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Childhood maltreatment and adulthood victimization: An evidence-based model.

There is ample evidence showing that childhood maltreatment increases two to three fold the risk of victimization in adulthood. Various risk factors, including posttraumatic stress disorder (PTSD) symptoms, dissociation, self-blame, and alcohol abuse are related to revictimization. Although previous research examined associations between risk factors for revictimization, the evidence is limited and the proposed models mostly include a handful of risk factors. Therefore, it is critical to investigate a more comprehensive model explaining the link between childhood maltreatment and adulthood (re)victimization. Accordingly, this study tested a data-driven theoretical path model consisting of 33 variables (and their associations) that could potentially enhance understanding of factors explaining revictimization. Cross-sectional data derived from a multi-wave study were used for this investigation. Participants (N=2156, age mean=19.94, SD=2.89) were first-year female psychology students in the Netherlands and New Zealand, who responded to a battery of questionnaires and performed two computer tasks. The path model created by structural equation modelling using modification indices showed that peritraumatic dissociation, PTSD symptoms, trauma load, loneliness, and drug use were important mediators. Attachment styles, maladaptive schemas, meaning in life, and sex motives connected childhood maltreatment to adulthood victimization via other factors (i.e., PTSD symptoms, risky sex behavior, loneliness, emotion dysregulation, and sex motives). The model indicated that childhood maltreatment was associated with cognitive patterns (e.g., anxious attachment style), which in turn were associated with emotional factors (e.g., emotion dysregulation), and then with behavioral factors (e.g., risky sex behavior) resulting in revictimization. The findings of the study should be interpreted in the light of the limitations. In particular, the cross-sectional design of the study hinders us from ascertaining that the mediators preceded the outcome variable.

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Comorbidity of anxiety/affective, conduct/antisocial, attention deficit, and alcohol use disorders with suicidal behaviors in an American Indian community sample of adults and adolescents.

To study the associations of anxiety/affective disorders, conduct/antisocial disorders (ASPD/CD), attention deficit disorders (ADHD), and alcohol use disorders (AUD) with suicidal behaviors in an American Indian (AI) community sample of adolescents and adults. Participants were AI (360 adolescents, 925 adults) recruited from reservations who were assessed with the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA). Among AI adults (mean age=33 years), 17% percent reported lifetime experiences of suicidal thoughts (ideation and/or plans) and 14% reported suicidal acts (including either a suicide attempt history or verified death by suicide; n=19 deaths). Among AI adolescents (mean age=15 years), 20% experienced suicidal thoughts and 9% experienced suicidal acts (including 3 deaths). In logistic regression analyses, suicidal thoughts were significantly associated with lifetime diagnoses of affective disorder, CD and ADHD in adolescents, and with anxiety disorder, affective disorder, and ASPD/CD in adults. Suicidal acts were associated with affective disorder, ADHD, and alcohol drinking in adolescents and with anxiety disorder, ASPD/CD and AUD in adults. The number of comorbid disorders greatly increased the risk of both suicidal thoughts and acts among both adolescents and adults. In addition to affective disorders, both ADHD and CD in adolescents, and ASPD in adults, demonstrated an association with suicidal thoughts. Alcohol use by adolescents and AUD among adults also were associated with suicidal attempts in this AI sample. These findings suggest need for additional research and potential integration of alcohol in screening and intervention programs focused on the prevention of suicide among AI.

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Latent profiles of posttraumatic stress disorder symptoms and sleep disturbances in relation to drinking to cope motives among college students.

Posttraumatic stress disorder (PTSD), sleep disturbances, and problematic alcohol use are frequently comorbid. Research shows that individuals with more PTSD symptom severity and poorer sleep are highly susceptible to drinking alcohol to cope with negative affect. The current study examined the number and nature of different subgroups of trauma-exposed college students based on endorsed PTSD symptoms and sleep disturbances; and how such subgroups relate to drinking to cope motives. The sample included 474 trauma-exposed college students (Mage=20.69 years; 75.50% female) who completed self-report surveys. Latent profile analyses revealed three subgroups: High PTSD-Sleep Disturbances (n=71), Moderate PTSD-Sleep Disturbances (n=135), and Low PTSD-Sleep Disturbances (n=268). Results indicated that college students in the Low PTSD-Sleep Disturbances group endorsed the lowest amount of coping-related drinking motives; however, college students in the Moderate PTSD-Sleep Disturbances group did not endorse significantly different levels of coping-related drinking motives than college students in the High PTSD-Sleep Disturbances group. College students with subclinical presentations of psychopathology are at risk for endorsing risky drinking motives. As they adjust to a stressful environment with a culture of heavy drinking, providing context-relevant intervention efforts such as adaptive coping strategies, relaxation skills designed to facilitate restful sleep, and trauma-informed care may be highly beneficial for college students.

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From 'mental fog' to post-acute COVID-19 syndrome's executive function alteration: Implications for clinical approach.

