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An important challenge in mental health research is to translate findings from cognitive neuroscience and neuroimaging research into effective treatments that target the neurobiological alterations involved in psychiatric symptoms. To address this challenge, in this review we propose a heuristic neurocircuit-based taxonomy to guide the treatment of obsessive–compulsive disorder (OCD). We do this by integrating information from several sources. First, we provide case vignettes in which patients with OCD describe their symptoms and discuss different clinical profiles in the phenotypic expression of the condition. Second, we link variations in these clinical profiles to underlying neurocircuit dysfunctions, drawing on findings from neuropsychological and neuroimaging studies in OCD. Third, we consider behavioral, pharmacological, and neuromodulatory treatments that could target those specific neurocircuit dysfunctions. Finally, we suggest methods of testing this neurocircuit-based taxonomy as well as important limitations to this approach that should be considered in future research.

Episodic memory is the ability to learn, store and recall new information. The prefrontal cortex (PFC) is a crucial area engaged in this ability. Cognitive training has been demonstrated to improve episodic memory in adults and older subjects. However, there are no studies examining the effects of cognitive training on episodic memory encoding in typically developing children and adolescents. This study investigated the behavioral effects and neural correlates of semantic categorization strategy training in children and adolescents during verbal episodic memory encoding using functional magnetic resonance imaging (fMRI). Participants with age range: 7-18 years were scanned before and after semantic categorization training during encoding of word lists. Results showed improved memory performance in adolescents, but not in children. Deactivation of the anterior medial PFC/anterior cingulate and higher activation of the right anterior and lateral orbital gyri, right frontal pole and right middle frontal gyrus activation were found after training in adolescents when compared to children. These findings suggest different maturational paths of brain regions, especially in the PFC, and deactivation of default mode network areas, which are involved in successful memory and executive processes in the developing brain.

Although it has been suggested that the hippocampus and amygdala (HA) are involved in the neurobiology of obsessive–compulsive disorder (OCD), volumetric findings have been inconsistent, and little work has been undertaken on the volumetry of the heterogeneous anatomic units of HA, with their specific functions and cytoarchitecture, in OCD. We sought to explore potential sources of heterogeneity in brain volumes by performing a separate analysis for people with and without psychotropic medication use, as well as the association of subfield volumes with OCD symptom severity. We segmented T1-weighted images from people with OCD and healthy controls in the OCD Brain Imaging Consortium to produce 12 hippocampal subfields and 9 amygdala subfields using Free-Surfer 6.0. We assessed between-group differences in subfield volume using a mixed-effects model adjusted for age and quadratic effects of age, sex, site, and whole HA volume. We also performed subgroup analyses to examine subfield volume in relation to comorbid anxiety and depression, medication status, and symptom severity. We corrected all analyses for multiple comparisons using the false discovery rate (FDR). We included images from 381 people with OCD and 338 healthy controls. These groups did not significantly differ in HA subfield volumes. However, medicated people with OCD had significantly smaller volumes in the hippocampal dentate gyrus (pFDR = 0.04, d = −0.26) and molecular layer (pFDR = 0.04, d = −0.29), and larger volumes in the lateral (pFDR = 0.049, d = 0.23) and basal (pFDR = 0.049, d = 0.25) amygdala subfields, than healthy controls. Unmedicated people with OCD had significantly smaller volumes in the hippocampal cornu ammonis sector 1 (pFDR = 0.02, d = −0.28) than controls. We did not detect associations between any subfield volume and OCD severity. We used cross-sectional data, which limits the interpretation of our analysis. Differences in HA subfields between people with OCD and healthy controls are dependent on medication status, in line with previous work on other brain volumetric alterations in OCD. This emphasizes the importance of considering psychotropic medication in neuroimaging studies of OCD.

