Psychological Medicine最新文献

Background: Racial, ethnic, and socioeconomic disparities persist in posttraumatic stress disorder (PTSD), which are partly attributed to minoritized women being trauma-exposed, while also contending with harmful contextual stressors. However, few have used analytic strategies that capture the interplay of these experiences and their relation to PTSD. The current study used a person-centered statistical approach to examine heterogeneity in trauma and contextual stress exposure, and their associations with PTSD and underlying symptom dimensions, in a diverse sample of low-income postpartum women.

Methods: Using a community-based sample of Black, Hispanic/Latina, and White postpartum women recruited from five U.S. regions (n = 1577), a latent class analysis generated profiles of past-year exposure to traumatic events and contextual stress at one month postpartum. Regression analyses then examined associations between class membership and PTSD symptom severity at six months postpartum as a function of race/ethnicity.

Results: A four-class solution best fit the data, yielding High Contextual Stress, Injury/Illness, Violence Exposure, and Low Trauma/Contextual Stress classes. Compared to the Low Trauma/Contextual Stress class, membership in any of the other classes was associated with greater symptom severity across nearly all PTSD symptom dimensions (all ps < 0.05). Additionally, constellations of exposures were differentially linked to total PTSD symptom severity, reexperiencing, and numbing PTSD symptoms across racial/ethnic groups (ps < 0.05).

Conclusions: A person-centered approach to trauma and contextual stress exposure can capture heterogeneity of experiences in diverse, low-income women. Moreover, racially/ethnically patterned links between traumatic or stressful exposures and PTSD symptom dimensions have implications for screening and intervention in the perinatal period.

Background: Psychostimulants and nonstimulants have partially overlapping pharmacological targets on attention-deficit/hyperactivity disorder (ADHD), but whether their neuroimaging underpinnings differ is elusive. We aimed to identify overlapping and medication-specific brain functional mechanisms of psychostimulants and nonstimulants on ADHD.

Methods: After a systematic literature search and database construction, the imputed maps of separate and pooled neuropharmacological mechanisms were meta-analyzed by Seed-based d Mapping toolbox, followed by large-scale network analysis to uncover potential coactivation patterns and meta-regression analysis to examine the modulatory effects of age and sex.

Results: Twenty-eight whole-brain task-based functional MRI studies (396 cases in the medication group and 459 cases in the control group) were included. Possible normalization effects of stimulant and nonstimulant administration converged on increased activation patterns of the left supplementary motor area (Z = 1.21, p < 0.0001, central executive network). Stimulants, relative to nonstimulants, increased brain activations in the left amygdala (Z = 1.30, p = 0.0006), middle cingulate gyrus (Z = 1.22, p = 0.0008), and superior frontal gyrus (Z = 1.27, p = 0.0006), which are within the ventral attention network. Neurodevelopmental trajectories emerged in activation patterns of the right supplementary motor area and left amygdala, with the left amygdala also presenting a sex-related difference.

Conclusions: Convergence in the left supplementary motor area may delineate novel therapeutic targets for effective interventions, and distinct neural substrates could account for different therapeutic responses to stimulants and nonstimulants.

Background: Childhood adversity has been associated with increased peripheral inflammation in adulthood. However, not all individuals who experience early adversity develop these inflammatory outcomes. Separately, there is also a link between various internalizing emotional distress conditions (e.g. depression, anxiety, and fear) and inflammation in adulthood. It is possible the combination of adult emotional distress and past childhood adversity may be uniquely important for explaining psychopathology-related immune dysfunction at midlife.

Methods: Using data from the Midlife in the United States (MIDUS) study (n = 1255), we examined whether internalizing, defined as past 12-month emotional distress symptomatology and trait neuroticism, moderated associations between childhood adversity and heightened inflammation in adulthood. Using latent variable modeling, we examined whether transdiagnostic or disorder-specific features of emotional distress better predicted inflammation.

Results: We observed that childhood adversity only predicted adult inflammation when participants also reported adult internalizing emotional distress. Furthermore, this moderation effect was specific to the transdiagnostic factor of emotional distress rather than the disorder-specific features.

Conclusions: We discuss the possibility that adult internalizing symptoms and trait neuroticism together may signal the presence of temporally stable vulnerabilities that amplify the impact of childhood adversity on midlife immune alterations. The study highlights the importance of identifying emotional distress in individuals who have experienced childhood adversity to address long-term immune outcomes and enhance overall health.

