The involvement of parietal and frontal brain areas in the inference of self-agency

2013 ◽  
Author(s):  
Neeltje E. M. van Haren ◽  
Robert A. Renes ◽  
Henk Aarts ◽  
Matthijs Vink
Keyword(s):  
2019 ◽  
Vol 50 (5) ◽  
pp. 799-807 ◽  
Author(s):  
Esther D. A. van Duin ◽  
Jenny Ceccarini ◽  
Jan Booij ◽  
Zuzana Kasanova ◽  
Claudia Vingerhoets ◽  
...  

AbstractBackgroundThe 22q11.2 deletion syndrome (22q11DS) is caused by a deletion on chromosome 22 locus q11.2. This copy number variant results in haplo-insufficiency of the catechol-O-methyltransferase (COMT) gene, and is associated with a significant increase in the risk for developing cognitive impairments and psychosis. The COMT gene encodes an enzyme that primarily modulates clearance of dopamine (DA) from the synaptic cleft, especially in the prefrontal cortical areas. Consequently, extracellular DA levels may be increased in prefrontal brain areas in 22q11DS, which may underlie the well-documented susceptibility for cognitive impairments and psychosis in affected individuals. This study aims to examine DA D2/3 receptor binding in frontal brain regions in adults with 22q11DS, as a proxy of frontal DA levels.MethodsThe study was performed in 14 non-psychotic, relatively high functioning adults with 22q11DS and 16 age- and gender-matched healthy controls (HCs), who underwent DA D2/3 receptor [18F]fallypride PET imaging. Frontal binding potential (BPND) was used as the main outcome measure.ResultsBPND was significantly lower in adults with 22q11DS compared with HCs in the prefrontal cortex and the anterior cingulate gyrus. After Bonferroni correction significance remained for the anterior cingulate gyrus. There were no between-group differences in BPND in the orbitofrontal cortex and anterior cingulate cortex.ConclusionsThis study is the first to demonstrate lower frontal D2/3 receptor binding in adults with 22q11DS. It suggests that a 22q11.2 deletion affects frontal dopaminergic neurotransmission.


2021 ◽  
Author(s):  
Fabio Campanella ◽  
Thomas West ◽  
Corrado Corradi-Dell'Acqua ◽  
Miran Skrap

Extensive neuroimaging literature suggests that understanding others' thoughts and emotions engages a wide network encompassing parietal, temporal and medial frontal brain areas. However, the causal role played by these regions in social inferential abilities is still unclear. Moreover very little is known about ToM deficits in brain tumours and whether potential anatomical substrates are comparable to those identified in fMRI literature. This study evaluated the performance of 105 tumour patients, before and immediately after brain surgery, on a cartoon-based non-verbal task evaluating Cognitive (Intention Attribution) and Affective (Emotion Attribution) ToM, as well as a non-social control condition (Causal Inference). Across multiple analyses, we found converging evidence of a double dissociation between patients with right superior parietal damage, selectively impaired in Intention Attribution, and those with right antero-medial temporal lesion, exhibiting deficits only in Emotion attribution. Instead, patients with damage to the frontal cortex were impaired in all kinds of inferential processes, including those from the non-social control conditions. Overall, our data provides novel reliable causal evidence of segregation between different aspects of the ToM network from both the cognitive and also the anatomical point of view.


2021 ◽  
Vol 164 ◽  
pp. 71-86
Author(s):  
Rob H.J. Van der Lubbe ◽  
Jagna Sobierajewicz ◽  
Marijtje L.A. Jongsma ◽  
Willem B. Verwey ◽  
Anna Przekoracka-Krawczyk

2019 ◽  
Author(s):  
Son Ta Dinh ◽  
Moritz M. Nickel ◽  
Laura Tiemann ◽  
Elisabeth S. May ◽  
Henrik Heitmann ◽  
...  

