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Common transdiagnostic cognitive deficits among people with psychiatric disorders exposed to childhood maltreatment: a meta-analysis
Abstract
Introduction:
Previous meta-analyses have shown a moderate negative impact of maltreatment on the neuropsychological functioning of people with or without psychiatric disorders compared to healthy groups. The objectives of the present meta-analysis were to (1) investigate the impact of maltreatment on neuropsychological functioning of people with psychiatric disorders and to (2) evaluate the moderating effect of age, at the time of the cognitive assessment, on neuropsychological functioning.
Methods:
Seventeen studies published between 1970 and July 2017 were included.
Results:
The results showed a negative impact of maltreatment with a small effect size (g = -0.25) on the neuropsychological performances in the group with psychiatric disorders with a history of exposure to childhood maltreatment compared to the group with psychiatric disorders without a history of exposure to childhood maltreatment. Cognitive domains that are significantly affected by maltreatment are: working memory (g = -0.56), verbal episodic memory (g = -0.39), intelligence (g = -0.27) and processing speed (g = -0.21). The impact of childhood maltreatment on the cognitive profile is greater in adults than young people.
Conclusions:
Clinicians should consider these common cognitive deficits using a transdiagnostic approach in cognitive interventions.
... The same issues of high levels of symptom heterogeneity, cross-disorder homogeneity and comorbidity in adult psychopathology has led to a shift toward using symptom dimensions rather than singular diagnostic labels to understand these complex conditions (Cuthbert & Insel, 2013;Owen, 2014). This transdiagnostic approach opens up the possibility of tailoring interventions to the constellation of needs of the individual rather than to a single and potentially ill-fitting diagnostic label, with promising applications of this approach in the areas of depression, anxiety, and psychosis (e.g., Mercier, Masson, Bussières, & Cellard, 2018;Newby, Mc-Kinnon, Kuyken, Gilbody, & Dalgleish, 2015;Reininghaus et al., 2019;Sakiris & Berle, 2019;Titov et al., 2011). ...
... Although the value of extending this approach to neurodevelopmental disorders has been widely recognized (Casey et al., 2014;Sonuga-Barke, Cortese, Fairchild, & Stringaris, 2016;Sonuga-Barke & Coghill, 2014;Zhao & Castellanos, 2016), the majority of studies espousing this approach over the past decade have compared cognitive or behavioral symptoms across groups of children with conventionally defined disorders such as reading difficulties, math difficulties, ADHD, or ASD with typically developing individuals (de Jong, Bitter, van Setten, & Marinus, 2009;Hobson, 2014;Karalunas et al., 2014;Mercier et al., 2018;Willcutt et al., 2013). ...
... A latent variable approach was adopted to identify the primary cognitive dimensions of the sample, in line with data-driven approaches recently adopted in other transdiagnostic, dimensional studies (e.g., Kotov et al., 2017;Mercier et al., 2018;Reininghaus et al., 2019;Sokolova et al., 2017). This approach side-steps debates about which of two different measures sharing common variance represents the core deficit (e.g., phonological processing or verbal STM in reading difficulties). ...
A data-driven, transdiagnostic approach was used to identify the cognitive dimensions linked with learning in a mixed group of 805 children aged 5 to 18 years recognised as having problems in attention, learning and memory by a health or education practitioner. Assessments included phonological processing, information processing speed, short-term and working memory, and executive functions, and attainments in word reading, spelling, and maths. Data reduction methods identified three dimensions of phonological processing, processing speed and executive function for the sample as a whole. This model was comparable for children with and without ADHD. The severity of learning difficulties in literacy was linked with phonological processing skills, and in maths with executive control. Associations between cognition and learning were similar across younger and older children and individuals with and without ADHD, although stronger links between learning-related problems and both executive skills and processing speed were observed in children with ADHD. The results establish clear domain-specific cognitive pathways to learning that distinguish individuals in the heterogeneous population of children struggling to learn.
... Interestingly, several studies report that the childhood trauma might accentuate these deficits (Jiménez et al., 2017;Masson et al., 2016;Quide et al., 2017;Russo et al., 2015). Thus, the cognitive impairments observed in these individuals could be related to the effects of childhood trauma to neurodevelopment (Alexandra et al., 2018;Brietzke et al., 2012;Tendolkar et al., 2018). ...
... The first five years of life is the period when the brain develops with greater intensity, although its complete maturation only occurs during early adult life. Therefore, the impact of this hormonal imbalance may affect the normal course of brain development (Danese et al., 2017;Malarbi et al., 2017), what could explain the association between childhood trauma and alterations on prefrontal cortex, corpus callosum amygdala, hippocampus, and hypothalamic-pituitary-adrenal axis (Aas et al., 2012;Alexandra et al., 2018;Brietzke et al., 2012;Glaser, 2000 Consequently, these brain abnormalities are linked to cognitive impairments. Two meta-analyses that investigated the impact of childhood maltreatment on cognition found deficits in working memory, verbal episodic memory, processing speed, attention, executive function, and intelligence. ...
... Two meta-analyses that investigated the impact of childhood maltreatment on cognition found deficits in working memory, verbal episodic memory, processing speed, attention, executive function, and intelligence. Moreover, they emphasized that the combination of mental disorder diagnosis and maltreatment can accentuate these deficits (Alexandra et al., 2018;Masson et al., 2016). However, what may be more critical to deficits in working memory, verbal episodic memory and intelligence is the exposure to childhood maltreatment and not the psychiatric diagnosis itself (Alexandra et al., 2018). ...
Maltreatments in childhood may have implications for neurodevelopment that could remain throughout life. Childhood trauma seems to be associated with the onset of bipolar disorder (BD), and its occurrence might accentuate the overall disease impairments related to cognitive deficits in BD. We aimed to evaluate the effects of a history of childhood trauma to estimated intellectual functioning (IQ) of individuals with BD. We included 72 subjects with BD during euthymia. Participants underwent a clinical interview and were assessed through the Childhood Trauma Questionnaire (CTQ) and Wechsler Abbreviated Scale of Intelligence (WASI). Most prevalent trauma subtypes were emotional abuse and neglect (54.1%). A linear regression model that included perceived childhood trauma, family history of severe mental disorders, age at diagnosis and psychotic symptoms during the first episode as main factors showed that only childhood trauma had a significant effect in predicting estimated IQ. Therefore, the history of childhood trauma in individuals with BD may play a role in intellectual development, suggesting that adversities during development result in decreased general cognitive abilities. These results reinforce the need to promote early interventions to protect childhood and to promote the well-being of children, contributing to the growth of healthy adults.
... Similarly, PTEs have been extensively and independently linked to mental health problems (Gardner et al., 2019;Kessler et al., 2010;R.-Mercier et al., 2018), substance use disorders (Puetz and McCrory, 2015;Sebalo et al., 2023), and neurocognitive difficulties (Hawkins et al., 2021;Kavanaugh et al., 2017;Lund et al., 2020;Puetz and McCrory, 2015;R.-Mercier et al., 2018). Many PTEs do not result in direct structural brain damage (e.g., emotional neglect will not lesion the brain) but can hel ...
... Similarly, PTEs have been extensively and independently linked to mental health problems (Gardner et al., 2019;Kessler et al., 2010;R.-Mercier et al., 2018), substance use disorders (Puetz and McCrory, 2015;Sebalo et al., 2023), and neurocognitive difficulties (Hawkins et al., 2021;Kavanaugh et al., 2017;Lund et al., 2020;Puetz and McCrory, 2015;R.-Mercier et al., 2018). Many PTEs do not result in direct structural brain damage (e.g., emotional neglect will not lesion the brain) but can help rewire brain circuitry, leading to challenges in mental health, substance use, and neurocognition. ...
Purpose
Traumatic brain injury (TBI) and potentially traumatic events (PTEs) contribute to increased substance use, mental health issues, and cognitive impairments. However, there's not enough research on how TBI and PTEs combined impact mental heath, substance use, and neurocognition.
Methods
This study leverages a subset of The National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) multi-site dataset with 551 adolescents to assess the combined and distinctive impacts of TBI, PTEs, and TBI+PTEs (prior to age 18) on substance use, mental health, and neurocognitive outcomes at age 18.
Results
TBI, PTEs, and TBI+PTEs predicted greater lifetime substance use and past-year alcohol and cannabis use. PTEs predicted greater internalizing symptoms, while TBI+PTEs predicted greater externalizing symptoms. Varying effects on neurocognitive outcomes included PTEs influencing attention accuracy and TBI+PTEs predicting faster speed in emotion tasks. PTEs predicted greater accuracy in abstraction-related tasks. Associations with working memory were not detected.
Conclusion
This exploratory study contributes to the growing literature on the complex interplay between TBI, PTEs, and adolescent mental health, substance use, and neurocognition. The developmental implications of trauma via TBIs and/or PTEs during adolescence are considerable and worthy of further investigation.
... CM can be divided into abuse, which is an exposure to threatening behaviours, and neglect, a deprivation of cognitive and psychosocial stimulation. CM is associated with deficits in memory and executive function (Majer, Nater, Lin, Capuron, & Reeves, 2010;Nikulina & Widom, 2013), independent of psychopathology (R-Mercier, Masson, Bussières, & Cellard, 2018). Thus, neurobiological consequences of CM may be deemed as a potential explanation for poor cognitive functioning in MDD (Gould et al., 2012;Kaczmarczyk, Wingenfeld, Kuehl, Otte, & Hinkelmann, 2018). ...
... Early exposure to stress has been mostly related to an increased risk for the development of psychopathology after experiencing subsequent stressors in adulthood (Heim, Newport et al., 2008). This is because early life stress alters corticolimbic brain systems that regulate stress and anxiety, disrupts the acquisition of appropriate coping styles, induces alterations in baseline activity as well as stress reactivity of the HPA axis, diminishes the volumes of the hippocampus and the prefrontal cortex (Stein, Koverola, Hanna, Torchia, & McClarty, 1997;Van Harmelen et al., 2010), and impairs cognition (Heim, Newport et al., 2008;Majer et al., 2010;McEwen, 2007;Nikulina & Widom, 2013;Pryce, Dettling, Spengler, Spaete, & Feldon, 2004;Pryce et al., 2005), independent of psychopathology (R-Mercier et al., 2018). There is evidence that prior exposure to moderate (but not minimal or substantial) stress levels, which are challenging enough to evoke acute anxiety and transiently activate the HPA axis, fosters the development of resilience to subsequent stressors encountered later in life (Parker, Buckmaster, Hyde, Schatzberg, & Lyons, 2019;Parker & Maestripieri, 2011). ...
Background: Childhood maltreatment (CM) is associated with impaired hypothalamic-pituitary-adrenal (HPA) axis negative feedback and cognitive dysfunction, resembling those abnormalities linked to major depressive disorder (MDD).
Objectives: We aimed to assess the potential modulating effects of MDD diagnosis or HPA axis function in the association between different types of CM and cognitive performance in adulthood.
Methods: Sixty-eight MDD patients and 87 healthy controls were recruited. CM was assessed with the Childhood Trauma Questionnaire. We obtained three latent variables for neuropsychological performance (verbal memory, visual memory and executive function/processing speed) after running a confirmatory factor analysis with cognitive tests applied. Dexamethasone suppression test ratio (DSTR) was performed using dexamethasone 0.25 mg.
Results: Different types of CM had different effects on cognition, modulated by MDD diagnosis and HPA axis function. Individuals with physical maltreatment and MDD presented with enhanced cognition in certain domains. The DSTR differentially modulated the association between visual memory and physical neglect or sexual abuse.
