Cingulate Cortex

The cingulate cortex is a paired region located on the medial surface of the cerebral hemispheres, arching above the corpus callosum. It encompasses both the cingulate gyrus and the cingulate sulcus, and is often regarded as part of the limbic lobe and limbic system.

Anterior vs. Posterior Cingulate Cortex

The anterior cingulate cortex (ACC) occupies the front portion (Brodmann areas 24, 32, and 33) and is crucial for cognitive functions such as attention, conflict monitoring, emotion, and decision-making.

The posterior cingulate cortex (PCC), situated behind the ACC (areas 23 and 31), is a central hub in the brain’s default mode network.

It is highly metabolically active and plays key roles in episodic memory retrieval, awareness, and pain processing.

The Four-Region Model

Researchers often divide the cingulate cortex more finely. Vogt (2005) proposed a four-region model:

• Anterior cingulate cortex (ACC): Areas 24 and 32, split into a dorsal “cognitive” zone and a rostral-ventral “affective” zone.
• Midcingulate cortex (MCC): The middle section. Its anterior part links to conflict monitoring and negative affect, its posterior part to orienting toward pain.
• Posterior cingulate cortex (PCC): The default-mode and memory hub described above.
• Retrosplenial cortex (RSC): Lies directly behind the splenium of the corpus callosum and is closely tied to the hippocampal formation.

This finer map matters. A conflict study and a pain study may both report “ACC activation” yet describe different subregions of the same gyrus. That is one reason findings across the ACC literature can look inconsistent.

Cell Structure and Von Economo Neurons

The regions also differ in tissue structure. The anterior and midcingulate cortex are agranular or dysgranular, meaning they lack a well-developed granular layer IV, like much of the limbic cortex.

The posterior cingulate and retrosplenial cortex are more granular and resemble neocortex proper. This gradient tracks function.

Anterior regions couple more tightly to limbic, autonomic, and motivational circuitry. Posterior regions couple to the parietal and medial temporal systems that support memory and spatial cognition.

One cell type is concentrated almost exclusively in the ACC. Layer Vb contains von Economo neurons (VENs): unusually large, spindle-shaped neurons with one thick, sparsely branched dendrite at each pole.

Nimchinsky and colleagues (1999) found VENs only in the anterior cingulate cortex of humans and great apes. Allman and colleagues (2005) proposed that the VEN’s size and sparse branching may allow unusually fast transmission of socially relevant signals. That could support rapid, intuitive appraisal of complex social situations.

Connections with Other Brain Regions and the Limbic System

The cingulate cortex is deeply interconnected within the limbic system. It receives input from thalamic nuclei and neocortex. It also communicates with the entorhinal cortex via the cingulum bundle, a white-matter tract running the length of the cingulate gyrus.

The ACC connects strongly with the orbitofrontal cortex, amygdala, and other limbic-related structures. This allows it to integrate emotion and reward signals.

Meanwhile, the PCC links extensively with medial temporal memory regions (e.g., hippocampus, parahippocampal gyrus) and association cortices. This supports memory, self-awareness, and high-level cognitive integration.

The Papez Circuit and the Limbic System

Papez (1937) proposed the first systematic account. His circuit linked the hippocampus, the mammillary bodies of the hypothalamus, the anterior nucleus of the thalamus, and the cingulate cortex in a closed loop.

Papez suggested that the felt experience of emotion arises when activity reaches the cingulate cortex. He argued that the hypothalamus governs the outward expression of emotion more directly.

MacLean (1949) later added the amygdala and other structures. He called the result the “visceral brain”, then proposed the broader term limbic system.

The circuit’s core connections have held up well. The idea that the cingulate cortex is dedicated to the conscious experience of emotion has not. Contemporary evidence credits it with a much wider portfolio, including cognitive control, attention, pain, and memory.

Functions of the Cingulate Cortex

Emotion Regulation and Processing

The cingulate cortex, especially its anterior part (ACC), plays a central role in emotion regulation by integrating emotional input with cognitive control.

