential moderating role of genes associated with hypothalamic-pituitary-adrenal axis reactivity. Participants included children (8-14 years old) of mothers with (n = 81) and without (n = 81) a history of depression. Eye movements were recorded while children passively viewed arrays of angry, happy, sad, and neutral faces. DNA was obtained from buccal cells. Children of depressed mothers exhibited more sustained attention to sad faces than did children of nondepressed mothers. However, it is important that this relation was moderated by childrens genotype. Specifically, children of depressed mothers who carried reactive genotypes across the corticotropin-releasing hormone type 1 receptor (CHRH1) TAT haplotype and FK506 binding protein 5 (FKBP5) rs1360780 (but not the solute carrier family C6 member 4 [SLC6A4] of the serotonin transporter linked polymorphic region [5-HTTLPR]) exhibited less sustained attention to sad faces and more sustained attention to happy faces. These findings highlight the role played by specific genetic influences and suggest that previous mixed findings may have been due to genetic heterogeneity across the samples.

Neural correlates of rumination in adolescents with remitted major depressive disorder and healthy controls

The aim of the present study was to use fMRI to examine the neural correlates of engaging in rumination among a sample of remitted depressed adolescents, a population at high risk for future depressive relapse. A rumination induction task was used to assess differences in the patterns of neural activation during rumination versus a distraction condition among 26 adolescents in remission from major depressive disorder (rMDD) and in 15 healthy control adolescents. Self-report depression and rumination, as well as clinician-rated depression, were also assessed among all participants. All of the participants recruited regions in the default mode network (DMN), including the posterior cingulate cortex, medial prefrontal cortex, inferior parietal lobe, and medial temporal gyrus, during rumination. Increased activation in these regions during rumination was correlated with increased self-report rumination and symptoms of depression across all participants. Adolescents with rMDD also exhibited greater activation in regions involved in visual, somatosensory, and emotion processing than did healthy peers. The present findings suggest that during ruminative thought, adolescents with rMDD are characterized by increased recruitment of regions within the DMN and in areas involved in visual, somatosensory, and emotion processing.

Vulnerability to Depression in Youth: Advances from Affective Neuroscience

Vulnerability models of depression posit that individual differences in trait-like vulnerabilities emerge early in life and increase risk for the later development of depression. In this review, we summarize advances from affective neuroscience using neural measures to assess vulnerabilities in youth at high risk for depression due to parental history of depression or temperament style, as well as prospective designs evaluating the predictive validity of these vulnerabilities for symptoms and diagnoses of depression across development. Evidence from multiple levels of analysis indicates that healthy youth at high risk for depression exhibit abnormalities in components of the Research Domain Criteria (RDoC) positive valence systems, including blunted activation in the striatum during reward anticipation and feedback, and that some of these measures can be used to predict later symptoms. In addition, alterations in components of RDoCs negative valence systems, including neural processing of sadness, loss, and threat, have been observed in risk for depression, though effects appear to be more task and method dependent. Within the social processes domain, preliminary evidence indicates that neural processing of social feedback, including heightened reactivity to exclusion and blunted response to social reward, may be related to depression vulnerability. These studies indicate that affective neuroscience can inform understanding of developmental pathways to depression and identify altered emotional processing among youth at high risk. We provide an integrated summary of consistent findings from this literature, along with recommendations for future directions and implications for early intervention.

Sensitivity in detecting facial displays of emotion: Impact of maternal depression and oxytocin receptor genotype

The current study examined sensitivity in detecting emotional faces among children of depressed and non-depressed mothers. A second goal was to examine the potential moderating role of the oxytocin receptor gene (OXTR rs53576), which has been linked to emotion recognition in the past. Participants included 247 children (ages 8–14). Children completed a forced choice emotion identification task. Maternal history of major depressive disorder during childrens lives was associated with childrens sensitivity in detecting emotional faces among children homozygous for the OXTR rs53576 G allele, but not among carriers of the A allele. Among G homozygotes, children of depressed mothers exhibited increased sensitivity in detecting sad faces, and reduced sensitivity in detecting happiness, compared to children of non-depressed mothers.