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Background: How cognition is influenced by electroconvulsive treatment (ECT) and major depressive disorder (MDD) is still debated. The development and etiology of neurocognitive impairment in MDD were examined by investigating the cognitive profile following ECT related to the state, scar, and trait perspectives, with the former predicting improvements parallel with depressive symptoms, while the two latter expected persisting impairments. Executive functions (EF) and attention are central to cognition and alterations in these functions could influence other domains like memory. The main aims of the present study were to examine the short and long-term effects of ECT on EF and attention in patients with major depressive disorder by exploiting the rapid antidepressant effect of this treatment., Methods: A case-control longitudinal follow-up design was used to investigate the effects of unilateral brief-pulse ECT on EF and attention in patients with depression (n = 36) compared to untreated healthy controls (n = 16). EF and attention were measured pre-treatment, approximately two weeks, and six months post-treatment., Results: The patient group showed significantly worse performance on most tests compared to healthy controls pre-treatment, and no short- or long-term worsening of EF and attention following ECT was found. Significant improvement was identified in patients' attention, processing speed and inhibition after ECT., Conclusions: The present study showed that there was no cognitive worsening after ECT treatment. An improvement in several of the tests measuring inhibition, attention, and processing speed was parallel to symptom reduction, with the former showing associations to symptom change, suggesting state-related effects from improved mood. Still, the patient group performed significantly worse on most measures both pre-treatment and at the short and long-term follow-ups, indicating prevailing trait or scar effects on cognitive functions and potential lack of practice effects., Clinical Trial Number: NCT04348825 (14.04.20)., Competing Interests: Declarations. Ethics approval and consent to participate: Written and informed consent from participants was collected in advance of participation. All participants consented to participation in the study. The study was approved by the Regional Committee for Medical and Health Research Ethics, South East, ID: 2013/1032 ECT and neurology. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Executive functions and emotion regulation develop from early childhood to adolescence and are predictive of important psychosocial outcomes. However, despite the correlation between the two regulatory capacities, whether they are prospectively related in school-aged children remains unknown, and the direction of effects is uncertain. In this study, a sample drawn from two birth cohorts in Norway was biennially examined between the ages of 6 and 14 (n = 852, 50.1% girls, 93% Norwegian). Parents completed the Emotion Regulation Checklist, and teachers completed the Behavior Rating Inventory of Executive Function. A random intercept cross-lagged panel model revealed that improved emotion regulation predicted increased executive functioning to the same extent throughout development, whereas enhanced executive functioning was unrelated to future changes in emotion regulation., (© 2024 The Authors. Child Development published by Wiley Periodicals LLC on behalf of Society for Research in Child Development.)

According to prominent models of child development, parental factors may contribute to individual differences in children's executive functioning (EF). Here, we examine the relative importance of parents' socio-economic status, mental health, and parenting as predictors of EF development, drawing on a large (n = 1,070) community sample of Norwegian children who received biennial EF assessments from 6 to 10 years of age. We measure EF by means of the Behavior Rating Inventory of Executive Function. We assess parenting through observer ratings of parent-child interactions and parental mental health via the Beck Anxiety Inventory, Beck Depression Inventory, and Hopkins Symptom Checklist. When we adjust for all time-invariant unmeasured confounders, higher parental education predicts superior EF development, whereas harsh parenting forecasts poorer EF development. However, parenting does not mediate the effect of parental education. These results indicate that harsh parenting should be targeted in interventions aimed at improving EF. Statement of contribution What is already known on this subject? Parental factors seem to affect child development of executive functions (EF). Specifically, parental socio-economic status, mental health, and their parenting seem to influence the developmental course of child EF. What does this study add? To what degree the parental influence on EF development is likely to be driven by time-invariant factors, for example, genetics. The relative influence of positive and negative parenting on EF development., (© 2019 The British Psychological Society.)

