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Identification of Common Neural Circuit Disruptions in Cognitive Control Across Psychiatric Disorders.

ABSTRACT: Cognitive deficits are a common feature of psychiatric disorders. The authors investigated the nature of disruptions in neural circuitry underlying cognitive control capacities across psychiatric disorders through a transdiagnostic neuroimaging meta-analysis.A PubMed search was conducted for whole-brain functional neuroimaging articles published through June 2015 that compared activation in patients with axis I disorders and matched healthy control participants during cognitive control tasks. Tasks that probed performance or conflict monitoring, response inhibition or selection, set shifting, verbal fluency, and recognition or working memory were included. Activation likelihood estimation meta-analyses were conducted on peak voxel coordinates.The 283 experiments submitted to meta-analysis included 5,728 control participants and 5,493 patients with various disorders (schizophrenia, bipolar or unipolar depression, anxiety disorders, and substance use disorders). Transdiagnostically abnormal activation was evident in the left prefrontal cortex as well as the anterior insula, the right ventrolateral prefrontal cortex, the right intraparietal sulcus, and the midcingulate/presupplementary motor area. Disruption was also observed in a more anterior cluster in the dorsal cingulate cortex, which overlapped with a network of structural perturbation that the authors previously reported in a transdiagnostic meta-analysis of gray matter volume.These findings demonstrate a common pattern of disruption across major psychiatric disorders that parallels the "multiple-demand network" observed in intact cognition. This network interfaces with the anterior-cingulo-insular or "salience network" demonstrated to be transdiagnostically vulnerable to gray matter reduction. Thus, networks intrinsic to adaptive, flexible cognition are vulnerable to broad-spectrum psychopathology. Dysfunction in these networks may reflect an intermediate transdiagnostic phenotype, which could be leveraged to advance therapeutics.

SUBMITTER: McTeague LM

PROVIDER: S-EPMC5543416 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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Identification of Common Neural Circuit Disruptions in Cognitive Control Across Psychiatric Disorders.

McTeague Lisa M LM Huemer Julia J Carreon David M DM Jiang Ying Y Eickhoff Simon B SB Etkin Amit A

The American journal of psychiatry 20170321 7

<h4>Objective</h4>Cognitive deficits are a common feature of psychiatric disorders. The authors investigated the nature of disruptions in neural circuitry underlying cognitive control capacities across psychiatric disorders through a transdiagnostic neuroimaging meta-analysis.<h4>Method</h4>A PubMed search was conducted for whole-brain functional neuroimaging articles published through June 2015 that compared activation in patients with axis I disorders and matched healthy control participants d ...[more]

PMID: 28320224

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Project description:OBJECTIVE:Disrupted emotional processing is a common feature of many psychiatric disorders. The authors investigated functional disruptions in neural circuitry underlying emotional processing across a range of tasks and across psychiatric disorders through a transdiagnostic quantitative meta-analysis of published neuroimaging data. METHODS:A PubMed search was conducted for whole-brain functional neuroimaging findings published through May 2018 that compared activation during emotional processing tasks in patients with psychiatric disorders (including schizophrenia, bipolar or unipolar depression, anxiety, and substance use) to matched healthy control participants. Activation likelihood estimation (ALE) meta-analyses were conducted on peak voxel coordinates to identify spatial convergence. RESULTS:The 298 experiments submitted to meta-analysis included 5,427 patients and 5,491 control participants. ALE across diagnoses and patterns of patient hyper- and hyporeactivity demonstrated abnormal activation in the amygdala, the hippocampal/parahippocampal gyri, the dorsomedial/pulvinar nuclei of the thalamus, and the fusiform gyri, as well as the medial and lateral dorsal and ventral prefrontal regions. ALE across disorders but considering directionality demonstrated patient hyperactivation in the amygdala and the hippocampal/parahippocampal gyri. Hypoactivation was found in the medial and lateral prefrontal regions, most pronounced during processing of unpleasant stimuli. More refined disorder-specific analyses suggested that these overall patterns were shared to varying degrees, with notable differences in patterns of hyper- and hypoactivation. CONCLUSIONS:These findings demonstrate a pattern of neurocircuit disruption across major psychiatric disorders in regions and networks key to adaptive emotional reactivity and regulation. More specifically, disruption corresponded prominently to the "salience" network, the ventral striatal/ventromedial prefrontal "reward" network, and the lateral orbitofrontal "nonreward" network. Consistent with the Research Domain Criteria initiative, these findings suggest that psychiatric illness may be productively formulated as dysfunction in transdiagnostic neurobehavioral phenotypes such as neurocircuit activation.