Conclusions: HPA axis-related neurobiological mechanisms leading to cognitive impairment might differ depending upon the type of CM. Our results suggest a need for early assessment and intervention on cognition and resilience mechanisms in individuals exposed to CM to minimize its deleterious and lasting effects.
... These neurobiological alterations are accompanied by functional deficits in various cognitive domains. While deteriorating effects of CM on working memory, attention, and intelligence have been reported consistently [10][11][12], there are mixed results regarding episodic memory, processing speed, and executive functioning [10,11,13]. Previous metaanalyses seem to disagree on whether CM-associations with cognitive functioning are evident nonspecifically across cognitive domains or differ across domains. ...
... One meta-analysis comparing healthy CM and non-CM groups found widespread cognitive deficits in the CM group irrespective of the cognitive domains [11]. Another meta-analysis investigating samples with several psychiatric diagnoses found that largest effects of CM on cognition were evident in the attention and visual episodic memory domains, while no associations were observed for visuospatial working memory and executive functioning [13]. On the contrary, Masson et al. (2016) found in their meta-analysis that the strongest associations between CM and cognition were evident in the executive functioning domain [14]. ...
Childhood maltreatment is associated with cognitive deficits that in turn have been predictive for therapeutic outcome in psychiatric patients. However, previous studies have either investigated maltreatment associations with single cognitive domains or failed to adequately control for confounders such as depression, socioeconomic environment, and genetic predisposition. We aimed to isolate the relationship between childhood maltreatment and dysfunction in diverse cognitive domains, while estimating the contribution of potential confounders to this relationship, and to investigate gene–environment interactions. We included 547 depressive disorder and 670 healthy control participants (mean age: 34.7 years, SD = 13.2). Cognitive functioning was assessed for the domains of working memory, executive functioning, processing speed, attention, memory, and verbal intelligence using neuropsychological tests. Childhood maltreatment and parental education were assessed using self-reports, and psychiatric diagnosis was based on DSM-IV criteria. Polygenic scores for depression and for educational attainment were calculated. Multivariate analysis of cognitive domains yielded significant associations with childhood maltreatment (η²p = 0.083, P < 0.001), depression (η²p = 0.097, P < 0.001), parental education (η²p = 0.085, P < 0.001), and polygenic scores for depression (η²p = 0.021, P = 0.005) and educational attainment (η²p = 0.031, P < 0.001). Each of these associations remained significant when including all of the predictors in one model. Univariate tests revealed that maltreatment was associated with poorer performance in all cognitive domains. Thus, environmental, psychopathological, and genetic risk factors each independently affect cognition. The insights of the current study may aid in estimating the potential impact of different loci of interventions for cognitive dysfunction. Future research should investigate if customized interventions, informed by individual risk profiles and related cognitive preconditions, might enhance response to therapeutic treatments.
Variable effect sizes are compared in a reduced model with only one predictor while controlling for age and sex (dark gray), and in a full model controlling for age, sex, MDD diagnosis, PE, and polygenic scores for MDD and EdA (light gray). CM childhood maltreatment, MDD major depressive disorder, PE parental education, PGS polygenic score, EdA educational attainment.
... CM can be divided into abuse, which is an exposure to threatening behaviours, and neglect, a deprivation of cognitive and psychosocial stimulation. CM is associated with deficits in memory and executive function (Majer, Nater, Lin, Capuron, & Reeves, 2010;Nikulina & Widom, 2013), independent of psychopathology (R-Mercier, Masson, Bussières, & Cellard, 2018). Thus, neurobiological consequences of CM may be deemed as a potential explanation for poor cognitive functioning in MDD (Gould et al., 2012;Kaczmarczyk, Wingenfeld, Kuehl, Otte, & Hinkelmann, 2018). ...
... Early exposure to stress has been mostly related to an increased risk for the development of psychopathology after experiencing subsequent stressors in adulthood (Heim, Newport et al., 2008). This is because early life stress alters corticolimbic brain systems that regulate stress and anxiety, disrupts the acquisition of appropriate coping styles, induces alterations in baseline activity as well as stress reactivity of the HPA axis, diminishes the volumes of the hippocampus and the prefrontal cortex (Stein, Koverola, Hanna, Torchia, & McClarty, 1997;Van Harmelen et al., 2010), and impairs cognition (Heim, Newport et al., 2008;Majer et al., 2010;McEwen, 2007;Nikulina & Widom, 2013;Pryce, Dettling, Spengler, Spaete, & Feldon, 2004;Pryce et al., 2005), independent of psychopathology (R-Mercier et al., 2018). There is evidence that prior exposure to moderate (but not minimal or substantial) stress levels, which are challenging enough to evoke acute anxiety and transiently activate the HPA axis, fosters the development of resilience to subsequent stressors encountered later in life (Parker, Buckmaster, Hyde, Schatzberg, & Lyons, 2019;Parker & Maestripieri, 2011). ...
Obesity and the metabolic syndrome (MetS) predispose to multiple diseases and to accelerated cell aging as indexed by accelerated shortening of telomeres in peripheral blood mononuclear cells (PBMC's). Major depressive disorder (MDD) is often associated with MetS and is also associated with increased disease risk and PBMC telomere shortening. A potential role of leptin in telomere shortening has been suggested, but prior results have been inconsistent and no study has yet assessed this relationship in MDD. The goal of this study was to assess the relationship between serum leptin concentrations and PBMC telomere length in MDD and in controls and to assess whether this relationship is mediated by body-mass index (BMI) or the homeostatic model assessment of insulin resistance (HOMA-IR), two principal components of the MetS.Eighteen medication-free MDD subjects (11 female, 7 male, mean age 37.1 + 2.7 years) and 17 healthy controls (11 female, 6 male, mean age 37.8 + 3.0 years) had blood drawn for assay of fasting morning levels of leptin, glucose, and insulin and PBMC telomere length. The groups did not differ on BMI (24.66 + 3.72 vs. 24.77 + 4.29, respectively, n.s.). Analyses were co-varied for age and sex, with and without BMI.In the combined group, serum leptin concentrations were inversely correlated with telomere length (r= − 0.33, p<0.02), with and without co-varying for BMI. This relationship remained significant in the MDD group alone (r= − 0.54, p<0.04) but missed significance in the controls (r= − 0.23, ns). Hierarchical linear regression, entering BMI and HOMA-IR prior to leptin (with telomere length the dependent variable) showed that BMI and HOMA-IR were not significantly correlated with telomere length (t=1.04, p>0.30, and t=1.49, p>0.10, respectively), but leptin concentrations remained significantly correlated with telomere length (t= − 2.88, p=0.007).Relatively high leptin concentrations, in the presence or absence of increased BMI and insulin resistance, may be a risk factor for telomere shortening. While this was demonstrated here in individuals with MDD, a similar relationship in non-depressed individuals cannot be ruled out because of the small sample size.
... doubting one's memories. Despite this common assumption, the impact of gaslighting on memory has yet to be empirically tested. Assessing the impact of gaslighting on memory is particularly important in light of extensive evidence that other forms of interpersonal victimization, such as abuse, result in profound memory deficits (Masson et al., 2016;R.-Mercier et al., 2018;Su et al., 2019) and biases (Ayoub et al., 2006;Vrijsen et al., 2017). Given that general interpersonal victimization can impact memory, it is plausible that very intense gaslighting experiences (i.e., those that approach being traumatic or abusive) may have especially pronounced effects on memory. Memory deficits can be debilitating and ...
Gaslighting is a form of psychological manipulation where victims are led to doubt their own thoughts, perception of reality, or memories. Despite the growing popularity of the term and purported harmful implications, empirical efforts to operationalize and define gaslighting remain sparse. This study aimed to define common features and themes of self-reported gaslighting experiences. Young adults (N=250) completed several questionnaires and open-ended prompts relating to gaslighting experiences. Using a variety of natural language processing techniques, we explore the gaslighting construct using a data-driven approach from the perspective of self-reported targets of gaslighting. These data confirm that gaslighting is a type of interpersonal manipulation aimed at making a person feel 'crazy' or doubt their memories. Romantic partners were reported to be the most common perpetrators of gaslighting, and both beneficial (e.g., awareness of manipulative people) and detrimental (e.g., self-doubt) consequences of experiencing gaslighting appear to be long-lasting. Additionally, we found that more severe, frequent, and long-lasting gaslighting experiences are associated with broader subjective memory deficits, even extending to other memories outside of the gaslighting event itself. This study highlights pervasive cognitive and psychological impacts of gaslighting, and underscores the need for further empirical research and informed clinical strategies.
... Consistent with data-driven approaches adopted across transdiagnostic studies (e.g., Holmes et al., 2021;Kotov et al., 2017;Mercier et al., 2018;Reininghaus et al., 2019;Sokolova et al., 2017) a latent variable approach was used to identify dimensions of difficulty in the whole sample, and then to test whether these dimensions differed in structure and severity between boys and girls. Identifying dimensions side-steps debates about which of two different measures sharing common variance represents a core deficit or difference, and instead identifies the major sources of variance across all measures in a dataset. ...
Background:
Fewer girls than boys are identified as struggling at school for suspected problems in attention, learning and/or memory. The objectives of this study were to: i) identify dimensions of cognition, behaviour and mental health in a unique transdiagnostic sample of struggling learners; ii) test whether these constructs were equivalent for boys and girls, and; iii) compare their performance across the dimensions.
Methods:
805 school-aged children, identified by practitioners as experiencing problems in cognition and learning, completed cognitive assessments, and parents/carers rated their behaviour and mental health problems.
Results:
Three cognitive [Executive, Speed, Phonological], three behavioural [Cognitive Control, Emotion Regulation, Behaviour Regulation], and two mental health [Internalising, Externalising] dimensions distinguished the sample. Dimensions were structurally comparable between boys and girls, but differences in severity were present: girls had greater impairments on performance-based measures of cognition; boys were rated as having more severe externalising problems.
Conclusions:
Gender biases to stereotypically male behaviours are prevalent among practitioners, even when the focus is on identifying cognitive and learning difficulties. This underscores the need to include cognitive and female-representative criteria in diagnostic systems to identify girls whose difficulties could go easily undetected.
... -Mercier et al., 2018;Reininghaus et al., 2019;Titov et al., 2011), but there is widespread recognition of its value for characterising developmental disorders in terms of underlying dimensions of symptoms(Casey et al., 2014;Snowling & Hulme, 2012; Sonuga-Barke et al., 2016b;Sonuga-Barke & Coghill, 2014;Zhao & Castellanos, 2016). One of the most common methods for understanding how symptoms are related uses latent variable models, a statistical method that groups variables based on shared variance to derive underlying dimensions of difficulties(Kotov et al., 2017; see Chapter I, Section 2.3.1 for a detailed description of this approach) This technique has been used to identify dimensions of phonological and non-phonological skills in children with diagnosed DLD and dyslexia(Ramus et al., 2013); and separate latent constructs for inattention and hyperactivity in children with ADHD(Martel et al., 2010).Network analysis offers an alternative approach to understanding symptom interrelations. ...
Neurodevelopmental difficulties can have a substantial impact on children’s lives and often have lasting effects in adult life. The scientific study of the causes and consequences of neurodevelopmental difficulties has arguably been slowed by the overreliance on case-control designs, which fail to capture the overlap across different neurodevelopmental disorders and the heterogeneity within them. The work presented in this thesis applies a transdiagnostic framework to large developmental datasets to advance our understanding of neurodevelopmental diversity. Three empirical studies were conducted with a cohort of children with a range of diagnosed and undiagnosed needs. The first study explored the interrelationships between language, communication, cognitive, and behavioural difficulties using network science (Chapter I). A subsequent study investigated how children vary in their relative strengths and weakness across these domains, and how this variation relates to socio-emotional functioning, academic skills, and neural white matter organisation (Chapter II). The third study compared the pattern of interrelationships between cognitive and academic skills observed in this cohort to those found in a community sample (Chapter III). Collectively, the studies presented in this thesis demonstrate the value of studying neurodevelopmental diversity transdiagnostically. I argue that the field needs to move away from studying groups of children with restricted difficulties and dedicate more effort towards understanding how multiple developmental factors interact to shape individual trajectories over developmental time.
