Major depressive disorder (MDD) is marked by significant changes to the local synchrony of spontaneous neural activity across various brain regions. However, many methods for assessing this local connectivity use fixed or arbitrary neighborhood sizes, resulting in a decreased capacity to capture smooth changes to the spatial gradient of local correlations. A newly developed method sensitive to classical anatomo-functional boundaries, Iso-Distant Average Correlation (IDAC), was therefore used to examine depression associated alterations to the local functional connectivity of the brain.

One-hundred and forty-seven adolescents and young adults with MDD and 94 healthy controls underwent a resting-state functional magnetic resonance imaging (fMRI) scan. Whole-brain functional connectivity maps of intracortical neural activity within iso-distant local areas (5–10, 15–20, and 25–30 mm) were generated to characterize local fMRI signal similarities.

Across all spatial distances, MDD participants demonstrated greater local functional connectivity of the bilateral posterior hippocampus, retrosplenial cortex, dorsal insula, fusiform gyrus, and supplementary motor area. Local connectivity alterations in short and medium distances (5–10 and 15–20 mm) in the mid insula cortex were additionally associated with expressive suppression use, independent of depressive symptom severity.

Our study identified increased synchrony of the neural activity in several regions commonly implicated in the neurobiology of depression. These effects were relatively consistent across the three distances examined. Longitudinal investigation of this altered local connectivity will clarify whether these differences are also found in other age groups and if this relationship is modified by increased disease chronicity.

Severe mental disorders experience premature mortality mostly from physical causes. When a patient with a history of bipolar disorder is admitted to the emergency room (ER) for psychiatric symptoms, these are routinely interpreted as a psychiatric disturbance. However, a careful history should be performed to correctly interpret key clinical information to rule out somatic etiology and establish adequate diagnosis.

To describe a patient whose presenting symptoms were misdiagnosed as psychiatric relapse, rather than serious somatic comorbidity debut.

A 70-year-old man, with a history of type I bipolar disorder and multiple cardiovascular conditions, was admitted to the ER for self-referred nervousness, depressed mood, insomnia, and suicidal thoughts. Symptoms had greatly worsened the previous week to his consultation with paroxysmal episodes of severe anxiety, feelings of strangeness, and sensations of unpleasant odors.

During observation, the patient was found lying down with loss of consciousness, urinary incontinence, and amnesia of the event. Generalized tonic-clonic seizures were observed by neurologists while mental status examination was being performed. After symptoms were oriented as having a neurological etiology, the patient suffered cardiac arrest and defibrillation was required. After admittance to the intensive care unit and inpatient cardiology care, the patient was discharged from the hospital with the diagnosis of ventricular fibrillation due to drug-induced QT prolongation. There was no evidence of mixed depression or seizures once the cardiac dysfunction was identified and treated.

The psychiatric symptoms were the clinical manifestation of a generalized seizure-like activities that were attributed to transient cerebral hypoperfusion secondary to ventricular fibrillation.

No significant relationships.

Intensive home-treatment (IHT) for people experiencing a mental health crisis has been progressively established in many European countries as an alternative to in-ward treatment. However, the management of acute episodes at home can cause burden in the caregivers of these patients.

To create a brief group intervention (BGI) to reduce burden in the caregivers of the patients admitted to an IHT unit.

A preliminary version of the BGI (BGI 1.0) was designed based on literature’s review. It consisted of 4 sessions of 90 minutes (one per week), on-line (COVID-19), focused on caregivers burden, stress and self-care, communication skills, and self-compassion. All the caregivers of the patients admitted for IHT from 10/01/2020 to 06/01/2021 were offered the BGI 1.0. At the end of the intervention, participants (caregivers and therapists) were asked about their opinion on its contents and usefulness.

A total of 31 caregivers received the BGI 1.0. Most of them felt satisfied with the intervention. Opinions varied as to which contents should be expanded or included. The therapists thought that the number of sessions should be increased to take a closer look at some contents or to include new ones. They also believed that the on-line format hindered the adherence and the interaction between the participants.