Background: Recent stressful life events (SLE) are a risk factor for psychosis, but limited research has explored how SLEs affect individuals at clinical high risk (CHR) for psychosis. The current study investigated the longitudinal effects of SLEs on functioning and symptom severity in CHR individuals, where we hypothesized CHR would report more SLEs than healthy controls (HC), and SLEs would be associated with poorer outcomes.

Methods: The study used longitudinal data from the EU-GEI High Risk study. Data from 331 CHR participants were analyzed to examine the effects of SLEs on changes in functioning, positive and negative symptoms over a 2-year follow-up. We compared the prevalence of SLEs between CHR and HCs, and between CHR who did (CHR-T) and did not (CHR-NT) transition to psychosis.

Results: CHR reported 1.44 more SLEs than HC (p < 0.001), but there was no difference in SLEs between CHR-T and CHR-NT at baseline. Recent SLEs were associated with poorer functioning and more severe positive and negative symptoms in CHR individuals (all p < 0.01) but did not reveal a significant interaction with time.

Conclusions: CHR individuals who had experienced recent SLEs exhibited poorer functioning and more severe symptoms. However, as the interaction between SLEs and time was not significant, this suggests SLEs did not contribute to a worsening of symptoms and functioning over the study period. SLEs could be a key risk factor to becoming CHR for psychosis, however further work is required to inform when early intervention strategies mitigating against the effects of stress are most effective.

Background: Late-life depression (LLD) is characterized by repeated recurrent depressive episodes even with maintenance treatment. It is unclear what clinical and cognitive phenotypic characteristics present during remission predict future recurrence.

Methods: Participants (135 with remitted LLD and 69 comparison subjects across three institutions) completed baseline phenotyping, including psychiatric, medical, and social history, psychiatric symptom and personality trait assessment, and neuropsychological testing. Participants were clinically assessed every two months for two years while receiving standard antidepressant treatment. Analyses examined group differences in phenotypic measure using general linear models. Concurrent associations between phenotypic measures and diagnostic groups were examined using LASSO logistic regression.

Results: Sixty (44%) LLD participants experienced a relapse over the two-year period. Numerous phenotypic measures across all domains differed between remitted LLD and comparison participants. Only residual depressive symptom severity, rumination, medical comorbidity, and executive dysfunction significantly predicted LLD classification. Fewer measures differed between relapsing and sustained remission LLD subgroups, with the relapsing group exhibiting greater antidepressant treatment intensity, greater fatigue, rumination, and disability, higher systolic blood pressure, greater life stress and lower instrumental social support. Relapsing group classification was informed by antidepressant treatment intensity, lower instrumental social support, and greater life stress.

Conclusions: A wide range of phenotypic factors differed between remitted LLD and comparison groups. Fewer measures differed between relapsing and sustained remission LLD subgroups, with less social support and greater stress informing vulnerability to subsequent relapse. This research suggests potential targets for relapse prevention and emphasizes the need for clinically translatable relapse biomarkers to inform care.

Background: The mechanisms underlying generalized forms of dissociative ('psychogenic') amnesia are poorly understood. One theory suggests that memory retrieval is inhibited via prefrontal control. Findings from cognitive neuroscience offer a candidate mechanism for this proposed retrieval inhibition. By applying predictions based on these experimental findings, we examined the putative role of retrieval suppression in dissociative amnesia.

Methods: We analyzed fMRI data from two previously reported cases of dissociative amnesia. Patients had been shown reminders from forgotten and remembered time periods (colleagues and school friends). We examined the neuroanatomical overlap between regions engaged in the unrecognized compared to the recognized condition, and the regions engaged during retrieval suppression in laboratory-based tasks. Effective connectivity analyses were performed to test the hypothesized modulatory relationship between the right anterior dorsolateral prefrontal cortex (raDLPFC) and the hippocampus. Both patients were scanned again following treatment, and analyses were repeated.

Results: We observed substantial functional alignment between the inhibitory regions engaged during laboratory-based retrieval suppression tasks, and those engaged when patients failed to recognize their current colleagues. This included significant activation in the raDLPFC and right ventrolateral prefrontal cortex, and a corresponding deactivation across autobiographical memory regions (hippocampus, medial PFC). Dynamic causal modeling confirmed the hypothesized modulatory relationship between the raDLPFC and the hippocampus. This pattern was no longer evident following memory recovery in the first patient, but persisted in the second patient who remained amnesic.