The present pilot study investigated neuronal correlates of executive functioning in patients previously diagnosed with recurrent major depressive disorder (MDD). The aim of the study was to examine a partially remitted and remitted MDD patient group with functional magnetic resonance imaging (fMRI) using a cognitive activation paradigm in order to probe aspects of response inhibition, attention shift, and working memory. Twenty MDD patients and 19 healthy controls, matched for age and sex, participated in the study. A working memory n-back task with single presentations of incongruent Stroop words was used, with the instruction to either remember the color of the ink the word was written in, or the color word itself, presented two or three words back in the presentation series. MR images were acquired on a 1.5-T GE Signa HD MR scanner. In addition to MR data, response time (RT) and response accuracy (RA) behavioral data were recorded. The behavioral results showed longer RT and lower RA in the MDD group compared to the control group across instruction conditions and working memory load. Based on previous studies of executive function, a composite region of interest (ROI) mask of the anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (DLPFC), caudate, and putamen was used in statistical analysis. Significant activation was observed in controls throughout this corticostriatal network. When compared to controls, patients showed no significant difference in the level of activation in the ACC and the DLPFC. However, in the putamen and caudate, hypoactivation in the patient group was observed. It was concluded that these effects could be due to a scar effect as a result of previous episodes of MDD., (© 2016 The Institute of Psychology, Chinese Academy of Sciences and John Wiley & Sons Australia, Ltd.)

Major Depressive Disorder (MDD) is often associated with high levels of stress and disturbances in the Hypothalamic Pituitary Adrenal (HPA) system, yielding high levels of cortisol, in addition to cognitive dysfunction. Previous studies have shown a relationship between cortisol profile and cognitive functioning in recurrent MDD in general. More specifically, the association between hypercortisolism and cognitive functioning, such as memory and Executive Functioning (EF), and also more recently cortisol suppression has been explored. However, no studies have investigated these relationships in patients diagnosed with first episode MDD. The aim of the present study was to examine the relationship between cortisol levels before and after the Dexamethasone suppression test (DST) and cognitive function in first episode MDD patients. Twenty-one patients meeting the DSM-IV criteria for a first episode of MDD diagnosis were included in the study. The control group was matched for age, gender and education level. Cortisol was measured in saliva collected with Salivette sampling devices. Saliva samples were collected 4 times during a 24 hours period over two consecutive days: at awakening, after 45 minutes, after 7 hours and at 11 pm. Dexamethasone (1.0 mg) was given orally on Day 1 at 11 pm. The neuropsychological test battery consisted of standardized tests measuring executive functioning (EF) and memory functioning. Cortisol levels did not differ significantly between patients and controls on Day 1, except for the last sample before Dexamethasone administration, where the control group showed higher levels. Both groups showed suppression after Dexamethasone. On Day 2 there was a significant difference between groups at the third sample, showing a significantly lower level in the control group, suggesting that the controls have a more effective suppression profile than the patients. There were no significant correlations between cortisol levels before or after Dexamethasone and cognitive measures. The results indicate impairment on HPA-axis functioning in first episode MDD patients, with less suppression functioning compared to healthy controls, but no relationship between cortisol profile and cognitive functioning in EF or Memory., (© 2015 Scandinavian Psychological Associations and John Wiley & Sons Ltd.)

Introduction: Executive Functions (EF) has been documented to be impaired in patients with recurrent Major Depressive Disorder (MDD) in several studies. Longitudinal studies have suggested that these impairments may be a result of several episodes of depression or they may represent stable traits in this patient group. However, few studies have addressed these issues and investigated cognitive functioning with a particular focus on EF in patients who experience MDD for the first time., Methods: In the present study, the executive functions of inhibition, verbal fluency, mental flexibility, and planning and problem solving were investigated in a group of patients diagnosed with first episode MDD. Thirty patients and 30 control subjects were included in the study., Results: The patient group performed significantly more poorly in the cognitive functions of inhibition and semantic fluency. In addition, the patient group showed a reduced speed of mental processing on some of the measures. However, the results showed that reduced processing speed alone could not account for the poor performance in inhibition and semantic fluency. There were no differences between the two groups in the other measures of EF, indicating that functioning of mental flexibility, phonemic fluency, planning, and problem solving was intact in the patient group., Conclusions: The results show that impaired inhibition and semantic fluency are present early in the course of MDD. The present findings indicate that poor inhibition and performance in semantic fluency may represent stable traits in MDD, independent of symptom severity and the number of depressive episodes.

