Defining the impact of childhood adversities on cognitive deficits in psychosis: An exploratory analysis

Schalinski, Inga; Teicher, Martin H.; Carolus, Almut M.; Rockstroh, Brigitte

doi:10.1016/j.schres.2017.05.014

Cited by 50 publications

(59 citation statements)

References 44 publications

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“…Similar deficits in working memory and inhibitory control are noted in human studies (Table 4; although see Feeney et al, 2013), with some indication that selective attention may also be impaired in adults reporting chronic exposure to juvenile stressors (e.g. Schalinski et al, 2017; Viola et al, 2013, although this latter study was complicated by simultaneous treatment for crack cocaine use). As discussed in section 3.2, these facets of executive function are dependent on PFC function.…”

Section: Impact Of Chronic Juvenile Stress On Prefrontal Cortex Ansupporting

confidence: 63%

“…In addition, the majority of preclinical studies assessing the effects of pre- and adolescent stress exposure on later executive function and reward processing are conducted using social-based stressors. Furthermore, human studies rarely either distinguish the different types of stressors experienced by participants or establish the precise age of stress exposure (Tables 2 & 4; but see Schalinski et al, 2017). Additional confounds arise from differences between preclinical and clinical studies in the type of reward used to assess changes in reward processing following juvenile exposure to chronic stress, with animal studies primarily focusing on responses to drugs of abuse, whereas monetary rewards have typically been used for humans.…”

Section: Discussionmentioning

confidence: 99%

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Impact of juvenile chronic stress on adult cortico-accumbal function: Implications for cognition and addiction

Watt

Weber

Davies

et al. 2017

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Repeated exposure to stress during childhood is associated with increased risk for neuropsychiatric illness, substance use disorders and other behavioral problems in adulthood. However, it is not clear how chronic childhood stress can lead to emergence of such a wide range of symptoms and disorders in later life. One possible explanation lies in stress-induced disruption to the development of specific brain regions associated with executive function and reward processing, deficits in which are common to the disorders promoted by childhood stress. Evidence of aberrations in prefrontal cortex and nucleus accumbens function following repeated exposure of juvenile (pre- and adolescent) organisms to a variety of different stressors would account not only for the similarity in symptoms across the wide range of childhood stress-associated mental illnesses, but also their persistence into adulthood in the absence of further stress. Therefore, the goal of this review is to evaluate the current knowledge regarding disruption to executive function and reward processing in adult animals or humans exposed to chronic stress over the juvenile period, and the underlying neurobiology, with particular emphasis on the prefrontal cortex and nucleus accumbens. First, the role of these brain regions in mediating executive function and reward processing is highlighted. Second, the neurobehavioral development of these systems is discussed to illustrate how juvenile stress may exert long-lasting effects on prefrontal cortex-accumbal activity and related behavioral functions. Finally, a critical review of current animal and human findings is presented, which strongly supports the supposition that exposure to chronic stress (particularly social aggression and isolation in animal studies) in the juvenile period produces impairments in executive function in adulthood, especially in working memory and inhibitory control. Chronic juvenile stress also results in aberrations to reward processing and seeking, with increased sensitivity to drugs of abuse particularly noted in animal models, which is in line with greater incidence of substance use disorders seen in clinical studies. These consequences are potentially mediated by monoamine and glutamatergic dysfunction in the prefrontal cortex and nucleus accumbens, providing translatable therapeutic targets. However, the predominant use of male subjects and social-based stressors in preclinical studies points to a clear need for determining how both sex differences and stressor heterogeneity may differentially contribute to stress-induced changes to substrates mediating executive function and reward processing, before the impact of chronic juvenile stress in promoting adult psychopathology can be fully understood.

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Section: Impact Of Chronic Juvenile Stress On Prefrontal Cortex Ansupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Impact of juvenile chronic stress on adult cortico-accumbal function: Implications for cognition and addiction

Watt

Weber

Davies

et al. 2017

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

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“…However, this meta‐analysis examined only studies of nonsocial cognition, and did not explore whether different types of adversity or the timing of adversity (e.g., neglect vs. trauma, early vs. late childhood) has differential effects on cognition in schizophrenia. Notably, findings from recent studies suggest that social cognitive impairment is more related to neglect than other types of adversity.…”

Section: Recent Developments and Future Directions For Research On Comentioning

confidence: 99%

Nonsocial and social cognition in schizophrenia: current evidence and future directions

