scholarly journals The neural correlates of grandmaternal caregiving

2021 ◽  
Vol 288 (1963) ◽  
Author(s):  
James K. Rilling ◽  
Amber Gonzalez ◽  
Minwoo Lee

In many societies, grandmothers are important caregivers, and grandmaternal investment is often associated with improved grandchild well-being. Here, we present, to our knowledge, the first study to examine grandmaternal brain function. We recruited 50 grandmothers with at least one biological grandchild between 3 and 12 years old. Brain function was measured with functional magnetic resonance imaging as grandmothers viewed pictures of their grandchild, an unknown child, the same-sex parent of the grandchild, and an unknown adult. Grandmothers also completed questionnaires to measure their degree of involvement with and attachment to their grandchild. After controlling for age and familiarity of stimuli, viewing grandchild pictures activated areas involved with emotional empathy (insula and secondary somatosensory cortex) and movement (motor cortex and supplementary motor area). Grandmothers who more strongly activated areas involved with cognitive empathy (temporo-parietal junction and dorsomedial prefrontal cortex) when viewing pictures of the grandchild desired greater involvement in caring for the grandchild. Finally, compared with results from an earlier study of fathers, grandmothers more strongly activated regions involved with emotional empathy (dorsal anterior cingulate cortex, insula and secondary somatosensory cortex), and motivation (nucleus accumbens, ventral pallidum and caudate nucleus). All in all, our findings suggest that emotional empathy may be a key component of grandmaternal responses to their grandchildren.

2019 ◽  
Vol 117 (2) ◽  
pp. 950-958 ◽  
Author(s):  
Yilu Wang ◽  
Jianqiao Ge ◽  
Hanqi Zhang ◽  
Haixia Wang ◽  
Xiaofei Xie

Engaging in altruistic behaviors is costly, but it contributes to the health and well-being of the performer of such behaviors. The present research offers a take on how this paradox can be understood. Across 2 pilot studies and 3 experiments, we showed a pain-relieving effect of performing altruistic behaviors. Acting altruistically relieved not only acutely induced physical pain among healthy adults but also chronic pain among cancer patients. Using functional MRI, we found that after individuals performed altruistic actions brain activity in the dorsal anterior cingulate cortex and bilateral insula in response to a painful shock was significantly reduced. This reduced pain-induced activation in the right insula was mediated by the neural activity in the ventral medial prefrontal cortex (VMPFC), while the activation of the VMPFC was positively correlated with the performer’s experienced meaningfulness from his or her altruistic behavior. Our findings suggest that incurring personal costs to help others may buffer the performers from unpleasant conditions.


2017 ◽  
Vol 30 (1) ◽  
pp. 179-189 ◽  
Author(s):  
Tomer Shechner ◽  
Nathan A. Fox ◽  
Jamie A. Mash ◽  
Johanna M. Jarcho ◽  
Gang Chen ◽  
...  

AbstractBehavioral inhibition (BI) is a temperament identified in early childhood that is associated with risk for anxiety disorders, yet only about half of behaviorally inhibited children manifest anxiety later in life. We compared brain function and behavior during extinction recall in a sample of nonanxious young adults characterized in childhood with BI (n = 22) or with no BI (n = 28). Three weeks after undergoing fear conditioning and extinction, participants completed a functional magnetic resonance imaging extinction recall task assessing memory and threat differentiation for conditioned stimuli. While self-report and psychophysiological measures of differential conditioning and extinction were similar across groups, BI-related differences in brain function emerged during extinction recall. Childhood BI was associated with greater activation in subgenual anterior cingulate cortex in response to cues signaling safety. This pattern of results may reflect neural correlates that promote resilience against anxiety in a temperamentally at-risk population.


Psych ◽  
2019 ◽  
Vol 1 (1) ◽  
pp. 482-490 ◽  
Author(s):  
Steven M. Platek ◽  
Judson C. Hendry

Human kin recognition activates substrates of the extended facial processing network, notably the right-hemisphere structures involved in self-face recognition and posterior medial cortical substrates. To understand the mechanisms underlying prosociality toward kin faces in comparison to other familiar faces, we investigated the neural correlates of implicit trustworthiness ratings to faces of actual kin and personal friends, controlling for activation to distracter faces. When controlling for activation associated with unknown faces, trustworthiness ratings of faces of kin, compared to friends, were associated with increased activation in the dorsal anterior cingulate cortex, posterior cingulate, and precuneous. On the other hand, trustworthiness ratings of friend faces, relative to kin faces, were associated with the lateral occipital gyrus and insular cortex. Trustworthiness ratings for unknown faces were only associated with activation in the fusiform gyrus. These findings suggest that we should employ medial cortical substrates known to be part of the self-other network when making implicit social judgements about kin, but not other classes of facial stimuli.


2019 ◽  
Vol 286 (1908) ◽  
pp. 20191016 ◽  
Author(s):  
Amir-Homayoun Javadi ◽  
Eva Zita Patai ◽  
Eugenia Marin-Garcia ◽  
Aaron Margois ◽  
Heng-Ru M. Tan ◽  
...  

