Research-Practice Partnership to Develop and Implement Routine Mental Health Symptom Tracking Tool Among Older Adults During COVID-19.

OBJECTIVE: Older adults are disproportionally impacted by the COVID-19 pandemic, causing a mental health crisis in late life, due to physical restrictions (e.g., quarantine), limited access to services, and lower literacy and access to technology. Despite established benefits, systematic screening of mental health needs of older adults in community and routine care settings is limited and presents multiple challenges. Cross-disciplinary collaborations are essential for identification and evaluation of mental health needs and service delivery. METHODS: Using a research-practice partnership model, we developed and implemented a routine mental health needs identification and tracking tool at a community-based social services organization. Repeated screenings were conducted remotely over 5 months and included depression, anxiety, perceived loneliness, social support, and related domains such as sleep quality, resilience, and trauma symptoms linked to COVID-19. We examined symptomatic distress levels and associations between different domains of functioning. RESULTS: Our project describes the process of establishing a research-practice partnership during the COVID-19 pandemic. We collected 292 screenings from 124 individuals; clients were mildly to moderately depressed and anxious, reporting large amounts of time alone and moderate levels of loneliness. Those reporting higher depressive symptoms reported higher anxiety symptoms, poorer sleep quality, lower quality of life, lower capacity to adapt to challenging situations, and greater trauma symptoms due to COVID-19. CONCLUSION: Our routine screening tool can serve as a blueprint for case management agencies and senior centers nationwide, beyond the pressing mental health crisis due to COVID-19, to continue identifying needs as they emerge in the community.

The impact of white matter hyperintensities on the structural connectome in late-life depression: Relationship to executive functions.

BACKGROUND: White matter hyperintensities (WMH) represent ischemic white matter damage in late-life depression (LLD) and are associated with cognitive control dysfunction. Understanding the impact of WMH on the structural connectivity of gray matter and the cognitive control correlates of WMH-related structural dysconnectivity can provide insight into the pathophysiology of LLD. METHODS: We compared WMH burden and performance on clinical measures of cognitive control in patients with LLD (N = 44) and a control group of non-depressed older adults (N = 59). We used the Network Modification (NeMo) Tool to investigate the impact of WMH on structural dysconnectivity in specific gray matter regions, and how such connectivity was related to cognitive control functions. RESULTS: Compared to the control group, LLD participants had greater WMH burden, poorer performance on Trail Making Test (TMT) A & B, and greater self-reported dysexecutive behavior on the Frosntal Systems Behavior Scale-Executive Function subscale (FrSBe-EF). Within the LLD group, disrupted connectivity in the left supramarginal gyrus, paracentral lobule, thalamus, and pallidum was associated with psychomotor slowing (TMT-A). Altered connectivity in the left supramarginal gyrus, paracentral lobule, precentral gyrus, postcentral gyrus, thalamus, and pallidum was associated with poor attentional set-shifting (TMT-B). A follow-up analysis that isolated set-shifting ability (TMT-B/A ratio) confirmed the association with dysconnectivity in the bilateral paracentral lobule, right thalamus, left precentral gyrus, postcentral gyrus, and pallidum; additionally, it revealed associations with dysconnectivity in the right posterior cingulate, and left anterior cingulate, middle frontal cortex, and putamen. CONCLUSIONS: In LLD, WMH are associated with region-specific disruptions in cortical and subcortical gray matter areas involved in attentional aspects of cognitive control systems and sensorimotor processing, which in turn are associated with slower processing speed, and reduced attentional set-shifting. CLINICAL TRIALS REGISTRATION: https://clinicaltrials.gov/ct2/show/NCT01728194.

Emergency department visits for depression in the United States from 2006 to 2014.

BACKGROUND: Patients with depression frequently seek care in the emergency department (ED), especially in the context of suicidal ideation (SI) and self-harm (SH). However, the prevalence and trends in the United States (US) of ED visits for depression have not yet been characterized using a nationally representative sample. This study evaluates ED trends for depression in the US from 2006 to 2014. METHODS: Data was obtained from the Nationwide Emergency Department Sample (NEDS) in 2006 and 2014 using a primary ICD-9 diagnosis of depression or a primary diagnosis of suicidal ideation (SI) and a secondary diagnosis of depression. RESULTS: Between 2006 and 2014, there was a 25.9% increase in visits to the ED for depression, which was higher than the 14.8% increase in total ED visits during this time period. The mean inflation adjusted charges associated with depression-related ED visits increased by 107.7%, which was higher than the increase in mean charges for all ED visits in the same time period (40.47%). Visit rates were bimodally distributed with respect to age, with peaks in adolescence and middle age. Notably there was a 61.3% increase in ED visits for depression in individuals younger than 20 between 2006 and 2014. Over half of patients were admitted for inpatient care with a mean length of stay of 5.6 days in both years. Inpatient charges increased 71.8% between 2006 and 2014. CONCLUSIONS: ED visits for depression in the United States rose 25.9% between 2006 and 2014, which was higher than the 14.8% increase in total ED visits during this time period. Over half of ED depression visits were admitted to inpatient stay (mean 5.6 days both years).