It responds to rewards, monitors conflict and errors, and helps modulate emotional experiences such as empathy, pain, and social evaluation.

The ACC also influences autonomic functions like heart rate and blood pressure in emotional contexts.

Bush, Luu, and Posner (2000) reviewed neuroimaging findings. They proposed a cognitive-affective split. The dorsal ACC responds most to demanding tasks involving attention, working memory, response selection, and conflict.

The rostral and ventral ACC, closer to the orbitofrontal cortex and amygdala, responds most to emotionally salient material. During emotional processing, the two zones deactivate reciprocally.

Reappraisal: Changing How a Situation Feels

Ochsner and Gross (2005, 2008) synthesised imaging evidence on cognitive reappraisal. This means deliberately reinterpreting a situation to change how it feels. Successful reappraisal recruits the prefrontal cortex and ACC to turn down amygdala activity. Thinking differently can genuinely change how it feels.

Automatic Regulation and Mindfulness

Not all emotion regulation is deliberate. Mauss, Bunge, and Gross (2007) reviewed automatic emotion regulation, which occurs without conscious intent or awareness.

They highlighted the subgenual cingulate cortex (Brodmann area 25), a small ventral part of the ACC, in automatic mood control.

Using PET imaging, Zubieta and colleagues (2003) found that anterior cingulate µ-opioid neurotransmission varies with the intensity of sustained emotional experience. This ties emotion to the brain’s own opioid system.

Mindfulness training offers a third route, sharpening cingulate activity rather than dampening it.

Teper, Segal, and Inzlicht (2013) reviewed evidence that experienced meditators show an amplified error-related negativity (ERN). The ERN is an electrical brain signal, linked to the ACC, that appears within about 100 milliseconds of a mistake. Meditators also make fewer Stroop errors.

Meditators exposed to a painful stimulus show reduced amygdala activity alongside increased anterior cingulate activity, relative to non-meditators.

Structural change follows too. After an eight-week mindfulness-based stress reduction course, Hölzel and colleagues (2011) found increased posterior cingulate gray-matter density, relative to a wait-list control group.

Attention, Focus, and Decision-Making

The ACC is vital for attention allocation, performance monitoring, and decision-making.

Conflict Monitoring and Error Detection

Detecting conflict is the best-established function of the dorsal ACC. It notices when a response is difficult, error-prone, or competes with another response, such as during the Stroop or Flanker tasks. It then evaluates errors and signals that more cognitive control is needed.

This finding anchored conflict-monitoring theory. Botvinick, Cohen, and Carter (2004) later proposed that the ACC detects conflict between competing responses and signals the prefrontal cortex, which then increases top-down control.

Electrical recordings agree. The error-related negativity (ERN) is a frontocentral brain signal appearing within about 100 milliseconds of an error. Its main source is widely attributed to the ACC.

Posterior Cingulate and the Default Mode Network

The posterior cingulate cortex (PCC) plays a key role in activities of the default mode network, such as internal focus and episodic memory retrieval. It also balances internal against external attention.

Raichle and colleagues (2001) found that the PCC and medial prefrontal cortex are more active at rest than during externally focused tasks. They proposed that this reflects an organised baseline of self-referential and monitoring activity, not mere idling.

The PCC is not a passive hub, however. A later review by Leech and Sharp (2014) argued that it actively regulates the balance between internally and externally directed attention.

PCC activity typically falls during demanding external tasks and rises during mind-wandering, autobiographical memory retrieval, and self-referential thought. The dorsal ACC shows the opposite pattern.

Memory, Learning, and Spatial Awareness

The PCC receives spatial and action-related information from parietal regions. It exchanges information with the hippocampal system via the parahippocampal and entorhinal cortices. This supports spatial awareness, episodic memory retrieval, and action–outcome learning.

The cingulate cortex acts as a bridge between neocortical input (both “what” and “where” streams) and the hippocampus, facilitating associative learning and memory formation.

The retrosplenial cortex, just behind the rear end of the corpus callosum (the splenium), is closely linked to the PCC and the hippocampal formation. It contributes to spatial memory and navigation (Vogt, 2005). This connectivity also makes the region vulnerable in memory-related neurodegenerative disease, discussed below.

