Neural correlates of prediction error in patients with schizophrenia: evidence from an fMRI meta-analysis.

Abnormal processes of learning from prediction errors, i.e. the discrepancies between expectations and outcomes, are thought to underlie motivational impairments in schizophrenia. Although dopaminergic abnormalities in the mesocorticolimbic reward circuit have been found in patients with schizophrenia, the pathway through which prediction error signals are processed in schizophrenia has yet to be elucidated. To determine the neural correlates of prediction error processing in schizophrenia, we conducted a meta-analysis of whole-brain neuroimaging studies that investigated prediction error signal processing in schizophrenia patients and healthy controls. A total of 14 studies (324 schizophrenia patients and 348 healthy controls) using the reinforcement learning paradigm were included. Our meta-analysis showed that, relative to healthy controls, schizophrenia patients showed increased activity in the precentral gyrus and middle frontal gyrus and reduced activity in the mesolimbic circuit, including the striatum, thalamus, amygdala, hippocampus, anterior cingulate cortex, insula, superior temporal gyrus, and cerebellum, when processing prediction errors. We also found hyperactivity in frontal areas and hypoactivity in mesolimbic areas when encoding prediction error signals in schizophrenia patients, potentially indicating abnormal dopamine signaling of reward prediction error and suggesting failure to represent the value of alternative responses during prediction error learning and decision making.

The differential neural substrates for reward choice under gain-loss contexts and risk in alcohol use disorder: Evidence from a voxel-based meta-analysis.

BACKGROUND: Making a risky decision is a complex process that involves the evaluation of both the values of the options and the associated risk level; this process is distinct from reward processing in gain versus loss contexts. Although disrupted reward processing in mesolimbic dopamine circuitry is suggested to underlie pathological incentive processing in patients with alcohol use disorder (AUD), the differential neural processes subserving these motivational tendencies for risk situations or gain/loss choices in decision-making have not been identified. METHODS: To examine the common or distinct neural mechanisms in the evaluation of risk versus outcomes for AUD, we conducted two separate coordinate-based meta-analyses of functional neuroimaging studies by using Seed-Based d Mapping software to evaluate 13 studies investigating gain and loss processing and 10 studies investigating risky decision-making. RESULTS: During gain and loss processing, relative to healthy controls, AUD patients showed reduced activation in the mesocortical-limbic circuit, including the orbital prefrontal cortex (OFC), dorsal striatum, insula, hippocampus, cerebellum, cuneus cortex and superior temporal gyrus, but hyperactivation in the inferior temporal gyrus and paracentral lobule (extending to the middle cingulate cortex (MCC) and precuneus). During decision-making under risk, AUD patients exhibited hypoactivity of the prefrontal and cingulate cortices, including the posterior cingulate cortex (extending to the MCC), middle frontal gyrus, medial prefrontal cortex, dorsolateral prefrontal cortex, OFC and anterior cingulate cortex. CONCLUSIONS: Our results extend existing neurological evidence by showing that a reduced response in the mesocortical-limbic circuit is found in gain versus loss processing, with decreased responsivity in cortical regions in risk decision-making. Our results implicate dissociable neural circuit responses for gain-loss processing and risk decision-making, which contribute to a better understanding of the pathophysiological mechanism underlying nondrug incentive and risk processing in individuals with AUD.

The brain activity pattern in alcohol-use disorders under inhibition response Task.

BACKGROUND: Inhibitory control impairment in alcohol use disorder (AUD) may indicate detrimental effects of chronic alcohol use on different functional systems in the brain, but the current studies lack consistency. This study aims to identify the most consistent response inhibition-related brain dysfunction based on existing data. METHODS: We performed systematic searches of the PubMed, Embase, Web of Science, and PsychINFO databases for available studies. Anisotropic effect-size signed differential mapping was used to quantitatively analyze the differences in response inhibition-related brain activation between AUD patients and HCs. Meta regression was used to explore the relationship between brain alterations and clinical variables. RESULTS: The brain hypoactivation or hyperactivation in AUD patients compared with HCs during the response inhibition tasks was mainly located in the prefrontal cortex including the superior frontal gyrus, inferior frontal gyrus, and middle frontal gyrus, anterior cingulate gyrus (ACC), superior temporal gyrus, occipital gyrus, and somatosensory areas including postcentral gyrus and supramarginal gyrus. The meta-regression revealed that older patients were more likely to present activation in the left superior frontal gyrus when performing the response inhibition tasks. CONCLUSIONS: The response inhibitive dysfunctions in a distinct prefrontal-cingulate cortices may presumably reflect the core impairment in cognitive control abilities. Dysfunction in the occipital gyrus and somatosensory areas may indicate an abnormal motor-sensory and visual function in AUD. Such functional abnormalities may represent neurophysiological correlates of the executive deficits observed in AUD patients. This study has been registered in PROSPERO (number CRD42022339384).

