Internalizing disorders (INTs), including anxiety (AD) and depressive disorders (DD), frequently emerge during adolescence. Studies suggest that certain core domains of executive functioning (EF), i.e. inhibition, shifting and working memory (WM) may show selectively lower performance in certain INTs. This systematic review aimed to evaluate the evidence of associations between INTs and EF in adolescents. A systematic search was conducted in Medline, Psych-INFO, Scopus, and Web of Science in May 2023. Inclusion focused on adolescents (12–17) with AD (including obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD)) or DD. After screening 2,551 titles/abstracts, 818 records underwent full-text review, on which independent reviewers reached 93

BackgroundCognitive rigidity and working memory impairment are established features of internalizing syndromes. Growing evidence suggests that deficits in affective control –cognitive control in the context of emotion – may underpin elevated emotion-related impulsivity in various psychiatric disorders.ObjectiveThis study examines two components of affective control (affective flexibility and emotional working memory) as potential neurocognitive processes linking emotion-related impulsivity to internalizing psychopathology.MethodUndergraduate participants (analysis n = 120) completed the Memory and Affective Flexibility Task (MAFT), a novel behavioral assessment designed to assess hot cognition in affective flexibility and emotional working memory performance, alongside self-report measures of impulsivity and symptoms of internalizing disorders.ResultsStructural equation modeling suggested that less accurate working memory during neutral trials (cool cognition) was associated with more symptoms of internalizing psychopathology. However, effects of hot working memory and affective flexibility were not significantly related to emotion-related impulsivity or psychopathology scores.ConclusionsAlthough findings provide no support for the validity of MAFT indices of hot cognition, these results replicate and extend work on the importance of cool working memory and emotion-related impulsivity as correlates of psychopathology.

INTRODUCTION:Major depressive disorder (MDD) is a major global healthcare challenge. This is, in part, due to the lack of treatment response and chronic course of MDD. Such a course of illness is often termed treatment-resistant depression (TRD) and is seen in over one-third of people with MDD. Reasons for treatment resistance are not well established, nor is the definition of TRD. Duration and severity of depression, however, are associated with TRD and are also associated with cognitive deficits. Thus, TRD could be particularly prone to cognitive deficits and at heightened risk for neuroprogression. While the cognitive profile of MDD has been investigated in several systematic reviews, no systematic review of cognition in TRD exists to date. The present study will fill this gap in the literature. It is expected that TRD will show more severe cognitive deficits than generally reported in MDD and deficits in all cognitive functions are expected. METHODS AND ANALYSIS:A systematic review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines will be performed of the databases Embase, Pubmed/MEDLINE, PsychINFO and Cochrane including peer-reviewed studies on humans using standardised cognitive tests. Pilot searching was performed in January 2025 and the full search will be commenced in June 2025, with additional searches following completion. Where sufficient data are reported, a meta-analysis comparing deficits in TRD with MDD and healthy control participants will be performed; alternatively, effects based on norms will be calculated. Meta-regression, subgroup and sensitivity analyses will be conducted to explore moderators that are sufficiently reported in the literature. The quality of studies will be assessed by the Newcastle-Ottawa Scale. ETHICS AND DISSEMINATION:Ethical approval is not necessary to perform the study, and results will be presented at a suitable conference and published in a peer-reviewed journal. PROSPERO REGISTRATION NUMBER:CRD42024538898.

