Predictors of psychiatric treatment-seeking attitudes in older adults.

OBJECTIVES: Understanding the factors that contribute to treatment-seeking attitudes among older adults-a growing population with frequent mental health concerns-is vital. Although past research has identified some demographic and belief-based predictors of mental health treatment attitudes among this population, previous studies are limited by only evaluating these variables in isolation and not distinguishing between different types of treatment (e.g. medication and psychotherapy). METHODS: In a pre-registered online survey of 606 older adults (age 60 years and older), we evaluated stigmatizing attitudes, etiological beliefs about depression, psychological symptoms, and health literacy as well as attitudes about psychotherapy and medication separately. RESULTS: Pre-registered linear regression analyses showed that greater stigmatizing attitudes uniquely predicted more negative attitudes for both therapy and medication treatment seeking over and above gender, education, income, extrinsic barriers, health literacy, depression, and anxiety. Additionally, loneliness was a significant predictor of less favorable medication attitudes. Exploratory analysis revealed that attributing depression to a chemical imbalance predicted positive attitudes about medication, but not psychotherapy. CONCLUSION: These findings indicate that older adults' treatment-seeking behaviors are separately influenced by stigma, etiological beliefs, and loneliness.

Depression self-labeling in U.S. college students: Associations with perceived control and coping strategies.

BACKGROUND: Research on mental illness labeling has demonstrated that self-labeling (identifying with a mental illness label, e.g., "I have depression") is associated with internalized stigma, maladaptive responses to that stigma, and lower quality of life. However, research has not yet examined the link between self-labeling and how individuals cope with emotional distress. It is important to understand this relationship because adaptive and maladaptive methods of coping can lead to positive and negative mental illness outcomes. METHODS: This cross-sectional study examined the link between depression self-labeling, depression symptoms, and three constructs related to depression self-management (perceived control over depression, cognitive emotion regulation strategies, and help-seeking beliefs) in a large (N = 1423) sample of U.S. college students. RESULTS: Approximately one-fifth of students (22.2 %) self-labeled as having depression, while 39.0 % were estimated to meet diagnostic criteria for MDD. After controlling for depression symptom severity, self-labeling was associated with lower levels of perceived control over depression (p = .002), more catastrophizing (p = .013), less perspective taking, refocusing, reappraisal, and planning (ps < 0.05), and more positive help-seeking attitudes towards medication (p < .001) but not therapy. LIMITATIONS: Results are non-causal and may not generalize to non-college populations. CONCLUSIONS: Self-labeling may inform how individuals cope with emotional distress, with the potential for positive and negative effects on clinical outcomes. This is consistent with well-established research on self-labeling with regards to stigma, but extends this research in important new directions.

Framing depression as a functional signal, not a disease: Rationale and initial randomized controlled trial.

Depression is often framed as a disease or dysfunctional syndrome, yet this framing has unintended negative consequences including increased stigma. Here, we consider an alternative messaging framework - that depression serves an adaptive function. We describe the historical development of popular messages about depression and draw from the fields of evolutionary psychiatry and social cognition to describe the alternative framework that depression is a "signal" that serves a purpose. We then present data from a pre-registered, online randomized-controlled study in which participants with self-reported depression histories viewed a series of videos that explained depression as a "disease like any other" with known biopsychosocial risk factors (BPS condition), or as a signal that serves an adaptive function (Signal condition). In the entire sample (N = 877), three of the six hypotheses were supported: The Signal condition led to less self-stigma, greater offset efficacy, and more adaptive beliefs about depression. Exploratory analyses revealed these Signal effects were stronger among females (N = 553), who also showed a greater growth mindset of depression after the Signal explanation. Results suggest that framing depression as an adaptive signal can benefit patients and avoid harmful consequences of popular etiological presentations. We conclude that alternative framings of depression are worthy of further study.

Relative Effects of Sexual Assault and Temperament Traits on Cognitive Characteristics of Histrionic Personality Disorder.

