scholarly journals Neocortical substrates of feelings evoked with music in the ACC, insula, and somatosensory cortex

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Stefan Koelsch ◽  
Vincent K. M. Cheung ◽  
Sebastian Jentschke ◽  
John-Dylan Haynes

AbstractNeurobiological models of emotion focus traditionally on limbic/paralimbic regions as neural substrates of emotion generation, and insular cortex (in conjunction with isocortical anterior cingulate cortex, ACC) as the neural substrate of feelings. An emerging view, however, highlights the importance of isocortical regions beyond insula and ACC for the subjective feeling of emotions. We used music to evoke feelings of joy and fear, and multivariate pattern analysis (MVPA) to decode representations of feeling states in functional magnetic resonance (fMRI) data of n = 24 participants. Most of the brain regions providing information about feeling representations were neocortical regions. These included, in addition to granular insula and cingulate cortex, primary and secondary somatosensory cortex, premotor cortex, frontal operculum, and auditory cortex. The multivoxel activity patterns corresponding to feeling representations emerged within a few seconds, gained in strength with increasing stimulus duration, and replicated results of a hypothesis-generating decoding analysis from an independent experiment. Our results indicate that several neocortical regions (including insula, cingulate, somatosensory and premotor cortices) are important for the generation and modulation of feeling states. We propose that secondary somatosensory cortex, which covers the parietal operculum and encroaches on the posterior insula, is of particular importance for the encoding of emotion percepts, i.e., preverbal representations of subjective feeling.

2019 ◽  
Vol 316 (5) ◽  
pp. G615-G622
Author(s):  
Patrick Sanvanson ◽  
Zhixin Li ◽  
Ling Mei ◽  
Venelin Kounev ◽  
Mark Kern ◽  
...  

Esophageal acid sensory signals are transmitted by both vagal and spinal pathways to the cerebral cortex. The influence and interplay of these pathways on esophageal acid-related functional connectivity has been elusive. Our aim was to evaluate the esophageal acid exposure-related effect on the anterior cingulate cortex (ACC) functional connectivity networks using functional MRI-guided functional connectivity MRI (fcMRI) analysis. We studied six Sprague-Dawley rats for fcMRI experiments under dexmedetomidine hydrochloride anesthesia. Each rat was scanned for 6 min before and after esophageal hydrochloric acid infusion (0.1 N, 0.2 ml/min). The protocol was repeated before and after bilateral cervical vagotomy on the same rat. Seed-based fcMRI analysis was used to examine ACC networks and acid-induced network alterations. Three-factor repeated-measures ANOVA analysis among all four subgroups revealed that the interaction of acid infusion and bilateral vagotomy was mainly detected in the hypothalamus, insula, left secondary somatosensory cortex, left parietal cortex, and right thalamus in the left ACC network. In the right ACC network, this interaction effect was detected in the caudate putamen, insula, motor, primary somatosensory cortex, secondary somatosensory cortex, and thalamic regions. These regions in the ACC networks showed decreased intranetwork connectivity due to acid infusion. However, after bilateral vagotomy, intranetwork connectivity strength inversed and became stronger following postvagotomy acid infusion. Signals transmitted through both the vagal nerve and spinal nerves play a role in esophageal acid-related functional connectivity of the ACC. The vagal signals appear to dampen the acid sensation-related functional connectivity of the ACC networks. NEW & NOTEWORTHY These studies show that esophageal acid-induced brain functional connectivity changes are vagally mediated and suggest that signals transmitted through both the vagal nerve and spinal nerves play a role in esophageal acid-related functional connectivity of the anterior cingulate cortex. This paper focuses on the development of a novel rat functional MRI model fostering improved understanding of acid-related esophageal disorders.


Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 230-230 ◽  
Author(s):  
Shaheen Ahmed ◽  
Sven Vanneste

Abstract INTRODUCTION Minimally invasive neuromodulation such as spinal cord stimulation (SCS) and occipital nerve stimulation (ONS) have shown to be successful for treatment of different types of pain such as chronic back or leg pain, complex regional pain syndrome (CRPS), and fibromyalgia. Recently, novel stimulation paradigm called burst stimulation was developed that suppresses pain to better extent than classical tonic stimulation. From clinical point of view, burst stimulation is very promising; however, little is known about its underlying mechanism. Hence, in this work we investigate mechanism of action for burst stimulation in different patient groups and controls using different neuroimaging multimodalities such as EEG, fMRI and PET. METHODS Control subjects and patients with chronic back or leg pain, CRPS, or fibromyalgia enrolled for study. Both controls and patients received SCS or ONS and sham, tonic, and burst stimulation in fMRI, PET, and EEG. RESULTS >EEG shows significant changes for burst stimulation compared to tonic and sham stimulation; evident by increased activity at dorsal anterior cingulate cortex (dACC), dorsolateral prefrontal cortex (dPFC), primary somatosensory cortex, and posterior cingulate cortex (PSC) in alpha frequency band. PET further confirmed by showing increased tracer capitation for burst in dACC, pregenual anterior cingulate cortex (pgACC), parahippocampus, and fusiform gyrus. Furthermore, fMRI showed burst changes in dACC, dPFC, pgACC, cerebellum, hypothalamus, and premotor cortex. A conjunction analysis between tonic and burst stimulation demonstrated theta activity is commonly modulated in somatosensory cortex and PSC. CONCLUSION Our data suggest that burst and tonic stimulation modulate ascending lateral and descending pain inhibitory pathways. Burst stimulation adds by modulating the medial pain pathway, possibly by direct modulation of spinothalamic pathway, as suggested by animal research. Burst normalizes an imbalance between ascending pain via medial system and descending pain inhibitory activity, which could be a plausible reason it's better than to tonic stimulation.


1999 ◽  
Vol 82 (4) ◽  
pp. 1934-1943 ◽  
Author(s):  
Robert C. Coghill ◽  
Christine N. Sang ◽  
Jose Ma. Maisog ◽  
Michael J. Iadarola

Functional imaging studies of human subjects have identified a diverse assortment of brain areas that are engaged in the processing of pain. Although many of these brain areas are highly interconnected and are engaged in multiple processing roles, each area has been typically considered in isolation. Accordingly, little attention has been given to the global functional organization of brain mechanisms mediating pain processing. In the present investigation, we have combined positron emission tomography with psychophysical assessment of graded painful stimuli to better characterize the multiregional organization of supraspinal pain processing mechanisms and to identify a brain mechanism subserving the processing of pain intensity. Multiple regression analysis revealed statistically reliable relationships between perceived pain intensity and activation of a functionally diverse group of brain regions, including those important in sensation, motor control, affect, and attention. Pain intensity–related activation occurred bilaterally in the cerebellum, putamen, thalamus, insula, anterior cingulate cortex, and secondary somatosensory cortex, contralaterally in the primary somatosensory cortex and supplementary motor area, and ipsilaterally in the ventral premotor area. These results confirm the existence of a highly distributed, bilateral supraspinal mechanism engaged in the processing of pain intensity. The conservation of pain intensity information across multiple, functionally distinct brain areas contrasts sharply with traditional views that sensory-discriminative processing of pain is confined within the somatosensory cortex and can account for the preservation of conscious awareness of pain intensity after extensive cerebral cortical lesions.


2019 ◽  
Vol 29 ◽  
pp. S141-S142
Author(s):  
L. Herrmann ◽  
V. Kasties ◽  
Y. Fan ◽  
L. Danyeli ◽  
T. Tar ◽  
...  

2021 ◽  
Author(s):  
Ting-Peng Liang ◽  
Yuwen Li ◽  
Nai-Shing Yen ◽  
Ofir Turel ◽  
Sen-Mou Hsu