The BGI 1.0 seems to be a good starting point to design the final version of the intervention. However, an exhaustive assessment of the construct of burden in a larger sample of caregivers should be performed prior to its design.

No significant relationships.

Electroconvulsive therapy (ECT) is the most effective and fast acting therapy for treatment-resistant depression (TRD). Animal research has consistently pointed to neuroplasticity as a central mechanism of ECT action (1), however evidence in humans remains scarce (2; 3).

We assessed two independent samples of TRD patients referred for ECT. The Barcelona-sample included 13 subjects treated with bitemporal ECT and 10 healthy volunteers (HV). Four successive 3T structural MRIs were acquired: baseline, 24-48 hours after the 1st ECT session, 24-48 hours after the 9th ECT, and two weeks after ECT course completion. HV were scanned twice five weeks apart. Within the framework of the Barcelona-Sydney Clinical Imaging Collaboration, we also scanned 10 patients treated mainly with right unilateral ECT (Sydney-sample). Whole-brain longitudinal grey matter (GM) changes were measured using intra-subject diffeomorphic registration, within SPM12b.

In the Barcelona-sample, over the course of treatment bitemporal ECT produced a linear increase of GM volume in the limbic system (involving bilateral hippocampi and amygdalae). Additionally, volumetric increase within the right subgenual cortex was detected from baseline to the 9th ECT session. Such volume changes were not observed in HV. Furthermore, GM volume expansion correlated positively with depressive symptom improvement and neurocognitive performance (memory and executive function). Hippocampal and amygdalar volume increases were replicated in the Sydney-sample, although limited to the stimulated hemisphere.

ECT effects described here could be accounted for by the induction of regionally specific structural plasticity. Nevertheless, other mechanisms such as neurovascular changes should not be discarded.

The growing concern about cannabis use, the most used illicit drug worldwide, has led to an increase in the number of cannabis studies using neuroimaging techniques to determine its effect on brain structure and function.

We conducted a systematic review to assess the evidence of the impact of chronic cannabis use on brain structure and function in adults and adolescents.

Papers published until August 2012 were included from EMBASE, Medline, PubMed and LILACS databases following a comprehensive search strategy and pre-determined set of criteria for article selection. Only neuroimaging studies involving chronic cannabis users with a matched control group were considered.

One hundred and forty-two studies were identified, of which 43 met the established criteria. Eight studies were in adolescent population. Neuroimaging studies provide evidence of morphological brain alterations in both population groups, particularly in the medial temporal and frontal cortices, as well as the cerebellum. These effects may be related to the amount of cannabis exposure. Functional neuroimaging studies suggest different patterns of resting global and brain activity during the performance of several cognitive tasks also in both groups, which may indicate compensatory effects in response to chronic cannabis exposure. The results pointed out methodological limitations among studies and high heterogeneity in the findings.

Chronic cannabis use may alter brain structure and function in adult and adolescent population. Further studies should consider the use of convergent and multimodal methodology, prospective large samples involving adolescent to adulthood subjects, and data-sharing initiatives. Grants: PNSD/2011/050, PNSD2006/101, SGR2009/1435.

Neuropsychological and neuroimaging studies of response inhibition in cannabis users have reported inconsistent results. The age of onset of cannabis use and individual genetic differences may play a critical role in the regulation of inhibition in cannabis users.

We examine the influence of COMT Val158Met functional polymorphism on the response inhibition brain network in a group of early-onset chronic cannabis users compared with healthy controls.

fMRI data was acquired from 27 chronic cannabis users who began use cannabis before 16 years of age, and 29 non-using control subjects matched in terms of age, educational level and intelligence quotient while undergoing the Multi-Source Interference Task (MSIT). Participants were male, Caucasians aged between 18 and 30 years. All were assessed by a structured psychiatric interview (PRISM) to exclude any lifetime Axis-I disorder (DSM-IV). COMT genotyping was performed and resonance imaging data was analysed by voxel-based morphometry (VBM).

