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BACKGROUND Irritable mood is a transdiagnostic clinical feature that is present in multiple psychiatric disorders. Although irritability is frequently examined as a unitary construct, two dimensions of irritability, tonic (i.e., irritable mood) and phasic (i.e., temper outbursts), have been hypothesized. However, few studies have examined whether tonic and phasic irritability are empirically separable and predict different forms of psychopathology. METHODS We utilized data from a longitudinal study of a community sample of 550 girls (age 13.5-15.5 years) followed at 9-month intervals for 3 years. We conducted exploratory factor analysis (EFA) using items from three self-report inventories: the International Personality Item Pool Anger scale, Temperament and Affectivity Inventory Anger scale, and Buss-Perry Aggression Questionnaire Anger scale. RESULTS The EFA identified dimensions that were consistent with tonic and phasic irritability. Tonic irritability at baseline independently predicted the development of depressive disorders and generalized anxiety disorder (GAD) in subsequent waves. Phasic irritability independently predicted a decreased probability of GAD, but an increased probability of oppositional defiant, conduct, and substance use disorder, and greater risky sexual behavior and relational aggression during the follow-up. CONCLUSIONS Tonic and phasic irritability appear to be separable constructs with unique implications for later psychopathology and related behavior among adolescent girls. It is important to consider this distinction in research on the etiology and pathophysiology of irritability and developing effective treatments.

Objective:At first hospitalization, a long duration of untreated psychosis (DUP) predicts illness severity and worse treatment outcomes. The mechanism of this association, however, remains unclear....

Background Evidence supports the notion that early-life stress and trauma impact cortical development and increase vulnerability to depression. However, it remains unclear whether common stressful life events in community-dwelling adolescents have similar consequences for cortical development. Methods A total of 232 adolescent girls (mean age 15.29 ± 0.65 years) were assessed with the Stressful Life Events Schedule (a semistructured interview of stressors in the previous 9 months) and underwent a magnetic resonance imaging scan. FreeSurfer 5.3.0 was used to perform whole-brain surface-based morphometry. Dysphoria was assessed at the time of imaging and prospectively at three 9-month follow-up appointments using the Inventory of Depression and Anxiety Symptoms II. Results At least one stressful life event was reported in 90% of the adolescent participants during the 9 months preceding imaging. Greater burden of recent life stress was associated with less left precuneus and left postcentral cortical thickness and smaller left superior frontal and right inferior parietal volume (all p Conclusions Consistent with evidence from imaging studies of trauma-exposed youths and preclinical stress models, a heavy burden of recent common life stress in community-dwelling adolescent girls was associated with altered frontal/parietal cortical morphology. Stress-linked precuneus cortical thickness represents a candidate prospective biomarker of adolescent depression.

Salivary markers of immune function are increasingly commonly used in studies of human health. Yet, few studies have examined the short-term or long-term reliability or stability of these biomarkers, making their measurement properties unclear. We addressed this issue in the present study by collecting two saliva samples, two hours apart, from 426 adolescent girls during a baseline laboratory visit. Then, eighteen months later, we collected the same samples again from a subset of these participants (n = 113). The correlations between the two samples collected at each session were generally high (mean r = 0.67). In contrast, although single saliva samples were only weakly correlated across 18 month (mean rs = 0.18), averaging the two quantifications within a session considerably improved the reliability (mean r = 0.27). In short, salivary immune markers exhibited strong short-term test-retest correlations, and averaging across multiple assessments notably improved long-term test-retest correlations. Additional research is needed to establish the health relevance and mechanisms underlying these potentially useful, non-invasive biomarkers.

Background Research on a putative link between apolipoprotein-e4 allele (APOE-e4) and schizophrenia has been inconclusive. However, prior studies have not investigated the association between APOE-e4 and symptom trajectories, nor has the existing literature taken into account the potentially moderating effect of age in genetic association studies. Methods The association between APOE-e4 and four symptom dimensions was investigated in a longitudinal study of 116 individuals with schizophrenia initially assessed during their first admission for psychosis and evaluated five times over the following 20 years. A meta-analysis identified 29 case-control studies of APOE-e4 allele frequency in schizophrenia, which were analyzed using random-effects meta-regression to test the potentially moderating effect of age. Results Longitudinal models identified a specific association between APOE-e4 and symptom trajectories, showing that APOE-e4 portends worsening severity of hallucinations and delusions in late adulthood among people with schizophrenia, at a rate of a 0.46 standard deviation increase per decade. Meta-analysis showed a significant effect of age: the association between APOE-e4 and schizophrenia was not detectable in younger people but became pronounced with age, such that APOE-e4 increased the odds of diagnosis by 10% per decade. Conclusions Taken together, the meta-analysis and longitudinal analysis implicate APOE-e4 as an age-related risk factor for worsening hallucinations and delusions, and suggest APOE-e4 may play an age-mediated pathophysiological role in schizophrenia. The presence of an APOE-e4 allele may also identify a subgroup of patients who require intensive monitoring and additional targeted interventions, especially in mid-to late-life.