Pain Processing in the Cingulate Cortex

Pain has a sensory side and an affective side. The sensory side covers where the pain is and how intense it feels.

The affective side covers how unpleasant it is and how strongly it demands avoidance. Here the cingulate cortex matters most.

Together with the amygdala and insula, it is central to the affective side. The anterior and midcingulate cortex track the unpleasantness of pain and the urge to avoid it. Posterior regions contribute more to spatial and orienting aspects (Vogt, 2005; Fuchs et al., 2014).

Fuchs and colleagues (2014) reviewed the evidence. They drew together anatomical, electrophysiological, and lesion findings on the ACC. They concluded that ACC neurons encode the affective salience of painful stimuli.

Placebo analgesia and hypnotic suggestion reduce cingulate activity without necessarily reducing primary somatosensory activity. The person still registers the stimulus. Its emotional sting is dampened.

Empathy, Rejection, and Love

Social rejection also hurts in a neural sense. Eisenberger, Lieberman, and Williams (2003) scanned participants during a ball-tossing game from which they were deliberately excluded. Exclusion activated the ACC in a pattern that tracked self-reported distress. This suggests that physical pain and rejection share neural systems.

At the opposite emotional pole, Bartels and Zeki (2000) scanned people viewing photographs of their romantic partners. They found a distinctive pattern of activation, including the ACC and subcortical reward regions.

Psychological Pain Management

Because the cingulate cortex carries much of pain’s emotional sting, it is a natural target for psychological pain treatments.

Mindfulness, cognitive reappraisal, and biofeedback are used on the premise that they can lower cingulate and limbic reactivity to pain. The painful stimulus itself stays the same.

Disorders and Dysfunctions of the Cingulate Cortex

Devinsky, Morrell, and Vogt (1995) reviewed cases of bilateral anterior cingulate injury caused by tumours, stroke, surgical lesions, and cingulotomy. They described a consistent syndrome. Signs may include the following:

• Autonomic changes: Irregular heart rate, blood pressure, or digestion.
• Flat affect: Reduced emotional expression.
• Loss of empathy: Difficulty resonating with others’ feelings.
• Poor decisions: Impaired judgment and risk-reward evaluation.
• Attention deficits: Trouble focusing or resolving conflict.
• Emotional instability: Impulsivity or inappropriate reactions.
• Akinetic mutism: A severe reduction in speech and movement. Patients can still speak and move but lose the drive to do so.
• Memory and spatial problems: Difficulty retrieving memories or navigating environments, more closely linked to posterior and retrosplenial damage.

Mental and Psychiatric Disorders

• The subgenual anterior cingulate cortex (sgACC) is heavily implicated in major depression. It has been tested as a deep-brain-stimulation target in treatment-resistant cases, with mixed results.
• In OCD, the ACC shows abnormal neurochemistry (e.g., altered glutamate/GABA balance) and structural changes like reduced grey matter.
• Schizophrenia patients often have reduced ACC volume and lower metabolic activity in both anterior and posterior segments.
• Anxiety and other neuropsychiatric disorders are associated with dysfunction in cingulate-related networks.

OCD and the Overactive Error Alarm

In OCD, neuroimaging and neurochemical studies repeatedly implicate overactivity in loops linking the cortex, striatum, and thalamus that include the ACC. Milad and Rauch (2012) argued that OCD reflects dysfunction distributed across cognitive-control and affective circuitry, not one segregated loop.

That may explain OCD’s abnormally large error-related negativity. It is as if the brain’s error alarm is stuck on, generating persistent doubt about whether a checking or washing task is really done.

Depression and Deep Brain Stimulation

The subgenual cingulate (Brodmann area 25) is one of the most intensively studied targets in treatment-resistant depression research. Deep brain stimulation (DBS) delivers continuous electrical stimulation through implanted electrodes.

That open-label pilot generated optimism, but a larger, stronger trial was more sobering.

The contrast shows why open-label promise and blinded, randomised confirmation are different kinds of evidence.