The negativity bias predicts response rate to Behavioral Activation for depression.

BACKGROUND AND OBJECTIVES: This treatment study investigated the extent to which asymmetric dimensions of affective responding, specifically the positivity offset and the negativity bias, at pretreatment altered the rate of response to Behavioral Activation treatment for depression. METHOD: Forty-one depressed participants were enrolled into 16 weekly sessions of BA. An additional 36 lifetime healthy participants were evaluated prospectively for 16 weeks to compare affective responding between healthy and remitted patients at post-treatment. All participants were assessed at Weeks 0, 8 and 16 using repeated measures, involving a structured clinical interview for DSM-IV Axis I disorders, questionnaires, and a computerized task designed to measure affective responses to unpleasant, neutral, and pleasant images. RESULTS: The negativity bias at pre-treatment predicted the rate of response to BA, while the positivity offset did not. LIMITATIONS: Only one treatment condition was used in this study and untreated depressed participants were not enrolled, limiting our ability to compare the effect of BA. CONCLUSIONS: Baseline negativity bias may serve as a signal for patients to engage in and benefit from the goal-directed BA strategies, thereby accelerating rate of response.

Twice the negativity bias and half the positivity offset: Evaluative responses to emotional information in depression.

BACKGROUND AND OBJECTIVES: Humans have the dual capacity to assign a slightly pleasant valence to neutral stimuli (the positivity offset) to encourage approach behaviors, as well as to assign a higher negative valence to unpleasant images relative to the positive valence to equally arousing and extreme pleasant images (the negativity bias) to facilitate defensive strategies. We conducted an experimental psychopathology study to examine the extent to which the negativity bias and the positivity offset differ in participants with and without major depression.. METHOD: Forty-one depressed and thirty-six healthy participants were evaluated using a structured clinical interview for DSM-IV Axis I disorders, questionnaires, and a computerized task designed to measure implicit affective responses to unpleasant, neutral, and pleasant stimuli. RESULTS: The negativity bias was significantly higher and the positivity offset was significantly lower in depressed relative to healthy participants.. LIMITATIONS: Entry criteria enrolling medication-free participants with minimal DSM-IV comorbidity may limit generalizability of the findings. CONCLUSIONS: This study advances our understanding of the positive and negative valence systems in depression, highlighting the irregularities in the positive valence system..

Differences in the neural correlates of affective responses in depressed and healthy women.

We aimed to characterize the extent to which there were differences in neural activation between female participants who were diagnosed with or without depression while viewing negative and neutral imagery. The study enrolled 105 medication-free, right-handed female participants between 17 and 63 years who met criteria for current Major Depressive Disorder (n=47) or no prior psychiatric diagnoses (n=58). All participants completed a clinical assessment and underwent a functional Magnetic Resonance Imaging (fMRI) scan while responding to an implicit affect task that required them to identify the location of ideographs embedded in one of four corners of each valenced image. When unpleasant (termed negative) stimuli were presented, depressed relative to healthy participants showed significantly decreased activation of the left amygdala and right Inferior Parietal Lobe (IPL). When activation was assessed during the negative versus neutral condition, depressed relative to healthy participants showed significantly increased activation in the Anterior Cingulate Cortex (ACC) and the left IPL. Notably, within-group analyses of healthy participants under the negative condition showed that depressive severity was positively correlated with activation in the left amygdala and left IPL. Our findings suggest that depression influences bottom-up and top-down processing of unpleasant information.

Affective information processing in pregnancy and postpartum with and without major depression.

Adults with clinical depression exhibit systematic errors in their recognition and interpretation of affective stimuli. This study investigated the extent to which depression and phases of pregnancy and postpartum influence affective processing of positive and negative information, and the extent to which affective information processing in pregnancy predicts depressive symptoms in postpartum. Data were collected from 80 unmedicated women, diagnosed with major depressive disorder (MDD) or with no psychiatric disorder and between ages 18 and 44 years, during 32-36 weeks of pregnancy and during 6-8 weeks postpartum. All completed a Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) Axis I review, symptom reports, and a computer task measuring affective information processing. Significant group differences were found in which postpartum women with major depression were less responsive to negative stimuli, with lower ratings of intensity and reactions to negative pictorial stimuli, compared with postpartum healthy women. Also, lower ratings of the intensity and reactions to negative stimuli during pregnancy among depressed women predicted postpartum depression severity, even after controlling for depressive severity and affect ratings in pregnancy. Blunted affective reactivity to negative stimuli is a characteristic of depression that was observed among depressed women during pregnancy and postpartum in our study.

Training-associated changes and stability of attention bias in youth: Implications for Attention Bias Modification Treatment for pediatric anxiety.