Introduction:Major depressive disorder (MDD) is associated with cognitive impairment, including verbal memory. Limited knowledge exists following memory performance in first episode (FE) MDD. This study investigated verbal memory, depressive symptoms, and relapse in FE MDD over five years, from the trait, state, and scar perspectives. These perspectives suggests that deficits in memory either preexists, manifest in MDD, or exacerbates with every MDD episode, respectively. Methods:Thirty patients and 30 healthy matched controls (HC) were assessed using the California Verbal Learning Test, second edition (CVLT-II) across three test occasions; in the acute phase (Y0), at one-year (Y1) and five-year (Y5) follow-up. The relationship between CVLT-II scores and depression severity (measured by the Montgomery Åsberg Depression Rating Scale) and relapse at the five-year follow-up, was assessed. Results:The FE MDD group demonstrated significantly poorer performance on List A, Trial 1 immediate free recall at Y0 compared to HC, however correction for multiple comparisons the difference did not reach significance. No differences were observed in any other condition at any time point. Further, the PG had a significant improvement on List A, trial 1 from Y0 to Y5. No associations were found between symptom severity and verbal memory, and no performance differences were identified between patients with and without relapse in a five -year perspective. Discussion:In conclusion, individuals with FE MDD show normal verbal memory performance, but exhibit impaired performance on List A, Trial 1 immediate free recall in the acute phase improving in remission, indicative of a state-related deficit in auditory attention. No evidence of scarring deficits in the FE MDD group was observed in the follow-up period.

Background Inhibitory deficits are common in psychopathology. Emotion-related impulsivity (ERI) and rumination are general risk factors for psychiatric distress that are similarly associated with dysfunctional inhibition—particularly in affective contexts. A number of cognitive remediation procedures have been developed to improve inhibitory control; however, most remediation programs focus on “cold” cognition independent of affective processing. This pilot trial will gather preliminary evidence for a new cognitive training intervention targeting “hot” affective control (ie, inhibitory functions during elevated emotional arousal) in a transdiagnostic sample of adults who report heightened emotion dysregulation. Objective This manuscript describes a protocol for a pilot randomized waitlist-controlled trial to assess changes in ERI and rumination after neurobehavioral affective control training (N-ACT), an 8-week cognitive training intervention designed to improve emotional response inhibition and emotional working memory. Our primary aim is to evaluate the efficacy, feasibility, and acceptability of N-ACT in reducing rumination and ERI, which we respectively conceptualize as complementary cognitive and behavioral consequences of emotion dysregulation. Secondarily, we will examine whether N-ACT leads to improvements in inhibitory control and, more distally, psychopathology symptoms. Methods The final sample will comprise 80 adults who report high ERI or rumination. Participants will be randomized to (1) begin the N-ACT program without delay or (2) join a waitlist condition and then complete N-ACT. Exclusion criteria include active alcohol or substance use disorders, psychosis, and suicide risk. At the baseline and postintervention time points, participants will complete measures of emotion dysregulation and psychiatric symptoms, as well as a neuropsychological assessment of inhibitory control. Individuals assigned to the control group will undergo an identical assessment before joining the waitlist, followed by parallel assessments before and after N-ACT. Results This trial is funded by support from the University of California Board of Regents and the Peder Sather Foundation (funding period: October 2022-September 2025). Recruitment is scheduled to begin in spring 2025. We will begin data analysis once data collection is complete, which is planned to occur in fall 2025. Conclusions This pilot randomized waitlist-controlled trial is designed to assess the initial efficacy, feasibility, and acceptability of N-ACT, a novel cognitive remediation approach developed to address 2 key contributors to psychopathology: ERI and rumination. The N-ACT program uses computerized adaptive behavioral tasks to strengthen the affective control processes theoretically and empirically linked to ERI and rumination. We hope this work will help inform future studies with sufficient statistical power to ascertain whether enhancing affective control through cognitive training (N-ACT) produces downstream reductions in psychiatric symptoms via improved emotion regulation. Trial Registration ClinicalTrials.gov NCT06226467; https://www.clinicaltrials.gov/study/NCT06226467; Open Science Framework Registry rak5z; https://osf.io/rak5z International Registered Report Identifier (IRRID) PRR1-10.2196/54221