Histrionic personality disorder (HPD) is a common and problematic form of personality pathology involving excessive attention-seeking, often through overly sexualized means. Much of the research on HPD has involved the association between HPD characteristics and basic temperament traits. Given the sometimes hypersexualized presentation of HPD, another potential influence on HPD characteristics may be exposure to sexual assault. However, there is little research on the association between sexual assault and HPD in general or with respect to temperament traits in particular. In this study, we examine the relative associations of sexual assault and temperament traits with the cognitive characteristics of HPD in a large sample of college students (N = 965) using a Bayesian approach to the analysis of covariance. Results suggest that sexual assault is associated with HPD cognitive characteristics over and above the robust influence of temperament traits. The study findings have implications for future research on and clinical intervention with people with HPD.

Limited impacts of biogenetic messaging on neural correlates of cognitive control and beliefs about depression.

During the past 60 years, perceptions about the origins of mental illness have shifted toward a biomedical model, depicting depression as a biological disorder caused by genetic abnormalities and/or chemical imbalances. Despite benevolent intentions to reduce stigma, biogenetic messages promote prognostic pessimism, reduce feelings of agency, and alter treatment preferences, motivations, and expectations. However, no research has examined how these messages influence neural markers of ruminative activity or decision-making, a gap this study sought to fill. In this pre-registered, clinical trial (NCT03998748), 49 participants with current or past depressive experiences completed a sham saliva test and were randomly assigned to receive feedback that they either have (gene-present; n = 24) or do not have (gene-absent; n = 25) a genetic predisposition to depression. Before and after receiving the feedback, resting-state activity and neural correlates of cognitive control (error-related negativity [ERN] and error positivity [Pe]) were measured using high-density electroencephalogram (EEG). Participants also completed self-report measures of beliefs about the malleability and prognosis of depression and treatment motivation. Contrary to hypotheses, biogenetic feedback did not alter perceptions or beliefs about depression, nor did it alter EEG markers of self-directed rumination nor neurophysiological correlates of cognitive control. Explanations of these null findings are discussed in the context of prior studies.

Chemical imbalance and etiological beliefs about depression among college students.

Etiological beliefs of depression have differing impacts on motivation, hope, and treatment expectations. However, it is unclear where people are exposed to these beliefs. Objective: This study examined beliefs about depression and their relations to symptoms, attitudes about depression, and treatment preferences. Participants: 426 undergraduates attending a large midwestern university. Methods: Participants completed an online survey asking about causes of depression, if and where they had heard about the "chemical imbalance" explanation of depression, attitudes about depression, as well as measures of their symptoms, treatment history, and hypothetical treatment preferences. Results: Sixty-two percent of the sample had heard of the chemical imbalance explanation, most commonly from the classroom. Biochemical beliefs about depression were most strongly endorsed among participants with a family history of depression and who had had personal experience with treatment. The chemical imbalance belief was uniquely related to dysfunctional beliefs about depression. Etiological beliefs were largely unrelated to treatment preferences. Conclusion: College students are exposed to models of mental health that may not be ideal for treatment and recovery.

Targeting cognitive control to reduce anxiety in very young children: A proof of concept study.

OBJECTIVE: Underdeveloped cognitive control (CC)-the capacity to flexibly adjust to changing environments-may predispose some children to early onset anxiety disorders and represents a promising intervention target. The current study established and pilot-tested "Camp Kidpower"-a novel group-based, interactive CC training intervention-and assessed its impacts on behavioral and neurophysiological indices of CC among preschool children with elevated anxiety symptoms. METHODS: Forty-four anxious children (4-6 years) were enrolled in Camp Kidpower, delivered in four sessions over 10 days. Before and after camp, children's capacity for CC was measured using well-validated, non-trained behavioral tasks and error-related negativity (ERN). Child anxiety symptoms were measured by parent report on the Spence Preschool Anxiety Scale. RESULTS: Thirty-two children completed the study, as defined by completion of pre- and follow-up assessments and at least three camp sessions. From baseline to after camp, performance on behavioral tests of CC improved, ERN amplitude increased, and anxiety symptoms decreased. CONCLUSION: Results provide initial evidence that play-based cognitive training targeted to behavioral and brain markers of CC reduces anxiety in preschoolers.