Heart rate variability (HRV) is reduced in patients who suffer from panic disorder (PD). Reduced HRV is related to hypoactivity in the prefrontal cortex (PFC), which negatively affects executive functioning. The present study assessed the relationships between vagally mediated HRV at baseline and measures of executive functioning in 36 patients with PD. Associations between these physiological and cognitive measures and panic-related variables were also investigated. HRV was measured using HF-power (ms(2)), and executive functions were assessed with the Wisconsin Card Sorting Test (WCST) and the Color-Word Interference Test (CWIT) from the Delis-Kaplan Executive Function System (D-KEFS). Panic-related variables comprised panic frequency, panic-related distress, and duration of PD. Performance on the neuropsychological measures correlated significantly with HRV. Both panic-related distress and duration of PD were inversely related with measures of HRV and cognitive inhibition. The current findings support the purported relationship between HRV and executive functions involving the PFC., (Copyright © 2012 Elsevier B.V. All rights reserved.)

BACKGROUND: Generalised anxiety disorder (GAD) is a frequent and severe anxiety disorder among older adults. GAD increases the risk of developing other disorders such as depression and coronary heart disease. Older adults with GAD exhibit a poorer response to cognitive behaviour therapy (CBT) compared to younger patients with GAD. The normal age-related cognitive decline can be a contributor to reduced treatment efficacy. One strategy for improving treatment efficacy is to combine CBT with adjunctive interventions targeted at improving cognitive functions. Physical exercise is a viable intervention in this regard. Increased levels of brain-derived neurotrophic factor may mediate improvement in cognitive function. The present study aims to investigate the proposed effects and mechanisms related to concomitant physical exercise. METHODS: The sample comprises 70 participants aged 60-75 years, who have GAD. Exclusion criteria comprise substance abuse and unstable medication; inability to participate in physical exercise; and conditions which precludes GAD as primary diagnosis. The interventions are individual treatment in the outpatient clinic at the local psychiatric hospital, with two experimental arms: (1) CBT + physical exercise and (2) CBT + telephone calls. The primary outcome measure is symptom reduction on the Penn State Worry Questionnaire. Other measures include questionnaires, clinical interviews, physiological, biological and neuropsychological tests. A subset of 40 participants will undergo magnetic resonance imaging (MRI). After inclusion, participants undergo baseline testing, and are subsequently randomized to a treatment condition. Participants attend five sessions of the add-on treatment in the pre-treatment phase, and move on to interim testing. After interim testing, participants attend 10 sessions of CBT in parallel with continued add-on treatment. Participants are tested post-intervention within 2 weeks of completing treatment, with follow-up testing 6 and 12 months later. DISCUSSION: This study aims to develop better treatment for GAD in older adults. Enhancing treatment response will be valuable from both individual and societal perspectives, especially taking the aging of the general population into account. TRIAL REGISTRATION: ClinicalTrials.gov, NCT02690441 . Registered on 24 February 2016.

Abstract PTSD symptomatology is known to be associated with executive dysfunction. Inhibitory control is a core component of executive functioning, and inhibitory skills are essential both for adequate functioning in everyday life and important in situations following trauma. The aim of the present study was to examine the relationship between trauma exposure, inhibitory control and PTSD symptomatology in adolescent survivors of the terror attack at Utøya, Norway on the 22nd of July, 2011. In this cross-sectional case-control study, 20 trauma exposed adolescents and 20 healthy controls matched in age and gender were compared on a neuropsychological test of cognitive inhibition (Color-Word Interference Test) and a self-report measure of inhibition ability (BRIEF-A). Our analyses revealed that the trauma exposed group differed significantly on the self-reported measure of inhibitory control compared to the control group, but there were no differences between groups on the objective measures of cognitive inhibition. Follow-up analyses with subgroups in the trauma exposed group based on PTSD symptomatology (PTSD + and PTSD-) and the control group revealed that the PTSD- group showed significantly better results than both the PTSD + and the control group on the measures of inhibitory control. Moreover, the follow-up analyses showed that the PTSD + group showed significantly poorer results from the other two groups on the measures of inhibitory control and self-reported inhibition. We conclude that impaired inhibitory control, measured both objectively and by self-reported questionnaire, is related to PTSD symptomatology. Findings suggest that inhibitory dysfunctions may be a vulnerability factor for the development of PTSD symptomatology in trauma exposed adolescents, and thus it seems that the ability to exhibit inhibitory control could be a possible resilience factor to prevent the development of PTSD symptoms. [ABSTRACT FROM AUTHOR]