Successful navigation can require realizing the current path choice was a mistake and the best strategy is to retreat along the recent path: ‘back-track’. Despite the wealth of studies on the neural correlates of navigation little is known about backtracking. To explore the neural underpinnings of backtracking we tested humans during functional magnetic resonance imaging on their ability to navigate to a set of goal locations in a virtual desert island riven by lava which constrained the paths that could be taken. We found that on a subset of trials, participants spontaneously chose to backtrack and that the majority of these choices were optimal. During backtracking, activity increased in frontal regions and the dorsal anterior cingulate cortex, while activity was suppressed in regions associated with the core default-mode network. Using the same task, magnetoencephalography and a separate group of participants, we found that power in the alpha band was significantly decreased immediately prior to such backtracking events. These results highlight the importance for navigation of brain networks previously identified in processing internally-generated errors and that such error-detection responses may involve shifting the brain from default-mode states to aid successful spatial orientation.


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.


2014 ◽  
Vol 45 (3) ◽  
pp. 589-600 ◽  
Author(s):  
J. Gilleen ◽  
S. S. Shergill ◽  
S. Kapur

BackgroundPatients with schizophrenia have substantially reduced subjective well-being (SW) compared to healthy individuals. It has been suggested that diminished SW may be related to deficits in the neural processing of reward but this has not been shown directly. We hypothesized that, in schizophrenia, lower SW would be associated with attenuated reward-related activation in the reward network.MethodTwenty patients with schizophrenia with a range of SW underwent a functional magnetic resonance imaging (fMRI) reward task. The brain activity underlying reward anticipation and outcome in schizophrenia was examined and compared to that of 12 healthy participants using a full factorial analysis. Region of interest (ROI) analyses of areas within the reward network and whole-brain analyses were conducted to reveal neural correlates of SW.ResultsReward-related neural activity in schizophrenia was not significantly different from that of healthy participants; however, the patients with schizophrenia showed significantly diminished SW. Both ROI and whole-brain analyses confirmed that SW scores in the patients correlated significantly with activity, specifically in the dorsal anterior cingulate cortex (dACC), during both reward anticipation and reward outcome. This association was not seen in the healthy participants.ConclusionsIn patients with schizophrenia, reduced activation of the dACC during multiple aspects of reward processing is associated with lower SW. As the dACC has been widely linked to coupling of reward and action, and the link to SW is apparent over anticipation and outcome, these findings suggest that SW deficits in schizophrenia may be attributable to reduced integration of environmental rewarding cues, motivated behaviour and reward outcome.


2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Sven Vanneste ◽  
Dirk De Ridder

Abstract Chronic pain is pain that persists beyond the expected period of healing. The subjective experience of chronic pain results from pathological brain network interactions, rather than from persisting physiological sensory input of nociceptors. We hypothesize that pain is an imbalance between pain evoking dorsal anterior cingulate cortex and somatosensory cortex and pain suppression (i.e. pregenual anterior cingulate cortex). This imbalance can be measured objectively by current density ratios between pain input and pain inhibition. A balance between areas involved in pain input and pain suppression requires communication, which can be objectively identified by connectivity measures, both functional and effective connectivity. In patients with chronic neuropathic pain, electroencephalography is performed with source localization demonstrating that pain is reflected by an abnormal ratio between the dorsal anterior cingulate cortex, somatosensory cortex and pregenual anterior cingulate cortex. Functional connectivity demonstrates decreased communication between these areas, and effective connectivity puts the culprit at the dorsal anterior cingulate cortex, suggesting that the problem is related to abnormal behavioral relevance attached to the pain. In conclusion, chronic pain can be considered as an imbalance between pain input and pain suppression.


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.


Author(s):  
Karin Vadovičová ◽  
Roberto Gasparotti

We propose that dorsal anterior cingulate cortex (dACC), anterior insula (AI) and adjacent caudolateral orbitofrontal cortex (clOFC), project to lateral habenula (LHb) and D2 loop of ventral striatum (VS), forming a functional adversity processing circuit, directed towards inhibitory avoidance and self-control. This circuit learns what is bad or harmful to us, evaluates and predicts risks - to stop us from selecting and going/moving for the bad or suboptimal choices that decrease our well-being and survival chances. Proposed role of dACC is to generate a WARNING signal when things are going (or might end) bad or wrong to prevent negative consequences: pain, harm, loss or failure. The AI signals about bad, low, noxious and aversive qualities, which might make us sick or cause discomfort. These cortical adversity processing regions activate directly and indirectly (via D2 loop of VS) the LHb, which then inhibits dopamine and serotonin release (and is reciprocally inhibited by VTA/SNc, DRN) to avoid choosing and doing things leading to harm or loss, but also to make us feel worse, even down when overstimulated. We propose that dopamine attenuates output of the adversity processing circuit, thus decreasing inhibitory avoidance and self-control, while serotonin attenuates dACC, AI, clOFC, D1 loop of VS, LHb, amygdala and pain pathway. Thus, by reciprocal inhibition, by causing dopamine and serotonin suppression - and by being suppressed by them, the adversity processing circuit competes with reward processing circuit for control of choice behaviour and affective states. We propose stimulating effect of dopamine and calming inhibitory effect of serotonin on the active avoidance circuit involving amygdala, linked to threat processing, anger, fear, self-defense and violence. We describe causes and roles of dopamine and serotonin signaling in health and in mental dysfunctions. We add new idea on ventral ACC role in signaling that we are doing well and inducing serotonin, when we gain/reach safety, comfort, valuable resources (social or biological rewards), affection and achieve goals.


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