Both groups did not differ on their behavioural performance and brain responses during the MSIT task. A significant group-by-genotype interaction was observed on task-related brain activation (and on MSIT reaction times), in which met carrier load was associated with increased activation in cannabis users and val carrier load with increased activation in controls. The interaction pattern included the medial frontal cortex, ACC, inferior frontal gyrus, ventral striatum, anterior mesencephalon, inferior parietal and superior temporal cortices and the PCC.

Chronic cannabis exposure interacts with the genetically driven dopamine function in the modulation of the neural mechanisms related to response inhibition.

Grants:PNSD/2011/050, PNSD2006/101, SGR2009/1435.

Automated surveillance of healthcare-associated infections reduces workload and improves standardization, but it has not yet been adopted widely. In this study, we assessed the performance and feasibility of an easy implementable framework to develop algorithms for semiautomated surveillance of deep incisional and organ-space surgical site infections (SSIs) after orthopedic, cardiac, and colon surgeries.

Retrospective cohort study in multiple countries.

European hospitals were recruited and selected based on the availability of manual SSI surveillance data from 2012 onward (reference standard) and on the ability to extract relevant data from electronic health records. A questionnaire on local manual surveillance and clinical practices was administered to participating hospitals, and the information collected was used to pre-emptively design semiautomated surveillance algorithms standardized for multiple hospitals and for center-specific application. Algorithm sensitivity, positive predictive value, and reduction of manual charts requiring review were calculated. Reasons for misclassification were explored using discrepancy analyses.

The study included 3 hospitals, in the Netherlands, France, and Spain. Classification algorithms were developed to indicate procedures with a high probability of SSI. Components concerned microbiology, prolonged length of stay or readmission, and reinterventions. Antibiotics and radiology ordering were optional. In total, 4,770 orthopedic procedures, 5,047 cardiac procedures, and 3,906 colon procedures were analyzed. Across hospitals, standardized algorithm sensitivity ranged between 82% and 100% for orthopedic surgery, between 67% and 100% for cardiac surgery, and between 84% and 100% for colon surgery, with 72%–98% workload reduction. Center-specific algorithms had lower sensitivity.

Using this framework, algorithms for semiautomated surveillance of SSI can be successfully developed. The high performance of standardized algorithms holds promise for large-scale standardization.

Pathological worry is a hallmark feature of generalised anxiety disorder (GAD), associated with dysfunctional emotional processing. The ventromedial prefrontal cortex (vmPFC) is involved in the regulation of such processes, but the link between vmPFC emotional responses and pathological v. adaptive worry has not yet been examined.

To study the association between worry and vmPFC activity evoked by the processing of learned safety and threat signals.

In total, 27 unmedicated patients with GAD and 56 healthy controls (HC) underwent a differential fear conditioning paradigm during functional magnetic resonance imaging.

Compared to HC, the GAD group demonstrated reduced vmPFC activation to safety signals and no safety–threat processing differentiation. This response was positively correlated with worry severity in GAD, whereas the same variables showed a negative and weak correlation in HC.

Poor vmPFC safety–threat differentiation might characterise GAD, and its distinctive association with GAD worries suggests a neural-based qualitative difference between healthy and pathological worries.

None.

The assessment of inter-regional functional connectivity (FC) has allowed for the description of the putative mechanism of action of treatments such as deep brain stimulation (DBS) of the nucleus accumbens in patients with obsessive–compulsive disorder (OCD). Nevertheless, the possible FC alterations of other clinically-effective DBS targets have not been explored. Here we evaluated the FC patterns of the subthalamic nucleus (STN) and the bed nucleus of the stria terminalis (BNST) in patients with OCD, as well as their association with symptom severity.

Eighty-six patients with OCD and 104 healthy participants were recruited. A resting-state image was acquired for each participant and a seed-based analysis focused on our two regions of interest was performed using statistical parametric mapping software (SPM8). Between-group differences in FC patterns were assessed with two-sample t test models, while the association between symptom severity and FC patterns was assessed with multiple regression analyses.