Background: Malfunctioning of executive functions correlates with psychopathology in children. However, the directionality, the extent to which the relation varies for various disorders, and whether prospective relations afford causal interpretations are not known. Methods: A community sample of Norwegian children (n = 874) was studied biennially from the age of 6 to 14 years. Executive functions were assessed using the Behavior Rating Inventory of Executive Function Teacher‐report and symptoms of psychopathology were assessed using the Preschool Age Psychiatric Assessment (age 6; parents) and Child and Adolescent Psychiatric Assessment (ages 8–14; children and parents). Prospective reciprocal relations were examined using a random intercept cross‐lagged panel model that adjusts for all unobserved time‐invariant confounders. Results: Even when time‐invariant confounders were accounted for, reduced executive functions predicted increased symptoms of depressive disorders, anxiety disorders, attention‐deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) 2 years later, even when previous changes in these symptoms were adjusted for. The level of prediction (B =.83, 95% CI [.37, 1.3]) was not different for different disorders or ages. Conversely, reduced executive functions were predicted by increased symptoms of all disorders (B =.01, 95% CI [.01,.02]). Conclusions: Reduced executive functioning may be involved in the etiology of depression, anxiety, ADHD, and ODD/CD to an equal extent. Moreover, increased depression, anxiety, ADHD, and ODD/CD may negatively impact executive functioning. [ABSTRACT FROM AUTHOR]

Introduction: Remission from major depressive disorder (MDD) is associated with residual symptoms related to reduced functioning, quality of life, and relapse risk. Previous studies have raised questions about mechanisms involved-in and affected by cognitive training. This study investigated the associations and changes among depressive symptoms, rumination, processing speed (PS), executive functioning (EF), and emotional working memory (e-WM) pre- post computerized working memory training (CWMT). Method: Twenty-nine remitted participants were included in a pre- post pilot study of within-subject effects of online CWMT. A total of 20 participants completed the intervention and pre- post tests of EF and PS, e-WM, in addition to symptom and rumination measures. Associations between changes in symptoms and cognition were investigated pre- post. Associations between improvements in CWMT, depression history, and changes in cognition were explored. Hypotheses and statistics were preregistered before data were analyzed. Results: Manipulation of negatively valanced stimuli in e-WM showed an inverse association with rumination pre-intervention, but the association disappeared post-intervention. Cognitive functioning improved in most conditions with largest effects in EF. Symptoms did not change in the remitted sample. CWMT improvements were related to improvements in some aspects of EF and PS, but also to worse self-reported attention. Depression history was related to less improvement in EF. Limitations: Sample size was small and there was dropout from the study. There was no control group, thus precluding practice and placebo effects and causal relationships. Conclusions: Computerized WM training improves cognitive functions and could influence associations between e-WM and rumination. This could counteract functional impairment following MDD. [ABSTRACT FROM AUTHOR]

Increasingly, studies have investigated cognitive functioning from the perspective of acute state - to remitted phases of Major Depressive Disorder (MDD). Some cognitive deficits observed in the symptomatic phase persist in remission as traits or scars. The etiological origin and clinical consequences of the neurocognitive profiles reported in the literature are still unclear and may vary across populations. Deficits are suspected to influence the association between MDD and neurodegenerative disorders and could thus be of particular clinical consequence. The aim of this review is to describe the clinical neuropsychological profile in MDD and how it is related to research during the past decade on cognitive deficits in MDD from a state, trait, and scar perspective. This review, with a clinical perspective, investigates research from the past decade regarding cognitive functioning in MDD in a long-term perspective. We focus on the clinical manifestation of deficits, and the potential neurodegenerative consequences of the neurocognitive profile in MDD. Searches in Medline, PsycINFO and Embase were conducted targeting articles published between 2010 and 2020. Examination of the evidence for long-lasting neurocognitive deficits in major depression within the cognitive domains of Memory, Executive Functions, Attention, and Processing Speed was conducted and was interpreted in the context of the State, Scar and Trait hypotheses. Defining the neurocognitive profiles in MDD will have consequences for personalized evaluation and treatment of residual cognitive symptoms, and etiological understanding of mood disorders, and treatments could potentially reduce or delay the development of neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

