Cognitive impairment in patients with eating disorders was reported by the majority of studies addressing this issue. However, heterogeneous patterns of cognitive dysfunctions were observed and, in a minority of studies, no impairment was found. The present study was aimed to define the pattern of neurocognitive impairment in a large sample of bulimia nervosa (BN) patients and to demonstrate that neuroendocrine, personality and clinical characteristics influence neurocognitive performance in BN.

Attention, executive control, conditional and incidental learning were evaluated in 83 untreated female patients with BN and 77 healthy controls. Cortisol and 17β-estradiol plasma levels were assessed. Cloninger's Temperament and Character Inventory-Revised (TCI-R), the Eating Disorder Inventory-2 and the Montgomery-Asberg Depression Rating Scale were administered.

No impairment of cognitive performance was found in subjects with BN vs. healthy controls. The higher the cortisol level and “Self-directedness” scores the better the performance on conditional learning, while 17β-estradiol levels showed an opposite pattern of association; “Reward dependence” scores were associated to a worse performance on incidental learning; depressive symptomatology negatively influenced the performance on the WCST.

No cognitive impairment was found in untreated patients with BN in the explored cognitive domains. An influence of neuroendocrine, personality and clinical variables on neurocognitive functioning was found, which might explain discrepancies in literature findings.

Prenatal risk factors, such as gestational complications and exposure to stress during pregnancy, may have a role in the development of many psychiatric disorders including eating disorders.

To investigate the impact of prenatal stress exposure on the development and clinical features of anorexia nervosa.

One hundred and nine patients with a lifetime diagnosis of anorexia nervosa and 118 healthy controls underwent a clinical assessment, which included interviews, questionnaires and a neuropsychological battery. The mothers of the patients and controls underwent a specific interview focused on stressful life events, which occurred during pregnancy. Obstetric and neonatal records were consulted.

The mothers of patients experienced more severe stressful episodes during pregnancy than the mothers of controls and the perceived distress showed significant positive correlation with both total number of obstetrical complications and placental weight. In patients, the severity of stressful events was strongly associated to cognitive rigidity and perseverance.

Prenatal stress exposure might be a risk factor for the development of anorexia nervosa and it is associated with cognitive traits of rigidity and perseverance.

The authors have not supplied their declaration of competing interest.

The possibility of evaluating cortical morphological and structural features on the basis of their covariance patterns is becoming increasingly important in clinical neuroscience, because their organizational principles reveal an inter-regional structural dependence which derive from a complex mixture of developmental, genetic and environmental factors.

In this study, we describe cortical network organization in anorexia nervosa using a MRI morpho-structural covariance analysis based on cortical thickness, gyrification and fractal dimension.

Aim of the research is to evaluate any alterations in structural network properties measured with graph theory from multi-modal imaging data in AN.

Thirty-eight patients with acute AN, 38 healthy controls and 20 patients in full remission from AN underwent MRI scanning. Surface extraction was completed using FreeSurfer package. Graph analysis was performed using graph analysis toolbox.

In acute patients, the covariance analysis among cortical thickness values showed a more segregated pattern and a reduction of global integration indexes. In the recovered patients group, we noticed a similar global trend without statistically significant differences for any single parameter. According to gyrification indexes, the covariance network showed a trend towards high segregation both in acute and recovered patients. We did not observe any significant difference in the covariance networks in the analysis of fractal dimension.

The presence of increased segregation properties in cortical covariance networks in AN may be determined by a retardation of neurodevelopmental trajectories or by an energy saving adaptive response. The differences between the analyzed parameters likely depend on their different morpho-functional meanings.

The authors have not supplied their declaration of competing interest.

Neuropsychological impairments in anorexia nervosa (AN) have been considered both as putative risk factors and as a target for treatment. However, the role of neuropsychological variables as predictors of outcome is not clear.

Our aim is to investigate the role of neuropsychological variables as predictors of response to treatment in a group of individuals affected by AN.

The study sample consisted of 144 patients diagnosed with acute AN, according to the DSM-5 criteria, referred to the Eating Unit of the Hospital of Padova, Italy. All participants were assessed by means of a neuropsychological and clinical test battery at intake and followed during outpatient treatment for an average of 531 days. Eighty-three percent of the patients underwent cognitive behavioral therapy, the families of 75% of the patients were included in the treatment and 48% of the patients took antidepressants (SSRI).

Both body mass index at assessment and illness duration appeared to be independent factors significantly affecting the outcome. The role of neuropsychological variables was explored including cognitive performance in a multivariate analysis including BMI at intake, duration of illness and diagnostic subtype. The inclusion in the model of the Wisconsin Sorting Card Task performance and the central coherence index (calculated by the Rey Figure Test) significantly increased the prediction ability of the model for full remission at the end of treatment.

This is the first study to show that neuropsychological characteristics may predict treatment response in AN. These data support the implementation of cognitive remediation techniques in the treatment of AN.

The authors have not supplied their declaration of competing interest.

