Transient and sustained BOLD signal time courses affect the detection of emotion-related brain activation in fMRI

NeuroImage ◽  
2014 ◽  
Vol 103 ◽  
pp. 522-532 ◽  
Author(s):  
Christian Paret ◽  
Rosemarie Kluetsch ◽  
Matthias Ruf ◽  
Traute Demirakca ◽  
Raffael Kalisch ◽  
...  
Author(s):  
Dimitra Flouri ◽  
Daniel Lesnic ◽  
Constantina Chrysochou ◽  
Jehill Parikh ◽  
Peter Thelwall ◽  
...  

Abstract Introduction Model-driven registration (MDR) is a general approach to remove patient motion in quantitative imaging. In this study, we investigate whether MDR can effectively correct the motion in free-breathing MR renography (MRR). Materials and methods MDR was generalised to linear tracer-kinetic models and implemented using 2D or 3D free-form deformations (FFD) with multi-resolution and gradient descent optimization. MDR was evaluated using a kidney-mimicking digital reference object (DRO) and free-breathing patient data acquired at high temporal resolution in multi-slice 2D (5 patients) and 3D acquisitions (8 patients). Registration accuracy was assessed using comparison to ground truth DRO, calculating the Hausdorff distance (HD) between ground truth masks with segmentations and visual evaluation of dynamic images, signal-time courses and parametric maps (all data). Results DRO data showed that the bias and precision of parameter maps after MDR are indistinguishable from motion-free data. MDR led to reduction in HD (HDunregistered = 9.98 ± 9.76, HDregistered = 1.63 ± 0.49). Visual inspection showed that MDR effectively removed motion effects in the dynamic data, leading to a clear improvement in anatomical delineation on parametric maps and a reduction in motion-induced oscillations on signal-time courses. Discussion MDR provides effective motion correction of MRR in synthetic and patient data. Future work is needed to compare the performance against other more established methods.


2000 ◽  
Vol 44 (1) ◽  
pp. 137-143 ◽  
Author(s):  
Wen-Ming Luh ◽  
Eric C. Wong ◽  
Peter A. Bandettini ◽  
B. Douglas Ward ◽  
James S. Hyde

1998 ◽  
Vol 16 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Alistair M. Howseman ◽  
David A. Porter ◽  
Chloe Hutton ◽  
Oliver Josephs ◽  
Robert Turner

2020 ◽  
Author(s):  
M.E. Hoeppli ◽  
H. Nahman-Averbuch ◽  
W.A. Hinkle ◽  
E. Leon ◽  
J. Peugh ◽  
...  

AbstractPain is a uniquely individual experience. Previous studies have highlighted changes in brain activation and morphology associated with inter- and intra-individual pain perception. In this study we sought to characterize brain mechanisms associated with individual differences in pain in a large sample of healthy participants (N = 101). Pain ratings varied widely across individuals. Moreover, individuals reported changes in pain evoked by small differences in stimulus intensity in a manner congruent with their pain sensitivity, further supporting the utility of subjective reporting as a measure of the true individual experience. However, brain activation related to inter-individual differences in pain was not detected, despite clear sensitivity of the BOLD signal to small differences in noxious stimulus intensities within individuals. These findings raise questions about the utility of fMRI as an objective measure to infer reported pain intensity.


2017 ◽  
Author(s):  
S. Saalasti ◽  
J. Alho ◽  
J.M. Lahnakoski ◽  
M. Bacha-Trams ◽  
E. Glerean ◽  
...  

ABSTRACTOnly a few of us are skilled lipreaders while most struggle at the task. To illuminate the poorly understood neural substrate of this variability, we estimated the similarity of brain activity during lipreading, listening, and reading of the same 8-min narrative with subjects whose lipreading skill varied extensively. The similarity of brain activity was estimated by voxel-wise comparison of the BOLD signal time courses. Inter-subject correlation of the time courses revealed that lipreading and listening are supported by the same brain areas in temporal, parietal and frontal cortices, precuneus and cerebellum. However, lipreading activated only a small part of the neural network that is active during listening/reading the narrative, demonstrating that neural processing during lipreading vs. listening/reading differs substantially. Importantly, skilled lipreading was specifically associated with bilateral activity in the superior and middle temporal cortex, which also encode auditory speech. Our novel results both confirm previous results from few previous studies using isolated speech segments as stimuli but also extend in an important way understanding of neural mechanisms of lipreading.