Effects of modafinil on electroencephalographic microstates in healthy adults.

RATIONALE: Modafinil has been proposed as a potentially effective clinical treatment for neuropsychiatric disorders characterized by cognitive control deficits. However, the precise effects of modafinil, particularly on brain network functions, are not completely understood. OBJECTIVES: To address this gap, we examined the effects of modafinil on resting-state brain activity in 30 healthy adults using microstate analysis. Electroencephalographic (EEG) microstates are discrete voltage topographies generated from resting-state network activity. METHODS: Using a placebo-controlled, within-subjects design, we examined changes to microstate parameters following placebo (0 mg), low (100 mg), and high (200 mg) modafinil doses. We also examined the functional significance of these microstates via associations between microstate parameters and event-related potential indexes of conflict monitoring and automatic error processing (N2 and error-related negativity) and behavioral responses (accuracy and RT) from a subsequent flanker interference task. RESULTS: Five microstates emerged following each treatment condition, including four canonical microstates (A-D). Modafinil increased microstate C proportion and occurrence regardless of dose, relative to placebo. Modafinil also decreased microstate A proportion and microstate B proportion and occurrence relative to placebo. These modafinil-related changes in microstate parameters were not associated with similar changes in flanker ERPs or behavior. Finally, modafinil made transitions between microstates A and B less likely and transitions from A and B to C more likely. CONCLUSIONS: Previous fMRI work has correlated microstates A and B with auditory and visual networks and microstate C with a salience network. Thus, our results suggest modafinil may deactivate large-scale sensory networks in favor of a higher order functional network during resting-state in healthy adults.

A multi-pronged investigation of option generation using depression, PET and modafinil.

Option generation is a critical process in decision making, but previous studies have largely focused on choices between options given by a researcher. Consequently, how we self-generate options for behaviour remain poorly understood. Here, we investigated option generation in major depressive disorder and how dopamine might modulate this process, as well as the effects of modafinil (a putative cognitive enhancer) on option generation in healthy individuals. We first compared differences in self-generated options between healthy non-depressed adults [n = 44, age = 26.3 years (SD 5.9)] and patients with major depressive disorder [n = 54, age = 24.8 years (SD 7.4)]. In the second study, a subset of depressed individuals [n = 22, age = 25.6 years (SD 7.8)] underwent PET scans with 11C-raclopride to examine the relationships between dopamine D2/D3 receptor availability and individual differences in option generation. Finally, a randomized, double-blind, placebo-controlled, three-way crossover study of modafinil (100 mg and 200 mg), was conducted in an independent sample of healthy people [n = 19, age = 23.2 years (SD 4.8)] to compare option generation under different doses of this drug. The first study revealed that patients with major depressive disorder produced significantly fewer options [t(96) = 2.68, P = 0.009, Cohen's d = 0.54], albeit with greater uniqueness [t(96) = -2.54, P = 0.01, Cohen's d = 0.52], on the option generation task compared to healthy controls. In the second study, we found that 11C-raclopride binding potential in the putamen was negatively correlated with fluency (r = -0.69, P = 0.001) but positively associated with uniqueness (r = 0.59, P = 0.007). Hence, depressed individuals with higher densities of unoccupied putamen D2/D3 receptors in the putamen generated fewer but more unique options, whereas patients with lower D2/D3 receptor availability were likely to produce a larger number of similar options. Finally, healthy participants were less unique [F(2,36) = 3.32, P = 0.048, partial η2 = 0.16] and diverse [F(2,36) = 4.31, P = 0.021, partial η2 = 0.19] after taking 200 mg versus 100 mg and 0 mg of modafinil, while fluency increased linearly with dosage at a trend level [F(1,18) = 4.11, P = 0.058, partial η2 = 0.19]. Our results show, for the first time, that option generation is affected in clinical depression and that dopaminergic activity in the putamen of patients with major depressive disorder may play a key role in the self-generation of options. Modafinil was also found to influence option generation in healthy people by reducing the creativity of options produced.