Nonsuicidal self-injury (NSSI) is prevalent and affects mainly the youth population. It is prospectively associated with suicide attempts, making it a target for suicide prevention. Recently, several studies have investigated neural pathways of NSSI using neuroimaging. However, there is a lack of systematized appraisal of these findings. This systematic review aims to identify and summarize the main neuroimaging findings of NSSI in youth. We followed PRISMA statement guidelines and searched MEDLINE, APA PsycInfo, and Google Scholar databases for neuroimaging studies, irrespective of imaging modality, specifically investigating NSSI in samples with a mean age of up to 25 years old. Quality assessment was made using the Newcastle–Ottawa and Joanna Briggs Institute scales. The initial search retrieved 3030 articles; 21 met inclusion criteria, with a total of 938 subjects. Eighteen studies employed functional neuroimaging techniques such as resting-state and task-based fMRI (emotional, interpersonal exposure/social exclusion, pain, reward, and cognitive processing paradigms). Three studies reported on structural MRI. An association of NSSI behavior and altered emotional processing in cortico-limbic neurocircuitry was commonly reported. Additionally, alterations in potential circuits involving pain, reward, interpersonal, self-processing, and executive function control processes were identified. NSSI has complex and diverse neural underpinnings. Future longitudinal studies are needed to understand its developmental aspects better.

Psychiatric disorders affect close to 30% of the global population and account for more than 7% of the global burden of disease. To address this problem, new treatment approaches are required that target the heterogeneity of psychiatric conditions and their underlying neurobiological bases. In this article, we use obsessive-compulsive disorder (OCD) as an example to summarize recent conceptual work that has attempted to offer solutions to better understanding heterogeneity and improving effectiveness of psychiatric treatments. Specifically, we highlight hypothetical “clinical profiles” of OCD that are based on neurocognitive alterations (eg, dysregulated fear), which are underpinned by dysfunctions in specific neurocircuits (eg, hyperactive frontolimbic circuit function) and could be ameliorated with neurocircuit-based treatments. While this model of OCD is not yet ready for clinical use, this approach to understanding OCD may be helpful for clinicians in understanding individual patients under their care and the mechanisms involved in different treatments for OCD. [Psychiatr Ann. 2022;52(4);152–156.]

Objectives We describe the harmonized MRI acquisition and quality assessment of an ongoing global OCD study, with the aim to translate representative, well‐powered neuroimaging findings in neuropsychiatric research to worldwide populations. Methods We report on T1‐weighted structural MRI, resting‐state functional MRI, and multi‐shell diffusion‐weighted imaging of 140 healthy participants (28 per site), two traveling controls, and regular phantom scans. Results Human image quality measures (IQMs) and outcome measures showed smaller within‐site variation than between‐site variation. Outcome measures were less variable than IQMs, especially for the traveling controls. Phantom IQMs were stable regarding geometry, SNR, and mean diffusivity, while fMRI fluctuation was more variable between sites. Conclusions Variation in IQMs persists, even for an a priori harmonized data acquisition protocol, but after pre‐processing they have less of an impact on the outcome measures. Continuous monitoring IQMs per site is valuable to detect potential artifacts and outliers. The inclusion of both cases and healthy participants at each site remains mandatory.

Sensory phenomena (SP) are uncomfortable feelings, including bodily sensations, sense of inner tension, “just-right” perceptions, feelings of incompleteness, or “urge-only” phenomena, which have been described to precede, trigger or accompany repetitive behaviours in individuals with obsessive–compulsive disorder (OCD). Sensory phenomena are also observed in individuals with tic disorders, and previous research suggests that sensorimotor cortex abnormalities underpin the presence of SP in such patients. However, to our knowledge, no studies have assessed the neural correlates of SP in patients with OCD. We assessed the presence of SP using the University of São Paulo Sensory Phenomena Scale in patients with OCD and healthy controls from specialized units in São Paulo, Brazil, and Barcelona, Spain. All participants underwent a structural magnetic resonance examination, and brain images were examined using DARTEL voxel-based morphometry. We evaluated grey matter volume differences between patients with and without SP and healthy controls within the sensorimotor and premotor cortices. We included 106 patients with OCD and 87 controls in our study. Patients with SP (67% of the sample) showed grey matter volume increases in the left sensorimotor cortex in comparison to patients without SP and bilateral sensorimotor cortex grey matter volume increases in comparison to controls. No differences were observed between patients without SP and controls. Most patients were medicated. Participant recruitment and image acquisition were performed in 2 different centres. We have identified a structural correlate of SP in patients with OCD involving grey matter volume increases within the sensorimotor cortex; this finding is in agreement with those of tic disorder studies showing that abnormal activity and volume increases within this region are associated with the urges preceding tic onset.