Neurodegenerative and Neurological Conditions

• Early Alzheimer’s disease involves atrophy and disrupted connectivity in the posterior cingulate and cingulum bundle.
• Autism Spectrum Disorder (ASD) features functional differences and altered connectivity in the PCC.
• Dysfunction within the cingulate is also implicated in ADHD, affecting attention and executive function via default-mode network instability.

Early Alzheimer’s Disease

Posterior cingulate changes often appear before the more widely recognised medial temporal atrophy becomes obvious.

This finding has shaped PET-based diagnostic criteria for early Alzheimer’s disease ever since.

Von Economo Neurons in Dementia and Healthy Ageing

Von Economo neurons turn out to be a disease-specific casualty. Seeley and colleagues (2006) used stereological cell counts in post-mortem anterior cingulate tissue to compare behavioural-variant frontotemporal dementia, Alzheimer’s disease, and healthy controls.

VEN density was about three-quarters lower in frontotemporal dementia. Alzheimer’s disease cases showed essentially normal VEN counts, despite extensive tangle pathology in the same tissue.

This matches the clinical pictures. Frontotemporal dementia erodes empathy and social judgement before memory, whereas early Alzheimer’s disease follows a posterior, memory-first course.

Not every finding points to vulnerability. Gefen and colleagues (2015) studied SuperAgers, people over 80 whose episodic memory matches adults decades younger. Their anterior cingulate cortex was significantly thicker than that of 50 to 65-year-old controls.

Post-mortem counts told a similar story. They showed roughly three to five times the VEN density of age-matched controls and of people with amnestic mild cognitive impairment. This positions the anterior cingulate as a candidate site of cognitive reserve, not only of age-related vulnerability.

ADHD and the Default Mode Network

Castellanos and Proal (2012) reviewed evidence that ADHD is better understood as a difference in large-scale brain-system coordination. It is not a difference in the prefrontal-striatal circuit alone.

They highlighted atypical interaction between the default mode network, in which the PCC is a hub, and networks that support focused, externally directed attention.

On this account, some ADHD attention and mind-wandering patterns reflect default-mode activity that stays active when a task demands sustained external attention.

How do researchers study the cingulate cortex?

Researchers explore the cingulate cortex using a range of advanced techniques combining structure, function, and computation:

• Functional MRI (fMRI): Maps cingulate engagement via the BOLD signal, a blood-oxygen marker of neural activity, during tasks or at rest, especially within the default mode network.
• Diffusion MRI (DTI/tractography) and parcellation methods: Reveal structural connectivity within cingulate subregions and with other brain areas.
• Functional MRS (fMRS): Measures dynamic changes in metabolites such as glutamate or GABA in the anterior cingulate during activation or pain studies.
• Electrophysiology & Electrocorticography (ECoG): Provide high-resolution, direct recordings of neural activity from the cortical surface or depth electrodes, offering unparalleled temporal and spatial detail.
• MEG and EEG: Noninvasive ways to map temporal brain dynamics, especially useful for oscillatory and synchrony studies.
• Positron emission tomography (PET): Maps regional glucose metabolism or receptor binding. It revealed early posterior cingulate hypometabolism in Alzheimer’s disease (Minoshima et al., 1997).
• Lesion and neurosurgical case studies: Damage from tumours, stroke, or surgery gives causal evidence that imaging cannot, but the samples are small and varied (Devinsky et al., 1995).
• Functional ultrasound (fUS): Emerging technology that maps blood flow, and thus activity, with high spatial and temporal precision, currently most advanced in animal and neonatal brain studies.

These tools collectively enable researchers to dissect the cingulate cortex’s anatomy, functionality, metabolism, connectivity, and real-time neural dynamics with increasing precision.

Critical Evaluation of Cingulate Cortex Research

Cingulate research is rich. It also has clear limits, and recent large studies have tested earlier optimism. Popular and even textbook accounts often describe “the ACC” as if it does one thing.