... Previous findings in patients across a range of various disorders, including psychosis, and healthy controls on reduced cognitive abilities when childhood maltreatment had occurred [13][14][15][16][17]69] support our results for the subtype of childhood maltreatment physical abuse. Further, the current study revealed that being in a CHR state was associated with lower scores in verbal memory. ...
Introduction:
Childhood maltreatment is associated with both reduced cognitive functioning and the development of psychotic symptoms. However, the specific relationship between childhood maltreatment, cognitive abilities and (pre)psychotic symptoms remains unclear. Therefore, the aim of this study was to investigate the association between childhood maltreatment and tasks of verbal memory and processing speed in a help-seeking sample of an early detection of psychosis service.
Methods:
A total of 274 participants consisting of 177 clinical high risk (CHR) for psychosis subjects and 97 clinical controls (CC) with subthreshold CHR underwent a battery of neurocognitive assessments measuring the latent variables verbal memory and processing speed. Additionally, the Trauma and Distress Scale (TADS) was administered to assess varying childhood maltreatment subtypes. Structural equation modeling (SEM) was used to examine associations between verbal memory, processing speed, and maltreatment subtypes. Other factors in the model were age, gender, clinical group (CHR or CC), and the presence of different CHR criteria.
Results:
Physical abuse was associated with lower scores in verbal memory and processing speed. The explained variance in the SEM reached up to 9.5% for verbal memory and 24.9% for processing speed. Both latent variables were each associated with the presence of cognitive-perceptive basic symptoms. Lower verbal memory was additionally associated with the clinical high-risk group, and processing speed capacity was associated with higher age and female gender.
Conclusion:
Childhood physical abuse in particular was associated with poorer performance on verbal memory and processing speed across both groups of CHR and CC with subthreshold CHR symptoms. This adds to the current literature on reduced cognitive abilities when childhood maltreatment had occurred, albeit subtype dependent. Our findings, together with high prevalence rates of childhood maltreatment in patients with psychosis or CHR states, along with the presence of cognitive deficits in these patients, highlight the importance of not only assessing cognition but also childhood maltreatment in managing these patients. Future research should investigate the specific biological mechanisms of childhood maltreatment on verbal memory and processing speed in CHR subjects, as neurobiological alterations might explain the underlying mechanisms.
... Neurocognitive deficits are considered a core feature of many psychiatric disorders. Patients with psychiatric disorders, who also have a history of ACEs have greater deficits compared to those without history of ACEs (R. -Mercier et al., 2018). A meta-analysis of 23 studies with a total of 3315 patients with psychotic disorders (Vargas et al., 2019), examined the relationship between ACEs and overall neurocognitive functioning for four subdomains (working memory, executive function, verbal/visual memory, and attention/processing speed). ...
Background: Neurocognitive deficits are considered an endophenotype for several psychiatric disorders, typically studied in unaffected first-degree relatives (FDRs). Environmental factors such as adverse childhood experiences (ACEs) may also affect neurocognition. This study examines the effect of ACEs on neurocognitive performance in FDRs of patients with severe mental illness in order to determine whether familial risk has a moderating effect on the relationship between ACEs and neurocognition.
Methods: The sample consists of a total of 512 individuals composed of unaffected FDRs from multiplex families with severe mental illnesses (schizophrenia, bipolar disorder, obsessive-compulsive disorder or alcohol use disorder) and healthy controls (with no familial risk). Neurocognitive tests included processing speed (Color Trails), new learning (Auditory Verbal Learning Test), working memory (N-Back), and Theory of Mind (SOCRATIS). ACEs were measured using the WHO ACE-International Questionnaire (ACE-IQ). Regression models adjusted for age, gender and education were done to predict each neurocognitive domain by the effect of familial risk, ACE-IQ Total Score and the interaction (familial risk x ACE-IQ Total score).
Results: When all FDRs were examined as a group, the main effect of familial risk predicted poor performance in all domains of neurocognition (p <0.01), and the ACEs x familial risk interaction had a significant negative association with global neurocognition, processing speed & working memory. This interaction effect was driven predominantly by the familial risk of AUD. In FDRs of schizophrenia & bipolar disorder, only the main effects of familial risk were significant (working memory, theory of mind & global neurocognition), with no impact of ACEs or its interaction in both these sub-groups.
Conclusions: The impact of childhood adversity on neurocognition is moderated by familial risk of psychiatric disorders. Genetic or familial vulnerability may play a greater role in disorders such as schizophrenia and bipolar disorder, while the interaction between ACEs and family history may be more relevant in the case of disorders with greater environmental risk, such as substance use.
... Crucially, it maps all measures in a multidimensional space (all indicators load on all components at each level of the hierarchy), and allows each level of the hierarchy to retain all the variance in the patterns of covariation among the symptoms. In retaining what is shared between indicators at each level of hierarchy, this approach is congruent with transdiagnostic approaches that aim to understand the shared mechanisms underlying symptoms that co-occur across traditional categorical disorders (e.g., Cuthbert & Insel, 2013;R-Mercier et al., 2018;Newby et al., 2015;Owen, 2014;Reininghaus et al., 2019;Sakiris & Berle, 2019;Titov et al., 2011). ...
Hierarchical dimensional models of psychopathology derived for adult and child community populations offer more informative and efficient methods for assessing and treating symptoms of mental ill health than traditional diagnostic approaches. It is not yet clear how many dimensions should be included in models for youth with neurodevelopmental conditions. The aim of this study was to delineate the hierarchical dimensional structure of psychopathology in a transdiagnostic sample of children and adolescents with learning-related problems, and to test the concurrent predictive value of the model for clinically, socially, and educationally relevant outcomes. A sample of N = 403 participants from the Centre for Attention Learning and Memory (CALM) cohort were included. Hierarchical factor analysis delineated dimensions of psychopathology from ratings on the Conner's Parent Rating Short Form, the Revised Children's Anxiety and Depression Scale, and the Strengths and Difficulties Questionnaire. A hierarchical structure with a general p factor at the apex, broad internalizing and broad externalizing spectra below, and three more specific factors (specific internalizing, social maladjustment, and neurodevelopmental) emerged. The p factor predicted all concurrently measured social, clinical, and educational outcomes, but the other dimensions provided incremental predictive value. The neurodevelopmental dimension, which captured symptoms of inattention, hyperactivity, and executive function and emerged from the higher-order externalizing factor, was the strongest predictor of learning. This suggests that in struggling learners, cognitive and affective behaviors may interact to influence learning outcomes. (PsycInfo Database Record (c) 2021 APA, all rights reserved).
... Therefore, these predictors should be validated in prospective controlled studies, focusing on long-term outcomes to build on the findings presented here. In addition, there may be other important predictors that were not included in this study, e.g., the therapeutic relationship [93], motivational processes [94][95][96], and patient adherence [97,98], childhood maltreatment [99], and expectations [100]. Future studies should routinely collect data on therapist variables (e.g., experience as indicated by years of training, level of competence as indicated by interpersonal skill set) and the therapeutic relationship using adequate measures. ...
The objectives of this study were to investigate the naturalistic effectiveness of routine inpatient treatment for patients with obsessive–compulsive disorder (OCD) and to identify predictors of treatment outcome. A routinely collected data set of 1,596 OCD inpatients (M = 33.9 years, SD = 11.7; 60.4% female) having received evidence-based psychotherapy based on the cognitive–behavioral therapy (CBT) in five German psychotherapeutic clinics was analyzed. Effect sizes (Hedges' g) were calculated for several outcome variables to determine effectiveness. Predictor analyses were performed on a subsample (N = 514; M = 34.3 years, SD = 12.2; 60.3% female). For this purpose, the number of potential predictors was reduced using factor analysis, followed by multiple regression analysis to identify robust predictors. Effect sizes of various outcome variables could be classified as large (g = 1.34 of OCD–symptom change). Predictors of changes in OCD and depressive symptoms were symptom severity at admission and general psychopathological distress. In addition, patients with higher social support and more washing compulsions benefited more from treatment. Subgroup analyses showed a distinct predictor profile of changes in compulsions and obsessions. The results indicate that an evidence-based psychotherapy program for OCD can be effectively implemented in routine inpatient care. In addition to well-established predictors, social support, and washing compulsions in particular were identified as important positive predictors. Specific predictor profiles for changes in obsessions and compulsions are discussed.
... Over the past decade, there has been a broad shift away from diagnosis-specific deficits toward identifying dimensions that cut across disorders conventionally considered to be distinct [14,15]. This approach has been applied most widely to adult psychiatric conditions [16][17][18], but there is widespread recognition of its value for characterising developmental disorders in terms of underlying dimensions of symptoms [19][20][21][22][23]. One of the most common methods for understanding how symptoms are related uses latent variable models, a statistical method that groups variables based on shared variance to derive underlying dimensions of difficulties [24]. ...
Background:
Communication, behavioural, and executive function problems often co-occur in childhood. Previous attempts to identify the origins of these comorbidities have typically relied on comparisons of different deficit groups and/or latent variable models. Here we apply a network approach to a heterogeneous sample of struggling learners to conceptualise these comorbidities as a dynamic system of interacting difficulties.
Methods:
714 children struggling with attention, learning, and/or memory were included. The sample consisted of children with both diagnosed (41%) and undiagnosed difficulties. The conditional independence network of parent ratings of everyday behaviour, cognition, and communication was estimated.
Results:
A clustering coefficient identified four interconnected areas of difficulty: (1) structural language and learning; (2) pragmatics and peer relationships; (3) behavioural and emotional problems; and (4) cognitive skills. Emotional and behavioural symptoms shared multiple direct connections with pragmatic abilities and cognitive problems, but not with structural language skills or learning problems. Poor structural language and cognitive skills were associated with learning problems. Centrality indices highlighted working memory and language coherence as symptoms bridging different problem areas.
Conclusion:
The network model identified four areas of difficulty and potential bridging symptoms. Although the current analytic framework does not provide causal evidence, it is possible that bridging symptoms may be the origins of comorbidities observed on a dimensional level; problems in these areas may cascade and activate problems in other areas of the network. The potential value of applying a dynamic systems network approach to symptoms of developmental disorders is discussed.
Cognitive impairment is experienced by many individuals with major depressive disorder (MDD) and is significantly related to sustained disability. Recent work has begun to explore the relationship between childhood adversity (CA) and cognitive impairment in MDD, but this work is limited by unreliable measures of CA. Furthermore, no previous research has examined whether CA relates to cognitive remediation response. The current study clarifies how CA and clinical characteristics of illness explain cognitive variance. In addition, we investigate whether CA is associated with response to cognitive remediation. Thirty-nine individuals who completed cognitive remediation were rerecruited to complete a retrospective interview on CA. Results showed that CA, repeated depressive episodes, and earlier age at diagnosis were associated with poorer cognition. We did not observe a difference in treatment response based on CA. Findings suggest that CA is an important variable to consider when examining the expression of depressive illness and areas for intervention.
