UNASSIGNED: A systematic overview of underlying mechanisms in the new disruptive mood dysregulation disorder (DMDD) diagnosis is needed. The Research Domain Criteria (RDoC) represent a system of six domains of human functioning, which aims to structure the understanding of the nature of mental illnesses. By means of the RDoC framework, the objective of this systematic review is to synthesize available data on children and youths <18 years suffering from DMDD as reported in peer reviewed papers.
UNASSIGNED: A literature search guided by PRISMA was conducted using Medline, PsychInfo, and Embase, while the RDoC domains were employed to systematize research findings. Risk of bias in the included studies was examined.
UNASSIGNED: We identified 319 studies. After study selection, we included 29 studies. Twenty-one of these had findings relating to >1 RDoC domain. The risk of bias assessment shows limitations in the research foundation of current knowledge on mechanisms of DMDD.
UNASSIGNED: Reviewing self-report, behavior and neurocircuit findings by means of RDoC domains, we suggest that DMDD youths have a negative interpretation bias in social processes and valence systems. In occurrence of a negative stimuli interpretation, aberrant cognitive processing may arise. However, current knowledge of DMDD is influenced by lack of sample diversity and open science practices.
UNASSIGNED: We found the six RDoC domains useful in structuring current evidence of the underlying mechanisms of DMDD. Important opportunities for future studies in this field of research are suggested. In clinical practice, this comprehensive summary on DMDD mechanisms can be used in psychoeducation and treatment plans.

It is well-established that addiction is typically associated with a distinct pattern of neurocognitive functioning with a consensus that it is typified by impaired top-down executive control and aberrant risk-reward processing. Despite a consensus that neurocognition plays an important role in characterizing and maintaining addictive disorders, there is a lack of systematic, bottom-up synthesis of quantitative evidence showing that neurocognition predicts addictive behaviors, and which neurocognitive constructs have the best predictive validity. This systematic review aimed to assess whether cognitive control and risk-reward processes as defined by the Research Domain Criteria (RDoC) predict the development and maintenance of addictive behaviors specifically, consumption, severity, and relapse. The findings from this review expose the substantial lack of evidence for neurocognition predicting addiction outcomes. However, there is evidence that suggests reward-related neurocognitive processes may be important for the detection of early risk for addiction, as well as a potentially viable target for designing novel, more effective interventions.

Changes in reward processing are hypothesized to play a role in the onset and maintenance of binge eating (BE). However, despite an increasing number of studies investigating the neurobiological reward system in individuals who binge eat, no comprehensive systematic review exists on this topic. Therefore, this review has the following objectives: (1) identify structural and functional changes in the brain reward system, either during rest or while performing a task; and (2) formulate directions for future research.
A search was conducted of articles published until March 31, 2022. Neuroimaging studies were eligible if they wanted to study the reward system and included a group of individuals who binge eat together with a comparator group. Their results were summarized in a narrative synthesis.
A total of 58 articles were included. At rest, individuals who binge eat displayed a lower striatal dopamine release, a change in the volume of the striatum, frontal cortex, and insula, as well as a lower frontostriatal connectivity. While performing a task, there was a higher activity of the brain reward system when anticipating or receiving food, more model-free reinforcement learning, and more habitual behavior. Most studies only included one patient group, used general reward-related measures, and did not evaluate the impact of comorbidities, illness duration, race, or sex.
Confirming previous hypotheses, this review finds structural and functional changes in the neurobiological reward system in BE. Future studies should compare disorders, use measures that are specific to BE, and investigate the impact of confounding factors.
This systematic review finds that individuals who binge eat display structural and functional changes in the brain reward system. These changes could be related to a higher sensitivity to food, relying more on previous experiences when making decisions, and more habitual behavior. Future studies should use a task that is specific to binge eating, look across different patient groups, and investigate the impact of comorbidities, illness duration, race, and sex.
Se plantea la hipótesis de que los cambios en el procesamiento de la recompensa desempeñan un papel en el inicio y mantenimiento de los atracones (BE). Sin embargo, a pesar de un número creciente de estudios que investigan el sistema de recompensa neurobiológica en individuos que comen en atracones, no existe una revisión sistemática exhaustiva sobre este tema. Por lo tanto, esta revisión tiene los siguientes objetivos: (1) identificar cambios estructurales y funcionales en el sistema de recompensa cerebral, ya sea en reposo o mientras se realiza una tarea; (2) formular direcciones para futuras investigaciones. MÉTODOS: Se realizó una búsqueda de artículos publicados hasta el 31 de marzo de 2022. Los estudios de neuroimagen eran elegibles si querían estudiar el sistema de recompensa e incluían a un grupo de individuos que comían en atracón junto con un grupo de comparación. Sus resultados se resumieron en una síntesis narrativa.
Se incluyeron un total de 58 artículos. En reposo, los individuos que comen en atracón mostraron una menor liberación de dopamina estriatal, un cambio en el volumen del cuerpo estriado, la corteza frontal y la ínsula, así como una menor conectividad frontostriatal. Al realizar una tarea, hubo una mayor actividad del sistema de recompensa cerebral al anticipar o recibir alimentos, más aprendizaje de refuerzo sin modelos y un comportamiento más habitual. La mayoría de los estudios sólo incluyeron un grupo de pacientes, utilizaron medidas generales relacionadas con la recompensa y no evaluaron el impacto de las comorbilidades, la duración de la enfermedad, la raza o el sexo. DISCUSIÓN: Confirmando hipótesis anteriores, esta revisión encuentra cambios estructurales y funcionales del sistema de recompensa neurobiológica en BE. Los estudios futuros deben comparar los trastornos, utilizar medidas que sean específicas para el comer en atracones e investigar el impacto de los factores de confusión.