Background Adolescent-onset depressive disorders (DDs) are associated with deficits in the regulation of negative affect across modalities (self-report, behavioral paradigms, and neuroimaging), which may manifest prior to first-onset DDs. Whether the neurocircuitry governing emotional regulation predates DDs is unclear. This study tested whether a critical pathway for emotion regulation (rostral anterior cingulate cortex–amygdala structural connectivity) predicts first-onset DDs in adolescent females. Methods Diffusion tensor imaging data were acquired on adolescent females (n = 212) without a history of DDs and the cohort was reassessed for first-onset DDs over the next 27 months. Results A total of 26 girls developed first onsets of DDs in the 27 months after imaging. Multivariate logistic regression showed that lower weighted average fractional anisotropy of uncinate fasciculus tracts between the rostral anterior cingulate cortex and amygdala prospectively predicted first onset of DDs (adjusted odds ratio = 0.44, p = .005), above and beyond established risk factors including baseline depression symptom severity, history of anxiety disorders, parental history of depression, parental education, and age. Conclusions This study provides evidence for the first time showing that aberrant structural connectivity between the rostral anterior cingulate cortex and amygdala prospectively predates first onset of DDs in adolescent females. These results highlight the importance of a well-established neural circuit implicated in the regulation of negative affect as a likely etiological factor and a promising target for intervention and prevention of DDs.

Background: First onsets of depression are especially common in adolescent females and often develop into chronic/recurrent illness. Surprisingly few studies have comprehensively evaluated multiple domains of etiologically-informative risk factors for first onset in adolescents from the community. We investigated whether clinical, cognitive, personality, interpersonal, and biological risk factors prospectively predict a first onset of depressive disorder (DD), and of DD with a chronic/recurrent course, in a community sample of adolescent girls. Methods: 479 girls (13.5–15.5 years) with no history of DD completed baseline assessments of risk factors and five diagnostic assessments over 3 years. Baseline measures were analyzed separately and jointly to prospectively predict first-onset DD and first-onset chronic/recurrent DD. Results: Most risk factors predicted first-onset DD (n = 93), including depressive symptoms, anxiety disorders, rumination, personality traits, blunted neural response (late positive potential [LPP]) to unpleasant pictures, peer victimization, parental criticism, and parental mood disorder. Depressive symptoms, rumination, parental mood disorder, and parental criticism were independently associated with first onsets. Nearly all measures, including a blunted neural response to rewards (reward positivity [RewP]), also predicted first-onset chronic/recurrent DD (n = 52), with depressive symptoms, low extraversion, poor peer relationships, and blunted RewP emerging as independent risk factors. Limitations: This study focused on adolescent females and therefore does not provide information on males. Conclusions: Multiple domains of risk factors in early adolescence are prospectively associated with first-onset DD and chronic/recurrent DD. A smaller subset of risk factors uniquely contributing to first onsets may represent core vulnerabilities for adolescent-onset depression and promising prevention targets.

BackgroundPerformance monitoring entails rapid error detection to maintain task performance. Impaired performance monitoring is a candidate pathophysiological process in psychotic disorders, which may explain the broader deficit in executive function and its known associations with negative symptoms and poor functioning. The current study models cross-sectional pathways bridging neurophysiological measures of performance monitoring with executive function, symptoms, and functioning.MethodsData were from the 20-year assessment of the Suffolk County Mental Health Project. Individuals with psychotic disorders (N = 181) were originally recruited from inpatient psychiatric facilities. Data were also collected from a geographically and demographically matched group with no psychosis history (N = 242). Neural measures were the error-related negativity (ERN) and error positivity (Pe). Structural equation modeling tested mediation pathways.ResultsBlunted ERN and Pe in the clinical cohort related to impaired executive function (r = 0.26–0.35), negative symptom severity (r = 0.17–0.25), and poor real-world functioning (r = 0.17–0.19). Associations with executive function were consistent across groups. Multiple potential pathways were identified in the clinical cohort: reduced ERN to inexpressivity was mediated by executive function (β = 0.10); reduced Pe to global functioning was mediated by executive function and avolition (β = 0.10).ConclusionsThis supports a transdiagnostic model of psychotic disorders by which poor performance monitoring contributes to impaired executive function, which contributes to negative symptoms and poor real-world functioning. If supported by future longitudinal research, these pathways could inform the development of targeted interventions to address cognitive and functional deficits that are central to psychotic disorders.

Individual with substance use disorders have well-recognized impairments in cognitive control, including in behavioral adaptation after mistakes. One way in which this impairment manifests is via diminished post-error slowing, the increase in reaction time following a task-related error that is posited to reflect cautionary or corrective behavior. Yet, in the substance use disorder literature, findings with regard to post-error slowing have been inconsistent, and thus could benefit from quantitative integration. Here, we conducted a meta-analysis of case-control studies examining post-error slowing in addiction. Twelve studies with 15 unique comparisons were identified, comprising 567 substance users and 384 healthy controls across three broad types of inhibitory control paradigms (go-no/go, conflict resolution, and stop signal tasks, respectively). Results of the random-effects meta-analysis revealed a moderate group difference across all studies (Cohen's d = 0.31), such that the individuals with substance use disorder had diminished post-error slowing compared with controls. Despite this omnibus effect, there was also large variability in the magnitude of the effects, explained in part by differences between studies in task complexity. These findings suggest that post-error slowing may serve as a promising and easy-to-implement measure of cognitive control impairment in substance use disorder, with potential links to aberrant brain function in cognitive control areas such as the anterior cingulate cortex.