Cognitive deficits such as difficulties with attention, memory, and executive functions are frequently reported during remission from depression and relates to adverse functioning in daily life and risk of relapse. There is therefore a need for interventions targeting cognitive deficits after depression. However, few randomized controlled trials have investigated the efficacy of interventions targeting subjective residual cognitive deficits in adults remitted from depression. This randomized crossover trial aimed to investigate the efficacy of an internet-delivered cognitive enhancement intervention on subjective residual cognitive deficits. Forty-four formerly depressed adults (89 % female;mean age = 39 years) were included. Twenty-three participants received the intervention, and 21 participants were assigned to a waitlist control group. The waitlist control group received the intervention after seven weeks. Analyses of follow-up assessment after six months were conducted for the combined sample. Significant differences were found between the intervention and waitlist control group in subjective cognitive functioning (d = 1.83) and rumination (d = 1.65). There was a difference in symptoms of depression between the groups (d = 1.22), whereas symptoms of depression increased in the waitlist control, but not in the intervention group. Fewer participants in the waitlist control group (43 %), compared to the intervention group (78 %) showed reliable improvement in self-reported cognitive deficits after receiving the intervention. Findings should be interpreted with caution due to the small sample, and lack of an active control group. Internet-delivered cognitive enhancement interventions may improve subjective cognitive deficits. Waiting time to receive cognitive enhancement interventions may worsen symptoms and treatment response. • The intervention was associated with improvement of self-reported residual cognitive deficits and rumination. • Symptoms of depression increased in the waitlist control group but were unchanged in the intervention group. • Fewer participants from the waitlist control group showed reliable improvement compared to the intervention group. [ABSTRACT FROM AUTHOR]

Objective: Major Depressive Disorder (MDD) is associated with cognitive impairment in general, and Executive Functioning (EF) in particular, even in remitted phase of the disorder, suggesting residual cognitive symptoms. The aim of the present study was to investigate self-reported EF 1 year after the first episode of MDD and to explore this in relation to depressive mood symptoms, remission and relapse. Method: The study included data from 24 patients and 23 healthy control subjects 1 year after the patients' initial first episode of MDD. All participants completed the Behavior Rating Inventory of Executive Functioning-Adult version (BRIEF-A), a standardized self-report measure of perceived EF in everyday life, measuring nine different EF. Total index scores for metacognitive functions, behavior/emotional regulation functions and a global EF score is also calculated. Results: The patient group in total, independent of symptom status, reported significantly lower EF in all indexes compared to the healthy controls 1 year after the initial episode. However, higher depressive mood symptom load correlated with self-reported difficulties in metacognitive functions and poor global EF scores. Regulatory control of behavior and emotional responses did not show such strong association with mood symptoms, but low self-report scores on this measure was associated with relapse during the first year after the initial episode. Conclusion: First-episode patients report significant lower executive functioning in everyday life compared to individually matched healthy controls, 1 year after onset, independent of symptom load. Residual cognitive symptoms seem to be evident and associated with risk of relapse and should be targeted in treatment and prevention of recurrence in MDD. [ABSTRACT FROM AUTHOR]