Delay discounting paradigms have gained widespread popularity across clinical research. Given the prevalence in the field, researchers have set lofty expectations for the importance of delay discounting as a key transdiagnostic process and a \'core\' process underlying specific domains of dysfunction (e.g. addiction). We believe delay discounting has been prematurely reified as, in and of itself, a core process underlying psychological dysfunction, despite significant concerns with the construct validity of discounting rates. Specifically, high delay discounting rates are only modestly related to measures of psychological dysfunction and therefore are not \'core\' to these more complex behavioral problems. Furthermore, discounting rates do not appear to be specifically related to any disorder(s) or dimension(s) of psychopathology. This raises fundamental concerns about the utility of discounting, if the measure is only loosely associated with most forms of psychopathology. This stands in striking contrast to claims that discounting can serve as a \'marker\' for specific disorders, despite never demonstrating adequate sensitivity or specificity for any disorder that we are aware of. Finally, empirical evidence does not support the generalizability of discounting rates to other decisions made either in the lab or in the real-world, and therefore discounting rates cannot and should not serve as a summary measure of an individual\'s decision-making patterns. We provide recommendations for improving future delay discounting research, but also strongly encourage researchers to consider whether the empirical evidence supports the field\'s hyper-focus on discounting.

Deficits in social processing (SP) have been proposed to underpin interpersonal dysfunction in both Borderline Personality Disorder (BPD) and Substance Use Disorders (SUD). This study aimed to explore potential transdiagnostic cognitive and behavioral phenotypes of these disorders utilizing the NIMH Research Domain Criteria \'Systems for Social Processes\'. A systematic review and meta-analysis of the published research was conducted on 134 studies identified through our database searches. Four meta-analyses were conducted, which revealed significant overlapping deficits in the ability to identify facial emotions and infer the mental states of others in both BPD and SUD. Further, people with BPD displayed a higher ostracism effect following perceived social exclusion. Systematically reviewed studies also revealed significant dysfunction amongst individuals with BPD and SUD across both self and other SP constructs, which were broadly similar in magnitude. Taken together, these results support the proposition that SP dysfunction may be considered a core transdiagnostic phenotype of BPD and SUD.

More than one-thousand trials with functional magnetic resonance imaging (fMRI) as an outcome measure were registered in clinicaltrials.gov at the time of writing this article. However, 93% of these registered trials are still not completed with published results and there is no picture available about methodological dimensions of these ongoing trials with fMRI as an outcome measure.
We collected trials that use fMRI as an outcome measure in the ClinicalTrials.gov registry on 13 October 2018 and reviewed each trial\'s record entry. Eligible trials\' characteristics were extracted and summarized.
In total, 1,386 clinical trials were identified that reported fMRI in their outcome measures with fMRI as the only primary outcome in 33% of them. 82% of fMRI trials were started after 2011. The most frequent intervention was drug (pharmacological intervention) (29%). 57% of trials had parallel assignment design and 20% were designed for cross-over assignment. For task-based fMRI, cognitive systems (46%) based on Research Domain Criteria (RDoC) was the most frequent domain of tasks. Less than one-third of trials (28%) registered at least one region of interest for their analysis. Food cue reactivity task, pain perception task, n-back task, and monetary incentive delay task were recruited in more than 25 registered trials.
The number of fMRI trials (fMRI as an outcome measure) with both task and rest protocols is growing rapidly. Our study suggests a growing need for harmonization and standardized checklists on both methods and analysis for preregistration of fMRI-based outcomes in clinical trials.

Risk for suicidal behavior may fluctuate across the menstrual cycle. Here, we use the RDoC framework to review potential mechanisms by which the cycle may increase acute suicide risk.
The menstrual cycle impacts the majority of RDoC constructs linked to suicide risk, particularly among hormone-sensitive women, such as those with premenstrual dysphoric disorder or premenstrual exacerbation of a psychiatric disorder. Despite this, there are no published studies examining suicidal ideation, planning, or behavior longitudinally across the cycle. More work is needed to understand how hormone sensitivity may relate to both trait and state suicide risk. Intensive multilevel investigations of cyclical hormone effects on suicide risk through specific RDoC mechanisms are suggested. This is a fertile research area and may provide key insights regarding the mechanisms of acute suicide risk.