OBJECTIVE: An increased neural response to making mistakes has emerged as a potential biomarker of anxiety across development. The error-related negativity is an event-related potential elicited when people make mistakes on simple laboratory-based reaction time tasks that has been associated with risk for anxiety. The present study examined whether the error-related negativity prospectively predicted the first onset of generalized anxiety disorder (GAD) over 1.5 years in adolescent girls. METHODS: The sample included 457 girls between the ages of 13.5 and 15.5 years, with no history of GAD. At baseline, the error-related negativity was measured using a flankers task. Psychiatric history of the adolescent and biological parent were assessed with diagnostic interviews, and the adolescent completed a self-report questionnaire regarding anxiety symptoms. Approximately 1.5 years later, adolescents completed the same interview. RESULTS: An increased neural response to errors at baseline predicted first-onset GAD over 1.5 years. The error-related negativity was a significant predictor independent of other prominent risk factors, including baseline anxiety and depression symptoms and parental lifetime psychiatric history. Jointly the error-related negativity and social anxiety symptoms provided the greatest power for predicting first-onset GAD. CONCLUSIONS: The current study provides evidence for the utility of the error-related negativity as a biomarker of risk for GAD during a key developmental period.

Purpose The aim of present study was to test the diathesis-stress model of depression using baseline cortisol, prospective assessment of depression symptoms, and stressful life events. Methods The sample consisted of 527 adolescent girls aged 13.5–15.5 years without major depressive disorder. At baseline, saliva samples were collected at waking, 30 minutes after waking, and 8 p.m. on 3 consecutive days. Diurnal cortisol was indexed by cortisol awakening response (CAR) and area under the curve with respect to ground (AUCg). Stressful events during the preceding interval and current depressive symptoms were assessed 18 months following baseline. Results Stressful events and the interaction of CAR or AUCg with stressful events predicted depressive symptoms at 18 months, even after controlling for baseline depressive symptoms. Specifically, in the face of high levels of stress, baseline blunted CAR or smaller AUCg were associated with future depressive symptoms. This was more apparent for CAR than AUCg. The effect was reversed at low levels of stress, with heightened CAR associated with more severe depressive symptoms. Conclusions Blunted CAR and less daily cortisol output at baseline appear to accentuate the depressogenic effects of stressful events after 18 months, consistent with the diathesis-stress model of hypothalamic-pituitary-adrenal axis function in depression.

Background Major depressive disorder is a leading cause of disability worldwide; however, little is known about pathological mechanisms involved in its development. Research in adolescent depression has focused on reward sensitivity and striatal mechanisms implementing it. The contribution of loss sensitivity to future depression, as well as the orbitofrontal cortex (OFC) mechanisms critical for processing losses and rewards, remains unexplored. Furthermore, it is unclear whether OFC functioning interacts with familial history in predicting future depression. Methods In this longitudinal study, we recorded functional magnetic resonance imaging data while 229 female adolescents with or without parental history of depression completed a monetary gambling task. We examined whether OFC blood oxygen level–dependent response and functional connectivity during loss and win feedback was associated with depression symptoms concurrently and prospectively (9 months later) and whether this relationship was moderated by parental history of depression. Results Reduced OFC response during loss was associated with higher depression symptoms concurrently and prospectively, even after controlling for concurrent depression, specifically in adolescents with parental history of depression. Similarly, increased OFC-posterior insula connectivity during loss was associated with future depression symptoms, but this relationship was not moderated by parental history of depression. Conclusions This study provides the first evidence for loss-related alterations in OFC functioning and its interaction with familial history of depression as possible mechanisms in the development of depression. While the current functional magnetic resonance imaging literature has mainly focused on reward, the current findings underscore the need to include prefrontal loss processing in existing developmental models of depression.

BackgroundIndividual differences in neuroticism, extraversion, and conscientiousness are associated with, and may predict onset of, internalizing disorders. These general traits can be parsed into facets, but there is a surprising paucity of research on facet risk for internalizing disorders. We examined general traits and facets of neuroticism, extraversion, and conscientiousness in predicting first onsets of depressive and anxiety disorders.MethodsA community sample of 550 adolescent females completed general and facet-level personality measures and diagnostic interviews. Interviews were re-administered 18 months later.ResultsFirst onsets of depressive disorders were predicted by neuroticism, extraversion, and conscientiousness. Facets predicting first onset of depression included depressivity (neuroticism facet) and lower positive emotionality and sociability (extraversion facets). First onsets of generalized anxiety disorder (GAD) were predicted by neuroticism, and particularly the facet of anxiousness. First onsets of social phobia were predicted at the facet level by anxiousness. First onsets of specific phobia were predicted by neuroticism, low conscientiousness, and all neuroticism facets. In multivariate analyses, first onsets of depression were uniquely predicted by depressivity, and onsets of GAD and social phobia were uniquely predicted by anxiousness over and above the general trait of neuroticism.ConclusionsGeneral traits predict first onsets of depressive and anxiety disorders. In addition, more specific associations are evident at the facet level. Facets can refine our understanding of the links between personality and psychopathology risk, and provide finer-grained targets for personality-informed interventions.