Findings can look inconsistent. One study reports ACC activity during pain, another during conflict, another during reward. Often these reflect different subregions, or different computations such as value versus conflict, lumped under one label (Vogt, 2005; Shenhav et al., 2013).

A more precise, subregion-specific vocabulary is needed before cross-study comparisons can be taken at face value. The same caution applies within a single diagnosis.

Correlation, Lesions, and Animal Models

Correlational imaging cannot show which way causation runs. Loh and Kanai (2014) scanned 75 healthy adults.

They found that heavier media multitasking went with smaller gray-matter density in the ACC. The design could not show whether multitasking shrinks the ACC, whether a smaller ACC encourages multitasking, or whether a third factor drives both.

A longitudinal design would be needed to settle it.

Lesion studies speak to causation more directly. Yet human cingulate lesions are rare, vary in size and location, and are never randomly assigned (Devinsky et al., 1995).

Much causal evidence on cingulate pain and reward processing also comes from rodents and non-human primates (Vogt, 2005; Fuchs et al., 2014). Extrapolating to the larger human cingulate, with its expanded midcingulate and retrosplenial territories, is not guaranteed.

Competing Models of Cognitive Control

Conflict monitoring remains the dominant account of dorsal ACC function. Its strength is converging evidence from fMRI, lesion, and ERP studies.

Its limit is clear. It says little about why the ACC tracks conflict rather than a broader signal that conflict merely correlates with.

A rival account addresses that gap. Expected Value of Control (EVC) theory proposes that the ACC computes the expected net value of allocating cognitive control (Shenhav et al., 2013). Anticipated benefits, such as better performance or larger reward, are weighed against the mental effort cost.

Conflict is one input among several. EVC can explain when people choose to invest effort at all, including ACC responses that track anticipated reward with no response conflict.

EVC subsumes conflict monitoring as a special case. The two are best read as successive layers of one research programme, not rival camps.

Contemporary Research

Recent work has moved from showing that the cingulate cortex matters toward asking how reliably and how causally it does so. The deep brain stimulation trials above show the same lesson: a large sham-controlled trial tempered early open-label promise.

Are ERN and Reward Positivity Reliable Biomarkers?

The ERN and a related reward-sensitive signal, the reward positivity (RewP), are altered in anxiety, OCD, and depression. That raised hopes that they could serve as objective markers of risk.

A pre-registered power analysis sits higher in the evidence hierarchy than the small correlational studies it reviews. It deserves more weight than the raw count of significant results.

Does Reappraisal Work the Same Way in Anxiety and Depression?

Cui and colleagues (2024) combined a meta-analysis of behavioural reappraisal studies with a meta-analysis of reappraisal neuroimaging studies.

People with depressive disorders reduced negative reactivity through reappraisal less well than healthy controls. People with anxiety disorders did about as well as controls.

The imaging results told close to the opposite story. Anxiety samples showed weaker recruitment of cognitive-control regions, including the median cingulate (Brodmann area 24), whereas depressive samples showed broadly typical activation.

This double dissociation undercuts any assumption that a diagnosis predicts one uniform pattern of ACC dysfunction.

References

Allman, J. M., Watson, K. K., Tetreault, N. A., & Hakeem, A. Y. (2005). Intuition and autism: A possible role for Von Economo neurons. Trends in Cognitive Sciences, 9(8), 367–373. https://doi.org/10.1016/j.tics.2005.06.008

Bartels, A., & Zeki, S. (2000). The neural basis of romantic love. NeuroReport, 11(17), 3829–3834. https://doi.org/10.1097/00001756-200011270-00046

Botvinick, M. M., Cohen, J. D., & Carter, C. S. (2004). Conflict monitoring and anterior cingulate cortex: An update. Trends in Cognitive Sciences, 8(12), 539–546. https://doi.org/10.1016/j.tics.2004.10.003

Bush, G., Luu, P., & Posner, M. I. (2000). Cognitive and emotional influences in anterior cingulate cortex. Trends in Cognitive Sciences, 4(6), 215–222. https://doi.org/10.1016/S1364-6613(00)01483-2