Electroconvulsive therapy (ECT)-mediated hippocampal volumetric increase is consistently reported, though its clinical relevance remains debated. This study evaluates if ECT-related cognitive side effects are associated with regional volumetric changes along the hippocampal longitudinal axis. Longitudinal T1-weighted MRI scans in 435 patients (54.0 ± 15.0 years, 261 female) with major depression from the Global ECT-MRI Research Collaboration (GEMRIC) were used to measure changes in right global and longitudinal axis hippocampal subdivisions (head, body, tail) from baseline to post-treatment. Cognitive side effects were evaluated using pre-to-post treatment changes in two different verbal fluency tests available for 124 patients. Electric field modelling was applied to explore whether the regional hippocampal electric field strength related to individual changes in cognitive performance. Global hippocampal enlargement is observed pre-to-post ECT (pFDR < 0.001), but enlargement of the hippocampal head significantly exceeds the volumetric change in the hippocampal body and tail (pFDR < 0.001). Volumetric expansion of the hippocampal body and tail significantly associates with reduced verbal fluency scores (pFDR< 0.05). Moreover, volumetric reduction of the hippocampal tail at 6 months post-ECT associates with improved cognitive performance (pFDR < 0.05, N = 24). Finally, patients performing worse on verbal fluency tests following treatment have greater electric field during ECT in the right hippocampal body (puncorrected < 0.05). The findings support that cognitive performance following ECT relates to macrostructural changes in the posterior cognitive hippocampus. Thus, there may be a threshold of ECT induced posterior hippocampal volumetric change, beyond which cognitive side effects occur. Electroconvulsive Therapy (ECT) is a procedure that sends small electric currents through the brain and remains the most effective acute treatment for severe depressive episodes. However, we still do not fully understand how ECT works. Studies using brain scans (MRI) before and after ECT have shown that a part of the brain called the hippocampus often becomes larger after treatment. However, the clinical relevance of the volumetric change remains unknown. In this study, we looked at whether the increase in hippocampus size is linked to cognitive side effects. We found that a larger hippocampal volumetric increase after ECT was associated with reduced performance in verbal fluency tests, which measures our ability to rapidly produce words. These results suggest that big changes in the hippocampus after ECT may be related to short-term cognitive side effects. Ousdal et al. investigate whether global or regional hippocampal volume increase after Electroconvulsive therapy (ECT) for major depressive episodes relate to cognitive side effects. Their findings suggest that pronounced structural change in the posterior hippocampus (i.e., body and tail) associates with reduced cognitive performance following ECT.

The reasons why some individuals who experience trauma develop post-traumatic stress disorder (PTSD) while others do not remain poorly understood, highlighting the complex interplay of encoding-related and intrapersonal factors. This study aimed to examine factors predicting variability in trauma-related symptom development. Using a trauma film paradigm in a healthy sample (N = 32), we investigated how inhibitory control and peritraumatic responses relate to the development of intrusive memories and self-assessed event impact. Peritraumatic heart rate was associated with more frequent, vivid, and distressing memory intrusions during the week following trauma-analogue exposure. It also predicted hyperarousal and avoidance symptoms, with the latter further linked to lower inhibitory control. In a cognitive-interference task conducted approximately one day after trauma-analogue exposure, negative trauma reminders increased response latencies. This reduced interference control was predicted by both lower inhibitory control and higher peritraumatic heart rate, and it was especially pronounced in individuals who reported a heightened overall event impact. In conclusion, inhibitory control and peritraumatic heart rate emerged as predictors of subsequent reminder interference, intrusions, and self-assessed event impact. These findings provide insights into physiological and behavioural mechanisms underlying variability in the development of trauma-analogue symptoms and related cognitive interference when exposed to trauma reminders in a healthy sample without a trauma history.