Understanding whether and how the schizophrenia polygenic risk score (SZ PRS) predicts course of illness could improve diagnosis and prognostication in psychotic disorders. We tested whether the SZ PRS predicts symptoms, cognition, illness severity, and diagnostic changes over the 20 years following first admission. The Suffolk County Mental Health Project is an inception cohort study of first-admission patients with psychosis. Patients were assessed six times over 20 years, and 249 provided DNA. Geographically- and demographically-matched never psychotic adults were recruited at year 20, and 205 provided DNA. Symptoms were rated using the Schedule for the Assessment of Positive Symptoms and Schedule for the Assessment of Negative Symptoms. Cognition was evaluated with a comprehensive neuropsychological battery. Illness severity and diagnosis were determined by consensus of study psychiatrists. SZ PRS was significantly higher in first-admission than never psychotic groups. Within the psychosis cohort, the SZ PRS predicted more severe negative symptoms (β = 0.21), greater illness severity (β = 0.28), and worse cognition (β = −0.35), across the follow-up. The SZ PRS was the strongest predictor of diagnostic shifts from affective to non-affective psychosis over the 20 years (AUC = 0.62). The SZ PRS predicts persistent differences in cognition and negative symptoms. The SZ PRS also predicts who among those who appear to have a mood disorder with psychosis at first admission will ultimately be diagnosed with a schizophrenia spectrum disorder. These findings show potential for the SZ PRS to become a tool for diagnosis and treatment planning.

Effective suicide prevention is hindered by a limited understanding of the natural progression and neurobiology of the suicidal process. Our objective was to characterize the duration of the suicidal process and its relation to possible determinants: time judgment and cognitive impulsivity. In four groups of adults of both sexes including recent suicide attempters (n=57), suicidal ideators (n=131), non-suicidal depressed controls (n=51) and healthy controls (n=48) we examined time estimation and production, impulsivity and other cognitive variables. Duration of the suicidal process was recorded in suicide attempters. The suicide process duration, suicide contemplation and action intervals, had a bimodal distribution, ~40% of attempters took less than 5 minutes from decision to attempt. Time slowing correlated negatively with the suicidal action interval (time from the decision to kill oneself to suicide attempt) (p=.003). Individuals with suicide contemplation interval shorter than three hours showed increased time slowing, measured as shorter time production at 35 seconds (p=.011) and 43 seconds (p=.036). Delay discounting for rewards correlated with time estimation at 25 minutes (p=0.02) and 90 seconds (p=.01). Time slowing correlated positively with suicidal ideation severity, independently of depression severity (p

BackgroundClassic conceptual frameworks explaining the relationship of personality traits to depression include the precursor and predisposition models. The former hypothesizes that depression is predicted by traits alone whereas the latter hypothesizes that stress, together with personality, predicts depression. Dynamic vulnerability models (DVM) expand on these perspectives by incorporating fluctuations in personality over time. The stress generation model provides an alternative view, positing that depression generates stress, creating a self-perpetuating cycle. However, these conceptual models are rarely directly compared.MethodWe tested these models, focusing on neuroticism and stressful life events that the participant may have contributed to, using path analysis in a sample of 550 never-depressed, adolescent females assessed five times over 3 years.ResultsA dynamic precursor model with stress generation was best supported. For the precursor component, neuroticism predicted subsequent depression across four assessment intervals. For the dynamic trait component, stressful life events predicted subsequent neuroticism at three of four intervals. Finally, in line with stress generation, depression consistently predicted subsequent stressful life events, and life events then predicted depression.ConclusionsFinding support for the DVM is noteworthy, as this is the first comprehensive test of this model. Moreover, results supported integrating stress generation with trait vulnerability. Continued use of integrated approaches and refining the statistical implementation of these theories is necessary to advance understanding of the development of depression.

Background Adolescence is characterized by affective and cognitive changes that increase vulnerability to depression, especially in females. Neurodevelopmental models attribute adolescent depression to abnormal responses in amygdala, striatum, and prefrontal cortex (PFC). We examined whether the strength of functional brain networks involving these regions predicts depression symptoms in adolescent females. Methods In this longitudinal study, we recorded resting-state functional connectivity (RSFC) in 174 adolescent females. Using a cross-validation strategy, we related RSFC profiles that included (a) a network consisting of amygdala, striatum, and PFC (within-circuit model), (b) connectivity of this network to the whole brain (extended-circuit model), and (c) a network consisting of the entire brain (whole-brain model) to depression symptoms assessed concurrently and 18 months later. Results In testing subsets, the within-circuit RSFC profiles were associated with depression symptoms concurrently and 18 months later, while the extended-circuit and whole-brain model did not explain any additional variance in depression symptoms. Connectivity related to anterior cingulate and ventromedial prefrontal cortex contributed most to the association. Conclusions Our results demonstrate that RSFC-based brain networks that include amygdala, striatum, and PFC are stable neural signatures of concurrent and future depression symptoms, representing a significant step toward identifying the neural mechanism of depression in adolescence.

ObjectivesThis scoping review aims to facilitate psychometric developments in the field of digital media usage and well-being in young people by (1) identifying core concepts in the area of “screen time” and digital media use in children, adolescents, and young adults, (2) synthesising existing research paradigms and measurement tools that quantify these dimensions, and (3) highlighting important areas of need to guide future measure development.DesignA scoping review of 140 sources (126 database, 14 grey literature) published between 2014 and 2019 yielded 162 measurement tools across a range of domains, users, and cultures. Database sources from Ovid MEDLINE, PsycINFO and Scopus were extracted, in addition to grey literature obtained from knowledge experts and organisations relevant to digital media use in children. To be included, the source had to: (1) be an empirical investigation or present original research, (2) investigate a sample/target population that included children or young persons between the ages of 0 and 25 years of age, and (3) include at least one assessment method for measuring digital media use. Reviews, editorials, letters, comments and animal model studies were all excluded.MeasuresBasic information, level of risk of bias, study setting, paradigm, data type, digital media type, device, usage characteristics, applications or websites, sample characteristics, recruitment methods, measurement tool information, reliability and validity.ResultsSignificant variability in nomenclature surrounding problematic use and criteria for identifying clinical impairment was discovered. Moreover, there was a paucity of measures in key domains, including tools for young children, whole families, disadvantaged groups, and for certain patterns and types of usage.ConclusionThis knowledge synthesis exercise highlights the need for the widespread development and implementation of comprehensive, multi-method, multilevel, and multi-informant measurement suites.