Error-related Alpha Suppression: Scalp Topography and (Lack of) Modulation by Modafinil.

Errors in performance trigger cognitive and neural changes that are implemented to adaptively adjust to fluctuating demands. Error-related alpha suppression (ERAS)-which refers to decreased power in the alpha frequency band after an incorrect response-is thought to reflect cognitive arousal after errors. Much of this work has been correlational, however, and there are no direct investigations into its pharmacological sensitivity. In Study 1 (n = 61), we evaluated the presence and scalp distribution of ERAS in a novel flanker task specifically developed for cross-species assessments. Using this same task in Study 2 (n = 26), which had a placebo-controlled within-subject design, we evaluated the sensitivity of ERAS to placebo (0 mg), low (100 mg), and high (200 mg) doses of modafinil, a wakefulness promoting agent. Consistent with previous work, ERAS was maximal at parieto-occipital recording sites in both studies. In Study 2, modafinil did not have strong effects on ERAS (a significant Accuracy × Dose interaction emerged, but drug-placebo differences did not reach statistical significance after correction for multiple comparisons and was absent after controlling for accuracy rate). ERAS was correlated with accuracy rates in both studies. Thus, modafinil did not impact ERAS as hypothesized, and findings indicate ERAS may reflect an orienting response to infrequent events.

Post-error slowing in anxiety and obsessive-compulsive disorders.

Altered brain response to errors in anxiety and obsessive-compulsive disorders (OCD) suggests cognitive control abnormalities across both types of illness, but behavioral metrics of cognitive control function have yet to be compared in patients selected from these different diagnostic categories. Thus, we examined post-error slowing (PES), a behavioral adjustment that typically occurs after a mistake, in children and adolescents with and without a primary anxiety disorder (N = 103 anxiety and N = 28 healthy controls) and adolescents and adults with and without OCD (N = 118 OCD and N = 60 healthy controls) using a go/no-go task. Primary analyses tested for differences in PES between diagnostic groups (anxiety, OCD, healthy), controlling for age, overall reaction time, and overall accuracy. Results indicated that patients with anxiety disorders exhibited more post-error slowing than both patients with OCD and healthy volunteers. In contrast, participants with OCD did not differ from healthy volunteers in post-error slowing. In subgroup analyses restricted to adolescent participants (ages 13-17 years), more post-error slowing was observed in the anxiety disorders group compared with either the OCD or healthy groups. These data suggest that excessive post-error slowing, an index of behavioral adjustment following errors, may uniquely characterize patients with anxiety disorders relative to healthy individuals and those with OCD.

The effect of acute exercise for reducing cognitive alterations associated with individuals high in anxiety.

Single bouts of exercise have been observed to exhibit therapeutic benefits for reducing affective responses associated with anxiety. However, anxiety has also been found to relate to less efficient cognitive processing as well as a greater reliance on action monitoring processes. Given the extant body of evidence demonstrating that single bouts of exercise result in cognitive enhancements; the present investigation sought to determine the extent to which exercise might be effective at reducing these anxiety-related impairments in cognition. Using a randomized within-subjects crossover design in a sample of high-anxious and low-anxious college-aged adults, measures of inhibition, attention, and action monitoring were assessed before and after 20-min of either aerobic exercise or a cognitively engaging control condition during two separate, counterbalanced sessions. Findings from this investigation revealed that both high anxious and low anxious individuals exhibited enhancements in behavioral indices of performance on an inhibitory control task with faster and more accurate responses following 20 min of moderate intensity aerobic exercise. Additionally, both high anxious and low anxious individuals demonstrated exercise induced enhancements in the allocation of attentional resources (as indexed by P3 amplitude) as well as action monitoring (as indexed by ERN amplitude). Accordingly, these findings provide evidence consistent with broad-base claims regarding the benefits of exercise, suggesting that both high and low anxious individuals appear to incur cognitive benefits.

Concordant neurophysiological signatures of cognitive control in humans and rats.