A Meta-Analysis of Neural Correlates of Reward Anticipation in Individuals at Clinical Risk for Schizophrenia.

BACKGROUND: Aberrant striatal responses to reward anticipation have been observed in schizophrenia. However, it is unclear whether these dysfunctions predate the onset of psychosis and whether reward anticipation is impaired in individuals at clinical high risk for schizophrenia (CHR). METHODS: To examine the neural correlates of monetary anticipation in the prodromal phase of schizophrenia, we performed a whole-brain meta-analysis of 13 functional neuroimaging studies that compared reward anticipation signals between CHR individuals and healthy controls (HC). Three databases (PubMed, Web of Science, and ScienceDirect) were systematically searched from January 1, 2000, to May 1, 2022. RESULTS: Thirteen whole-brain functional magnetic resonance imaging studies including 318 CHR individuals and 426 HC were identified through comprehensive literature searches. Relative to HC, CHR individuals showed increased brain responses in the medial prefrontal cortex and anterior cingulate cortex and decreased activation in the mesolimbic circuit, including the putamen, parahippocampal gyrus, insula, cerebellum, and supramarginal gyrus, during reward anticipation. CONCLUSIONS: Our findings in the CHR group confirmed the existence of abnormal motivational-related activation during reward anticipation, thus demonstrating the pathophysiological characteristics of the risk populations. These results have the potential to lead to the early identification and more accurate prediction of subsequent psychosis as well as a deeper understanding of the neurobiology of high-risk state of psychotic disorder.

A meta-analysis of the neural substrates of monetary reward anticipation and outcome in alcohol use disorder.

The capacity to anticipate and detect rewarding outcomes is fundamental for the development of adaptive decision-making and goal-oriented behavior. Delineating the neural correlates of different stages of reward processing is imperative for understanding the neurobiological mechanism underlying alcohol use disorder (AUD). To examine the neural correlates of monetary anticipation and outcome in AUD patients, we performed two separate voxel-wise meta-analyses of functional neuroimaging studies, including 12 studies investigating reward anticipation and 7 studies investigating reward outcome using the monetary incentive delay task. During the anticipation stage, AUD patients displayed decreased activation in response to monetary cues in mesocortical-limbic circuits and sensory areas, including the ventral striatum (VS), insula, hippocampus, inferior occipital gyrus, supramarginal gyrus, lingual gyrus and fusiform gyrus. During the outcome stage, AUD patients exhibited reduced activation in the dorsal striatum, VS and insula, and increased activation in the orbital frontal cortex and medial temporal area. Our findings suggest that different activation patterns are associated with nondrug rewards during different reward processing stages, potentially reflecting a changed sensitivity to monetary reward in AUD.

Neural substrates of reward anticipation and outcome in schizophrenia: a meta-analysis of fMRI findings in the monetary incentive delay task.

Dysfunction of the mesocorticolimbic dopaminergic reward system is a core feature of schizophrenia (SZ), yet its precise contributions to different stages of reward processing and their relevance to disease symptomology are not fully understood. We performed a coordinate-based meta-analysis, using the monetary incentive delay task, to identify which brain regions are implicated in different reward phases in functional magnetic resonance imaging in SZ. A total of 17 studies (368 SZ and 428 controls) were included in the reward anticipation, and 10 studies (229 SZ and 281 controls) were included in the reward outcome. Our meta-analysis revealed that during anticipation, patients showed hypoactivation in the striatum, anterior cingulate cortex, median cingulate cortex (MCC), amygdala, precentral gyrus, and superior temporal gyrus compared with controls. Striatum hypoactivation was negatively associated with negative symptoms and positively associated with the proportion of second-generation antipsychotic users (percentage of SGA users). During outcome, patients displayed hyperactivation in the striatum, insula, amygdala, hippocampus, parahippocampal gyrus, cerebellum, postcentral gyrus, and MCC, and hypoactivation in the dorsolateral prefrontal cortex (DLPFC) and medial prefrontal cortex (mPFC). Hypoactivity of mPFC during outcome was negatively associated with positive symptoms. Moderator analysis showed that the percentage of SGA users was a significant moderator of the association between symptom severity and brain activity in both the anticipation and outcome stages. Our findings identified the neural substrates for different reward phases in SZ and may help explain the neuropathological mechanisms underlying reward processing deficits in the disorder.