Major depression (MDD) is associated with cognitive deficits in processing speed and executive function (EF) following first episode (FE). It is unclear whether deficits are state or trait related. Studies following FE MDD over longer periods are lacking, making it uncertain how cognition and symptoms develop after the initial episode. The present study assessed cognitive function and symptoms 5 years following FE MDD. In addition, the study explored relationships between MDD symptoms, rumination, and cognitive deficits with regards to the trait, state, and scar perspective. Twenty-three participants with previous FE MDD, and 20 matched control participants were compared on Delis-Kaplan Executive Function System measures of processing speed and EF, in a 5-year longitudinal follow-up study. Correlations between current symptoms- and history of MDD, rumination, cognition were investigated. Findings indicated that cognitive deficits persisted with no clear signs of exacerbation after initial episode. Inhibition appeared independent of current and previous symptoms of depression. Processing speed was related to depressive- symptoms and rumination. In conclusion, results indicated persisting, stable deficits in both EFs and processing speed. Findings further suggest that depressive symptoms could be related to deficits in processing speed, indicating state effects. There was limited support for worsening of cognition after initial episode. Some aspects of EF like Inhibition could show persistent deficits independent of depressive symptoms indicating trait effects. [ABSTRACT FROM AUTHOR]

AbstractExecutive functions (EF) decline with age and this decline in older adults with generalised anxiety disorder (GAD) may be influenced by heart rate variability (HRV), brain-derived neurotrophic factor (BDNF), and physical fitness. Understanding these relationships is important for tailored treatments in this population. In this study, 51 adults with GAD (M age = 66.46, SD = 4.08) and 51 healthy controls (M age = 67.67, SD = 4.04) were assessed on cognitive inhibition (Stroop task), shifting (Trails part 4), flexibility (Wisconsin Card Sorting Test – Perseverative errors), working memory (Digit Span Backwards), IQ (Wechsler Abbreviated Scale of Intelligence), high frequency HRV, serum mature BDNF levels, and VO2 max. Results indicated that participants with GAD exhibited better cognitive inhibition compared to controls, with no general reduction in EF. Cognitive inhibition was predicted by gender, HRV, and BDNF levels, while cognitive shifting was predicted by gender and IQ, and cognitive flexibility and working memory by IQ. The enhanced cognitive inhibition in GAD participants might stem from maladaptive use of this function, characteristic of GAD, or protection from EF decline due to normal HRV. Increased BDNF levels, possibly due to good fitness, or compensatory mechanisms related to the disorder, might also play a role. These findings highlight the complexity of EF and related mechanisms in GAD, highlighting the need for interventions that consider both cognitive and physiological factors for optimal outcomes. [ABSTRACT FROM AUTHOR]

Background: Generalised anxiety disorder (GAD) is a frequent and severe anxiety disorder among older adults. GAD increases the risk of developing other disorders such as depression and coronary heart disease. Older adults with GAD exhibit a poorer response to cognitive behaviour therapy (CBT) compared to younger patients with GAD. The normal age-related cognitive decline can be a contributor to reduced treatment efficacy. One strategy for improving treatment efficacy is to combine CBT with adjunctive interventions targeted at improving cognitive functions. Physical exercise is a viable intervention in this regard. Increased levels of brain-derived neurotrophic factor may mediate improvement in cognitive function. The present study aims to investigate the proposed effects and mechanisms related to concomitant physical exercise.Methods: The sample comprises 70 participants aged 60-75 years, who have GAD. Exclusion criteria comprise substance abuse and unstable medication; inability to participate in physical exercise; and conditions which precludes GAD as primary diagnosis. The interventions are individual treatment in the outpatient clinic at the local psychiatric hospital, with two experimental arms: (1) CBT + physical exercise and (2) CBT + telephone calls. The primary outcome measure is symptom reduction on the Penn State Worry Questionnaire. Other measures include questionnaires, clinical interviews, physiological, biological and neuropsychological tests. A subset of 40 participants will undergo magnetic resonance imaging (MRI). After inclusion, participants undergo baseline testing, and are subsequently randomized to a treatment condition. Participants attend five sessions of the add-on treatment in the pre-treatment phase, and move on to interim testing. After interim testing, participants attend 10 sessions of CBT in parallel with continued add-on treatment. Participants are tested post-intervention within 2 weeks of completing treatment, with follow-up testing 6 and 12 months later.Discussion: This study aims to develop better treatment for GAD in older adults. Enhancing treatment response will be valuable from both individual and societal perspectives, especially taking the aging of the general population into account.Trial Registration: ClinicalTrials.gov, NCT02690441 . Registered on 24 February 2016. [ABSTRACT FROM AUTHOR]