Although carotid endarterectomy (CEA) or carotid artery stenting (CAS) is recommended for symptomatic extracranial carotid stenosis of 50–99%, the COVID-19 pandemic significantly impacted resources. CAS therefore offered potential advantages as access to the angiosuite was seemingly easier than access to operating rooms. The primary objective was to determine the frequency of serious and non-serious complications following CAS before and during the COVID-19 pandemic.

We performed a retrospective cohort study of consecutive patients who received CAS at the Ottawa Hospital, Canada, from June 2019 to May 2021. We reviewed baseline demographics, imaging, as well as intraprocedural and postprocedural complications based on chart review. We performed multivariable logistic regression to determine associations between clinical and safety outcomes.

We included 47 patients in the pre-pandemic period and 93 patients in the pandemic period (mean age = 70.4 years; 54% female; P = 0.287 for age and P = 0.962 for sex, respectively). The combined rate of intraprocedural and postprocedural serious complications (ischemic stroke, intracerebral hemorrhage, myocardial infarction or death) was 7.1%. Eight strokes occurred, and one patient with a postprocedural ischemic stroke died 11 days after stenting. Complication rates were similar before and during the pandemic (aOR 1.040, 95% CI 0.466–2.321). The number of referrals for CEA during the pandemic period decreased by 50%.

In this cohort of consecutive patients undergoing CAS at a Canadian comprehensive stroke center before and during the COVID-19 pandemic, the rates of stroke and death were similar to pre-pandemic conditions and were generally consistent with the published literature.

Female gender is associated with a lower risk for aggressive behaviour and violent offending. Well established risk factors for aggressive behaviour are alcohol and other substance use, but previous studies focused mainly on male offenders and the general population. However, for therapeutic and prognostic reasons it is important to understand pathways to female offending.

To examine a sample of female forensic-psychiatric inpatients regarding the association of alcohol (AUD) and other substance use disorders (SUD) with violent offending (homicide, assault, robbery).

We conducted a retrospective cohort study of 334 female patients discharged before 01.01.2019 from a secure psychiatric hospital in Germany.

In total, 72% of the patients with AUD committed a violent crime, leading to admission to secure psychiatric treatment. In comparison a statistically significant lower rate (19%) of the SUD group was convicted of violent offending. Over 70% of the participants with AUD had a family history of AUD, and over 83% experienced physical violence in adulthood. We found no group differences (AUD vs. SUD) regarding aggressive behaviour during inpatient treatment.

According to our results, AUD compared to other SUD, is a significant risk factor for violent offending in women. A family background with AUD and a history of physical abuse might function as a risk factor for both: developing an AUD and violent offending. The comparable rates of aggression in both groups during inpatient treatment suggest that abstinence is a protective factor.

No significant relationships.

To present a multimodal analysis of psychopathology among African unaccompanied refugee minors (URMs) in Austria. These youths experience well documented war and flight related non-normative stressors on their way from Africa to Europe. We have previously reported 17% of PTSD, a number below expectations. We now report on trauma related personality variables which indicate that these youths are resilient but at high risk for decompensation. We tested the hypothesis that PTSD specific defenses would be high (most notably dissociation, conversion, projection, withdrawal and somatization).

Forty-one URMs participated in the study. The following standardized instruments were used: UCLA PTSD Index for DSM IV, Mini International Neuropsychiatric Diagnostic Interview for Children and Adolescents, Weinberger Adjustment Inventory, Response Evaluation Measure for the measurement of defenses.

Levels of psychopathology were below previously reported levels in URMs. By contrast, all defenses previously reported as elevated in PTSD (conversion, projection, dissociation, withdrawal and somatization) showed significant increases (p < 0.05), putting these defenses in the 80–95TH percentile for the norm population.

While syndromal illness was less than expected, indicators of trauma related habitual function were all elevated. The present findings reveal that URMs manage the extreme stress of their lives by defensive self-regulation. These findings have implications for diagnosis and management.

The present functional magnetic resonance imaging (fMRI) study investigated neural changes in relation to mood biased processing in depression, before and after cognitive behavioral therapy (CBT) using an emotional Stroop task.

Sixteen unmedicated patients (mean age 40 years), fulfilling DSM-IV diagnosis for unipolar major depression underwent fMRI, prior to and after 16 once-weekly sessions of CBT. Sixteen matched healthy volunteers were scanned at similar time intervals. In an emotional Stroop task negative and neutral words were presented in various colors and volunteers had to name the color of words. Latencies were recorded to determine behavioral emotional interference effects. MRI images were acquired using clustered image acquisition. Whole-brain and region of interest analysis examined the neural basis of interference and mood biased processing.

At baseline patients displayed increased latencies during color naming negative words, in comparison to neutral words and in relation to healthy volunteers. After treatment, latencies did not significantly differ between groups. With regard to neural activity, depressed patients showed increased activation at baseline in amygdala, dorsolateral prefrontal cortex (DLPFC), and ventrolateral prefrontal cortex (VLPFC), which normalized after CBT. Additionally, hyperactivation in the rostral anterior cingulate at baseline was positively correlated with symptom reduction after CBT.

Evidence was found for an emotional interference effect during acute states of depression which improved following CBT. The neural basis is associated with increased activity in the amygdala, DLPFC and VLPFC which normalized after treatment. CBT seems to affect behavioral biases and neural circuits involved in processing negative information.

There is considerable variation in the prevalence of breastfeeding, which allows for investigation of factors that influence the initiation and duration of breastfeeding and its association with well being of the mother infant dyad.

To better understand factors that influence (1) maternal breastfeeding status and (2) the “effects” of breastfeeding on mothers and infants.