Environmental factors such as adverse childhood experiences (ACEs) may affect neurocognition, an endophenotype for several mental illnesses. This study examines the effect of ACEs on neurocognitive performance in first-degree relatives (FDRs) of patients with severe mental illness to determine whether familial risk has a moderating effect on the relationship between ACEs and neurocognition. Unaffected FDRs from multiplex families with severe mental illnesses (schizophrenia, bipolar disorder, obsessive-compulsive disorder, or alcohol use disorder) (n = 324) and healthy controls (with no familial risk) (n = 188) underwent neurocognitive tests for processing speed, new learning, working memory and Theory of Mind. ACEs were measured using the WHO ACE-International Questionnaire (ACE-IQ). Regression models were done to predict each neurocognitive domain by the effect of familial risk, ACE-IQ Score and their interaction (familial risk*ACE-IQ score). The main effect of familial risk predicted poor performance in all domains of neurocognition (p < 0.01), and the interaction had negative association with global neurocognition (β = −0.093, p = 0.009), processing speed (β = −0.109, p = 0.003) and working memory (β = −0.092, p = 0.01). Among the ACEs sub-domains, only maltreatment, specifically the main effect of physical neglect, and interaction effect sexual abuse with familial risk predicted poorer neurocognition. In FDRs of schizophrenia and bipolar disorder, only the main effects of familial risk were significantly associated with neurocognition. We conclude that ACEs (especially maltreatment) are associated with neurocognition, but the relationship between childhood adversity and neurocognition is moderated by familial risk of mental illness. Genetic/familial vulnerability may have a stronger association with neurocognition in schizophrenia and bipolar disorder.
Importance:
Childhood adversities, including neglect, abuse, and other indicators of family dysfunction, are associated in adulthood with risk factors for poor cognitive and mental health. However, the extent to which these experiences are associated with adulthood cognition-related quality of life and risk for dementia is unknown.
Objective:
To determine the association of 10 adverse childhood experiences (ACEs) with neuropsychiatric outcomes among former National Football League (NFL) players.
Design, setting, and participants:
This cross-sectional analysis used data from the Football Player's Health Study at Harvard University, an ongoing longitudinal cohort study from January 30, 2015, to November 19, 2021, of former NFL players.
Exposures:
Ten ACEs were assessed using the Adverse Childhood Experiences Questionnaire.
Main outcomes and measures:
Dementia symptoms were assessed using the AD8: The Washington University Dementia Screening Test; cognition-related quality of life was assessed with the short form of the Quality of Life in Neurological Disorders; depression was assessed with the Patient Health Questionnaire-9; anxiety was assessed with the Generalized Anxiety Disorder-7; and pain intensity and pain interference in daily life were assessed with the Brief Pain Inventory. Risk ratios (RRs) assessing the association between ACEs and neuropsychiatric outcomes were estimated using generalized estimating equations, adjusted for age, race, and childhood socioeconomic status, and further adjusted for playing position, concussions incurred during football play, and number of seasons played in the NFL.
Results:
A total of 1755 men (mean [SD] age, 57.2 [13.5] years) who were former professional football players were included in the analysis. Five hundred twenty players (29.6%) identified as Black, 1160 (66.1%) identified as White, and 75 (4.3%) identified as other race or ethnicity. Players with 4 or more ACEs were at 48% greater risk of a positive screen for dementia (RR, 1.48 [95% CI, 1.22-1.79]), and at significantly greater risk of every other neuropsychiatric outcome except anxiety (RR range, 1.62 [95% CI, 1.09-2.39] to 1.74 [95% CI, 1.27-2.40]) compared with players with no ACEs. Further adjustment for concussions incurred during playing years attenuated these associations, although some were still significant (adjusted RR range, 1.32 [95% CI, 1.10-1.58] to 1.56 [95% CI, 1.15-2.11]). ACEs were also associated with concussion symptoms; players with 4 or more ACEs had a 60% increased risk of being in the top quartile of concussion symptoms (RR, 1.60; 95% CI, 1.12-2.28) compared with players with no ACEs.
Conclusions and relevance:
These findings suggest that ACEs may be associated with dementia symptoms among former NFL players. Moreover, ACEs should be investigated among professional football players and other populations as a prospective indicator of persons at high risk of concussion. These findings further suggest that treatment of psychological trauma in addition to treatment of physical injury may improve neuropsychiatric health in former NFL players.
Background
A routinely collected dataset was analyzed (1) to determine the naturalistic effectiveness of inpatient psychotherapy for depression in routine psychotherapeutic care, and (2) to identify potential predictors of change.
Methods
In a sample of 22,681 inpatients with depression, pre-post and pre-follow-up effect sizes were computed for various outcome variables. To build a probabilistic model of predictors of change, an independent component analysis generated components from demographic and clinical data, and Bayesian EFA extracted factors from the available pre-test, post-test and follow-up questionnaires in a subsample (N = 6377). To select the best-fitted model, the BIC of different path models were compared. A Bayesian path analysis was performed to identify the most important factors to predict changes.
Results
Effect sizes were large for the primary outcome and moderate for various secondary outcomes. Almost all pretreatment factors exerted significant influences on different baseline factors. Several factors were found to be resistant to change during treatment: suicidality, agoraphobia, life dissatisfaction, physical disability and pain. The strongest cross-loadings were observed from suicidality on negative cognitions, from agoraphobia on anxiety, and from physical disability on perceived disability.
Limitations
No causal conclusions can be drawn directly from our results as we only used cross-lagged panel data without control group.
Conclusions
The results indicate large effects of inpatient psychotherapy for depression in routine clinical care. The direct influence of pretreatment factors decreased over the course of treatment. However, some factors appeared stable and difficult to treat, which might hinder treatment outcome. Findings of different predictors of change are discussed.
Importance
Many studies have demonstrated an association between early-life adversity (ELA) and executive functioning in children and adolescents. However, the aggregate magnitude of this association is unknown in the context of threat and deprivation types of adversity and various executive functioning domains.
Objective
To test the hypothesis that experiences of deprivation are more strongly associated with reduced executive functioning compared with experiences of threat during childhood and adolescence.
Data Sources
Embase, ERIC, MEDLINE, and PsycInfo databases were searched from inception to December 31, 2020. Both forward and reverse snowball citation searches were performed to identify additional articles.
Study Selection
Articles were selected for inclusion if they (1) had a child and/or adolescent sample, (2) included measures of ELA, (3) measured executive functioning, (4) evaluated the association between adversity and executive functioning, (5) were published in a peer-reviewed journal, and (6) were published in the English language. No temporal or geographic limits were set. A 2-reviewer, blinded screening process was conducted.
Data Extraction and Synthesis
PRISMA guidelines were used to guide data extraction and article diagnostics (for heterogeneity, small study bias, and p-hacking). Article quality was assessed, and data extraction was performed by multiple independent observers. A 3-level meta-analytic model with a restricted maximum likelihood method was used. Moderator analyses were conducted to explore heterogeneity.
Main Outcomes and Measures
Primary outcomes included measures of the 3 domains of executive functioning: cognitive flexibility, inhibitory control, and working memory.
Results
A total of 91 articles were included, representing 82 unique cohorts and 31 188 unique individuals. Deprivation, compared with threat, was associated with significantly lower inhibitory control (F1,90 = 5.69; P = .02) and working memory (F1,54 = 5.78; P = .02). No significant difference was observed for cognitive flexibility (F1,36 = 2.38; P = .12). The pooled effect size of the association of inhibitory control with deprivation was stronger (Hedges g = −0.43; 95% CI, −0.57 to −0.29) compared with threat (Hedges g = −0.27; 95% CI, −0.46 to −0.08). The pooled effect size of the association of working memory with deprivation was stronger (Hedges g = −0.54; 95% CI, −0.75 to −0.33) compared with threat (Hedges g = −0.28; 95% CI, −0.51 to −0.05).
Conclusions and Relevance
Experiences of both threat and deprivation in childhood and adolescence were associated with reduced executive functioning, but the association was stronger for exposure to deprivation. Efforts to address the consequences of ELA for development should consider the associations between specific dimensions of adversity and specific developmental outcomes.
Cognitive function at middle age is of particular public health interest, as it strongly predicts later dementia. Children who have experienced abuse subsequently have worse cognitive function than those who have not. However, it remains unclear whether the association of abuse with cognitive function persists into middle age. In 2014–2016, 14,151 women ages 49–69 years who had previously responded to a childhood abuse questionnaire completed a cognitive battery. In models adjusted for childhood socioeconomic status and head trauma, combined physical, emotional, and sexual abuse was associated with lower scores on both Learning/Working Memory (severe abuse, lower scores similar to that observed in women 4.8 years older in our data) and Psychomotor Speed/Attention (severe abuse, lower scores similar to that observed in women to 2.9 years older in our data). Adjustment for adulthood socioeconomic status and health factors (e.g., smoking, hypertension) slightly attenuated associations. In exploratory analyses further adjusted for psychological distress, associations were attenuated. Women exposed versus unexposed to childhood abuse had poorer cognitive function at mid-life. Associations were particularly strong for learning and working memory and were not accounted for by adulthood health factors. Childhood abuse should be investigated as a potential risk factor for cognitive decline and dementia in old age.
Objective: The aims of this study were to determine the effectiveness of a routine clinical care treatment and to identify predictors of treatment outcome in PTSD inpatients. Methods: A routinely collected data set of 612 PTSD inpatients (M = 42.3 years [SD = 11.6], 75.7% female) having received trauma-focused psychotherapy was analyzed. Primary outcome was the clinical symptom severity change score, secondary outcomes were assessed using functional, anxiety, and depression change scores. Hedges g-corrected pre–post effect sizes (ES) were computed for all outcomes. Elastic net regulation as a data-driven, stability-based machine-learning approach was used to build stable clinical prediction models. Results: Hedges g ES indicated medium to large effects on all outcomes. The results of the predictor analyses suggested that a combined predictor model with sociodemographic, clinical, and psychometric variables contribute to predicting different treatment outcomes. Across the clinical and functional outcome, psychoticism, total number of diagnoses, and bronchial asthma consistently showed a stable negative predictive relationship to treatment outcome. Conclusion: Trauma-focused psychotherapy could effectively be implemented in a routine inpatient setting. Some important prognostic variables could be identified. If the proposed models of predictors are replicated, they may help personalize treatment for patients receiving routine clinical care.
Background
Patients with major depressive disorder (MDD) display cognitive deficits in acutely depressed and remitted states. Childhood maltreatment is associated with cognitive dysfunction in adults, but its impact on cognition and treatment related cognitive outcomes in adult MDD has received little consideration. We investigate whether, compared to patients without maltreatment and healthy participants, adult MDD patients with childhood maltreatment display greater cognitive deficits in acute depression, lower treatment-associated cognitive improvements, and lower cognitive performance in remission.
Methods
Healthy and acutely depressed MDD participants were enrolled in a multi-center MDD predictive marker discovery trial. MDD participants received 16 weeks of standardized antidepressant treatment. Maltreatment and cognition were assessed with the Childhood Experience of Care and Abuse interview and the CNS Vital Signs battery, respectively. Cognitive scores and change from baseline to week 16 were compared amongst MDD participants with (DM+, n = 93) and without maltreatment (DM−, n = 90), and healthy participants with (HM+, n = 22) and without maltreatment (HM−, n = 80). Separate analyses in MDD participants who remitted were conducted.
Results
DM+ had lower baseline global cognition, processing speed, and memory v. HM−, with no significant baseline differences amongst DM−, HM+, and HM− groups. There were no significant between-group differences in cognitive change over 16 weeks. Post-treatment remitted DM+, but not remitted DM−, scored significantly lower than HM− in working memory and processing speed.
Conclusions
Childhood maltreatment was associated with cognitive deficits in depressed and remitted adults with MDD. Maltreatment may be a risk factor for more severe and persistent cognitive deficits in adult MDD.