Error processing is impaired in psychosis, and numerous event-related potential studies have found reductions in the error-related negativity (ERN) and, more recently, the error positivity (Pe). The stability of reduced ERN/Pe in psychosis, however, is unknown. In a previous cross-sectional report, reduced ERN was associated with negative symptom severity and reduced Pe with a diagnosis of schizophrenia versus other psychosis. Here, we test the stability of impaired error processing over a four-year follow-up and relationships with subdimensions of negative symptoms. The ERN and Pe were recorded from individuals with psychotic disorders twice: 79 individuals were assessed 15 years after first hospitalization, and 69 were assessed at 19 years; 59 (26 with schizophrenia, 33 with other psychotic disorders) had data at both assessments. At 19 years the Pe was blunted in schizophrenia. The ERN and Pe exhibited temporal stability over the four years (r=.59 and .60, respectively). Reduced ERN and Pe correlated with the negative symptom subdimensions of inexpressivity and avolition, respectively, and not with psychotic or disorganized symptoms. Moreover, 15-year ERN predicted an increase in inexpressivity by year 19. No evidence was found for the reverse: negative symptoms did not predict change in ERN/Pe. Similar to non-clinical samples, the ERN and Pe show impressive four-year stability in late-phase psychosis. The ERN and Pe are promising neural measures for capturing individual differences in psychotic disorders, particularly with regard to negative symptomatology. They may prove to be useful clinically for forecasting illness course and as treatment targets.

Offspring with maternal PTSD are at increased risk of developing PTSD themselves. Alterations in the hypothalamus-pituitary-adrenal (HPA) axis may play a role and have been noted in offspring, although evidence is mostly from adult offspring with PTSD symptoms themselves. The present study of adolescent girls (N=472) and their mothers (n = 18 with lifetime PTSD versus n = 454 with no PTSD) sought to determine whether healthy, non-affected offspring of mothers with PTSD would exhibit altered HPA axis function. Saliva samples were collected from the adolescent girls at waking, 30 minutes after waking, and 8 pm on 3 consecutive days. Offspring whose mothers were diagnosed with PTSD demonstrated higher cortisol awakening response (CAR; Cohen's d = .58) and greater total cortisol output (Cohen's d = .62). In this preliminary study, higher cortisol levels during adolescence among offspring of mothers with PTSD may index a vulnerability in these at-risk youth.

The error-related negativity (ERN) currently appears as a physiological measure in relation to three Research Domain Criteria (RDoC) constructs: Cognitive Control, Sustained Threat, and Reward Learning. We propose a conceptual model in which variance in the ERN reflects individual differences in the degree to which errors are evaluated as threatening. We also discuss evidence for the placement of the ERN in the "Sustained Threat" construct, as well as evidence that the ERN may more specifically reflect sensitivity to endogenous threat. Following this, we present data from a sample of 515 adolescent females demonstrating a larger ERN in relation to self-reported checking behaviors, but only in older adolescents, suggesting that sensitivity to internal threat and the ERN-checking relationship may follow a developmental course as adolescents develop behavioral control. In contrast, depressive symptoms were linked to a smaller ERN, and this association was invariant with respect to age. Collectively, these data suggest that the magnitude of the ERN is sensitive both to specific anxiety-related processes and depression, in opposing directions that may reflect variation in internal threat sensitivity. We discuss directions for future research, as well as ways in which findings for the ERN complement and challenge aspects of the current RDoC matrix.

Abnormal patterns of attention to threat and reward have been proposed as potential mechanisms of dysfunction in anxiety and unipolar depressive disorders. However, few studies have simultaneously examined whether these patterns of attention are shared among disorders or distinguish between them. In the present study, we recorded the Late Positive Potential (LPP), an event-related potential and putative index of motivated attention, from 145 patients with anxiety and unipolar depressive disorders and 32 controls, as they viewed blocks of rewarding and threatening images, respectively. We found that a current diagnosis of depression was associated with a reduced LPP to rewarding visual stimuli. This appeared to be specific to a subgroup of individuals with early onset depression; this subgroup was also characterized by a reduced LPP to threatening images. Anxiety diagnosis and age of onset of anxiety, whether comorbid with depression or not, was unrelated to the magnitude of the LPP. Finally, a transdiagnostic symptom dimension measuring current severity of suicidal ideation was related to a reduced LPP to both rewarding and threatening images. These data suggest that dysfunction in neural markers of attention to threat and reward can effectively distinguish features of depression from anxiety, particularly early onset depression, and may track suicidal ideation across disorders.