Abstract Background: Escalation of commitment is a common bias in human decision making. The present study examined (1) differences in neural recruitment for escalation and de-escalation decisions of prior investments, and (2) how the activations of these brain networks are modulated by two factors that are often argued to modulate the behavior: (i) self-responsibility, and (ii) framing of the success probabilities. Results: Imaging data were obtained from functional magnetic resonance imaging (fMRI) applied to 29 participants. A whole-brain analysis was conducted to compare brain activations between conditions. ROI analysis, then, was used to examine if these significant activations were modulated by two contextual factors. Finally, mediation analysis was applied to explore how the contextual factors affect escalation decisions through brain activations. The findings showed that (1) escalation decisions are faster than de-escalation decisions, (2) the corresponding network of brain regions recruited for escalation (anterior cingulate cortex, insula and precuneus) decisions differs from this recruited for de-escalation decisions (inferior and superior frontal gyri), (3) the switch from escalation to de-escalation is primarily frontal gyri dependent, and (4) activation in the anterior cingulate cortex, insula and precuneus were further increased in escalation decisions, when the outcome probabilities of the follow-up investment were positively framed; and activation in the inferior and superior frontal gyri in de-escalation decisions were increased when the outcome probabilities were negatively framed. Conclusions: Escalation and de-escalation decisions recruit different brain regions. Framing of possible outcomes as negative leads to escalation decisions through recruitment of the inferior frontal gyrus. Responsibility for decisions affects escalation decisions through recruitment of the superior (inferior) gyrus, when the decision is framed positively (negatively).


2020 ◽  
pp. 1-13 ◽  
Author(s):  
Guang-Heng Dong ◽  
Min Wang ◽  
Hui Zheng ◽  
Ziliang Wang ◽  
Xiaoxia Du ◽  
...  

Abstract Background Studies of Internet gaming disorder (IGD) suggest an imbalanced relationship between cognitive control and reward processing in people with IGD. However, it remains unclear how these two systems interact with each other, and whether they could serve as neurobiological markers for IGD. Methods Fifty IGD subjects and matched individuals with recreational game use (RGU) were selected and compared when they were performing a cue-craving task. Regions of interests [anterior cingulate cortex (ACC), lentiform nucleus] were selected based on the comparison between brain responses to gaming-related cues and neutral cues. Directional connectivities among these brain regions were determined using Bayesian estimation. We additionally examined the posterior cingulate cortex (PCC) in a separate analysis based on data implicating the PCC in craving in addiction. Results During fixed-connectivity analyses, IGD subjects showed blunted ACC-to-lentiform and lentiform-to-ACC connectivity relative to RGU subjects, especially in the left hemisphere. When facing gaming cues, IGD subjects trended toward lower left-hemispheric modulatory effects in ACC-to-lentiform connectivity than RGU subjects. Self-reported cue-related craving prior to scanning correlated inversely with left-hemispheric modulatory effects in ACC-to-lentiform connectivity. Conclusions The results suggesting that prefrontal-to-lentiform connectivity is impaired in IGD provides a possible neurobiological mechanism for difficulties in controlling gaming-cue-elicited cravings. Reduced connectivity ACC-lentiform connectivity may be a useful neurobiological marker for IGD.


2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Zitong Xu ◽  
JunFan Fang ◽  
Xuaner Xiang ◽  
HaiJu Sun ◽  
SiSi Wang ◽  
...  

Objective. Electroacupuncture (EA) is reported effective in alleviating pain-related emotion; however, the underlying mechanism of its effects still needs to be elucidated. The NPS-NPSR system has been validated for the involvement in the modulation of analgesia and emotional behavior. Here, we aimed to investigate the role of the NPS-NPSR system in the anterior cingulate cortex (ACC), hypothalamus, and central amygdala (CeA) in the use of EA to relieve affective pain modeled by complete Freund’s adjuvant- (CFA-) evoked conditioned place aversion (C-CPA). Materials and Methods. CFA injection combined with a CPA paradigm was introduced to establish the C-CPA model, and the elevated O-maze (EOM) was used to test the behavioral changes after model establishment. We further explored the expression of NPS and NPSR at the protein and gene levels in the brain regions of interest by immunofluorescence staining and quantitative real-time PCR. Results. We observed that EA stimulation delivered to the bilateral Zusanli (ST36) and Kunlun (BL60) acupoints remarkably inhibited sensory pain, pain-evoked place aversion, and anxiety-like behavior. The current study showed that EA significantly enhanced the protein expression of this peptide system in the ACC and hypothalamus, while the elevated expression of NPSR protein alone was just confined to the affected side in the CeA. Moreover, EA remarkably upregulated the mRNA expression of NPS in CeA, ACC, and hypothalamus and NPSR mRNA in the hypothalamus and CeA. Conclusions. These data suggest the effectiveness of EA in alleviating affective pain, and these benefits may at least partially be attributable to the upregulation of the NPS-NPSR system in the ACC and hypothalamus.


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