Maltreatment-related childhood adversity is the leading preventable risk factor for mental illness and substance abuse. Although the association between maltreatment and psychopathology is compelling, there is a pressing need to understand how maltreatment increases the risk of psychiatric disorders. Emerging evidence suggests that maltreatment alters trajectories of brain development to affect sensory systems, network architecture and circuits involved in threat detection, emotional regulation and reward anticipation. This Review explores whether these alterations reflect toxic effects of early-life stress or potentially adaptive modifications, the relationship between psychopathology and brain changes, and the distinction between resilience, susceptibility and compensation. © 2016 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.
Systematic reviews and meta-analyses have become increasingly important in health care. Clinicians read them to keep up to date with their field [1],[2], and they are often used as a starting point for developing clinical practice guidelines. Granting agencies may require a systematic review to ensure there is justification for further research [3], and some health care journals are moving in this direction [4]. As with all research, the value of a systematic review depends on what was done, what was found, and the clarity of reporting. As with other publications, the reporting quality of systematic reviews varies, limiting readers' ability to assess the strengths and weaknesses of those reviews.
Several early studies evaluated the quality of review reports. In 1987, Mulrow examined 50 review articles published in four leading medical journals in 1985 and 1986 and found that none met all eight explicit scientific criteria, such as a quality assessment of included studies [5]. In 1987, Sacks and colleagues [6] evaluated the adequacy of reporting of 83 meta-analyses on 23 characteristics in six domains. Reporting was generally poor; between one and 14 characteristics were adequately reported (mean = 7.7; standard deviation = 2.7). A 1996 update of this study found little improvement [7].
In 1996, to address the suboptimal reporting of meta-analyses, an international group developed a guidance called the QUOROM Statement (QUality Of Reporting Of Meta-analyses), which focused on the reporting of meta-analyses of randomized controlled trials [8]. In this article, we summarize a revision of these guidelines, renamed PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses), which have been updated to address several conceptual and practical advances in the science of systematic reviews (Box 1).
Box 1: Conceptual Issues in the Evolution from QUOROM to PRISMA
Completing a Systematic Review Is an Iterative Process
The conduct of a systematic review depends heavily on the scope and quality of included studies: thus systematic reviewers may need to modify their original review protocol during its conduct. Any systematic review reporting guideline should recommend that such changes can be reported and explained without suggesting that they are inappropriate. The PRISMA Statement (Items 5, 11, 16, and 23) acknowledges this iterative process. Aside from Cochrane reviews, all of which should have a protocol, only about 10% of systematic reviewers report working from a protocol [22]. Without a protocol that is publicly accessible, it is difficult to judge between appropriate and inappropriate modifications.
Background:
Research documents a strong relationship between childhood maltreatment and depression. However, only few studies have examined the specific effects of various types of childhood abuse/neglect on depression. This meta-analysis estimated the associations between depression and different types of childhood maltreatment (antipathy, neglect, physical abuse, sexual abuse, and psychological abuse) assessed with the same measure, the Childhood Experience of Care and Abuse (CECA) interview.
Method:
A systematic search in scientific databases included use of CECA interview and strict clinical assessment for major depression as criteria. Our meta-analysis utilized Cohen's d and relied on a random-effects model.
Results:
The literature search yielded 12 primary studies (reduced from 44), with a total of 4372 participants and 34 coefficients. Separate meta-analyses for each type of maltreatment revealed that psychological abuse and neglect were most strongly associated with the outcome of depression. Sexual abuse, although significant, was less strongly related. Furthermore, the effects of specific types of childhood maltreatment differed across adult and adolescent samples.
Limitations:
Our strict criteria for selecting the primary studies resulted in a small numbers of available studies. It restricted the analyses for various potential moderators.
Conclusion:
This meta-analysis addressed the differential effects of type of childhood maltreatment on major depression, partially explaining between-study variance. The findings clearly highlight the potential impact of the more "silent" types of childhood maltreatment (other than physical and sexual abuse) on the development of depression.
Understanding the link between adverse childhood experiences (ACEs) and sexual victimization (SV) in adulthood may provide important information about the level of risk for adult SV and sexual re-victimization among childhood sexual abuse (CSA) survivors. In the present paper, we explore the relationship between ACEs, including CSA, and SV in adulthood. Data from the CDC-Kaiser ACE Study were used to examine the effect of experiences of early adversity on adult SV. Adult HMO members (n=7,272) undergoing a routine health exam provided detailed information about ACEs that occurred at age 18 or younger and their experiences of SV in adulthood. Analyses revealed that as ACE score increased, so did risk of experiencing SV in adulthood. Each of the ACE variables was significantly associated with adult SV, with CSA being the strongest predictor of adult SV. In addition, for those who reported CSA, there was a cumulative increase in adult SV risk with each additional ACE experienced. As such, early adversity is a risk factor for adult SV. In particular, CSA is a significant risk factor for sexual re-victimization in adulthood, and additional early adversities experienced by CSA survivors may heighten adult SV risk above and beyond the risk associated with CSA alone. Given the interconnectedness among various experiences of early adversity, adult SV prevention actions must consider how other violence-related and non-violence-related traumatic experiences may exacerbate the risk conferred by CSA on subsequent victimization.
Few studies have attempted to describe the range of cognitive impairments affecting people who have experienced child maltreatment. The aim of this meta-analysis was to examine the neuropsychological profile of these people and to determine the cognitive impacts of maltreatment from childhood to adulthood.
Fifty-two publications from 1970 to 2013 were included.
The affected cognitive domains were working memory (g = -.65), attention (g = -.63), intelligence (g = -.56) and speed of processing (g = -.49). The impact of maltreatment was greater in young children (g = -.71) and less pronounced in adults (g = -.26).
These results suggest that exposure to maltreatment has an impact on specific cognitive processes, regardless of age.
Few studies have attempted to describe the range of cognitive impairments in individuals with psychiatric disorders who experienced maltreatment as children. The aims of this meta-analysis were to establish the impact of maltreatment and psychiatric disorders on cognition, and to examine the change in impact from childhood to adulthood.
Twelve publications from 1970 to 2013 were included, with the following inclusion criteria: (a) individuals with a psychiatric disorder who experienced maltreatment, (b) use of at least 1 standardized neuropsychological measure, and (c) use of a control group without any psychiatric disorder or mistreatment. The majority of studies (10/12) were about posttraumatic stress disorder. Several effect sizes were calculated (Hedge's g) according to the cognitive domains.
The results of the meta-analysis demonstrate that the combination of psychiatric disorders and childhood maltreatment has a negative impact on global cognitive performance, with a moderate effect size (g = -0.59). The most affected cognitive domains for individuals aged 7- to 18-years-old were visual episodic memory (g = -0.97), executive functioning (g = -0.90), and intelligence (g = -0.68). For individuals over the age of 18-years-old, the most affected cognitive domains were verbal episodic memory (g = -0.77), visuospatial/problem solving (g = -0.73), and attention (g = -0.72). The impact of maltreatment and psychiatric disorders was greater in children than in adults (slope = 0.008, p < .002).
The results suggest that exposure to maltreatment and the presence of psychiatric disorders have a broad impact on cognition, with specific neuropsychological profile. (PsycINFO Database Record
(c) 2015 APA, all rights reserved).
We examined the hypothesis that exposure to childhood maltreatment increases the vulnerability to Adult Victimization (AV) in a homeless population (N = 500). We also investigated the effects of specific types (emotional, physical, and sexual) and cumulative experience of childhood maltreatment on AV, and whether gender moderates these relationships. All three groups with AV experience (emotional, physical, and sexual) indicated higher exposure to childhood abuse and cumulative maltreatment, and those who were sexually victimized as an adult showed higher exposure to childhood neglect. In addition, exposure to childhood maltreatment had type-specific and cumulative effects on AV. Exposure to all types of childhood abuse maintained a strong direct association with AV, regardless of demographic characteristics, including age, ethnicity, marital status, education level, and housing situation. In addition, exposure to physical neglect showed a significant relationship with Adult Sexual Victimization. Cumulative experience of childhood maltreatment was consistently associated with cumulative risk of experiencing AV. Gender had no significant effect on these relationships. Findings suggest that intervention programs in homeless population should consider the history of childhood maltreatment and its characteristics to increase the effectiveness of intervention strategies for AV in this population.
© The Author(s) 2015.
Objectives
We aimed to examine the association between childhood trauma and functional impairment in psychotic disorders, bipolar disorder and borderline personality disorder, to speculate on possible mechanisms that underlie this association and discuss the implications for clinical work.
Methods
Narrative review of the peer-reviewed English language literature in the area.
Results
High rates of childhood trauma in psychotic disorders, bipolar disorder and borderline personality disorder were identified. This was associated with impaired social and occupational functioning in both the premorbid and established phases of each of these psychiatric disorders over and above the deficits typically observed in these populations. Possible mechanisms mediating this relationship include neurocognitive deficits, insecure attachment, higher rates of comorbidities and problems with adherence and response to treatment.
Conclusions
Routine clinical inquiry about childhood maltreatment should be adopted within mental health settings. This has potentially important treatment implications for identifying those individuals at elevated risk of functional disability. While there is no clear guidance currently available on how to target childhood trauma in the treatment of psychotic disorders, bipolar disorder or borderline personality disorder, there are several promising lines of enquiry and further research is warranted.
Neurocognitive deficits are demonstrated in major depressive disorder (MDD) and most likely contribute to the functional impairment experienced by affected individuals. We systematically reviewed the evidence on neurocognitive deficits and their relationship(s) to psychosocial functioning in MDD.
English-language literature was searched in MEDLINE, EMBASE, Science Direct, and PsycInfo databases for the years 1980-October 15, 2013, with the following terms: (depressive disorder or depressive disorder, major) and permutations of (cognitive, neurocognitive, neuropsych*) with (impairment, deficit, performance, test) and (quality of life; functional outcomes; outcome assessment, health care) or (assessment, outcomes; assessment, patient outcomes; outcomes assessment; outcomes assessments, patient).
Inclusion criteria were (1) nongeriatric adults (< 60 years) with a primary diagnosis of MDD by DSM-IV, ICD-9, or ICD-10 criteria; (2) use of neuropsychological tests; and (3) use of a specific measure of social, occupational, or daily functioning. Of 488 articles identified in the initial search, 10 met the inclusion criteria.
Two independent appraisers assessed eligibility of the studies. Substantial heterogeneity in the samples and methods precluded a quantitative meta-analysis, so we performed a narrative descriptive review.
The included studies employed a variety of neurocognitive tests and assessments of psychosocial functioning. Overall, depressed samples had neurocognitive deficits in various domains that were associated with different measures of psychosocial functioning. However, these findings were constrained by methodological limitations of studies.
The limited evidence base suggests that neurocognitive functioning appears to be broadly associated with functional impairment in individuals with MDD, but the quality of evidence is weak. Further studies to clarify the relationship(s) between neurocognitive and psychosocial functioning in MDD will benefit from larger and more homogeneous samples, prospective designs with multivariate analyses, and use of comprehensive assessments of psychosocial functioning that are validated in depressed populations.
© Copyright 2014 Physicians Postgraduate Press, Inc.