2019

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Cognitive impairment in schizophrenia involves a broad array of nonsocial and social cognitive domains. It is a core feature of the illness, and one with substantial implications for treatment and prognosis. Our understanding of the causes, consequences and interventions for cognitive impairment in schizophrenia has grown substantially in recent years. Here we review a range of topics, including: a) the types of nonsocial cognitive, social cognitive, and perceptual deficits in schizophrenia; b) how deficits in schizophrenia are similar or different from those in other disorders; c) cognitive impairments in the prodromal period and over the lifespan in schizophrenia; d) neuroimaging of the neural substrates of nonsocial and social cognition, and e) relationships of nonsocial and social cognition to functional outcome. The paper also reviews the considerable efforts that have been directed to improve cognitive impairments in schizophrenia through novel psychopharmacology, cognitive remediation, social cognitive training, and alternative approaches. In the final section, we consider areas that are emerging and have the potential to provide future insights, including the interface of motivation and cognition, the influence of childhood adversity, metacognition, the role of neuroinflammation, computational modelling, the application of remote digital technology, and novel methods to evaluate brain network organization. The study of cognitive impairment has provided a way to approach, examine and comprehend a wide range of features of schizophrenia, and it may ultimately affect how we define and diagnose this complex disorder.

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“…Conventional analytic techniques, such as multiple regression, are not suitable because of marked collinearity in the degree of exposure to specific types of maltreatment at adjacent ages. Instead, we identified the most important cross-validated "predictors" associated with global network measures using random forest regression with conditional inference trees (RFR-CIT) (cforest in R package party), an artificial intelligence machine learning strategy that is highly resistant to collinearity, which we have used in an expanding series of sensitive period studies (Khan et al, 2015;Pechtel, Lyons-Ruth, Anderson, & Teicher, 2014;Schalinski, Breinlinger, Hirt, Teicher, Odenwald, & Rockstroh, 2017;Schalinski, Teicher, Carolus, & Rockstroh, 2018;Schalinski, Teicher, Nischk, Hinderer, Muller, & Rockstroh, 2016;Teicher, et al, 2018;Tomoda, Navalta, Polcari, Sadato, & Teicher, 2009a;Tomoda et al, 2012). Random forest regression predicts outcome by creating a forest of different decision trees with each tree generated from a different subset of the data and constrained in the number of predictors that can be considered at each branch point (Breiman, 2001).…”

Section: Identification Of Sensitive Exposure Periodsmentioning

confidence: 99%

Additional Insights into the Relationship Between Brain Network Architecture and Susceptibility and Resilience to the Psychiatric Sequelae of Childhood Maltreatment

2020

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Childhood maltreatment is associated with an increased risk for psychiatric and substance use disorders. However, some maltreated individuals appear resilient to these consequences while manifesting the same array of brain changes as maltreated individuals with psychopathology. Hence, a critical issue has been to identify compensatory brain alterations in these resilient individuals. We recently reported that maltreatment is associated with a more vulnerable structural brain network architecture. Resilient individuals have this same vulnerability but appeared to be able to effectively compensate due to reduced nodal efficiency (ability of a node to influence the global network) in 9 specific brain regions that moderate the relationship between maltreatment and psychopathology. Following up, we now report that network vulnerability increases progressively during late adolescence to plateau at about 21 years of age, which may help to explain age of onset of psychopathology. Further, we found that network vulnerability was most significantly affected by parental verbal abuse between 16 and 18 years of age and number of types of maltreatment during childhood. Asymptomatic individuals with no history of psychopathology had more prominent alterations in nodal efficiency than asymptomatic individuals with prior history, who specifically showed reduced nodal efficiency in the right amygdala and right subcallosal gyrus. Experiencing inadequate financial sufficiency during childhood increased the risk of susceptibility versus resilience by 2.98-fold (95% CI 1.49-5.97, p = 0.002) after adjusting for differences in exposure to maltreatment. Interestingly, adequate-to-higher financial sufficiency appeared to be protective and was associated with reduced nodal efficiency in the right postcentral gyrus and subcallosal gyrus "resilience" nodes. Keywords Childhood maltreatment. Abuse and neglect. Resilience. Brain networks. Graph theory. Neuroimaging Childhood maltreatment is the most important risk factor for psychopathology. Adverse childhood experiences in the form of maltreatment and household dysfunction account for about 33%, 54%, 64%, and 67% of the population attributable risk for anxiety disorders (

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Defining the impact of childhood adversities on cognitive deficits in psychosis: An exploratory analysis

Abstract: Abuse and neglect at periods when children spend substantial time in their families affect cognitive functioning, and hence aggravate dysfunction in psychosis. Results support the neurodevelopmental perspective on psychosis and the diagnostic value of type and timing of ACE.

Cited by 50 publications

References 44 publications

Impact of juvenile chronic stress on adult cortico-accumbal function: Implications for cognition and addiction

Impact of juvenile chronic stress on adult cortico-accumbal function: Implications for cognition and addiction

Nonsocial and social cognition in schizophrenia: current evidence and future directions

Additional Insights into the Relationship Between Brain Network Architecture and Susceptibility and Resilience to the Psychiatric Sequelae of Childhood Maltreatment

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