INTRODUCTION:Residual cognitive deficits are commonly reported by individuals in remission from depression, often affecting daily life functioning and mental health. To provide tailored and personalized cognitive enhancement interventions for this population, there is a need for a better understanding of the characteristics of those who benefit from such interventions. Therefore, this study aimed to identify predictors of changes in subjective executive functioning following an internet-delivered cognitive enhancement intervention for adults in remission from depression. METHODS:Data were collected from a randomized controlled trial investigating the efficacy of an internet-delivered cognitive enhancement intervention. Changes in subjective executive functioning from pre-treatment to the six-month follow-up were assessed in 44 participants in remission from depression, using the Behavior Rating Inventory of Executive Function Adult Global Executive Composite. Linear mixed model analyses were conducted to investigate the impact of demographic, clinical, and treatment credibility variables on change in subjective cognitive functioning over time. RESULTS:The results showed that shorter lifetime depression duration predicted greater improvements in subjective executive functioning (p = 0.031). Higher levels of treatment expectancy and credibility were related to greater improvements in subjective cognitive functioning (p = 0.024). Participants with a partner showed better treatment response than those without a partner (p < 0.001). CONCLUSION:This study builds on previous research on cognitive enhancement interventions in remitted depression, highlighting the impact of depression duration, treatment expectancy, and credibility on treatment response. Interventions targeting cognitive deficits appear most effective for those with a shorter lifetime duration of depression. Therefore, efforts should be made to enhance outcomes in those with a chronic course. To maximize engagement and outcomes, these interventions should be delivered in a way that individuals in remission from depression view them as credible and capable of reducing their deficits. Previous research has not found partner status to predict change in subjective executive functioning. The effect of partner status on treatment response should be investigated further.

INTRODUCTION:Generalised anxiety disorder (GAD) in older adults involves excessive worry and cognitive challenges. Verbal memory impairments is associated to hippocampal dysfunction, with cortisol and brain-derived neurotrophic factor (BDNF) being important in hippocampal integrity. Research on hippocampal volume and verbal memory in older adults with GAD is limited, with mixed findings. This study investigates verbal memory in older adults with GAD versus healthy controls, and relations with hippocampal volumes. METHODS:Participants included 49 adults with GAD (Mage = 65.82, SD = 3.94) and 49 controls (Mage = 67.73, SD = 4.11). Verbal memory was assessed using the California Verbal Learning Test Long Delay Free Recall, hippocampal volumes via MRI, BDNF from serum, and cortisol via saliva. We fitted a Bayesian multivariate linear regression with bilateral hippocampal volume as outcome measure, and predictors: age, gender, education, intracranial volume, IQ, BDNF, cortisol, SSRI use, CVLT Long Delay Free Recall (LD FR), CVLT Learning, and diagnostic status*CVLT LD FR interaction. RESULTS:A credible interaction showed better verbal memory associated to larger hippocampal volume in controls, but this relationship was attenuated in GAD. BDNF and cortisol were not credibly associated with hippocampal volume. CONCLUSION:Diagnostic status moderates verbal memory and hippocampal volume relations, suggesting a distinct neurocognitive profile in older adults with GAD compared to healthy controls.

Major depressive disorder (MDD) is associated with reduced quality of life and relapse risk. However, few studies have investigated how quality of life is associated with cognitive deficits following MDD and is affected by cognitive training. This study investigated the long-term effects of computer-based working memory training (CWMT) on health-related quality of life (HRQL) in remitted MDD, and the association between executive functions (EF) and HRQL. Twenty-nine remitted participants (M age 36.21, SD = 10.8) were included in a pre-post pilot study of CWMT with 1- and 2-year follow-up. Twenty participants completed 5 weeks of CWMT, 12 participants were included at the 1-year follow-up, and 10 participants returned for the 2-year follow-up. The 36-item Short-Form Health Survey was used to assess HRQL. Associations between subjective and objective cognitive EF and HRQL were measured by the Behavior Rating Inventory of Executive Function for Adults (BRIEF-A) and a neuropsychological test battery of EF. Significant moderate improvements were found in aspects of HRQL after 2 years (d = 0.66). There were negative correlations between HRQL and BRIEF-A pre-intervention (r = 0.47-0.65). However, the study did not find significant associations between improved EF and improved HRQL. Preliminary results indicate long-term improvements in HRQL following CWMT. Subjective EF deficits were associated with poorer HRQL. However, due to limitations including small sample size and multiple statistical comparisons, larger controlled studies are needed to investigate and replicate the potential effects of CWMT on HRQL.