Progress towards understanding neural mechanisms in humans relevant to psychiatric conditions has been hindered by a lack of translationally-relevant cognitive tasks for laboratory animals. Accordingly, there is a critical need to develop parallel neurophysiological assessments of domains of cognition, such as cognitive control, in humans and laboratory animals. To address this, we developed a touchscreen-based cognitive (Eriksen Flanker) task in rats and used its key characteristics to construct a novel human version, with similar testing parameters and endpoints across species. We obtained continuous electroencephalogram (EEG) recordings, including local field potentials in rats, and compared electrophysiological signatures locked to stimulus onset and responses across species. We also assessed whether behavioral or physiological task effects were modulated by modafinil, which enhances aspects of cognitive function in humans. In both species, the task elicited expected flanker interference effects (reduced accuracy) during high-conflict trials. Across homologous neuroanatomical loci, stimulus-locked increases in theta power during high-conflict trials as well as error-related negative potentials were observed. These endpoints were not affected by modafinil in either species. Despite some species-specific patterns, our findings demonstrate the feasibility of a rat Flanker task as well as cross-species behavioral and neurophysiological similarities, which may enable novel insights into the neural correlates of healthy and aberrant behavior and provide mechanistic insights relevant to treatment.

Mindsets in the clinic: Applying mindset theory to clinical psychology.

Beliefs about the malleability of attributes, also known as mindsets, have been studied for decades in social-personality psychology and education. Here, I review the many applications of mindset theory to clinical psychology and psychotherapy. First, I review social psychological and cognitive neuroscience evidence that mindsets and mindset-related messages are, to a large extent, focused on emotional tolerance. Specifically, the growth mindset, or the belief that attributes are malleable, encourages confronting and tolerating anxiety, frustration, and disappointment in healthy and adaptive ways that promote resilience, whereas the fixed mindset and related messages discourage the experience of these emotions and often leads to helplessness. Second, I review the emerging research on the anxiety mindset and discuss its relevance to clinical work. A model is proposed illustrating connections between mindsets, emotion regulation strategies, treatment preferences, and outcomes. Case examples are used to illustrate practical applications. I conclude that mindsets can inform psychotherapy, research, and public policy.

Cognitive Control in Pediatric Obsessive-Compulsive and Anxiety Disorders: Brain-Behavioral Targets for Early Intervention.

The DSM provides distinct criteria for obsessive-compulsive disorder (OCD) and various types of anxiety disorders, but phenomenological overlap, high rates of comorbidity, and early onset suggest common underlying mechanisms. This notion is further supported by use of the same treatments-cognitive behavioral therapy and serotonin reuptake inhibitor medication-for managing both OCD and non-OCD anxiety disorders in clinical settings. While early intervention with these gold standard treatments is recommended for pediatric OCD and anxiety disorders, young patients often remain symptomatic even after treatment. To guide the development of novel, mechanistically targeted treatments to better resolve OCD and anxiety symptoms, the identification of neural circuits underlying psychological constructs with relevance across disorders has been recommended. One construct that may be relevant for understanding pediatric OCD and anxiety disorders is cognitive control, given the difficulty that young patients experience in dismissing obsessions, compulsions, and worry despite recognition that these symptoms are excessive and unreasonable. In this review, we examine findings from a growing body of literature implicating brain-behavioral markers of cognitive control in pediatric OCD and anxiety disorders, including before and after treatment. We conclude by suggesting that interventions designed to enhance the functioning of the task control circuits underlying cognitive control may facilitate brain maturation to help affected youth overcome symptoms.

Empathy Mind-Set Moderates the Association Between Low Empathy and Social Aggression.

Empathy plays an important role in creating and maintaining adaptive interpersonal relationships. Accordingly, existing studies often report a negative correlation between empathy and interpersonal aggression. However, findings are sometimes inconsistent, and concerns have been raised about the size of the overall effect. Here, we examined the potential moderating role of empathy mind-sets-beliefs about the malleability of empathy. We hypothesized that the association between low empathy and aggression would be especially strong if individuals also believed that their levels of empathy were unchangeable (i.e., they endorsed a fixed mind-set about empathy); in contrast, a belief that empathy was malleable may weaken the association. Results supported this hypothesis, such that individuals with low levels of empathy were less likely to report aggression-social aggression in particular-if they also believed that empathy was changeable. These results point to a role for beliefs about the malleability of empathy as an important moderator and may point to ways to enhance empathy interventions by targeting mind-sets.