We investigated whether symptoms of attention-deficit/hyperactivity disorder (ADHD) are pathways through which deficits in inhibition and working memory are associated with teacher- and parent-rated social impairment in children. Participants were 64 children (55 % males; 53 % with ADHD) in grades 3-6. Consistent with our hypotheses, the association between inhibition and social impairment was mediated by hyperactivity/impulsivity and the association between working memory and social impairment was mediated by inattention. Support was not obtained for alternative models wherein the association between inhibition and social impairment was mediated by inattention, and the association between working memory and social impairment was mediated by hyperactivity/impulsivity. Further, tests of hierarchical models suggest that neither inhibition nor working memory is primary but, rather, that these cognitive processes are related to one another and that they collectively (but not uniquely) contribute to hyperactivity/impulsivity and inattention. These findings have implications for conceptual models of ADHD, for understanding factors that influence and sustain social impairment among youth with symptoms of the disorder, and for interventions aimed to addressing such impairment.
Objectives:
Impaired social, role, and neurocognitive functioning are preillness characteristics of people who later develop psychosis. In people with schizophrenia, neurocognition and negative symptoms are associated with functional impairment. We examined the relative contributions of neurocognition and symptoms to social and role functioning over time in clinically high-risk (CHR) individuals and determined if negative symptoms mediated the influence of cognition on functioning.
Methods:
Social, role, and neurocognitive functioning and positive, negative, and disorganized symptoms were assessed in 167 individuals at CHR for psychosis in the North American Prodrome Longitudinal Study Phase 1 (NAPLS-1), of whom 96 were reassessed at 12 months.
Results:
Regression analyses indicated that negative symptoms accounted for unique variance in social and role functioning at baseline and follow-up. Composite neurocognition accounted for unique, but modest, variance in social and role functioning at baseline and in role functioning at follow-up. Negative symptoms mediated the relationship between composite neurocognition and social and role functioning across time points. In exploratory analyses, individual tests (IQ estimate, Digit Symbol/Coding, verbal memory) selectively accounted for social and role functioning at baseline and follow-up after accounting for symptoms. When negative symptom items with content overlapping with social and role functioning measures were removed, the relationship between neurocognition and social and role functioning was strengthened.
Conclusion:
The modest overlap among neurocognition, negative symptoms, and social and role functioning indicates that these domains make substantially separate contributions to CHR individuals.
Objective:
This article reviews the conceptual basis, definitions, and evolution of cognitive training approaches for the treatment of mental disorders.
Method:
The authors review the current state of the knowledge on cognitive training in psychiatric illnesses, and its neural and behavioral targets, and summarize the factors that appear to relate to a successful response, including learner characteristics that influence clinical outcome. They also discuss methodological issues relevant to the development and testing of cognitive training approaches, with the goal of creating maximally efficient and effective approaches to training. Finally, they identify gaps in existing knowledge and outline key research directions for the future.
Results:
While much of the early research has been conducted in schizophrenia, cognitive training has more recently been applied to a widening range of neuropsychiatric illnesses, including attention deficit hyperactivity disorder, mood disorders, and substance use disorders. Cognitive training harnesses the inherent neuroplastic capacities of the brain, targeting neural system function across psychiatric disorders, thus improving the cognitive processes that play a role in emotion regulation, clinical symptoms, and adaptive community functioning.
Conclusions:
Cognitive training offers considerable promise, especially given the limited efficacy of pharmacological interventions in ameliorating cognitive deficits. However, more research is needed to understand the mechanisms underlying cognitive training, predictors of response, generalization and real-world applicability, and approaches to dissemination in practice settings.
Significance
Childhood maltreatment is a major risk factor for internalizing disorders including depression and anxiety, which cause significant disability. Altered connectivity of the brain’s fear circuitry represents an important candidate mechanism linking maltreatment and these disorders, but this relationship has not been directly explored. Using resting-state functional brain connectivity in adolescents, we show that maltreatment predicts lower prefrontal–hippocampal connectivity in females and males but lower prefrontal–amygdala connectivity only in females. Altered connectivity, in turn, mediated the development of internalizing symptoms. These results highlight the importance of fronto–hippocampal connectivity for both sexes in internalizing symptoms following maltreatment. The additional impact on fronto–amygdala connectivity in females may help explain their higher risk for anxiety and depression.
Background
Current diagnostic systems for mental disorders rely upon presenting signs and symptoms, with the result that current definitions do not adequately reflect relevant neurobiological and behavioral systems - impeding not only research on etiology and pathophysiology but also the development of new treatments.
Discussion
The National Institute of Mental Health began the Research Domain Criteria (RDoC) project in 2009 to develop a research classification system for mental disorders based upon dimensions of neurobiology and observable behavior. RDoC supports research to explicate fundamental biobehavioral dimensions that cut across current heterogeneous disorder categories. We summarize the rationale, status and long-term goals of RDoC, outline challenges in developing a research classification system (such as construct validity and a suitable process for updating the framework) and discuss seven distinct differences in conception and emphasis from current psychiatric nosologies.
Summary
Future diagnostic systems cannot reflect ongoing advances in genetics, neuroscience and cognitive science until a literature organized around these disciplines is available to inform the revision efforts. The goal of the RDoC project is to provide a framework for research to transform the approach to the nosology of mental disorders.
Background:
There is evidence to suggest that cognitive deficits might persist beyond the acute stages of illness in major depressive disorder (MDD). However, the findings are somewhat inconsistent across the individual studies conducted to date. Our aim was to conduct a systematic review and meta-analysis of existing studies that have examined cognition in euthymic MDD patients.
Method:
Following a systematic search across several publication databases, meta-analyses were conducted for 27 empirical studies that compared euthymic adult MDD patients (895 participants) and healthy controls (997 participants) across a range of cognitive domains. The influence of demographic variables and confounding factors, including age of onset and recurrent episodes, was examined.
Results:
Compared with healthy controls, euthymic MDD patients were characterized by significantly poorer cognitive functions. However, the magnitude of observed deficits, with the exception of inhibitory control, were generally modest when late-onset cases were excuded. Late-onset cases demonstrated significantly more pronounced deficits in verbal memory, speed of information processing and some executive functions.
Conclusions:
Cognitive deficits, especially poor response inhibition, are likely to be persistent features, at least of some forms, of adult-onset MDD. More studies are necessary to examine cognitive dysfunction in remitted psychotic, melancholic and bipolar spectrum MDD. Cognitive deficits overall appear to be more common among patients with late-onset depression, supporting the theories suggesting that possible vascular and neurodegenerative factors play a role in a substantial number of these patients.
Prior research has established the independent associations of depressive symptoms and childhood trauma to overgeneral memory (OGM); the present study addresses the potentially interactive effects between these two risk factors on OGM. In addition, the current study comprehensively evaluates whether executive functions (EF) mediate the relation between depressive symptoms and/or abuse to OGM in a child and adolescent sample. OGM was assessed among an inpatient-psychiatric sample of 49 youth (ages 7-17) with, and without, child abuse histories and depressive symptomatology. EF was assessed with standardized neuropsychological measures of verbal fluency, inhibition, and cognitive flexibility. There was a significant interaction of depressive symptoms and abuse in predicting OGM; the effect of depression on OGM was less pronounced among youth with abuse histories, who had elevated OGM at both low and high depressive symptoms relative to those with no abuse and low depressive symptoms. Among the EF measures, only category fluency was associated with OGM. An additive, rather than mediational, model was supported, whereby category fluency accounted for a significant proportion of variance in OGM above child abuse and depressive symptoms. The meaning of these findings for models of OGM and clinical practice are emphasized.
The purpose of the paper was to conduct a systematic review of early life stress and its association with psychiatric disorders in adulthood. The occurrence of early stress has lasting negative consequences on the individual, with psychopathology onset one of the most important consequences. The degree of early life stress is associated with the severity of psychiatric disorders and disability in adulthood. Methodology: We conducted a search of two databases (PubMed and SciELO), limited to the time span 1990-2010, using the following keywords: child abuse, maltreatment, early stress, and psychiatric disorders. Thirty-one papers were selected for this review. Results: We found that the subtypes of early life stress such as emotional and physical neglect and sexual, emotional, and physical abuse have associations with several psychiatric disorders, but the Borderline Personality Disorder and Mood Disorders are more associated with the categories listed. Conclusions: Exposure to adversities in childhood and adolescence is predictive of psychiatric disorders in adulthood. More studies are needed to understand the mechanisms by which early life stress is a risk factor for future psychopathology.
Adolescence is a period in which cognition and brain undergo dramatic parallel development. Whereas chronic use of alcohol and marijuana is known to cause cognitive impairments in adults, far less is known about the effect of these substances of abuse on adolescent cognition, including possible interactions with developmental processes.
Neuropsychological performance, alcohol use, and marijuana use were assessed in 48 adolescents (ages 12 to 18), recruited in 3 groups: a healthy control group (HC, n = 15), a group diagnosed with substance abuse or dependence (SUD, n = 19), and a group with a family history positive for alcohol use disorder (AUD) but no personal substance use disorder (FHP, n = 14). Age, drinks per drinking day (DPDD), percentage days drinking, and percentage days using marijuana were considered as covariates in a MANCOVA in which 6 neuropsychological composites (Verbal Reasoning, Visuospatial Ability, Executive Function, Memory, Attention, and Processing Speed) served as dependent variables.
More DPDD predicted poorer performance on Attention and Executive Function composites, and more frequent use of marijuana was associated with poorer Memory performance. In separate analyses, adolescents in the SUD group had lower scores on Attention, Memory, and Processing Speed composites, and FHP adolescents had poorer Visuospatial Ability.
In combination, these analyses suggest that heavy alcohol use in adolescence leads to reduction in attention and executive functioning and that marijuana use exerts an independent deleterious effect on memory. At the same time, premorbid deficits associated with family history of AUD appeared to be specific to visuospatial ability.
The investigation of putative effects of early life stress (ELS) in humans on later behavior and neurobiology is a fast developing field. While epidemiological and neurobiological studies paint a somber picture of negative outcomes, relatively little attention has been devoted to integrating the breadth of findings concerning possible cognitive and emotional deficits associated with ELS. Emerging findings from longitudinal studies examining developmental trajectories of the brain in healthy samples may provide a new framework to understand mechanisms underlying ELS sequelae.
The goal of this review was twofold. The first was to summarize findings from longitudinal data on normative brain development. The second was to utilize this framework of normative brain development to interpret changes in developmental trajectories associated with deficits in cognitive and affective function following ELS.
Five principles of normative brain development were identified and used to discuss behavioral and neural sequelae of ELS. Early adversity was found to be associated with deficits in a range of cognitive (cognitive performance, memory, and executive functioning) and affective (reward processing, processing of social and affective stimuli, and emotion regulation) functions.
Three general conclusions emerge: (1) higher-order, complex cognitive and affective functions associated with brain regions undergoing protracted postnatal development are particularly vulnerable to the deleterious effects of ELS; (2) the amygdala is particularly sensitive to early ELS; and (3) several deficits, particularly those in the affective domain, appear to persist years after ELS has ceased and may increase risk for later psychopathology.
Current versions of the DSM and ICD have facilitated reliable clinical diagnosis and research. However, problems have increasingly been documented over the past several years, both in clinical and research arenas (e.g., 1, 2). Diagnostic categories based on clinical consensus fail to align with findings emerging from clinical neuroscience and genetics. The boundaries of these categories have not been predictive of treatment response. And, perhaps most important, these categories, based upon presenting signs and symptoms, may not capture fundamental underlying mechanisms of dysfunction. One consequence has been to slow the development of new treatments targeted to underlying pathophysiological mechanisms.
Strong, graded relationships between exposure to childhood traumatic stressors and numerous negative health behaviors and outcomes, healthcare utilization, and overall health status inspired the question of whether these adverse childhood experiences (ACEs) are associated with premature death during adulthood.
This study aims to determine whether ACEs are associated with an increased risk of premature death during adulthood.