Conclusions: Findings are consistent with an inhibitory mechanism driving down activity across core memory regions to prevent the recognition of personally relevant stimuli.

Background: Attention-deficit/hyperactivity disorder (ADHD) patients exhibit characteristics of impaired working memory (WM) and diminished sensory processing function. This study aimed to identify the neurophysiologic basis underlying the association between visual WM and auditory processing function in children with ADHD.

Methods: The participants included 86 children with ADHD (aged 6-15 years, mean age 9.66 years, 70 boys, and 16 girls) and 90 typically developing (TD) children (aged 7-16 years, mean age 10.30 years, 66 boys, and 24 girls). Electroencephalograms were recorded from all participants while they performed an auditory discrimination task (oddball task). The visual WM capacity and ADHD symptom severity were measured for all participants.

Results: Compared with TD children, children with ADHD presented a poorer visual WM capacity and a smaller mismatch negativity (MMN) amplitude. Notably, the smaller MMN amplitude in children with ADHD predicted a less impaired WM capacity and milder inattention symptom severity. In contrast, the larger MMN amplitude in TD children predicted a better visual WM capacity.

Conclusions: Our results suggest an intimate relationship and potential shared mechanism between visual WM and auditory processing function. We liken this shared mechanism to a total cognitive resource limit that varies between groups of children, which could drive correlated individual differences in auditory processing function and visual WM. Our findings provide a neurophysiological correlate for reports of WM deficits in ADHD patients and indicate potential effective markers for clinical intervention.

Background: Prior studies suggest that childhood maltreatment is associated with altered hippocampal volume. However, longitudinal studies are currently scarce, making it difficult to determine how alterations in hippocampal volume evolve over time. The current study examined the relationship between childhood maltreatment and hippocampal volumetric development across childhood and adolescence in a community sample.

Methods: In this longitudinal study, a community sample of 795 participants underwent brain magnetic resonance imaging (MRI) in three waves spanning ages 6-21 years. Childhood maltreatment was assessed using parent-report and children´s self-report at baseline (6-12 years old). Mixed models were used to examine the relationship between childhood maltreatment and hippocampal volume across time.

Results: The quadratic term of age was significantly associated with both right and left hippocampal volume development. High exposure to childhood maltreatment was associated with reduced offset of right hippocampal volume and persistent reduced volume throughout adolescence.Critically, the relationship between childhood maltreatment and reduced right hippocampal volume remained significant after adjusting for the presence of any depressive disorder during late childhood and adolescence and hippocampal volume polygenic risk scores. Time-by-CM and Sex-by-CM interactions were not statistically significant.

Conclusions: The present study showed that childhood maltreatment is associated with persistent reduction of hippocampal volume in children and adolescents, even after adjusting for the presence of major depressive disorder and genetic determinants of hippocampal structure.

Background: This study evaluated the impact of 2015/2016 prescribing guidance on antidepressant prescribing choices in children.

Methods: A retrospective e-cohort study of whole population routine electronic healthcare records was conducted. Poisson regression was undertaken to explore trends over time for depression, antidepressant prescribing, indications and secondary care contacts. Time trend analysis was conducted to assess the impact of guidance.

Results: A total of 643 322 primary care patients in Wales UK, aged 6-17 years from 2010-2019 contributed 3 215 584 person-years of follow-up. Adjusted incidence of depression more than doubled (IRR for 2019 = 2.8 [2.5-3.2]) with similar trends seen for antidepressants. Fluoxetine was the most frequently prescribed first-line antidepressant. Citalopram comprised less than 5% of first prescriptions in younger children but 22.9% (95% CI 22.0-23.8; 95% CI 2533) in 16-17-year-olds. Approximately half of new antidepressant prescribing was associated with depression. Segmented regression analysis showed that prescriptions of 'all' antidepressants, Fluoxetine and Sertraline were increasing before the guidance. This upward trend flattened for both 'all' antidepressants and Fluoxetine and steepened for Sertraline. Citalopram prescribing was decreasing significantly pre guidance being issued with no significant change afterward.

Conclusions: Targeted intervention is needed to address rising rates of depression in children. Practitioners are partially adhering to local and national guidance. The decision-making process behind prescribing choices is likely to be multi-factorial. Activities to support implementation of guidance should be adopted in relation to safety in prescribing of antidepressants in children including timely availability of talking therapies and specialist mental health services.