Importance: It remains uncertain whether people with psychotic disorders experience progressive cognitive decline or normal cognitive aging after first hospitalization. This information is essential for prognostication in clinical settings, deployment of cognitive remediation, and public health policy. Objective: To examine long-term cognitive changes in individuals with psychotic disorders and to compare age-related differences in cognitive performance between people with psychotic disorders and matched control individuals (ie, individuals who had never had psychotic disorders). Design, Setting, and Participants: The Suffolk County Mental Health Project is an inception cohort study of first-admission patients with psychosis. Cognitive functioning was assessed 2 and 20 years later. Patients were recruited from the 12 inpatient facilities of Suffolk County, New York. At year 20, the control group was recruited by random digit dialing and matched to the clinical cohort on zip code and demographics. Data were collected between September 1991 and July 2015. Analysis began January 2016. Main Outcomes and Measures: Change in cognitive functioning in 6 domains: verbal knowledge (Wechsler Adult Intelligence Scale-Revised vocabulary test), verbal declarative memory (Verbal Paired Associates test I and II), visual declarative memory (Visual Reproduction test I and II), attention and processing speed (Symbol Digit Modalities Test-written and oral; Trail Making Test [TMT]-A), abstraction-executive function (Trenerry Stroop Color Word Test; TMT-B), and verbal fluency (Controlled Oral Word Association Test). Results: A total of 705 participants were included in the analyses (mean [SD] age at year 20, 49.4 [10.1] years): 445 individuals (63.1%) had psychotic disorders (211 with schizophrenia spectrum [138 (65%) male]; 164 with affective psychoses [76 (46%) male]; 70 with other psychoses [43 (61%) male]); and 260 individuals (36.9%) in the control group (50.5 [9.0] years; 134 [51.5%] male). Cognition in individuals with a psychotic disorder declined on all but 2 tests (average decline: d = 0.31; range, 0.17-0.54; all P

The five factor model (FFM) consists of cognitive-affective-behavioral trait dimensions (Neuroticism, Extraversion, Openness to experience, Agreeableness, and Conscientiousness) that are central to models of psychopathology. In adults, individual differences in three of the Big 5 traits, Neuroticism, Extraversion and Conscientiousness, have been linked to structural morphology and connectivity of the orbitofrontal cortex (OFC) and the amygdala, two brain regions critically involved in affective and regulatory processing. It is unclear whether these associations manifest in adolescence, a critical neurodevelopmental period during which many forms of psychiatric illness emerge. 223 adolescent girls (ages 14–16 years-old) completed a multimodal neuroimaging study that utilized T1-weighted structural MRI (e.g., cortical thickness and volume) and tractography-based diffusion tensor imaging (DTI; 64- direction). Cortical thickness and volume were extracted from the medial orbitofrontal cortex (mOFC) and amygdala and tractography-based fractional anisotropy (FA) was computed in the uncinate fasciculus (UF; the white matter tract connecting the OFC to the temporal lobe). We found that high Neuroticism was associated with less mOFC volume (bilateral), and low Conscientiousness was associated with higher white matter integrity in the UF, more amygdala volume, and less mOFC thickness (right-hemisphere). Extraversion was not observed to share associations with OFC markers. These OFC-amygdala structural correlations to personality do not match those reported in adult samples. Multi-modal neuroimaging techniques can help clarify the underpinnings of personality development between adolescence and adulthood.

Background Anxious youth are at increased risk for later depressive disorders, but not all anxious youth develop depression. Sequential comorbidity models emphasize shared risk factors and anxiety sequelae, but some anxious youth who later develop depression may have risk factors that are relatively specific to depression, in addition to a liability to anxiety. We examined several variables that appear relatively specific to risk for depression—the personality traits of low positive affectivity and high sadness, and an electrophysiological measure of blunted response to reward - in predicting first-onset depressive disorders and depressive symptoms in clinically anxious adolescent girls. Methods A sample of 114 adolescents with baseline anxiety disorders completed personality and psychopathology measures, psychophysiology tasks, and diagnostic interviews. Interviews and a measure of depressive symptoms were re-administered over 27 months. Results After controlling for baseline depressive symptoms, blunted reward sensitivity uniquely predicted first-onset depressive disorders and depressive symptoms 27 months later. Post-hoc analyses indicated that blunted reward sensitivity only predicted first-onset depressive disorders and depressive symptoms in girls with high social anxiety symptoms. Limitations Analyses were unable to account for concurrent anxiety symptoms and disorders. Conclusions The depression-specific risk factor, blunted reward sensitivity, may comprise one pathway to subsequent depressive disorders and symptoms in anxious youth and indicate which anxious youth need intervention to prevent later depression, particularly in socially anxious girls.

Several studies have reported differences between African Americans and Caucasians in relative proportion of psychotic symptoms and disorders, but whether this reflects racial bias in the assessment of psychosis is unclear. The purpose of this study was to examine the distribution of psychotic symptoms and potential bias in symptoms assessed via semi-structured interview using a cohort of 3,389 African American and 5,692 Caucasian participants who were diagnosed with schizophrenia, schizoaffective disorder, or bipolar disorder. In this cohort, the diagnosis of schizophrenia was relatively more common, and the diagnosis of bipolar disorder and schizoaffective disorder-bipolar type was less relatively common, among African Americans than Caucasians. With regard to symptoms, relatively more African Americans than Caucasians endorsed hallucinations and delusions symptoms, and this pattern was striking among cases diagnosed with bipolar disorder and schizoaffective-bipolar disorder. In contrast, the relative endorsement of psychotic symptoms was more similar among cases diagnosed with schizophrenia and schizoaffective disorder-depressed type. Differential item function analysis revealed that African Americans with mild psychosis over-endorsed "hallucinations in any modality" and under-endorsed "widespread delusions" relative to Caucasians. Other symptoms did not show evidence of racial bias. Thus, racial bias in assessment of psychotic symptoms does not appear to explain differences in the proportion of symptoms between Caucasians and African Americans. Rather, this may reflect ascertainment bias, perhaps indicative of a disparity in access to services, or differential exposure to risk factors for psychosis by race. © 2015 Wiley Periodicals, Inc.

