The neurobiology of aesthetic chills: How bodily sensations shape emotional experiences

Aesthetic chills (AC) are intense emotional responses to specific stimuli—such as music, films, speech, poetry, narratives, rituals—marked by discrete physiological responses (shivers and goosebumps) and a characteristic engagement of mesocorticolimbic reward circuits. Evidence suggests two symmetrical types: positive chills linked to high rewards and negative chills associated with high risks, both engaging the extended amygdala and processing of uncertainty. The dynamics of AC provide a window into the emergence of conscious feelings and how interoceptive bodily signals (e.g., shivers) temporally interact with awareness and valuation of external cues. Understanding AC may yield nonpharmacological strategies relevant to dopaminergic-related illnesses, reward learning, and maladaptive cognitions in depression.

The review synthesizes neuroimaging and neuromodulation evidence primarily from musical chills, acknowledging a paucity of studies for other stimuli (films, speech, narratives, rituals). Seven neuroimaging studies have examined AC, with early PET work (Blood & Zatorre, 2001) showing increased flow in ventral striatum, midbrain (VTA), insula, right orbitofrontal cortex, thalamus, anterior cingulate, supplementary motor area, cerebellum, and decreased flow in amygdala, left hippocampus, and vmPFC. Subsequent PET studies demonstrated dopamine release in dorsal/ventral striatum during peak musical pleasure (Salimpoor et al., 2011, 2013). TMS to left DLPFC modulated musical reward sensitivity and monetary valuation (Mas-Herrero et al., 2018). Pharmacology with dopamine precursors (levodopa) increased pleasure and chills incidence, while antagonists reduced them (Ferreri et al., 2019); naltrexone reduced arousal (pupil size) but did not alter self-reported pleasure (Laeng et al., 2021). High-density EEG revealed OFC theta activity correlated with emotional ratings during chills (Chabin et al., 2020). Structural connectivity studies linked trait propensity for chills to white-matter tract volume connecting posterior superior temporal gyrus, anterior insula, and medial prefrontal cortex (Sachs et al., 2016). Lesion and fMRI work in stroke patients implicated left anterior insula–temporal pole connectivity in coupling emotional arousal with bodily responses to chills stimuli (Witt et al., 2023). Personality (absorption, openness) and genetic factors contribute to individual differences, with twin data attributing ~36% of variance in AC to genetics (Bignardi et al., 2022). Theoretical accounts situate AC within predictive coding frameworks, precision-weighting of prediction errors by dopamine, and narrative/music-induced tension-resolution dynamics.

This theoretical review synthesizes findings across modalities to outline neurobiological mechanisms of aesthetic chills. Sources include PET and fMRI studies of musical pleasure and chills, high-density EEG, TMS neuromodulation experiments, pharmacological manipulations (dopamine precursors/antagonists; opioid antagonists), structural connectivity (DTI) and lesion-fMRI correlations in stroke, behavioral priming experiments manipulating coherence/surprisal, and preliminary clinical/behavioral studies using validated chills stimuli (ChillsDB) in populations with depressive symptoms. The authors frame results within predictive coding and precision-encoding accounts, integrating limbic, striatal, frontal, and interoceptive circuits to propose mechanistic roles for dopamine and bodily feedback in AC.