Carter, C. S., Braver, T. S., Barch, D. M., Botvinick, M. M., Noll, D., & Cohen, J. D. (1998). Anterior cingulate cortex, error detection, and the online monitoring of performance. Science, 280(5364), 747–749. https://doi.org/10.1126/science.280.5364.747

Castellanos, F. X., & Proal, E. (2012). Large-scale brain systems in ADHD: Beyond the prefrontal-striatal model. Trends in Cognitive Sciences, 16(1), 17–26. https://doi.org/10.1016/j.tics.2011.11.007

Clayson, P. E., Carbine, K. A., & Larson, M. J. (2020). A registered report of error-related negativity and reward positivity as biomarkers of depression: P-curving the evidence. International Journal of Psychophysiology, 150, 50–72. https://doi.org/10.1016/j.ijpsycho.2020.01.005

Cui, X., Ding, Q., Yu, S., Zhang, S., & Li, X. (2024). The deficit in cognitive reappraisal capacity in individuals with anxiety or depressive disorders: Meta-analyses of behavioral and neuroimaging studies. Clinical Psychology Review, 114, Article 102480. https://doi.org/10.1016/j.cpr.2024.102480

Devinsky, O., Morrell, M. J., & Vogt, B. A. (1995). Contributions of anterior cingulate cortex to behaviour. Brain, 118(1), 279–306. https://doi.org/10.1093/brain/118.1.279

Eisenberger, N. I., Lieberman, M. D., & Williams, K. D. (2003). Does rejection hurt? An fMRI study of social exclusion. Science, 302(5643), 290–292. https://doi.org/10.1126/science.1089134

Fuchs, P. N., Peng, Y. B., Boyette-Davis, J. A., & Uhelski, M. L. (2014). The anterior cingulate cortex and pain processing. Frontiers in Integrative Neuroscience, 8, Article 35. https://doi.org/10.3389/fnint.2014.00035

Gefen, T., Peterson, M., Papastefan, S. T., Martersteck, A., Whitney, K., Rademaker, A., Bigio, E. H., Weintraub, S., Rogalski, E., Mesulam, M.-M., & Geula, C. (2015). Morphometric and histologic substrates of cingulate integrity in elders with exceptional memory capacity. Journal of Neuroscience, 35(4), 1781–1791. https://doi.org/10.1523/JNEUROSCI.2998-14.2015

Holtzheimer, P. E., Husain, M. M., Lisanby, S. H., Taylor, S. F., Whitworth, L. A., McClintock, S., Slavin, K. V., Berman, J., McKhann, G. M., Patil, P. G., Rittberg, B. R., Abosch, A., Pandurangi, A. K., Holloway, K. L., Lam, R. W., Honey, C. R., Neimat, J. S., Henderson, J. M., DeBattista, C., . . . Mayberg, H. S. (2017). Subcallosal cingulate deep brain stimulation for treatment-resistant depression: A multisite, randomised, sham-controlled trial. The Lancet Psychiatry, 4(11), 839–849. https://doi.org/10.1016/S2215-0366(17)30371-1

Hölzel, B. K., Carmody, J., Vangel, M., Congleton, C., Yerramsetti, S. M., Gard, T., & Lazar, S. W. (2011). Mindfulness practice leads to increases in regional brain gray matter density. Psychiatry Research: Neuroimaging, 191(1), 36–43. https://doi.org/10.1016/j.pscychresns.2010.08.006

Leech, R., & Sharp, D. J. (2014). The role of the posterior cingulate cortex in cognition and disease. Brain, 137(1), 12–32. https://doi.org/10.1093/brain/awt162

Loh, K. K., & Kanai, R. (2014). Higher media multi-tasking activity is associated with smaller gray-matter density in the anterior cingulate cortex. PLOS ONE, 9(9), Article e106698. https://doi.org/10.1371/journal.pone.0106698

MacLean, P. D. (1949). Psychosomatic disease and the “visceral brain”: Recent developments bearing on the Papez theory of emotion. Psychosomatic Medicine, 11(6), 338–353.