Heterogeneity is a key feature of all psychiatric disorders that manifests on many levels, including symptoms, disease course, and biological underpinnings. These form a substantial barrier to understanding disease mechanisms and developing effective, personalized treatments. In response, many studies have aimed to stratify psychiatric disorders, aiming to find more consistent subgroups on the basis of many types of data. Such approaches have received renewed interest after recent research initiatives, such as the National Institute of Mental Health Research Domain Criteria and the European Roadmap for Mental Health Research, both of which emphasize finding stratifications that are based on biological systems and that cut across current classifications. We first introduce the basic concepts for stratifying psychiatric disorders and then provide a methodologically oriented and critical review of the existing literature. This shows that the predominant clustering approach that aims to subdivide clinical populations into more coherent subgroups has made a useful contribution but is heavily dependent on the type of data used; it has produced many different ways to subgroup the disorders we review, but for most disorders it has not converged on a consistent set of subgroups. We highlight problems with current approaches that are not widely recognized and discuss the importance of validation to ensure that the derived subgroups index clinically relevant variation. Finally, we review emerging techniques-such as those that estimate normative models for mappings between biology and behavior-that provide new ways to parse the heterogeneity underlying psychiatric disorders and evaluate all methods to meeting the objectives of such as the National Institute of Mental Health Research Domain Criteria and Roadmap for Mental Health Research.

Reduced capacity to cognitively regulate emotional responses is a common impairment across major neuropsychiatric disorders. Brain systems supporting one such strategy, cognitive reappraisal of emotion, have been investigated extensively in the healthy population, a research focus that has led to influential meta-analyses and literature reviews. However, the emerging literature on neural substrates underlying cognitive reappraisal in clinical populations is yet to be systematically reviewed. Therefore, the goal of the current review was to summarize the literature on cognitive reappraisal and highlight common and distinct neural correlates of impaired emotion regulation in clinical populations. We performed a two-stage systematic literature search, selecting 32 studies on cognitive reappraisal in individuals with mood disorders (n=12), anxiety disorders (n=14), addiction (n=2), schizophrenia (n=2), and personality disorders (n=5). Comparing findings across these disorders allowed us to determine underlying mechanisms that were either disorder-specific or common across disorders. Results showed that across clinical populations, individuals consistently demonstrated reduced recruitment of the ventrolateral prefrontal cortex (vlPFC) and dorsolateral prefrontal cortex (dlPFC) during downregulation of negative emotion, indicating that there may be a core deficit in selection, manipulation and inhibition during reappraisal. Further, in individuals with mood disorders, amygdala responses were enhanced during downregulation of emotion, suggesting hyperactive bottom-up responses or reduced modulatory capacity. In individuals with anxiety disorders, however, emotion regulation revealed reduced activity in the dorsal anterior cingulate cortex (dACC) and inferior/superior parietal cortex, possibly indicating a deficit in allocation of attention. The reviewed studies thus provide evidence for both disorder-specific and common deficits across clinical populations. These findings highlight the role of distinct neural substrates as targets for developing/assessing novel therapeutic approaches that are geared towards cognitive regulation of emotion, as well as the importance of transdiagnostic research to identify both disorder specific and core mechanisms.

In 2009, the U.S. National Institute of Mental Health (NIMH) proposed an approach toward the deconstruction of psychiatric nosology under the research domain criteria (RDoC) framework. The overarching goal of RDoC is to identify robust, objective measures of behavior, emotion, cognition, and other domains that are more closely related to neurobiology than are diagnoses. A preliminary framework has been constructed, which has connected molecules, genes, brain circuits, behaviors, and other elements to dimensional psychiatric constructs. Although the RDoC framework has salience in emerging studies, foundational literature that pre-dated this framework requires synthesis and translation to the evolving objectives and nomenclature of RDoC. Toward this end, we review the candidate-gene association, linkage, and genome-wide studies that have implicated a variety of loci and genetic polymorphisms in selected Positive Valence Systems (PVS) constructs. Our goal is to review supporting evidence to currently listed genes implicated in this domain and novel candidates. We systematically searched and reviewed literature based on keywords listed under the June, 2011, edition of the PVS matrix on the RDoC website (http://www.nimh.nih.gov/research-priorities/rdoc/positive-valence-systems-workshop-proceedings.shtml), which were supplemented with de novo keywords pertinent to the scope of our review. Several candidate genes linked to the PVS framework were identified from candidate-gene association studies. We also identified novel candidates with loose association to PVS traits from genome-wide studies. There is strong evidence suggesting that PVS constructs, as currently conceptualized under the RDoC initiative, index genetically influenced traits; however, future research, including genetic epidemiological, and psychometric analyses, must be performed.