Generalized anxiety disorder (GAD) is a severe and prevalent disorder among older adults. Cognitive behaviour therapy (CBT) is recommended treatment for GAD, but older adults benefit less than younger peers. Physical exercise has been suggested to improve treatment efficacy. We aimed to determine the efficacy of augmenting CBT with physical exercise for older adults with GAD. This randomised controlled trial included 50 participants (mean [SD] age 66.52 [4.09] years; 39 [78%] female) with GAD. Participants received individual CBT and were randomised to either physical exercise or telephone attention placebo. The main outcome measure was self-reported worry on the Penn State Worry Questionnaire (PSWQ). Secondary outcome measures were clinician-rated remission and self-reported symptoms of anxiety, depression, and quality of life. Although the interaction between time and condition was statistically nonsignificant, moderation analysis revealed that this interaction was significant for participants with low treatment credibility to CBT at baseline. Participants randomised to physical exercise were five times more likely to achieve reliable long-term worry-reduction than placebo control. We found significant differences in favour of physical exercise for secondary measures of depression and anxiety. Participants with better cognitive inhibition at baseline were more likely to achieve clinician-rated remission. Findings suggest that physical exercise augments CBT for older adults with GAD.

Background 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. Methods 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. Results 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. Limitations Findings should be interpreted with caution due to the small sample, and lack of an active control group. Conclusions Internet-delivered cognitive enhancement interventions may improve subjective cognitive deficits. Waiting time to receive cognitive enhancement interventions may worsen symptoms and treatment response.

IMPORTANCE Electroconvulsive therapy (ECT), wherein a generalized epileptic seizure is induced, is a treatment for major depressive disorder (MDD). Currently, it is unclear whether there is an association between seizure length and treatment outcome. OBJECTIVE To explore the association between seizure duration, potential confounding variables, and ECT treatment outcome. DESIGN, SETTING, AND PARTICIPANTS This population-based cohort study obtained data from the Swedish National Quality Register for ECT. Patients treated for unipolar MDD with unilateral electrode placement between January 1, 2012, and December 31, 2019, were included. The electroencephalographic (EEG) seizure duration from the first ECT treatment session for each patient was used for analysis. Data analyses were performed between March 2021 and May 2024. MAIN OUTCOMES AND MEASURESThe primary outcome was remission, defined as a cutoff score of less than 10 points on the self-assessment version of the Montgomery-& Aring;sberg Depression Rating Scale within 1 week after ECT. Multivariate logistic regression analysis was performed to calculate odds ratios (ORs) between different seizure duration groups. Furthermore, the associations between concomitant use of pharmacological treatments, seizure duration, and remission rate were explored. RESULTS Among the 6998 patients included, 4229 (60.4%) were female and the mean (SD) age was 55.2 (18.6) years. Overall, 2749 patients (39.3%) achieved remission after ECT. Patients with EEG seizure duration of 60 to 69 seconds had the highest remission rates compared with patients with seizure duration of less than 20 seconds (OR, 2.17; 95% CI, 1.63-2.88; P < .001). Anticonvulsant medications were associated with shorter seizure duration (eg, lamotrigine: beta coefficient [SE], -6.02 [1.08]; P < .001) and lower remission rates (eg, lamotrigine: adjusted OR, 0.67; 95% CI, 0.53-0.84; P < .001). CONCLUSIONS AND RELEVANCE This study found an association between seizure length and remission from MDD. Use of anticonvulsant medication during ECT was associated with shorter seizure duration and lower remission rates after ECT.