A common symptom of the neuropsychiatric Post-Acute COVID-19 syndrome (neuro-PACS) is the so called 'brain fog'. Patients describe the brain fog as problems with attention, memory and mental fatigue. Brain fog is experienced by 9-55% of people for months after having contracted SARS-CoV-2 virus. Several theories have been proposed to explain PACS's brain fog, including a neuroinflammatory hypothesis, but the hypothesis remains to be proven. Here, we examined inflammatory and immunological blood profile in a cohort of patients with PACS to investigate the association between executive functions and blood inflammatory markers. Executive function was assessed by the Trail Making Test (TMT) Part A and Part B, as well as the Barkley Deficits in Executive Functioning Scale (BDEFS), in 71 patients (36 men), average age of 40 years (range: 15-82, SD: 15.7). Impairment in executive functioning (BDEFS scores and TMT B scores) correlated with increased levels of Interleukin-6 (IL-6), fibrinogen and ferritin. Moreover, elevated levels of Il-6, fibrinogen, ferritin, tumor necrosis factor-alpha and C-reactive protein have been observed in PACS. These findings demonstrate that PACS is characterized by the presence of an immuno-inflammatory process, which is associated with diminished executive functioning. Here, we argue in favour of a shift from the non-descriptive definition of 'mental fog' to a characterization of a subtype of PACS, associated with alteration in executive functioning. Implication for clinical settings and prevention are discussed.

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Abnormal multi-layered dynamic cortico-subcortical functional connectivity in major depressive disorder and generalized anxiety disorder.

Comorbidity has been frequently observed between generalized anxiety disorder (GAD) and major depressive disorder (MDD), however, common and distinguishable alterations in the topological organization of functional brain networks remain poorly understood. We sought to determine a robust and sensitive functional connectivity marker for diagnostic classification and symptom severity prediction. Multi-layered dynamic functional connectivity including whole brain, network-node and node-node layers via graph theory and gradient analyses were applied to functional MRI resting-state data obtained from 31 unmedicated GAD and 34 unmedicated MDD patients as well as 33 age and education matched healthy controls (HC). GAD and MDD symptoms were assessed using Penn State Worry Questionnaire and Beck Depression Inventory II, respectively. Three network measures including global properties (i.e., global efficiency, characteristic path length), regional nodal property (i.e., degree) and connectivity gradients were computed. Results showed that both patient groups exhibited abnormal dynamic cortico-subcortical topological organization compared to healthy controls, with MDD>GAD>HC in degree of randomization. Furthermore, our multi-layered dynamic functional connectivity network model reached 77% diagnostic accuracy between GAD and MDD and was highly predictive of symptom severity, respectively. Gradients of functional connectivity for superior frontal cortex-subcortical regions, middle temporal gyrus-subcortical regions and amygdala-cortical regions contributed more in this model compared to other gradients. We found shared and distinct cortico-subcortical connectivity features in dynamic functional brain networks between GAD and MDD, which together can promote the understanding of common and disorder-specific topological organization dysregulations and facilitate early neuroimaging-based diagnosis.

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Testing anxiety and reward processing in anorexia nervosa as predictors of longitudinal clinical outcomes.

Anorexia nervosa (AN) is a psychiatric disorder with a tenuous longitudinal course marked by a high risk of relapse. Previous studies suggest that aberrant threat perception and reward processing operate in many with AN, and may produce obstacles to treatment engagement; therefore, these could potentially represent predictors for longitudinal clinical outcomes. In this study, anxiety and reward symptoms, behaviors, and neural circuit connectivity were measured in intensively treated AN-restrictive subtype patients (n=33) and healthy controls (n=31). Participants underwent an fMRI experiment using a monetary reward task in combination with either overlapping individually tailored anxiety-provoking words or neutral words. Behavioral/psychometric measures consisted of reaction times on the monetary reward task and self-ratings on anxiety symptoms at study entry. We tested multimodal, multivariate models based on neural, behavioral, and psychometric measures of reward and anxiety to predict physiological (Body Mass Index; BMI) and psychological (eating disorder symptom severity) longitudinal outcomes in AN over six months. Our results indicated that higher anxiety symptom psychometric scores significantly predicted BMI reductions at follow-up. Untreated anxiety after intensive treatment could put individuals with AN at heightened risk for weight loss. This represents a potentially modifiable risk factor that could be targeted more aggressively to help reduce the chance of future clinical worsening.

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Associations between parental depression and anxiety symptom severity and their Offspring's cortical thickness and subcortical volume.

Depression and anxiety are associated with grey matter changes in subcortical regions in adults and adolescents. Parent psychopathology is associated with offspring brain structure, but it's unclear whether altered brain structure in children is associated with severity of parental depression and anxiety symptoms. We examined 123 youth (Mean age=13.64; 62% female) with no clinically significant history of depression or anxiety and one parent diagnosed with current or past depressive or anxiety disorders. Parents completed the Mini International Neuropsychiatric Interview to assess diagnostic status and the Beck Depression Inventory-II, and the Generalized Anxiety Disorder-7 to assess current symptom severity. Youth underwent T1 weighted structural Magnetic Resonance Imaging scans. Bivariate analyses revealed higher parental depressive severity was not significantly associated with offspring grey matter. Parental anxiety severity was significantly associated with less left global surface area. When controlling for offspring age, sex and intracranial volume (ICV), offspring right surface area was negatively associated with parental depressive severity at a trend level. In previously depressed parents, greater parental depressive severity was significantly associated with offspring decreased left and right surface area. There were no significant associations between parental anxiety severity in previously depressed parents and offspring subcortical or cortical brain regions. These results highlight associations between parental depressive symptom severity and offspring brain structure and suggest that even within an already high-risk group of adolescents, there may be altered cortical surface area depending on parent symptom severity. This may help identify youth most at risk for developing a mood disorder and could help further early intervention and identification efforts.

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