Participants (n = 170) derive from a longitudinal Canadian study “Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN)”, a project designed to understand the pre- and postnatal influences on maternal health and child social-emotional development. Mothers provided data on breastfeeding status, early life adversity, oxytocin gene and oxytocin gene receptor polymorphisms, depression/anxiety, infant temperament and maternal sensitivity.

Early life adversity associated with a shorter breastfeeding duration and higher maternal depression levels. The relation between mothers’ early adversity and the duration of breastfeeding was mediated by mothers’ depression level, but only in women carrying one variant of the oxytocin rs2740210 gene marker (CC genotype). Mothers who breastfeed at 3 months acted more sensitively towards their infants when they were 6 months old and they in turn had infants who at 18 months showed reduced negative affectivity.

Women who have been exposed to early adversity are “living with the past” and they are, to certain extent, protected or more vulnerable to depression, depending on their genotype. Breastfeeding associated with higher maternal sensitivity, which associated with decreased negative emotionality in the infant at 18 months. Our results help to clarify associations between early life experiences, breastfeeding, and the mother-infant relationship.

The authors have not supplied their declaration of competing interest.

Maternal mental well being influences offspring development. Research suggests that an interplay between genetic and environmental factors underlies this familial transmission of mental disorders.

To explore an interaction between genetic and environmental factors to predict trajectories of maternal mental well being, and to examine whether these trajectories are associated with epigenetic modifications in mothers and their offspring.

We assessed maternal childhood trauma and rearing experiences, prenatal and postnatal symptoms of depression and stress experience from 6 to 72 months postpartum, and genetic and epigenetic variation in a longitudinal birth-cohort study (n = 262) (Maternal adversity, vulnerability and neurodevelopment project). We used latent class modeling to describe trajectories in maternal depressive symptoms, parenting stress, marital stress and general stress, taking polygenetic risk for major depressive disorder (MDD), a composite score for maternal early life adversities, and prenatal depressive symptoms into account.

Genetic risk for MDD associated with trajectories of maternal well being in the postpartum, conditional on the experience of early life adversities and prenatal symptoms of depression. We will explore whether these trajectories are also linked to DNA methylation patterns in mothers and their offspring. Preliminary analyses suggest that maternal early life adversities associate with offspring DNA methylation age estimates, which is mediated through maternal mental well being and maternal DNA methylation age estimates.

We found relevant gene-environment interactions associated with trajectories of maternal well being. Our findings inform research on mechanisms underlying familial transmission of vulnerability for psychopathology and might thus be relevant to prevention and early intervention programs.

The authors have not supplied their declaration of competing interest.

Bipolar disorder (BD) is a psychiatric disorder associated with increased rates of obesity and inflammation. Leptin is an adipokine that is mainly produced by the white adipose tissue in response to insulin. It stimulates the immune system, increasing the production of pro-inflammatory cytokines. There is currently uncertainty regarding possible alterations in peripheral leptin levels across the mood states in BD.

This study comprises a between-group meta-analysis comparing serum and plasma leptin levels in people with BD in mania, depression or euthymia and healthy controls. We conducted a systematic search for all possibly eligible-English and non-English peer-reviewed articles. We calculated the effect size (ES) utilizing Hedges’ adjusted g using random effects.

Eleven studies were included in the meta-analyses, providing data on 1118 participants. Serum and plasma leptin levels were not altered in subjects with BD when compared to healthy controls in mania (g = −0.99, 95% CI −2.43 to 0.43, P = 0.171), in depression (g = 0.17, 95% CI −0.45 to 0.79, P = 0.584), or in euthymia (g = 0.03, 95% CI −0.39 to 0.46, P = 0.882). However, we did observe a stronger association between leptin levels and both age and BMI in patients with BD in euthymia compared to healthy controls, such that the greater the age of the individuals, the greater the difference in leptin levels between BD and controls; and the higher the BMI, the greater the difference in leptin levels between BD and controls.

Our meta-analysis provides evidence that leptin levels are not altered in BD across the mood spectrum compared to healthy controls. The disproportionate increase of leptin levels with increase in BMI in BD speaks in favour of a potential inflammatory role of white adipose tissue in BD and a disproportionate increase of leptin levels with increase in age.

Animal and human studies suggest that individual differences in maternal parenting behaviour are transmitted from one generation to the next.

This study aimed to examine potential psychosocial mechanisms underlying an intergenerational transmission of conceptualization of parenting, including affect, cognition, and parental support.

In a subsample of 201 first-time mothers participating in the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project, we assessed maternal childhood rearing experiences, using the Parental Bonding Instrument and the Childhood Trauma Questionnaire. At 6 months postpartum, mothers completed questionnaires on parenting stress, symptoms of depression, internalization of maternal care regulation and current relationship with mother and father.

We found significant direct associations of maltreatment and rearing by the grandmother with parenting stress at 6 months. These associations were mediated through distinct psychosocial pathways: the association of maltreatment on higher parenting stress was fully mediated through more maternal symptoms of depression (z = 2.297; P = 022). The association between sub-optimal rearing provided by the mother and higher parenting stress was mediated through lower internalization of maternal care regulation (z = -2.155; P = 031) and to a lesser degree through more symptoms of depression (z = -1.842; P = 065). Finally, higher quality rearing by the grandfather was indirectly related to lower parenting stress through positive current relationship with the father (z = -2.617; P = 009).

There are distinct pathways by which early experiences manifest in parenting stress. By understanding the structure of dysregulated parenting, clinicians will have practical information to specifically target maternal motivation, social supports, and depressed mood to disrupt maladaptive parenting cognitions and practices.

The authors have not supplied their declaration of competing interest.