Baseline survey data on health behaviors, health status, and exposure to ACEs were collected from 17,337 adults aged >18 years during 1995-1997. The ACEs included abuse (emotional, physical, sexual); witnessing domestic violence; parental separation or divorce; and growing up in a household where members were mentally ill, substance abusers, or sent to prison. The ACE score (an integer count of the eight categories of ACEs) was used as a measure of cumulative exposure to traumatic stress during childhood. Deaths were identified during follow-up assessments (between baseline appointment date and December 31, 2006) using mortality records obtained from a search of the National Death Index. Expected years of life lost (YLL) and years of potential life lost (YPLL) were computed using standard methods. The relative risk of death from all causes at age < or =65 years and at age < or =75 years was estimated across the number of categories of ACEs using multivariable-adjusted Cox proportional hazards regression. Analysis was conducted during January-February 2009.
Overall, 1539 people died during follow-up; the crude death rate was 91.0 per 1000; the age-adjusted rate was 54.7 per 1000. People with six or more ACEs died nearly 20 years earlier on average than those without ACEs (60.6 years, 95% CI=56.2, 65.1, vs 79.1 years, 95% CI=78.4, 79.9). Average YLL per death was nearly three times greater among people with six or more ACEs (25.2 years) than those without ACEs (9.2 years). Roughly one third (n=526) of those who died during follow-up were aged < or =75 years at the time of death, accounting for 4792 YPLL. After multivariable adjustment, adults with six or more ACEs were 1.7 (95% CI=1.06, 2.83) times more likely to die when aged < or =75 years and 2.4 (95% CI=1.30, 4.39) times more likely to die when aged < or =65 years.
ACEs are associated with an increased risk of premature death, although a graded increase in the risk of premature death was not observed across the number of categories of ACEs. The increase in risk was only partly explained by documented ACE-related health and social problems, suggesting other possible mechanisms by which ACEs may contribute to premature death.
Both neurocognitive impairments and a history of childhood abuse are highly prevalent in patients with schizophrenia. Childhood trauma has been associated with memory impairment as well as hippocampal volume reduction in adult survivors. The aim of the following study was to examine the contribution of childhood adversity to verbal memory functioning in people with schizophrenia.
Eighty-five outpatients with a Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) diagnosis of chronic schizophrenia were separated into 2 groups on the basis of self-reports of childhood trauma. Performance on measures of episodic narrative memory, list learning, and working memory was then compared using multivariate analysis of covariance.
Thirty-eight (45%) participants reported moderate to severe levels of childhood adversity, while 47 (55%) reported no or low levels of childhood adversity. After controlling for premorbid IQ and current depressive symptoms, the childhood trauma group had significantly poorer working memory and episodic narrative memory. However, list learning was similar between groups.
Childhood trauma is an important variable that can contribute to specific ongoing memory impairments in schizophrenia.
Although common sense suggests that environmental influences increasingly account for individual differences in behavior as experiences accumulate during the course of life, this hypothesis has not previously been tested, in part because of the large sample sizes needed for an adequately powered analysis. Here we show for general cognitive ability that, to the contrary, genetic influence increases with age. The heritability of general cognitive ability increases significantly and linearly from 41% in childhood (9 years) to 55% in adolescence (12 years) and to 66% in young adulthood (17 years) in a sample of 11 000 pairs of twins from four countries, a larger sample than all previous studies combined. In addition to its far-reaching implications for neuroscience and molecular genetics, this finding suggests new ways of thinking about the interface between nature and nurture during the school years. Why, despite life's 'slings and arrows of outrageous fortune', do genetically driven differences increasingly account for differences in general cognitive ability? We suggest that the answer lies with genotype-environment correlation: as children grow up, they increasingly select, modify and even create their own experiences in part based on their genetic propensities.
Chronic exposure to stress hormones, whether it occurs during the prenatal period, infancy, childhood, adolescence, adulthood or aging, has an impact on brain structures involved in cognition and mental health. However, the specific effects on the brain, behaviour and cognition emerge as a function of the timing and the duration of the exposure, and some also depend on the interaction between gene effects and previous exposure to environmental adversity. Advances in animal and human studies have made it possible to synthesize these findings, and in this Review a model is developed to explain why different disorders emerge in individuals exposed to stress at different times in their lives.
This title proposes an insightful and original approach to understanding these disorders, one that focuses on what they have in common. Instead of examining in isolation, for example, obsessive compulsive disorders, insomnia, schizophrenia, it asks - what do patients with these disorders have in common? It takes each cognitive and behavioural process - attention, memory, reasoning, thought, behaviour, and examines whether it is a transdiagnostic process - i.e., serves to maintain a broad range of psychological disorders. Having shown how these disorders share several important processes, it then describes the practical implications of such an approach to diagnosis and treatment. Importantly it explores why the different psychological disorders can present so differently, despite being maintained by the same cognitive and behavioural processes. It also provides an account of the high rates of comorbidity observed among the different disorders.
Background
Psychotic disorders are associated with high rates of sustained unemployment, however, little is known about the long-term employment outcome of people at ultra-high risk (UHR) of developing psychosis. We sought to investigate the long-term unemployment rate and baseline predictors of employment status at follow-up in a large UHR cohort.
Method
268 UHR patients recruited from the Personal Assessment and Crisis Evaluation clinic in Melbourne, Australia were followed-up over 2–14 years after initial presentation to the service. Individuals in no form of employment or education were classed as unemployed. Logistic regression analyses were used to examine predictors of employment outcome.
Results
A high rate of unemployment was present at follow-up in this UHR sample (23%). At baseline, those who were unemployed at follow-up had a longer duration of untreated illness, more severe negative symptoms, lower IQ, poorer social and occupational functioning and reported more childhood trauma than the employed group. At follow-up, unemployed individuals exhibited significantly more severe symptoms on all measures and were more likely to have been diagnosed with a mood, anxiety, psychotic or substance use disorder. Childhood trauma and the duration of untreated illness at baseline were significant independent predictors of employment status at follow-up in the multivariate analyses.
Conclusions
Nearly a quarter of this UHR sample was unemployed at long-term follow-up. The duration of untreated illness and the effects of childhood trauma are potentially modifiable risk factors for long-term employment outcome in this group. Vocational support may be beneficial for many UHR patients presenting to services.
Background:
Childhood early life stress (ELS) increases risk of adulthood major depressive disorder (MDD) and is associated with altered brain structure and function. It is unclear whether specific ELSs affect depression risk, cognitive function and brain structure.
Method:
This cross-sectional study included 64 antidepressant-free depressed and 65 never-depressed individuals. Both groups reported a range of ELSs on the Early Life Stress Questionnaire, completed neuropsychological testing and 3T magnetic resonance imaging (MRI). Neuropsychological testing assessed domains of episodic memory, working memory, processing speed and executive function. MRI measures included cortical thickness and regional gray matter volumes, with a priori focus on the cingulate cortex, orbitofrontal cortex (OFC), amygdala, caudate and hippocampus.
Results:
Of 19 ELSs, only emotional abuse, sexual abuse and severe family conflict independently predicted adulthood MDD diagnosis. The effect of total ELS score differed between groups. Greater ELS exposure was associated with slower processing speed and smaller OFC volumes in depressed subjects, but faster speed and larger volumes in non-depressed subjects. In contrast, exposure to ELSs predictive of depression had similar effects in both diagnostic groups. Individuals reporting predictive ELSs exhibited poorer processing speed and working memory performance, smaller volumes of the lateral OFC and caudate, and decreased cortical thickness in multiple areas including the insula bilaterally. Predictive ELS exposure was also associated with smaller left hippocampal volume in depressed subjects.
Conclusions:
Findings suggest an association between childhood trauma exposure and adulthood cognitive function and brain structure. These relationships appear to differ between individuals who do and do not develop depression.
Advances in biology are providing deeper insights into how early experiences are built into the body with lasting effects on learning, behavior, and health. Numerous evaluations of interventions for young children facing adversity have demonstrated multiple, positive effects but they have been highly variable and difficult to sustain or scale. New research on plasticity and critical periods in development, increasing understanding of how gene-environment interaction affects variation in stress susceptibility and resilience, and the emerging availability of measures of toxic stress effects that are sensitive to intervention provide much-needed fuel for science-informed innovation in the early childhood arena. This growing knowledge base suggests 4 shifts in thinking about policy and practice: (1) early experiences affect lifelong health, not just learning; (2) healthy brain development requires protection from toxic stress, not just enrichment; (3) achieving breakthrough outcomes for young children facing adversity requires supporting the adults who care for them to transform their own lives; and (4) more effective interventions are needed in the prenatal period and first 3 years after birth for the most disadvantaged children and families. The time has come to leverage 21st-century science to catalyze the design, testing, and scaling of more powerful approaches for reducing lifelong disease by mitigating the effects of early adversity.
Background
Patients with a severe mental illness (SMI) are more likely to experience victimisation than the general population.AimsTo examine the prevalence of victimisation in people with SMI, and the relationship between symptoms, treatment facility and indices of substance use/misuse and perpetration, in comparison with the general population.Method
Victimisation was assessed among both randomly selected patients with SMI (n = 216) and the general population (n = 10 865).ResultsCompared with the general population, a high prevalence of violent victimisation was found among the SMI group (22.7% v. 8.5%). Compared with out-patients and patients in a sheltered housing facility, in-patients were most often victimised (violent crimes: 35.3%; property crimes: 47.1%). Risk factors among the SMI group for violent victimisation included young age and disorganisation, and risk factors for property crimes included being an in-patient, disorganisation and cannabis use. The SMI group were most often assaulted by someone they knew.Conclusions
Caregivers should be aware that patients with SMI are at risk of violent victimisation. Interventions need to be developed to reduce this vulnerability.
Childhood maltreatment is known to increase the risk of future psychiatric disorders. In the present study, we explored the impact of experienced maltreatment on the prevalence and comorbidity of psychiatric disorders in a high-risk population of adolescents in residential care units. We also studied the impact of poly-victimization. The participants of the study were adolescents in residential care units in Norway (n=335, mean age 16.8 years, girls 58.5%). A diagnostic interview (Child and Adolescent Psychiatric Assessment Interview) was used, yielding information about previous maltreatment (witnessing violence, victim of family violence, community violence, sexual abuse) and DSM-IV diagnoses present in the last three months. Exposure to maltreatment was reported by 71%, and in this group, we found significantly more Asperger's syndrome (AS) (p=.041), conduct disorder (CD) (p=.049), major depressive disorder (MDD) (p=.001), dysthymia (p=.030), general anxiety disorder (GAD) (p<.001), and having attempted suicide (p=.006). We found significantly more comorbid disorders in the maltreated group. Poly-victimization was studied by constructing a scale comprised of witnessing violence, victim of family violence, victim of sexual abuse and household dysfunction. We found that poly-victimization was associated with significantly increased risk of MDD, GAD, AS, CD, and having attempted suicide (p<.01). The complexity of the clinical outcomes revealed in this study suggest that longer-term treatment plans and follow-up by psychiatric services might be needed to a greater extend than for the rest of the child and adolescent population, and that trauma informed care is essential for adolescents in residential youth care.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Cross-section research suggests reported childhood abuse in schizophrenia spectrum disorders is linked with graver symptom levels and social dysfunction. To examine this prospectively, we compared biweekly ratings of positive and emotional discomfort symptoms and weekly accounts of hours worked over 4 months of rehabilitation of 12 participants with schizophrenia or schizoaffective disorder and childhood sexual abuse history and 31 with schizophrenia or schizoaffective disorder and no childhood sexual abuse history. Repeated-measures ANOVA revealed the abuse group had consistently higher levels of both symptom components and poorer participation in vocational rehabilitation. A time by group effect was observed for hours of work, with the abuse group working increasingly fewer hours over time. Participants reporting abuse also were more likely to perform poorly on a test of executive function and to have particularly higher levels of hallucinations and anxiety over time. Clinical and theoretical implications are discussed.