Attention Bias Modification Treatment (ABMT), an emerging treatment for anxiety disorders, is thought to modify underlying, stable patterns of attention. Therefore, ABMT research should take into account the impact of attention bias stability on attention training response, especially in pediatric populations. ABMT research typically relies on the dot-probe task, where individuals detect a probe following an emotional-neutral stimulus pair. The current research presents two dot-probe experiments relevant to ABMT and attention-bias stability. In Experiment 1, anxious youth receiving 8-weeks of cognitive-behavioral therapy (CBT) were randomly assigned to ABMT that trains attention towards happy faces (n=18) or placebo (n=18). Two additional comparison groups, anxious youth receiving only CBT (n=17) and healthy comparison youth (n=16), were studied. Active attention training towards happy faces did not augment clinician-rated response to CBT; however, individuals receiving training exhibited reductions on self-report measures of anxiety earlier than individuals receiving CBT only. In Experiment 2, healthy youth (n=12) completed a dot-probe task twice while undergoing functional magnetic resonance imaging. Intra-class correlation demonstrated stability of neural activation in response to attention bias in the ventrolateral prefrontal cortex and amygdala. Together, these two studies investigate the ways in which attention-bias stability may impact future work on ABMT.

Attention orientation in parents exposed to the 9/11 terrorist attacks and their children.

While trauma affects both parents and their children, minimal research examines the role of information-processing perturbations in shaping reactions to trauma experienced by parents and, in turn, the effect this trauma has on their children. This study examines familial associations among trauma, psychopathology, and attention bias. Specifically, group differences in psychopathology and attention bias were examined in both adults and their children based on trauma exposure. In addition, the association between attention bias in parents and attention bias in their children was examined. Parents exposed to the 9/11 World Trade Center attacks and their children were recruited from the New York City Metropolitan area. Levels of trauma exposure, psychiatric symptoms, and attention bias to threat, as measured with the dot-probe task, were each assessed in 90 subjects, comprising of 45 parents and one of their children. These measures were examined in parents and their children separately; each parent and child was categorized on the presence of high or low levels of trauma exposure. Although trauma exposure did not relate to psychopathology, parents who were highly exposed to trauma showed greater attention bias towards threat than parents with low trauma exposure. However, the children of high trauma-exposed parents did not show enhanced attention bias towards threat, though threat bias in the high trauma-exposed parents did negatively correlate with threat bias in their children. This association between trauma and attention bias in parents was found four-to-five years after 9/11, suggesting that trauma has enduring influences on threat processing. Larger, prospective studies might examine relationships within families among traumatic exposures, psychopathology, and information-processing functions.

Neural and behavioral responses to threatening emotion faces in children as a function of the short allele of the serotonin transporter gene.

Recent evidence suggests that a genetic polymorphism in the promoter region (5-HTTLPR) of the serotonin transporter gene (SLC6A4) mediates stress reactivity in adults. Little is known, however, about this gene-brain association in childhood and adolescence, generally conceptualized as a time of heightened stress reactivity. The present study examines the association between 5-HTTLPR allelic variation and responses to fearful and angry faces presented both sub- and supraliminally in participants, ages 9-17. Behaviorally, carriers of the 5-HTTLPR short (s) allele exhibited significantly greater attentional bias to subliminally presented fear faces than did their long (l)-allele homozygous counterparts. Moreover, s-allele carriers showed greater neural activations to fearful and angry faces than did l-allele homozygotes in various regions of association cortex previously linked to attention control in adults. These results indicate that in children and adolescents, s-allele carriers can be distinguished from l-allele homozygotes on the basis of hypervigilant behavioral and neural processing of negative material.

BDNF gene polymorphism (Val66Met) predicts amygdala and anterior hippocampus responses to emotional faces in anxious and depressed adolescents.

A polymorphism of the human Brain Derived Neurotrophic Factor (BDNF) gene that produces a valine-to-methionine substitution at codon 66 (Val66Met) is linked to adult anxiety and mood disorders, possibly through effects on brain circuitry function. Associations between BDNF gene variants and brain activity have not been explored in anxious and depressed adolescents. The current study investigated the association between BDNF genotype and amygdala-hippocampal responses to emotional stimuli in adolescents with anxiety disorders and/or major depressive disorder (MDD) and in healthy adolescents. Twenty-seven unmedicated patients with acutely-impairing current anxiety disorders and/or MDD and 31 healthy adolescents, matched on age, gender and IQ, rated their fear of fearful, angry, neutral and happy facial expressions during collection of fMRI data on the amygdala and hippocampus. Left and right amygdala and hippocampal responses were analyzed using repeated-measures analyses of variance models, with diagnosis (patients, healthy) and genotype (Met-carriers, Val/Val homozygotes) as between-group factors and facial expression (fearful, angry, neutral, happy) as a within-subject factor. Significant effects of diagnosis and diagnosis-by-genotype interactions (F's>4, p's<0.05) characterized activations in amygdala and anterior hippocampal regions. Greater activations in patients than healthy adolescents were found. Critically, these hyperactivations were modulated by BDNF genotype: Met-carriers showed greater neural responses of emotional faces than Val/Val homozygotes in patients only. These data are first to demonstrate the contribution of BDNF gene variants to the neural correlates of adolescent anxiety and depression. Early "gene-brain" linkages may lay the foundation for longer-term patterns of neural dysfunction in affective disorders.