2014 ◽  
Vol 4 (1) ◽  
pp. 6 ◽  
Author(s):  
Stephanie Boehme ◽  
Alexander Mohr ◽  
Michael PI Becker ◽  
Wolfgang HR Miltner ◽  
Thomas Straube

1998 ◽  
Vol 80 (6) ◽  
pp. 3312-3320 ◽  
Author(s):  
Carlo A. Porro ◽  
Valentina Cettolo ◽  
Maria Pia Francescato ◽  
Patrizia Baraldi

Porro, Carlo A., Valentina Cettolo, Maria Pia Francescato, and Patrizia Baraldi. Temporal and intensity coding of pain in human cortex. J. Neurophysiol. 80:3312–3320, 1998. We used a high-resolution functional magnetic resonance imaging (fMRI) technique in healthy right-handed volunteers to demonstrate cortical areas displaying changes of activity significantly related to the time profile of the perceived intensity of experimental somatic pain over the course of several minutes. Twenty-four subjects (ascorbic acid group) received a subcutaneous injection of a dilute ascorbic acid solution into the dorsum of one foot, inducing prolonged burning pain (peak pain intensity on a 0–100 scale: 48 ± 3, mean ± SE; duration: 11.9 ± 0.8 min). fMRI data sets were continuously acquired for ∼20 min, beginning 5 min before and lasting 15 min after the onset of stimulation, from two sagittal planes on the medial hemispheric wall contralateral to the stimulated site, including the cingulate cortex and the putative foot representation area of the primary somatosensory cortex (SI). Neural clusters whose fMRI signal time courses were positively or negatively correlated ( P < 0.0005) with the individual pain intensity curve were identified by cross-correlation statistics in all 24 volunteers. The spatial extent of the identified clusters was linearly related ( P < 0.0001) to peak pain intensity. Regional analyses showed that positively correlated clusters were present in the majority of subjects in SI, cingulate, motor, and premotor cortex. Negative correlations were found predominantly in medial parietal, perigenual cingulate, and medial prefrontal regions. To test whether these neural changes were due to aspecific arousal or emotional reactions, related either to anticipation or presence of pain, fMRI experiments were performed with the same protocol in two additional groups of volunteers, subjected either to subcutaneous saline injection (saline: n = 16), inducing mild short-lasting pain (peak pain intensity 23 ± 4; duration 2.8 ± 0.6 min) or to nonnoxious mechanical stimulation of the skin (controls: n = 16) at the same body site. Subjects did not know in advance which stimulus would occur. The spatial extent of neural clusters whose signal time courses were positively or negatively correlated with the mean pain intensity curve of subjects injected with ascorbic acid was significantly larger ( P < 0.001) in the ascorbic acid group than both saline and controls, suggesting that the observed responses were specifically related to pain intensity and duration. These findings reveal distributed cortical systems, including parietal areas as well as cingulate and frontal regions, involved in dynamic encoding of pain intensity over time, a process of great biological and clinical relevance.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 77-78
Author(s):  
J. Rech ◽  
K. Tascilar ◽  
H. Schenker ◽  
M. Hagen ◽  
M. Sergeeva ◽  
...  