IntroductionIndividual studiesThe summary effectHeterogeneity of effect sizesSummary points
Evidence on the relationship of adolescent exposure to violence (AEV) with adult physical and mental health problems is limited, with studies often focusing on earlier childhood rather than adolescence, and also on short term rather than long term outcomes. Information specifically on the relationship of AEV to seeking help for mental health problems in adulthood from either formal sources such as mental health professionals or informal sources such as friends and clergy is even more difficult to find. The present study investigates how adolescent exposure to violence (AEV), in the form of parental physical abuse, witnessing parental violence, and exposure to violence in the neighborhood, are related to self-reported adult physical problems and seeking formal or informal assistance with mental health, controlling for more general adolescent violent victimization and for self-reports and parent reports of mental health problems in adolescence. This study adds to the literature on AEV and adult physical problems, and provides a rare look at the relationship of AEV to adult help-seeking for mental health problems. The results suggest that AEV is associated with mental health problems in adolescence for both females and males, that for females AEV is related to physical problems and to seeking help for mental health problems in adulthood, but for males the only significant relationship involves inconsistent reports of witnessing parental violence and adult physical problems.
Schizophrenia results in cognitive impairments as well as positive, negative, and disorganized symptomatology. The present study examines the extent to which these cognitive deficits are generalized across domains, potential moderator variables, and whether the pattern of cognitive findings reported in schizophrenia has remained consistent over time and across cultural and geographic variation.
Relevant publications from 2006 to 2011 were identified through keyword searches in PubMed and an examination of reference lists. Studies were included if they (1) compared the cognitive performance of adult schizophrenia patients and healthy controls, (2) based schizophrenia diagnoses on contemporary diagnostic criteria, (3) reported information sufficient to permit effect size calculation, (4) were reported in English, and (5) reported data for neuropsychological tests falling into at least 3 distinct cognitive domains. A set of 100 non-overlapping studies was identified, and effect sizes (Hedge's g) were calculated for each cognitive variable.
Consistent with earlier analyses, patients with schizophrenia scored significantly lower than controls across all cognitive tests and domains (grand mean effect size, g=-1.03). Patients showed somewhat larger impairments in the domains of processing speed (g=-1.25) and episodic memory (g=-1.23). Our results also showed few inconsistencies when grouped by geographic region.
The present study extends findings from 1980 to 2006 of a substantial, generalized cognitive impairment in schizophrenia, demonstrating that this finding has remained robust over time despite changes in assessment instruments and alterations in diagnostic criteria, and that it manifests similarly in different regions of the world despite linguistic and cultural differences.
There is an overlap between the neurocognitive deficits observed in adult survivors of childhood trauma and individuals with psychosis. Few studies examine the relationship between trauma and neurocognition in psychosis. The purpose of this study was to examine this in a first episode population. Thirty individuals with first episode psychosis who had completed a battery of neurocognitive testing in the longitudinal Northern Ireland First Episode Psychosis Study were subsequently interviewed and separated into two groups on the basis of childhood trauma. Between groups analysis was used to compare differences on measures of memory, executive functioning and verbal fluency. Twenty-one (70%) participants reported childhood trauma and nine (30%) reported no such history. Participants with a history of childhood trauma had a significantly higher pre-morbid IQ than the no childhood trauma group and experienced a significant decline in IQ when pre-morbid IQ estimates were compared to current IQ estimates. After controlling for pre-morbid IQ on all domains, the childhood trauma group had significantly poorer performance on tasks of semantic fluency, delayed visual recall, and visuospatial working memory. Childhood trauma may contribute to specific neurocognitive deficits and may predict a lower level of functioning relative to pre-morbid ability.
Glass's estimator of effect size, the sample mean difference divided by the sample standard deviation, is studied in the context of an explicit statistical model. The exact distribution of Glass's estimator is obtained and the estimator is shown to have a small sample bias. The minimum variance unbiased estimator is obtained and shown to have uniformly smaller variance than Glass's (biased) estimator. Measurement error is shown to attenuate estimates of effect size and a correction is given. The effects of measurement invalidity are discussed. Expressions for weights that yield the most precise weighted estimate of effect size are also derived.
This study investigated the relationship between severe childhood abuse and cognitive functions in first-episode psychosis patients and geographically-matched controls. Reports of any abuse were associated with lower scores in the executive function domain in the control group. However, in contrast with our hypothesis, no relationships were found amongst cases.
Background:
Studies that have investigated the executive functions (EFs) in crack cocaine-dependence have focused on differences between groups of drug users and non-user controls. In this study, however, we employ a promising additional approach that considers individual differences, such as exposure to childhood neglect that might be related to the degree of cognitive impairment associated with addiction.
Objective:
We evaluated EFs in crack cocaine-dependent women who have reported a history of childhood physical neglect (CPN) and compared these measures with those of crack cocaine-dependent women who do not reported CPN.
Method:
The participants were divided into 2 groups: those with a history of CPN (CPN+) (n=37) and those without a history of CPN (CPN-) (n=48). Cold EFs were assessed with the Stroop Task, the Trail Making Test B, the Verbal Fluency Task, the N-Back Task and the Letter and Number Sequencing task. Hot EFs were assessed with the Iowa Gambling Task (IGT).
Results:
The CPN+ group exhibited lower performance in all of the tasks except the IGT. A multivariate analysis of covariance indicated significant group differences in EFs (F(6,63)=2.51, p=0.030), regardless of craving severity and premorbid IQ.
Conclusions:
CPN is associated with cognitive impairments in crack cocaine-dependent women specifically regarding EFs and working memory tasks.
Background: Both bipolar disorder (BD) and childhood trauma are associated with cognitive impairment. People with BD have high rates of childhood trauma, which confer greater overall disease severity, but, it is unknown if childhood trauma is associated with greater neurocognitive impairment in BD patients early in the course of their illnesses. In this study, we investigated the impact of childhood trauma on specific cognitive dysfunction in patients who recently recovered from their first episode of mania. Methods: Data were available for 64 patients and 28 healthy subjects matched by age, gender and pre-morbid IQ, recruited from a large university medical center. History of childhood trauma was measured using the Childhood Trauma Questionnaire. Cognitive function was assessed through a comprehensive neuropsychological test battery. Results: Trauma was associated with poorer cognitive performance in patients on cognitive measures of IQ, auditory attention and verbal and working memory, and a different pattern was observed in healthy subjects. Limitations: We had a modest sample size, particularly in the group of healthy subjects with trauma. Conclusions: Childhood trauma was associated with poorer cognition in BD patients who recently recovered from a first episode of mania compared to healthy subjects. The results require replication, but suggest that the co-occurrence of trauma and bipolar disorder can affect those cognitive areas that are already more susceptible in patients with BD.
Selective attention, the ability to focus our cognitive resources on information relevant to our goals, influences working memory (WM) performance. Indeed, attention and working memory are increasingly viewed as overlapping constructs. Here, we review recent evidence from human neurophysiological studies demonstrating that top-down modulation serves as a common neural mechanism underlying these two cognitive operations. The core features include activity modulation in stimulus-selective sensory cortices with concurrent engagement of prefrontal and parietal control regions that function as sources of top-down signals. Notably, top-down modulation is engaged during both stimulus-present and stimulus-absent stages of WM tasks; that is, expectation of an ensuing stimulus to be remembered, selection and encoding of stimuli, maintenance of relevant information in mind and memory retrieval.
This Technical Report was retired November 2021
Advances in fields of inquiry as diverse as neuroscience, molecular biology, genomics, developmental psychology, epidemiology, sociology, and economics are catalyzing an important paradigm shift in our understanding of health and disease across the lifespan. This converging, multidisciplinary science of human development has profound implications for our ability to enhance the life prospects of children and to strengthen the social and economic fabric of society. Drawing on these multiple streams of investigation, this report presents an ecobiodevelopmental framework that illustrates how early experiences and environmental influences can leave a lasting signature on the genetic predispositions that affect emerging brain architecture and long-term health. The report also examines extensive evidence of the disruptive impacts of toxic stress, offering intriguing insights into causal mechanisms that link early adversity to later impairments in learning, behavior, and both physical and mental well-being. The implications of this framework for the practice of medicine, in general, and pediatrics, specifically, are potentially transformational. They suggest that many adult diseases should be viewed as developmental disorders that begin early in life and that persistent health disparities associated with poverty, discrimination, or maltreatment could be reduced by the alleviation of toxic stress in childhood. An ecobiodevelopmental framework also underscores the need for new thinking about the focus and boundaries of pediatric practice. It calls for pediatricians to serve as both front-line guardians of healthy child development and strategically positioned, community leaders to inform new science-based strategies that build strong foundations for educational achievement, economic productivity, responsible citizenship, and lifelong health.
Previous research suggests that various types of childhood maltreatment frequently co-occur and confer risk for multiple psychiatric diagnoses. This non-specific pattern of risk may mean that childhood maltreatment increases vulnerability to numerous specific psychiatric disorders through diverse, specific mechanisms or that childhood maltreatment engenders a generalised liability to dimensions of psychopathology. Although these competing explanations have different implications for intervention, they have never been evaluated empirically.
We used a latent variable approach to estimate the associations of childhood maltreatment with underlying dimensions of internalising and externalising psychopathology and with specific disorders after accounting for the latent dimensions. We also examined gender differences in these associations.
Data were drawn from a nationally representative survey of 34 653 US adults. Lifetime DSM-IV psychiatric disorders were assessed using the AUDADIS-IV. Physical, sexual and emotional abuse and neglect were assessed using validated measures. Analyses controlled for other childhood adversities and sociodemographics.
The effects were fully mediated through the latent liability dimensions, with an impact on underlying liability levels to internalising and externalising psychopathology rather than specific psychiatric disorders. Important gender differences emerged with physical abuse associated only with externalising liability in men, and only with internalising liability in women. Neglect was not significantly associated with latent liability levels.
The association between childhood maltreatment and common psychiatric disorders operates through latent liabilities to experience internalising and externalising psychopathology, indicating that the prevention of maltreatment may have a wide range of benefits in reducing the prevalence of many common mental disorders. Different forms of abuse have gender-specific consequences for the expression of internalising and externalising psychopathology, suggesting gender-specific aetiological pathways between maltreatment and psychopathology.
to examine racial differences in (a) the prevalence of financial exploitation and psychological mistreatment since turning 60 and in the past 6 months and (b) the experience-perpetrator, frequency, and degree of upset-of psychological mistreatment in the past 6 months.
random digit dial telephone recruitment and population-based survey (telephone and in-person) of 903 adults aged 60 years and older in Allegheny County (Pittsburgh), Pennsylvania (693 non-African American and 210 African American). Covariates included sex, age, education, marital status, household composition, cognitive function, instrumental activities of daily living/activities of daily living difficulties, and depression symptoms.
prevalence rates were significantly higher for African Americans than for non-African Americans for financial exploitation since turning 60 (23.0% vs. 8.4%) and in the past 6 months (12.9% vs. 2.4%) and for psychological mistreatment since turning 60 (24.4% vs. 13.2%) and in the past 6 months (16.1% vs. 7.2%). These differences remained once all covariates were controlled in logistic regression models. There were also racial differences in the experience of psychological mistreatment in the past 6 months. Risk for clinical depression was also a consistent predictor of financial exploitation and psychological mistreatment.
although the results will need to be replicated in national surveys, the study suggests that racial differences in elder mistreatment are a potentially serious issue deserving of continued attention from researchers, health providers, and social service professionals.