Neurofunctional mapping of reward anticipation and outcome for major depressive disorder: a voxel-based meta-analysis.

Aberrations in how people form expectations about rewards and how they respond to receiving rewards are thought to underlie major depressive disorder (MDD). However, the underlying mechanism linking the appetitive reward system, specifically anticipation and outcome, is still not fully understood. To examine the neural correlates of monetary anticipation and outcome in currently depressed subjects with MDD, we performed two separate voxel-wise meta-analyses of functional neuroimaging studies using the monetary incentive delay task. During reward anticipation, the depressed patients exhibited an increased response in the bilateral middle cingulate cortex (MCC) extending to the anterior cingulate cortex, the medial prefrontal cortex, the left inferior frontal gyrus (IFG), and the postcentral gyrus, but a reduced response in the mesolimbic circuit, including the left striatum, insula, amygdala, right cerebellum, striatum, and IFG, compared to controls. During the outcome stage, MDD showed higher activity in the left inferior temporal gyrus, and lower activity in the mesocortical pathway, including the bilateral MCC, left caudate nucleus, precentral gyrus, thalamus, cerebellum, right striatum, insula, IFG, middle frontal gyrus, and temporal pole. Our findings suggest that cMDD may be characterised by state-dependent hyper-responsivity in cortical regions during the anticipation phase, and hypo-responsivity of the mesocortico-limbic circuit across the two phases of the reward response. Our study showed dissociable neural circuit responses to monetary stimuli during reward anticipation and outcome, which help to understand the dysfunction in different aspects of reward processing, particularly motivational v. hedonic deficits in depression.

Cases report: MRI findings of asymptomatically familial subependymal heterotopia with filamin A gene abnormality.

Subependymal heterotopia (SEH) is a rare neuronal migration disorder consisting of gray matter nodules along the lateral ventricular walls and is often associated with other brain malformations. Despite most SEH cases showing epilepsy during their lifetimes, very few patients with asymptomatically familial SEH tend to cause misdiagnosis or missed diagnosis. We present four familial SEH cases without any positive symptoms and medical history, including two fetuses, who were diagnosed by MRI and confirmed by genetic testing with mutation of filamin A. This report emphasizes the role of MRI in the recognition of SEH at an early age of gestation and in asymptomatically familial SEH. MRI provides a fast, repeatable, reliable, and cheap choice for detecting and screening familial SEH.

Voxel-Wise Quantitative Mapping of the Brain Association Ability.

The association cortices of the brain are essential for integrating multimodal information that subserves complex and high-order cognitive functions. To delineate the changing pattern of associative cortices can provide critical insight into brain development, aging, plasticity, and disease-triggered functional abnormalities. However, how to quantitatively characterize the association capability of the brain is elusive. Here, we developed a new method of association index (Asso) at the voxel level to quantitatively characterize the brain association ability. Using the Asso method, we found high Asso values in association cortical networks, and low values in visual and limbic networks, suggesting a pattern of significant gradient distribution in neural functions. The spatial distribution patterns of Asso show high similarities across different thresholds suggesting that Asso mapping is a threshold-free method. In addition, compared with functional connectivity strength, i.e., degree centrality method, Asso mapping showed different patterns for association cortices and primary cortices. Finally, the Asso method was applied to investigate aging effects and identified similar findings with previous studies. All these results indicated that Asso can characterize the brain association patterns effectively and open a new avenue to reveal a neural basis for development, aging, and brain disorders.

Neurobiological correlates of cue-reactivity in alcohol-use disorders: A voxel-wise meta-analysis of fMRI studies.

Altered brain responses to alcohol-associated stimuli are a neural hallmark of alcohol-use disorder (AUD) and a promising target for pharmacotherapy. However, findings in cue-reactivity based functional MRI (fMRI) studies are inconclusive. To investigate the neural substrates of cue-reactivity and their relevance to treatment outcomes, alcohol craving and relapse in AUD patients, we performed five meta-analyses using signed differential mapping software. Our meta-analysis revealed that alcohol cues evoke greater cue-reactivity than neutral cues in the mesocorticolimbic circuit and lower reactivity in the parietal and temporal regions in AUD patients. Compared to controls, AUD individuals displayed hyperactivations in the medial prefrontal cortex and anterior/middle part of the cingulate cortex. After receiving AUD treatment, AUD patients exhibited greater activations in the precentral gyrus but reduced activations in the bilateral caudate nucleus, insula, right DLPFC, and left superior frontal gyrus. No significant results were found in cue-reactivity correlates of alcohol craving and relapse. Our results implicate cue-induced abnormalities in corticostriatal-limbic circuits may underline the pathophysiology of AUD, and have translational value for treatment development.