The increased use of the MATRICS Consensus Cognitive Battery (MCCB) to investigate cognitive dysfunctions in schizophrenia fostered interest in its sensitivity in the context of family studies. As various measures of the same cognitive domains may have different power to distinguish between unaffected relatives of patients and controls, the relative sensitivity of MCCB tests for relative–control differences has to be established. We compared MCCB scores of 852 outpatients with schizophrenia (SCZ) with those of 342 unaffected relatives (REL) and a normative Italian sample of 774 healthy subjects (HCS). We examined familial aggregation of cognitive impairment by investigating within-family prediction of MCCB scores based on probands’ scores.

Multivariate analysis of variance was used to analyze group differences in adjusted MCCB scores. Weighted least-squares analysis was used to investigate whether probands’ MCCB scores predicted REL neurocognitive performance.

SCZ were significantly impaired on all MCCB domains. REL had intermediate scores between SCZ and HCS, showing a similar pattern of impairment, except for social cognition. Proband's scores significantly predicted REL MCCB scores on all domains except for visual learning.

In a large sample of stable patients with schizophrenia, living in the community, and in their unaffected relatives, MCCB demonstrated sensitivity to cognitive deficits in both groups. Our findings of significant within-family prediction of MCCB scores might reflect disease-related genetic or environmental factors.

Prenatal stress is hypothesized to have a disruptive impact on neurodevelopmental trajectories, but few human studies have been conducted on the long-term neural correlates of prenatal exposure to stress. The aim of this study was to explore the relationship between prenatal stress exposure and gray-matter volume and resting-state functional connectivity in a sample of 35 healthy women aged 14–40 years.

Voxel-based morphometry and functional connectivity analyses were performed on the whole brain and in specific regions of interest (hippocampus and amygdala). Data about prenatal/postnatal stress and obstetric complications were obtained by interviewing participants and their mothers, and reviewing obstetric records.

Higher prenatal stress was associated with decreased gray-matter volume in the left medial temporal lobe (MTL) and both amygdalae, but not the hippocampus. Variance in gray-matter volume of these brain areas significantly correlated with depressive symptoms, after statistically adjusting for the effects of age, postnatal stress and obstetric complications. Prenatal stress showed a positive linear relationship with functional connectivity between the left MTL and the pregenual cortex. Moreover, connectivity between the left MTL and the left medial-orbitofrontal cortex partially explained variance in the depressive symptoms of offspring.

In young women, exposure to prenatal stress showed a relationship with the morphometry and functional connectivity of brain areas involved in the pathophysiology of depressive disorders. These data provide evidence in favor of the hypothesis that early exposure to stress affects brain development and identified the MTL and amygdalae as possible targets of such exposure.

The study aims to explore, using indirect ecological measures of exposure, the role of viral infections in the development of anorexia nervosa (AN).

The cohort of participants consisted of all female subjects born in the Veneto region in the period between 1970 and 1984, and residing in the urban and suburban area of Padua (27 682 female subjects in an area of 424 km2). The main outcome measure was the diagnosis of AN resulting from the Public Mental Health Database, the Register of Hospital Admissions, and the Register of the Eating Disorders Unit (n=402, 1.4%). The number of cases of rubella, chickenpox, influenza and measles was ascertained for each month for the 15-year period.

Exposures during the sixth month of pregnancy to the peaks of chickenpox [odds ratio (OR) 1.6, 95% confidence interval (CI) 1.2–2.0] and rubella infections (OR 1.5, 95% CI 1.1–2.0) were significantly associated with an increased risk of developing AN, even after controlling for socio-economic status, urbanization and month of birth. We found weak evidence of a season-of-birth bias.

In utero exposure to viral infection could be a risk factor for developing AN. We need further epidemiological and serological studies to confirm this hypothesis.

Perinatal factors seem to be implicated in the pathogenesis of anorexia nervosa (AN) and may be involved in the programming of stress response systems in humans. Our aim was to explore one of the possible pathways to explain the association between perinatal complications and a psychiatric disorder. In particular, we tested the hypothesis that neonatal immaturity may confer an enhanced vulnerability to AN after exposure to a severe stressful event, such as childhood abuse.

The sample was composed of subjects who took part in a prevalence study carried out on a representative sample of the general population and cases of AN referred to an out-patient specialist unit. All subjects (n=663) were born in the two obstetric wards of Padua Hospital between 1971 and 1979. We analysed data using both a case-control and a cohort design.

We found that functional signs of neonatal dysmaturity, but not a low birthweight or prematurity, had a significant additive interaction with childhood abuse in determining the risk for this illness. In normal subjects, but not in subjects with AN, neonatal dysmaturity was associated with being small, short or thin for gestational age at birth.

The synergistic effect of neonatal dysmaturity and childhood abuse in increasing the risk for AN provides evidence for the hypothesis that a prenatal programming of stress response systems can result in an impairment of the individual's resilience to severe stressful events.