Although psychiatric symptom severity and impairment are overlapping but nevertheless distinct illness parameters, little research has examined whether variables found to be associated with the severity are also correlated with symptom-induced impairment. Parents and teachers completed ratings of symptom-induced impairment for DSM-IV-referenced syndromes, and parents completed a background questionnaire for a consecutively referred sample of primarily male (81 %) 6-to-12 year olds with autism spectrum disorder (ASD) (N = 221). Some clinical correlates (e.g., IQ

OBJECTIVE: Kraepelin considered declining course a hallmark of schizophrenia, but others have suggested that outcomes usually stabilize or improve after treatment initiation. The authors investigated this question in an epidemiologically defined cohort with psychotic disorders followed for 20 years after first hospitalization. METHOD: The Suffolk County Mental Health Project recruited first-admission patients with psychosis from all inpatient units of Suffolk County, New York (response rate, 72%). Participants were assessed in person six times over two decades; 373 completed the 20-year follow-up (68% of survivors); 175 had schizophrenia/schizoaffective disorder. Global Assessment of Functioning (GAF), psychotic symptoms, and mood symptoms were rated at each assessment. Month 6, when nearly all participants were discharged from the index hospitalization, was used as a reference. RESULTS: In the schizophrenia group, mean GAF scores declined from 49 at month 6 to 36 at year 20. Negative and positive symptoms also worsened (Cohen's d values, 0.45-0.73). Among participants without schizophrenia, GAF scores were higher initially (a mean of approximately 64) but declined by 9 points over the follow-up period. Worsening began between years 5 and 8. Neither aging nor changes in antipsychotic treatment accounted for the declines. In all disorders, depression improved and manic symptoms remained low across the 20 years. CONCLUSIONS: The authors found substantial symptom burden across disorders that increased with time and ultimately may undo initial treatment gains. Previous studies have suggested that better health care delivery models may preempt this decline. In the United States, these care needs are often not met, and addressing them is an urgent priority.

Affective personality traits, such as extraversion and neuroticism, are associated with individual differences in reward system functioning. The reward positivity (ΔRewP) is an event-related potential (ERP) component that indexes sensitivity to reward, and can be elicited by feedback indicating monetary gains relative to losses. In a sample of 508 adolescent girls, the current study examined the relationship between extraversion, neuroticism, and their respective facets and the ΔRewP. Results indicated an Extraversion × Neuroticism interaction, such that greater extraversion was associated with an increased ΔRewP, but only in the context of low neuroticism. This association was primarily due to the extraversion facet positive emotionality—high levels of positive emotionality were associated with an increased ΔRewP, but only in the context of low neuroticism. In addition, increased neuroticism diminished the age-related increase in the ΔRewP. The current study suggests that both extraversion and neuroticism are associated with reward system function in adolescence.

Examined the psychiatric and clinical correlates of loss of previously acquired skills (regression) as reported by parents of youth with autism spectrum disorder (ASD). Study sample comprised 6- to 18-year old (N = 213) children and adolescents with ASD. Parents reported regression in 77 (36%) youth. A more homogeneous subgroup with regression between 18 and 36 months (n = 48) had higher rates of intellectual disability, epilepsy, and special education, more socially restrictive educational settings, and more severe ASD communication deficits and schizophrenia spectrum symptoms than non-regressed youth (n = 136). Similar results were obtained for a more inclusive definition of regression (n = 77). A brief parent report of developmental regression may be a useful clinical indicator of later general functioning.

Background Reduced cortical thickness is a candidate biological marker of depression, although findings are inconsistent. This could reflect analytic heterogeneity, such as use of region-wise cortical thickness based on the Freesurfer Desikan–Killiany (DK) atlas or surface-based morphometry (SBM). The Freesurfer Destrieux (DS) atlas (more, smaller regions) has not been utilized in depression studies. This could also reflect differential gender and age effects. Methods Cortical thickness was collected from 170 currently depressed adults and 52 never-depressed adults. Visually inspected and approved Freesurfer-generated surfaces were used to extract cortical thickness estimates according to the DK atlas (68 regions) and DS atlas (148 regions) for region-wise analysis (216 total regions) and for SBM. Results Overall, except for small effects in a few regions, the two region-wise approaches generally failed to discriminate depressed adults from nondepressed adults or current episode severity. Differential effects by age and gender were also rare and small in magnitude. Using SBM, depressed adults showed a significantly thicker cluster in the left supramarginal gyrus than nondepressed adults (P = 0.047) but there were no associations with current episode severity. Conclusions Three analytic approaches (i.e., DK atlas, DS atlas, and SBM) converge on the notion that cortical thickness is a relatively weak discriminator of current depression status. Differential age and gender effects do not appear to represent key moderators. Robust associations with demographic factors will likely hinder translation of cortical thickness into a clinically useful biomarker. Hum Brain Mapp, 2017. © 2017 Wiley Periodicals, Inc.