In comparison with controls, patients with OCD showed: (1) increased FC between the left STN and the right pre-motor cortex, (2) decreased FC between the right STN and the lenticular nuclei, and (3) increased FC between the left BNST and the right frontopolar cortex. Multiple regression analyses revealed a negative association between clinical severity and FC between the right STN and lenticular nucleus.

This study provides a neurobiological framework to understand the mechanism of action of DBS on the STN and the BNST, which seems to involve brain circuits related with motor response inhibition and anxiety control, respectively.

Hippocampal abnormalities have been demonstrated in schizophrenia. It is unclear whether these abnormalities worsen with age, and whether they affect cognition and function.

To determine whether hippocampal abnormalities in chronic schizophrenia are associated with age, cognition and socio-occupational function.

Using 3 T magnetic resonance imaging we scanned 100 persons aged 19–82 years: 51 were out-patients with stable schizophrenia at least 2 years after diagnosis and 49 were healthy volunteers matched for age and gender. Automated analysis was used to determine hippocampal volume and shape.

There were differential effects of age in the schizophrenia and control samples on total hippocampal volume (group×age interaction:F (1,95) = 6.57, P = 0.012), with steeper age-related reduction in the schizophrenia group. Three-dimensional shape analysis located the age-related deformations predominantly in the mid-body of the hippocampus. In the schizophrenia group similar patterns of morphometric abnormalities were correlated with impaired cognition and poorer socio-occupational function.

Hippocampal abnormalities are associated with age in people with chronic schizophrenia, with a steeper decline than in healthy individuals. These abnormalities are associated with cognitive and functional deficits, suggesting that hippocampal morphometry may be a biomarker for cognitive decline in older patients with schizophrenia.

Despite knowledge of amygdala involvement in fear and anxiety, its contribution to the pathophysiology of obsessive–compulsive disorder (OCD) remains controversial. In the context of neuroimaging studies, it seems likely that the heterogeneity of the disorder might have contributed to a lack of consistent findings.

To assess the influence of OCD symptom dimensions on amygdala responses to a well-validated emotional face-matching paradigm.

Cross-sectional functional magnetic resonance imaging (fMRI) study of 67 patients with OCD and 67 age-, gender- and education-level matched healthy controls.

The severity of aggression/checking and sexual/religious symptom dimensions were significantly associated with heightened amygdala activation in those with OCD when responding to fearful faces, whereas no such correlations were seen for other symptom dimensions.

Amygdala functional alterations in OCD appear to be specifically modulated by symptom dimensions whose origins may be more closely linked to putative amygdala-centric processes, such as abnormal fear processing.

The size of particular sub-regions within the ventromedial prefrontal cortex (vmPFC) has been associated with fear extinction in humans. Exposure therapy is a form of extinction learning widely used in the treatment of obsessive-compulsive disorder (OCD). Here we investigated the relationship between morphometric measurements of different sub-regions of the vmPFC and exposure therapy outcome in OCD.

A total of 74 OCD patients and 86 healthy controls underwent magnetic resonance imaging (MRI). Cortical thickness and volumetric measurements were obtained for the rostral anterior cingulate cortex (rACC), the medial orbital frontal cortex and the subcallosal cortex. After MRI acquisition, patients were enrolled in an exposure therapy protocol, and we assessed the relationship between MRI-derived measurements and treatment outcome. Baseline between-group differences for such measurements were also assessed.

Compared with healthy controls, OCD patients showed a thinner left rACC (p = 0.008). Also, left rACC thickness was inversely associated with exposure therapy outcome (r – 0.32, p = 0.008), and this region was significantly thinner in OCD patients who responded to exposure therapy than in those who did not (p = 0.006). Analyses based on regional volumetry did not yield any significant results.

OCD patients showed cortical thickness reductions in the left rACC, and these alterations were related to exposure therapy outcome. The precise characterization of neuroimaging predictors of treatment response derived from the study of the brain areas involved in fear extinction may optimize exposure therapy planning in OCD and other anxiety disorders.