The Global ECT MRI Research Collaboration (GEMRIC) has collected clinical and neuroimaging data of patients treated with electroconvulsive therapy (ECT) from around the world. Results to date have focused on neuroimaging correlates of antidepressant response. GEMRIC sites have also collected longitudinal cognitive data. Here, we summarize the existing GEMRIC cognitive data and provide recommendations for prospective data collection for future ECT-imaging investigations. We describe the criteria for selection of cognitive measures for mega-analyses: Trail Making Test Parts A (TMT-A) and B (TMT-B), verbal fluency category (VFC), verbal fluency letter (VFL), and percent retention from verbal learning and memory tests. We performed longitudinal data analysis focused on the pre-/post-ECT assessments with healthy comparison (HC) subjects at similar timepoints and assessed associations between demographic and ECT parameters with cognitive changes. The study found an interaction between electrode placement and treatment number for VFC (F(1,107) = 4.14, p = 0.04). Higher treatment was associated with decreased VFC performance with right unilateral electrode placement. Percent retention showed a main effect for group, with post-hoc analysis indicating decreased cognitive performance among the HC group. However, there were no significant effects of group or group interactions observed for TMT-A, TMT-B, or VFL. We assessed the current GEMRIC cognitive data and acknowledge the limitations associated with this data set including the limited number of neuropsychological domains assessed. Aside from the VFC and treatment number relationship, we did not observe ECT-mediated neurocognitive effects in this investigation. We provide prospective cognitive recommendations for future ECT-imaging investigations focused on strong psychometrics and minimal burden to subjects.

Executive 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 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).

BACKGROUND:Electroconvulsive therapy (ECT) is an effective treatment for depression with potential transient cognitive side effects. However, subjective memory impairment can extend over a long period after ECT. OBJECTIVES:This study aimed to assess potential risk factors for long-term subjective memory impairment 6 months after ECT and to explore if the associations are mediated by depressive symptoms. METHODS:This registry-based study used the Swedish National Quality Register for ECT and other national registers. Long-term subjective memory worsening was defined as a minimum 2-step worsening on the memory item from the comprehensive psychopathological rating scale (CPRS-M) from before ECT to 6 months after ECT. Changes on the scale were also analyzed in continuous models. Statistical methods used were logistic regression and linear regression analyses in univariable and multivariable models. RESULTS:The study population consisted of 1498 patients. Subjective memory worsening occurred in 25.2 % of the population. Long-term subjective memory worsening was associated with more depressive symptoms and lower education levels. No association could be found related to ECT technical factors. The associations between age and psychiatric comorbidities with subjective memory worsening were mediated by depressive symptoms. CONCLUSION:Patients can be informed that depressive symptoms are one of the biggest contributing factors to long-term subjective memory impairment after ECT. A successful treatment is therefore important to minimize the long-term experience of memory deficits. The number of sessions or ECT technical factors do not seem to be associated with long-term subjective memory impairment.

It remains poorly understood why some individuals develop post-traumatic stress disorder (PTSD) while others do not. This study aimed to examine factors predicting variability in trauma-related symptom development. Using a trauma-film paradigm in a healthy sample (N = 32), we investigated how inhibitory control and peritraumatic responses relate to the development of intrusive memories and self-assessed event impact. Peritraumatic heart rate was associated with more frequent, vivid, and distressing memory intrusions during the week following trauma-analogue exposure. It also predicted hyperarousal and avoidance symptoms, with the latter further linked to lower inhibitory control. In a cognitive-interference task conducted approximately one day after trauma-analogue exposure, negative trauma reminders increased response latencies. This reduced interference control was predicted by both lower inhibitory control and higher peritraumatic heart rate, and it was especially pronounced in individuals who reported a heightened overall event impact. In conclusion, inhibitory control and peritraumatic heart rate emerged as predictors of subsequent reminder interference, intrusions, and self-assessed event impact. These findings provide insights into physiological and behavioural mechanisms underlying variability in the development of trauma-analogue symptoms and related cognitive interference when exposed to trauma reminders in a healthy sample without a trauma history.