IntroductionResearch on the relationship between digital media exposure and child development is complex, inconsistent and fraught with debate. A highlighted area of inadequacy surrounds the methodological limitations of measuring digital media use for both researchers and clinicians, alike. This protocol aims to (1) identify core concepts in the area of screen time and digital media use in children and adolescents (2) map existing research paradigms and screening/measurement tools that serve to underpin and operationalise core concepts and (3) provide an initial step in integrating these findings into a consolidated screening toolkit. It is expected this enterprise will help advance research and clinical evaluation in fields concerned with digital media use, namely medicine, child development and the social sciences.Methods and analysisThe planned scoping review will search relevant electronic databases, including Ovid MEDLINE, PsycINFO and Scopus, in addition to grey literature. All empirical investigations and presentation of original research will be considered, and measurement/screening tools for digital media usage in children and adolescents will be identified and reported on. Two reviewers will pilot test the screening criteria, and data extraction forms prior to independently screening all relevant literature and extracting the data. A three-stage synthesis process will be used to map the existent measurement and screening tools for digital media usage in children and adolescents.Ethics and disseminationThere are no ethical considerations for this scoping review. Plans for dissemination include publication in a top-tier, open-access journal, public presentations and conference proceedings. Presentation of the full scoping review has been accepted to the American Academy of Child & Adolescent Psychiatry 66th Annual Meeting.

Objective:\ud Social impairment is a long-recognized core feature of schizophrenia and is common in other psychotic disorders. Still, to date the long-term trajectories of social impairment in psychotic disorders have rarely been studied systematically.\ud \ud Methods:\ud Data came from the Suffolk County Mental Health Project, a 20-year prospective study of first-admission patients with psychotic disorders. A never-psychotic comparison group was also assessed. Latent class growth analysis was applied to longitudinal data on social functioning from 485 respondents with schizophrenia spectrum disorders and psychotic mood disorders, and associations of the empirically derived trajectories with premorbid social adjustment, diagnosis, and 20-year outcomes were examined.\ud \ud Results:\ud Four mostly stable trajectories of preserved (N=82; 59th percentile of comparison group sample distribution), moderately impaired (N=148; 17th percentile), severely impaired (N=181; 3rd percentile), and profoundly impaired (N=74; 1st percentile) functioning best described the 20-year course of social functioning across diagnoses. The outcome in the group with preserved functioning did not differ from that of never-psychotic individuals at 20 years, but the other groups functioned significantly worse. Differences among trajectories were already evident in childhood. The two most impaired trajectories started to diverge in early adolescence. Poorer social functioning trajectories were strongly associated with other real-world outcomes at 20 years. Multiple trajectories were represented within each disorder. However, more participants with schizophrenia spectrum disorders had impaired trajectories, and more with mood disorders had better functioning trajectories.\ud \ud Conclusions:\ud The results highlight substantial variability of social outcomes within diagnoses—albeit overall worse social outcomes in schizophrenia spectrum disorders—and show remarkably stable long-term impairments in social functioning after illness onset across all diagnoses.

A blunted neural response to rewards has recently emerged as a potential mechanistic biomarker of adolescent depression. The reward positivity, an event-related potential elicited by feedback indicating monetary gain relative to loss, has been associated with risk for depression. The authors examined whether the reward positivity prospectively predicted the development of depression 18 months later in a large community sample of adolescent girls.The sample included 444 girls 13.5-15.5 years old with no lifetime history of a depressive disorder, along with a biological parent for each girl. At baseline, the adolescents' reward positivity was measured using a monetary guessing task, their current depressive symptoms were assessed using a self-report questionnaire, and the adolescents' and parents' lifetime psychiatric histories were evaluated with diagnostic interviews. The same interview and questionnaire were administered to the adolescents again approximately 18 months later.A blunted reward positivity at baseline predicted first-onset depressive disorder and greater depressive symptom scores 18 months later. The reward positivity was also a significant predictor independent of other prominent risk factors, including baseline depressive symptoms and adolescent and parental lifetime psychiatric history. The combination of a blunted reward positivity and greater depressive symptom scores at baseline provided the greatest positive predictive value for first-onset depressive disorder.This study provides strong converging evidence that a blunted neural response to rewards precedes adolescent-onset depression and symptom emergence. Blunted neural response may therefore constitute an important target for screening and prevention.

Many previous studies have indicated that individuals who are depressed or at risk for depression are characterized by increased levels of morning cortisol and a greater cortisol awakening response (CAR). However, despite the high comorbidity between depressive and anxiety disorders, fewer studies have examined whether these diurnal cortisol abnormalities are also characteristic of anxiety or risk for anxiety.In the present study we examined cortisol in a community sample of 476 female adolescents and related it to maternal history of depression and/or anxiety disorders. Salivary cortisol was collected at waking, 30min post waking, and in the evening on three weekdays.Contrary to prior results, offspring at risk for depression did not have increased morning cortisol or CAR. However, offspring at risk for anxiety disorders had elevated 30min cortisol and total cortisol produced throughout the day; this effect was primarily driven by offspring of mothers with panic disorder or agoraphobia. Additionally, levels of cortisol were highest among offspring of mothers with multiple anxiety diagnoses.The study is limited to female adolescents and maternal diagnostic history. Additionally, some diagnoses could not be examined as a result of too few cases (e.g. GAD).Overall, these results underscore the importance of considering anxiety when examining the association of diurnal cortisol abnormalities with risk for psychopathology, as it may have influenced prior observations of elevated morning cortisol in depression.