Mauss, I. B., Bunge, S. A., & Gross, J. J. (2007). Automatic emotion regulation. Social and Personality Psychology Compass, 1(1), 146–167. https://doi.org/10.1111/j.1751-9004.2007.00005.x

Mayberg, H. S., Lozano, A. M., Voon, V., McNeely, H. E., Seminowicz, D., Hamani, C., Schwalb, J. M., & Kennedy, S. H. (2005). Deep brain stimulation for treatment-resistant depression. Neuron, 45(5), 651–660. https://doi.org/10.1016/j.neuron.2005.02.014

Milad, M. R., & Rauch, S. L. (2012). Obsessive-compulsive disorder: Beyond segregated cortico-striatal pathways. Trends in Cognitive Sciences, 16(1), 43–51. https://doi.org/10.1016/j.tics.2011.11.003

Minoshima, S., Giordani, B., Berent, S., Frey, K. A., Foster, N. L., & Kuhl, D. E. (1997). Metabolic reduction in the posterior cingulate cortex in very early Alzheimer’s disease. Annals of Neurology, 42(1), 85–94. https://doi.org/10.1002/ana.410420114

Nimchinsky, E. A., Gilissen, E., Allman, J. M., Perl, D. P., Erwin, J. M., & Hof, P. R. (1999). A neuronal morphologic type unique to humans and great apes. Proceedings of the National Academy of Sciences, 96(9), 5268–5273. https://doi.org/10.1073/pnas.96.9.5268

Ochsner, K. N., & Gross, J. J. (2005). The cognitive control of emotion. Trends in Cognitive Sciences, 9(5), 242–249. https://doi.org/10.1016/j.tics.2005.03.010

Ochsner, K. N., & Gross, J. J. (2008). Cognitive emotion regulation: Insights from social cognitive and affective neuroscience. Current Directions in Psychological Science, 17(2), 153–158. https://doi.org/10.1111/j.1467-8721.2008.00566.x

Papez, J. W. (1937). A proposed mechanism of emotion. Archives of Neurology and Psychiatry, 38(4), 725–743. https://doi.org/10.1001/archneurpsyc.1937.02260220069003

Raichle, M. E., MacLeod, A. M., Snyder, A. Z., Powers, W. J., Gusnard, D. A., & Shulman, G. L. (2001). A default mode of brain function. Proceedings of the National Academy of Sciences, 98(2), 676–682. https://doi.org/10.1073/pnas.98.2.676

Seeley, W. W., Carlin, D. A., Allman, J. M., Macedo, M. N., Bush, C., Miller, B. L., & DeArmond, S. J. (2006). Early frontotemporal dementia targets neurons unique to apes and humans. Annals of Neurology, 60(6), 660–667. https://doi.org/10.1002/ana.21055

Shenhav, A., Botvinick, M. M., & Cohen, J. D. (2013). The expected value of control: An integrative theory of anterior cingulate cortex function. Neuron, 79(2), 217–240. https://doi.org/10.1016/j.neuron.2013.07.007

Singer, T., Seymour, B., O’Doherty, J., Kaube, H., Dolan, R. J., & Frith, C. D. (2004). Empathy for pain involves the affective but not sensory components of pain. Science, 303(5661), 1157–1162. https://doi.org/10.1126/science.1093535

Teper, R., Segal, Z. V., & Inzlicht, M. (2013). Inside the mindful mind: How mindfulness enhances emotion regulation through improvements in executive control. Current Directions in Psychological Science, 22(6), 449–454. https://doi.org/10.1177/0963721413495869

Vogt, B. A. (2005). Pain and emotion interactions in subregions of the cingulate gyrus. Nature Reviews Neuroscience, 6(7), 533–544. https://doi.org/10.1038/nrn1704

Zubieta, J.-K., Ketter, T. A., Bueller, J. A., Xu, Y., Kilbourn, M. R., Young, E. A., & Koeppe, R. A. (2003). Regulation of human affective responses by anterior cingulate and limbic µ-opioid neurotransmission. Archives of General Psychiatry, 60(11), 1145–1153. https://doi.org/10.1001/archpsyc.60.11.1145