• Aesthetic chills engage mesocorticolimbic circuits: VTA dopaminergic projections to ventral striatum (NAcc), amygdala, hippocampus, OFC, vmPFC, insula, anterior cingulate, SMA, cerebellum; concurrent deactivations in amygdala, left hippocampus, vmPFC reported in PET (Blood & Zatorre, 2001).
• Dopamine release correlates with peak musical pleasure in dorsal/ventral striatum (Salimpoor et al., 2011) and with reward valuation of music (Salimpoor et al., 2013).
• Neuromodulation: Excitatory TMS to left DLPFC increased pleasure, arousal, and willingness to pay for music; inhibitory TMS decreased them (Mas-Herrero et al., 2018).
• Pharmacology: Levodopa increased pleasure and chills incidence; dopamine antagonists reduced these effects versus placebo (Ferreri et al., 2019). Opioid antagonism (naltrexone 50 mg) reduced pupil size (arousal) but not subjective pleasure (Laeng et al., 2021).
• Interoception: Insula involvement is critical; left anterior insula–temporal pole connectivity underpins coupling of emotional arousal with bodily responses. Stroke lesions affecting left insula impaired objective bodily chill responses but spared subjective experiences; reduced skin conductance correlated with lower temporal pole activation (Witt et al., 2023; Grunkina et al., 2017).
• Structural connectivity: Greater white-matter tract volume between auditory association cortex (pSTG), anterior insula, and mPFC predicts higher trait propensity for musical chills (Sachs et al., 2016).
• Predictive coding and precision: Dopamine encodes precision (reliability) of prediction errors, tuning attention and memory; incoherent/surprising primes disrupt AC (Schoeller & Perlovsky, 2016; Schoeller & Eskinazi, 2019). Novel musical systems become rewarding through learned predictions; fMRI shows auditory cortex prediction errors and auditory–mPFC connectivity tracking exposure and error signals (Kathios et al., 2023).
• Reward cycle positioning: AC may mark peak consummatory pleasure (Liking) and the transition toward satiety/learning, with striatal dopamine release during peak consumption (Small et al., 2003), NAcc firing pauses/unpauses around feeding transitions (Krause et al., 2010), and VTA lesions reducing overconsumption (Shimura et al., 2002).
• Arousal: Pre-exposure arousal predicts chills; chill-experiencers report roughly double pre-CS arousal versus non-chills participants (Schoeller et al., 2023b).
• Clinical/behavioral outcomes: In anhedonic depression, experiencing chills increased reward bias on the Probabilistic Reward Task compared with those without chills (p=0.004), indicating temporary mitigation of blunted reward learning; no difference in non-anhedonic depressed participants (Jain et al., 2023b). Chills shift self-reported valence and arousal (emotional drift) across groups, with high-anhedonia participants’ post-chills affect approaching non-anhedonic and control levels (Jain et al., 2023a, b). Chills exposure associated with increased psychological insight and emotional breakthrough, with intensity positively correlated with these measures, and co-occurring patterns of ego dissolution, connectedness, and moral elevation (Schoeller et al., 2023c, 2023d; Christov-Moore et al., 2023).
• Individual differences: Personality traits (absorption, openness) and genetic factors (~36% heritability) contribute to AC propensity (Silvia & Nusbaum, 2011; Silvia et al., 2015; McCrae, 2007; Bignardi et al., 2022). Potential serotonin–dopamine interactions are hypothesized but direct 5-HT2A evidence for AC is lacking.

The findings suggest that aesthetic chills arise from coordinated brain–body processes in which interoceptive signals (shivers/goosebumps mediated by insula and autonomic pathways) interface with dopaminergic precision-weighting of prediction errors across hierarchical cortical systems. This coordination shapes conscious feelings, motivation, and learning in response to resolving uncertainty in musical and narrative structures. AC appear to straddle reward phases, often peaking at consummation and initiating satiety-related learning, consistent with dopamine’s roles in incentive salience and memory consolidation via VTA–hippocampal projections. The observation that both appetitive (reward) and aversive (threat) systems are recruited aligns with accounts of awe/sublime as mixed valence and with amygdala’s context-dependent roles. Precision encoding provides a mechanistic bridge to observed enhancements in attention, memory, and valuation during AC, while disruptions in coherence can inhibit the phenomenon by degrading precision. Preliminary clinical data indicate AC may transiently normalize reward processing and affect in anhedonia and modulate maladaptive self-beliefs, pointing toward nonpharmacological avenues for disorders implicating dopaminergic precision-weighting (e.g., depression, schizophrenia, addiction).

Aesthetic chills provide a unique, measurable window into reward learning and conscious affect, engaging VTA-centered dopaminergic networks (NAcc, amygdala, frontal regions) and interoceptive circuitry (insula). Dopamine’s proposed role in precision encoding links AC to enhanced pleasure, motivation, attention, memory, and the transition within the reward cycle from wanting to liking and learning. Individual differences in AC are shaped by personality, structural connectivity, and genetics. Insights into AC neurobiology have translational relevance for psychiatric conditions characterized by dysfunctional precision-weighting of prediction errors. Preliminary evidence suggests AC can improve reward learning in anhedonia and positively shift maladaptive self-beliefs, motivating future research to expand stimuli beyond music, refine temporal measurements, probe neuromodulatory mechanisms (including acetylcholine and serotonin interactions), and assess clinical efficacy in targeted interventions.

• Current neuroimaging evidence on AC largely relies on musical stimuli; conclusions may not generalize to films, speech, narratives, rituals, or other chills stimuli.
• Only a small number of studies have directly examined neural correlates of AC; sample sizes and methodological heterogeneity limit firm mechanistic conclusions.
• fMRI temporal resolution and reliance on self-reported timing of chills may miss transient neural dynamics and introduce reporting bias.
• Pharmacological findings are mixed (e.g., opioid antagonism reducing arousal but not pleasure); direct links to specific serotonin receptor mechanisms (e.g., 5-HT2A) are currently absent.
• Clinical results (reward learning improvements, schema shifts) are preliminary and require replication, larger samples, and controlled trials.
• Theoretical models (precision encoding, learning-rate extrema) need empirical validation across diverse stimuli and populations.
• Lesion and structural connectivity findings emphasize left insula–temporal pole pathways, but causality and generalizability remain to be fully established.