Stressors and chemical imbalances: Beliefs about the causes of depression in an acute psychiatric treatment sample.

BACKGROUND: Public perceptions of mental illness are increasingly construed in neurobiological and genetic terms. Accumulating evidence suggests there are some unintended consequences of these explanations, including reduced optimism for recovery among individuals with depression. However, little is known about how these beliefs relate to treatment process and outcomes in a psychiatric treatment setting, a gap this study aimed to fill. METHODS: We examined etiological beliefs about depression in a sample of patients (N = 279) seeking acute treatment in a behaviorally-based therapy program at a psychiatric hospital and examined relations with treatment expectations and outcomes. RESULTS: We found that although psychosocial explanations of depression were most popular, biogenetic beliefs, particularly the belief that depression is caused by a chemical imbalance, were prevalent in this sample. Further, the chemical imbalance belief related to poorer treatment expectations. This relationship was moderated by symptoms of depression, with more depressed individuals showing a stronger relationship between chemical imbalance beliefs and lower treatment expectations. Finally, the chemical imbalance belief predicted more depressive symptoms after the treatment program ended for a 2-week measure of depression (but not for a 24-hour measure of depression), controlling for psychiatric symptoms at admission, inpatient hospitalizations, and treatment expectations. LIMITATIONS: The sample was homogenous in terms of race and ethnicity and we did not assess how patients came to their beliefs. CONCLUSIONS: Together, the results illustrate the correlates and possible impacts of etiological beliefs in a real-world clinical setting and invite a critical discussion about predominant messages about the etiology of depression.

Optimizing assessments of post-error slowing: A neurobehavioral investigation of a flanker task.

Appropriately adjusting to errors is essential for adaptive behavior. Post-error slowing (PES) refers to the increased reaction times on trials following incorrect relative to correct responses. PES has been used as a metric of cognitive control in basic cognitive neuroscience research as well as clinical contexts. However, calculation of PES varies widely among studies and has not yet been standardized, despite recent calls to optimize its measurement. Here, using behavioral and electrophysiological data from a modified flanker task, we considered different methods of calculating PES, assessed their internal consistency, examined their convergent correlations with behavioral performance and error-related event-related brain potentials (ERPs), and evaluated their sensitivity to task demands (e.g., presence of trial-to-trial feedback). Results indicated that the so-called robust measure of PES, calculated using only error-surrounding trials, provided an estimate of PES that was three times larger in magnitude than the traditional calculation. This robust PES correlated with the amplitude of the error positivity (Pe), an index of attention allocation to errors, just as well as the traditional method. However, all PES estimates had very weak internal consistency. Implications for measurement are discussed.

The Fixed Mindset of Anxiety Predicts Future Distress: A Longitudinal Study.

Mindsets, or beliefs about the malleability of self-attributes such as intelligence and personality, have been linked to a wide range of outcomes in educational and social psychology. There has been recent interest in exploring this construct in clinical psychological contexts. To that end, research has shown that the fixed mindset of anxiety-the belief that anxiety is fixed and unchangeable-is related to a variety of psychological distress symptoms, emotion regulation strategies, and treatment preferences. One outstanding question is whether the fixed mindset of anxiety predicts future psychological symptoms. To address this question, the current longitudinal study assessed weekly distress and anxiety mindset across 5 weeks. We found that fixed mindset of anxiety is predictive of future weekly distress, even after controlling for the previous week's distress, sex, socioeconomic status, baseline depression symptoms, and presence of psychiatric diagnosis. These findings add evidence to an emerging conceptual framework in which the fixed mindset of anxiety represents an important risk factor for the onset of future psychological problems.