Background:Tumor necrosis factor inhibitors have revolutionized the treatment of rheumatoid arthritis (RA). However, only about 50% of the patients respond well to TNF inhibitors. Therefore, markers that predict response to TNF inhibitors are valuable. Previously we demonstrated that central nervous system (CNS) response to nociceptive stimuli, measured by fMRI of the brain as blood oxygen level dependent (BOLD) signals, decreases already after 24 hours of anti-TNF administration a higher pre-treatment BOLD signal volume seems to predict clinical response to treatment with certolizumabpegol (CZP)1,2. We therefore hypothesized that the baseline volume of BOLD signal in the CNS could predict anti-TNF treatment response.Objectives:To perform a randomized placebo controlled trial in active RA patients to test the effect of TNF inhibition on arthritis induced pain activity in the brain and to test whether patients with high-level RA-related brain activation react differently to TNF-inhibitors than patients with low-level brain activation.Methods:Adult RA patients fulfilling the 2010 ACR/EULAR classification criteria with a DAS28>3.2 receiving stable DMARD treatment for at least 3 months were eligible. Patients underwent the first fMRI at screening measuring BOLD signal upon MCP joint compression and were stratified into low (< 700 units) and high (>700 units) voxel counts. Then patients were randomized to CZP or placebo with a 2:1 ratio. The second and third fMRI were performed after 12 and 24 weeks, respectively. Control stimulation was done by measuring brain activation after non-painful finger tapping.Results:156 RA patients with moderate-to-high disease activity participated in the study. In the finger tapping control, fMRI showed no significant changes in BOLD signal in the CZP-L and CZP-H arms, but a slight but significant decrease (p=0.043) was observed. After joint compression, the CZP-L group showed significant increase in the BOLD signal volume (p=0.043) in fMRI-2 as compared to fMRI-1 with no further significant changes. In contrast, in the CZP-H group, the BOLD signal volume significantly decreased (p=0.037) in fMRI-2 and continued to decrease further, p=0.007. No significant changes were observed in the placebo arm over time.Conclusion:TNF inhibition improves arthritis-related brain activity in the subgroup of RA patients with high baseline BOLD activity in the fMRI.References:[1]Hess, A.et al.PNAS (2011).[2]Rech, J. et al. Arthritis & Rheumatism (2013).Fig 1.BOLD fMRI responses to painful stimulationAcknowledgments:The study was supported by an unrestricted grant of UCB Biopharma SPRL Brussels, BelgiumDisclosure of Interests:Jürgen Rech Consultant of: BMS, Celgene, Novartis, Roche, Chugai, Speakers bureau: AbbVie, Biogen, BMS, Celgene, MSD, Novartis, Roche, Chugai, Pfizer, Lilly, Koray Tascilar: None declared, Hannah Schenker: None declared, Melanie Hagen: None declared, Marina Sergeeva: None declared, Mageshwar Selvakumar: None declared, Laura Konerth: None declared, Jutta Prade: None declared, Sandra Strobelt: None declared, Verena Schönau: None declared, Larissa Valor: None declared, Axel Hueber Grant/research support from: Novartis, Lilly, Pfizer, EIT Health, EU-IMI, DFG, Universität Erlangen (EFI), Consultant of: Abbvie, BMS, Celgene, Gilead, GSK, Lilly, Novartis, Speakers bureau: GSK, Lilly, Novartis, David Simon Grant/research support from: Else Kröner-Memorial Scholarship, Novartis, Consultant of: Novartis, Lilly, Arnd Kleyer Consultant of: Lilly, Gilead, Novartis, Abbvie, Speakers bureau: Novartis, Lilly, Frank Behrens Grant/research support from: Abbvie, Pfizer, Roche, Chugai, Janssen, Consultant of: Abbvie, Pfizer, Roche, Chugai, UCB, BMS, Celgene, MSD, Novartis, Biotest, Janssen, Genzyme, Lilly; Boehringer; Sandoz, Speakers bureau: Abbvie, Pfizer, Roche, Chugai, UCB, BMS, Celgene, MSD, Novartis, Biotest, Janssen, Genzyme, Lilly; Boehringer; Sandoz, Christoph Baerwald Consultant of: CGB received speaker or consulting fees from AbbVie, Paid instructor for: CGB received speaker or consulting fees from AbbVie, Speakers bureau: CGB received speaker or consulting fees from AbbVie, Stephanie Finzel: None declared, Reinhard Voll: None declared, Eugen Feist Consultant of: Novartis, Roche, Sobi, Lilly, Pfizer, Abbvie, BMS, MSD, Sanofi, Speakers bureau: Novartis, Roche, Sobi, Lilly, Pfizer, Abbvie, BMS, MSD, Sanofi, José Antonio P. da Silva Grant/research support from: Pfizer, Abbvie, Consultant of: Pfizer, AbbVie, Roche, Lilly, Novartis, Arnd Doerfler: None declared, Nemanja Damjanov Grant/research support from: from AbbVie, Pfizer, and Roche, Consultant of: AbbVie, Gedeon Richter, Merck, Novartis, Pfizer, and Roche, Speakers bureau: AbbVie, Gedeon Richter, Merck, Novartis, Pfizer, and Roche, Andreas Hess: None declared, Georg Schett Speakers bureau: AbbVie, BMS, Celgene, Janssen, Eli Lilly, Novartis, Roche and UCB


2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Atae Akhrif ◽  
Maximilian J. Geiger ◽  
Marcel Romanos ◽  
Katharina Domschke ◽  
Susanne Neufang

AbstractTranslational studies comparing imaging data of animals and humans have gained increasing scientific interests. With this upcoming translational approach, however, identifying harmonized statistical analysis as well as shared data acquisition protocols and/or combined statistical approaches is necessary. Following this idea, we applied Bayesian Adaptive Regression Splines (BARS), which have until now mainly been used to model neural responses of electrophysiological recordings from rodent data, on human hemodynamic responses as measured via fMRI. Forty-seven healthy subjects were investigated while performing the Attention Network Task in the MRI scanner. Fluctuations in the amplitude and timing of the BOLD response were determined and validated externally with brain activation using GLM and also ecologically with the influence of task performance (i.e. good vs. bad performers). In terms of brain activation, bad performers presented reduced activation bilaterally in the parietal lobules, right prefrontal cortex (PFC) and striatum. This was accompanied by an enhanced left PFC recruitment. With regard to the amplitude of the BOLD-signal, bad performers showed enhanced values in the left PFC. In addition, in the regions of reduced activation such as the parietal and striatal regions, the temporal dynamics were higher in bad performers. Based on the relation between BOLD response and neural firing with the amplitude of the BOLD signal reflecting gamma power and timing dynamics beta power, we argue that in bad performers, an enhanced left PFC recruitment hints towards an enhanced functioning of gamma-band activity in a compensatory manner. This was accompanied by reduced parieto-striatal activity, associated with increased and potentially conflicting beta-band activity.


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