AbstractChronic pain is a common and severely disabling disease whose treatment is often unsatisfactory. Insights into the brain mechanisms of chronic pain promise to advance the understanding of the underlying pathophysiology and might help to develop disease markers and novel treatments. Here, we systematically and comprehensively exploited the potential of electroencephalography (EEG) to determine abnormalities of brain function during the resting state in chronic pain. To this end, we performed state-of-the-art analyses of oscillatory brain activity, brain connectivity and brain networks in 101 patients of either sex suffering from chronic pain. The results show that global and local measures of brain activity did not differ between chronic pain patients and a healthy control group. However, we observed significantly increased connectivity at theta (4 – 8 Hz) and gamma (> 60 Hz) frequencies in frontal brain areas as well as global network reorganization at gamma frequencies in chronic pain patients. Furthermore, a machine learning algorithm could differentiate between patients and healthy controls with an above-chance accuracy of 57%, mostly based on frontal connectivity. These results implicate increased theta and gamma synchrony in frontal brain areas in the pathophysiology of chronic pain. While substantial challenges concerning accuracy, specificity and validity of potential EEG-based disease markers remain to be overcome, our study identifies abnormal frontal synchrony at theta and gamma frequencies as promising targets for non-invasive brain stimulation and/or neurofeedback approaches.


2015 ◽  
Vol 112 (20) ◽  
pp. E2695-E2704 ◽  
Author(s):  
Franz-Xaver Neubert ◽  
Rogier B. Mars ◽  
Jérôme Sallet ◽  
Matthew F. S. Rushworth

Reward-guided decision-making depends on a network of brain regions. Among these are the orbitofrontal and the anterior cingulate cortex. However, it is difficult to ascertain if these areas constitute anatomical and functional unities, and how these areas correspond between monkeys and humans. To address these questions we looked at connectivity profiles of these areas using resting-state functional MRI in 38 humans and 25 macaque monkeys. We sought brain regions in the macaque that resembled 10 human areas identified with decision making and brain regions in the human that resembled six macaque areas identified with decision making. We also used diffusion-weighted MRI to delineate key human orbital and medial frontal brain regions. We identified 21 different regions, many of which could be linked to particular aspects of reward-guided learning, valuation, and decision making, and in many cases we identified areas in the macaque with similar coupling profiles.


Author(s):  
Patrick Bach ◽  
Rilana Schuster ◽  
Anne Koopmann ◽  
Sabine Vollstaedt-Klein ◽  
Rainer Spanagel ◽  
...  

AbstractRecent studies on the pathophysiology of alcohol dependence suggest a link between peripheral calcium concentrations and alcohol craving. Here, we investigated the association between plasma calcium concentration, cue-induced brain activation, and alcohol craving. Plasma calcium concentrations were measured at the onset of inpatient detoxification in a sample of N = 115 alcohol-dependent patients. Alcohol cue-reactivity was assessed during early abstinence (mean 11.1 days) using a functional magnetic resonance imaging (fMRI) alcohol cue-reactivity task. Multiple regression analyses and bivariate correlations between plasma calcium concentrations, clinical craving measures and neural alcohol cue-reactivity (CR) were tested. Results show a significant negative correlation between plasma calcium concentrations and compulsive alcohol craving. Higher calcium levels predicted higher alcohol cue-induced brain response in a cluster of frontal brain areas, including the dorsolateral prefrontal cortex (dlPFC), the anterior prefrontal cortex (alPFC), and the inferior (IFG) and middle frontal gyri (MFG). In addition, functional brain activation in those areas correlated negatively with craving for alcohol during fMRI. Higher peripheral calcium concentrations during withdrawal predicted increased alcohol cue-induced brain activation in frontal brain areas, which are associated with craving inhibition and cognitive control functions. This might indicate that higher plasma calcium concentrations at onset of detoxification could modulate craving inhibition during early abstinence.Trial registration number: DRKS00003388; date of registration: 14.12.2011.


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