Cerebral Regional Homogeneity Alternation of Pregnant Women With Antenatal Depression During the Pandemic.

Purpose: The COVID-19 epidemic has been a threat to the health of people all over the world. Various precautions during COVID-19 in China have kept a large number of people in isolation, and this has inconvenienced and placed enormous stress on pregnant women. Pregnant women are more likely to suffer from antenatal depression (ANDP) with social isolation or low social support. This research aims to investigate the neurobiological mechanisms underlying ANDP, which impedes early detection and intervention in this disorder. Methods: A total of 43 singleton pregnant women who experienced isolation were recruited, including 21 treatment-naïve ANDP patients and 22 healthy pregnant women (HPW). To explore the intrinsic cerebral activity alternations in ANDP using resting-state functional MRI (rsfMRI), we assessed the local regional homogeneity (ReHo) differences in two groups using the voxel-based whole-brain analysis. The correlation between the regional functional abnormalities and clinical variables in ANDP patients was also examined. Results: Compared with HPW, ANDP patients showed decreased ReHo in the left dorsolateral prefrontal cortex, right insular and the cluster coving the right ventral temporal cortex (VTC), amygdala (AMG), and hippocampus (HIP). The Edinburgh Postnatal Depression Scale (EPDS) scores of ANDP patients negatively correlated with the ReHo in the right VTC, AMG, and HIP. Conclusion: Elucidating the neurobiological features of ANDP patients during COVID-19 is crucial for evolving adequate methods for early diagnosis, precaution, and intervention in a future epidemic.

Default mode network and frontolimbic gray matter abnormalities in patients with borderline personality disorder: A voxel-based meta-analysis.

Specific frontolimbic abnormalities are hypothesized to underlie the etiology of borderline personality disorder (BPD). However, findings from neuroimaging studies were inconsistent. In the current study, we aimed to provide a complete overview of cerebral microstructural alterations in gray matter (GM) of BPD patients. A total of 11 studies were enrolled, comprising 275 BPD patients and 290 healthy controls (HCs). A meta-analysis was conduct to quantitatively estimate regional GM abnormalities in BPD patients using the seed-based d mapping (SDM). Meta-regression was also conducted. Compared with HCs, the BPD patients exhibited increased GM mainly in bilateral supplementary motor area extending to right posterior cingulated cortex (PCC) and bilateral primary motor cortex, right middle frontal gyrus (MFG), and the bilateral precuneus extending to bilateral PCC. Decreased GM was identified in bilateral middle temporal gyri, right inferior frontal gyrus extending to right insular, left hippocampus and left superior frontal gyrus extending to left medial orbitofrontal cortex. The mean age of BPD patients were found nagativly associated with GM alterations in right MFG. Our findings suggested that BPD patients have significantly GM abnormalities in the default mode network and frontolimbic circuit. Our results provided further evidences in elucidating the underline neural mechanisms of BPD.

Cortical and subcortical gray matter shrinkage in alcohol-use disorders: a voxel-based meta-analysis.

Although gray matter (GM) damages caused by long term and excessive alcohol consumption have long been reported, the structural neuroimaging findings on alcohol-use disorders (AUD) are inconsistent. The aim of this study was to conduct a meta-analysis, using a novel voxel-based meta-analytic method effect-size signed differential mapping (ES-SDM), to characterize GM changes in AUD patients. Twelve studies including 433 AUD patients and 498 healthy controls (HCs) were retrieved. The AUD group demonstrated significant GM reductions in the corticostriatal-limbic circuits, including bilateral insula, superior temporal gyrus, striatum, dorsal lateral prefrontal cortex (DLPFC), precentral gyrus, anterior cingulate cortex (ACC), left thalamus and right hippocampus compared to HCs. GM reduction in the right striatum is significantly negatively related to duration of alcohol dependence, while GM shrinkage of the left superior, middle frontal gyrus, and left thalamus is related to lifetime alcohol consumption. The findings demonstrate that the GM abnormalities caused by AUD are in corticostriatal-limbic circuits whose dysfunctions may involve in craving and observed functional deficits.