Background Obsessive-compulsive disorder (OCD) has a lifetime prevalence of 2–3% and is a leading cause of global disability. Brain circuit abnormalities in individuals with OCD have been identified, but important knowledge gaps remain. The goal of the new global initiative described in this paper is to identify robust and reproducible brain signatures of measurable behaviors and clinical symptoms that are common in individuals with OCD. A global approach was chosen to accelerate discovery, to increase rigor and transparency, and to ensure generalizability of results. Methods We will study 250 medication-free adults with OCD, 100 unaffected adult siblings of individuals with OCD, and 250 healthy control subjects at five expert research sites across five countries (Brazil, India, Netherlands, South Africa, and the U.S.). All participants will receive clinical evaluation, neurocognitive assessment, and magnetic resonance imaging (MRI). The imaging will examine multiple brain circuits hypothesized to underlie OCD behaviors, focusing on morphometry (T1-weighted MRI), structural connectivity (Diffusion Tensor Imaging), and functional connectivity (resting-state fMRI). In addition to analyzing each imaging modality separately, we will also use multi-modal fusion with machine learning statistical methods in an attempt to derive imaging signatures that distinguish individuals with OCD from unaffected siblings and healthy controls (Aim #1). Then we will examine how these imaging signatures link to behavioral performance on neurocognitive tasks that probe these same circuits as well as to clinical profiles (Aim #2). Finally, we will explore how specific environmental features (childhood trauma, socioeconomic status, and religiosity) moderate these brain-behavior associations. Discussion Using harmonized methods for data collection and analysis, we will conduct the largest neurocognitive and multimodal-imaging study in medication-free subjects with OCD to date. By recruiting a large, ethno-culturally diverse sample, we will test whether there are robust biosignatures of core OCD features that transcend countries and cultures. If so, future studies can use these brain signatures to reveal trans-diagnostic disease dimensions, chart when these signatures arise during development, and identify treatments that target these circuit abnormalities directly. The long-term goal of this research is to change not only how we conceptualize OCD but also how we diagnose and treat it.

Socioeconomic disadvantage (SED) has been consistently associated with early life mental health problems. SED has been shown to impact multiple biological systems, including the regulation of neurotrophic proteins, immune-inflammatory and oxidative stress markers, which, conversely, have been reported to be relevant to physiological and pathological neurodevelopment This study investigated the relationship between SED, different domains of psychopathology, serum levels of interleukin-6 (IL6), thiobarbituric acid-reactive substance (TBARS) and brain-derived neurotrophic factor (BDNF). We hypothesized that a composite of socioeconomic risk would be associated with psychopathology and altered levels of peripheral biomarkers. In addition, we hypothesized that SED would moderate the associations between mental health problems, IL6, TBARS and BDNF. Using a cross-sectional design, we measured the serum levels of IL6, TBARS and BDNF in 495 children aged 6 to 12. We also investigated socio-demographic characteristics and mental health problems using the Child Behaviour Checklist (CBCL) DSM-oriented scales. SED was evaluated using a cumulative risk model. Generalized linear models were used to assess associations between SED, biomarkers levels and psychopathology. SED was significantly associated with serum levels of IL6 (RR = 1.026, 95% CI 1.004; 1.049, p = 0.020) and TBARS (RR = 1.077, 95% CI 1.028; 1.127, p = 0.002). The association between SED and BDNF was not statistically significant (RR = 1.031, 95% CI 0.997; 1.066, p = 0.077). SED was also significantly associated with all CBCL DSM-oriented scales (all p < 0.05), whereas serum biomarkers (i.e. IL6, TBARS, BDNF) were associated with specific subscales. Moreover, the associations between serum biomarkers and domains of psychopathology were moderated by SED, with stronger correlations between mental health problems, IL6, TBARS, and BDNF being observed in children with high SED. In children, SED is highly associated with mental health problems. Our findings suggest that this association may be moderated via effects on multiple interacting neurobiological systems.