Project description:Psychiatric disorders and common epilepsies are heritable disorders with a high comorbidity and overlapping symptoms. However, the causative mechanisms underlying this relationship are poorly understood. Here we aimed to identify overlapping genetic loci between epilepsy and psychiatric disorders to gain a better understanding of their comorbidity and shared clinical features. We analysed genome-wide association study data for all epilepsies (n = 44 889), genetic generalized epilepsy (n = 33 446), focal epilepsy (n = 39 348), schizophrenia (n = 77 096), bipolar disorder (n = 406 405), depression (n = 500 199), attention deficit hyperactivity disorder (n = 53 293) and autism spectrum disorder (n = 46 350). First, we applied the MiXeR tool to estimate the total number of causal variants influencing the disorders. Next, we used the conjunctional false discovery rate statistical framework to improve power to discover shared genomic loci. Additionally, we assessed the validity of the findings in independent cohorts, and functionally characterized the identified loci. The epilepsy phenotypes were considerably less polygenic (1.0 K to 3.4 K causal variants) than the psychiatric disorders (5.6 K to 13.9 K causal variants), with focal epilepsy being the least polygenic (1.0 K variants), and depression having the highest polygenicity (13.9 K variants). We observed cross-trait genetic enrichment between genetic generalized epilepsy and all psychiatric disorders and between all epilepsies and schizophrenia and depression. Using conjunctional false discovery rate analysis, we identified 40 distinct loci jointly associated with epilepsies and psychiatric disorders at conjunctional false discovery rate <0.05, four of which were associated with all epilepsies and 39 with genetic generalized epilepsy. Most epilepsy risk loci were shared with schizophrenia (n = 31). Among the identified loci, 32 were novel for genetic generalized epilepsy, and two were novel for all epilepsies. There was a mixture of concordant and discordant allelic effects in the shared loci. The sign concordance of the identified variants was highly consistent between the discovery and independent datasets for all disorders, supporting the validity of the findings. Gene-set analysis for the shared loci between schizophrenia and genetic generalized epilepsy implicated biological processes related to cell cycle regulation, protein phosphatase activity, and membrane and vesicle function; the gene-set analyses for the other loci were underpowered. The extensive genetic overlap with mixed effect directions between psychiatric disorders and common epilepsies demonstrates a complex genetic relationship between these disorders, in line with their bi-directional relationship, and indicates that overlapping genetic risk may contribute to shared pathophysiological and clinical features between epilepsy and psychiatric disorders.

Project description:BackgroundAutomatic biases, such as attentional biases and avoidance and interpretative biases, have been purported to be responsible for several psychiatric disorders. Gamification has been considered for cognitive bias modification, mainly to address the core issues of diminishing motivation to train over time, as bias modification intervention tasks tend to be highly repetitive. While a prior review has suggested how gamification strategies could be applied to such tasks, there remains a lack of systematic evaluation of gamified cognitive bias modification interventions in the literature.ObjectiveThe objective of this review is to understand the overall effectiveness of a gamified approach for cognitive bias modification and inform future research that seeks to integrate gamification technologies into existing conventional bias modification interventions.MethodsTo identify the relevant articles for our review, the following search terminologies were used: ("cognitive bias" OR "attention bias" OR "interpret* bias" OR "approach bias" OR "avoidance bias") AND ("training" OR "modification" OR "practice" OR "therapy") AND ("gamification" OR "game elements" OR "game" OR "gaming" OR "game mechanics"). PubMed, MEDLINE, PsycINFO, and Scopus databases were searched systematically for articles published after 2000. Articles were included if they described a gamified cognitive bias modification task and included participants with underlying psychopathological symptoms. Data were systematically extracted from the identified articles, and a qualitative synthesis was performed.ResultsFour studies evaluated gamified cognitive bias modification interventions. Two studies included participants with anxiety symptoms, one with affective symptoms, and one with alcohol problems. The conventional visual probe task paradigm was used in 3 studies, and the attentional visual search task paradigm was used in the last study. We found gaming elements incorporated to include that of animations, sounds, feedback, and a point-scoring system for response time and difficulty. Of the 4 identified studies, only 2 reported their gamified interventions to be effective.ConclusionsOur review is the first to systematically synthesize the evidence for gamified cognitive bias modification interventions. The results arising from our review should be considered in the future design and conceptualization of gamified cognitive bias modification interventions.International registered report identifier (irrid)RR2-10.2196/10154.

Dataset Information

Identification of Common Neural Circuit Disruptions in Cognitive Control Across Psychiatric Disorders.

Publications

Identification of Common Neural Circuit Disruptions in Cognitive Control Across Psychiatric Disorders.

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