Spontaneous fluctuations in neural responses to heartbeats predict visual detection

Journal name:
Nature Neuroscience
Volume:
17,
Pages:
612–618
Year published:
DOI:
doi:10.1038/nn.3671
Received
Accepted
Published online

Abstract

Spontaneous fluctuations of ongoing neural activity substantially affect sensory and cognitive performance. Because bodily signals are constantly relayed up to the neocortex, neural responses to bodily signals are likely to shape ongoing activity. Here, using magnetoencephalography, we show that in humans, neural events locked to heartbeats before stimulus onset predict the detection of a faint visual grating in the posterior right inferior parietal lobule and the ventral anterior cingulate cortex, two regions that have multiple functional correlates and that belong to the same resting-state network. Neither fluctuations in measured bodily parameters nor overall cortical excitability could account for this finding. Neural events locked to heartbeats therefore shape visual conscious experience, potentially by contributing to the neural maps of the organism that might underlie subjectivity. Beyond conscious vision, our results show that neural events locked to a basic physiological input such as heartbeats underlie behaviorally relevant differential activation in multifunctional cortical areas.

At a glance

Figures

  1. Experimental paradigm and rationale.
    Figure 1: Experimental paradigm and rationale.

    (a) Time course of a target-present trial. Subjects reported whether or not they saw a faint grating annulus. (b) Cardiac T waves (arrows) occurring between warning and stimulus onset and detected in single trials in the electrocardiogram. (c) Averaged MEG evoked fields locked on the T wave of the electrocardiogram (arrows) to test whether prestimulus neural events locked to heartbeats differed between hits and misses. The analysis focused on the time window free from cardiac artifact during the heart relaxation period after the T wave.

  2. Post-decisional heart slowing.
    Figure 2: Post-decisional heart slowing.

    Evolution of the mean interval between R peaks in hits and misses during a trial from the interbeat interval during which the warning cue appeared on the screen (warning) until the interbeat interval during which subjects responded (response) and intervals after the response (R+1 and R+2). Before stimulus onset, heart rate did not distinguish between hits and misses. In all trials, the heart slowed down after warning and accelerated after response delivery. Consciously seeing the stimulus further slowed down the heart, especially after subjects pressed the button to signal their decision (post hoc Bonferroni-corrected paired t test between hits and misses, R+1 t16 = 3.6, P = 0.012; R+2 t16 = 3.6, P = 0.012). Error bars represent the s.e.m. *P < 0.05, ***P < 0.0005, post hoc Bonferroni-corrected t test (n = 17) .

  3. Neural events locked to heartbeats before stimulus onset predicted conscious perception of the stimulus.
    Figure 3: Neural events locked to heartbeats before stimulus onset predicted conscious perception of the stimulus.

    (a) Topographical map of the heartbeat-evoked response (HER) difference between hits and misses grand averaged across 17 subjects in the 135–171 ms time window in which a significant difference was observed (Monte-Carlo P = 0.034 corrected for multiple comparisons in time and space) on magnetometer sensors. Larger black dots indicate the location of the magnetometers contributing to the significant cluster. (b) Prestimulus T-locked evoked magnetic fields averaged across the cluster (top) and at the sensor indicated by a white dot in a (bottom). The signal that was contaminated by the cardiac artifact, before +50 ms, appears in lighter color. The shaded area highlights the time window in which a significant difference was observed. (c) Amplitude of the prestimulus HER averaged across the cluster in the 135–171 ms time window in hits and misses and during a separate resting session with eyes open. HERs during rest were smaller than those preceding hits (P = 0.013) and larger than those preceding misses (P = 0.029, paired t tests; n = 17). (d) Perceptual performance as a function of prestimulus neural response to heartbeats. In each subject, we sorted single trials in three bins according to the amplitude of the neural response to heartbeats. Each dot corresponds to the mean amplitude in a given bin and in a given subject. When the neural response to heartbeats was larger, subjects were more likely to report seeing the stimulus. Thin gray lines represent the slope of the linear regression between change in hit rate and neural amplitude in each subject. The yellow line indicates the mean slope of the linear regression averaged across subjects. (e) The linear increase in hit rate (linear trend analysis; n = 17) with increasing HER amplitude (left) corresponded to an increase in sensitivity (middle; P = 0.049) without change in criterion (right; P = 0.99). AU, arbitrary units. Error bars represent the s.e.m. *P < 0.05, ***P < 0.0005. NS, not significant.

  4. Neural sources of the differential response to heartbeats.
    Figure 4: Neural sources of the differential response to heartbeats.

    (a) Differential activation by heartbeats in vACC-vmPFC bilaterally and rIPL in hits and misses before stimulus onset (criterion for visualization purpose, more than ten contiguous vertices with uncorrected P < 0.005, paired t test; n = 17). (b) Time course of the HER in vACC-vmPFC (top) and rIPL (bottom) separately in hits and misses grand averaged across subjects in absolute values of dipole currents (pA m), directly reflecting neural electrical activity. Signal that was contaminated by the cardiac artifact, before +50 ms, appears in lighter color. The shaded area highlights the time window in which we observed a significant difference (clustering procedure at the sensor level; n = 17). A larger neural response to heartbeats in hits occurred in both areas, with a more transient effect in rIPL than in vACC-vmPFC. (c) Hit-miss difference in cardiac interbeat interval after response delivery as a function of hit-miss difference in HER before stimulus onset in vACC-vmPFC. Each dot represents a subject. These two independent measures were significantly correlated (Pearson r = 0.65, P = 0.005; n = 17).

  5. Pupil diameter, alpha power and warning-evoked response do not predict detection (n = 17).
    Figure 5: Pupil diameter, alpha power and warning-evoked response do not predict detection (n = 17).

    (a) Pupil diameter during the 1.5 s preceding stimulus onset (left, time course; right, mean amplitude) did not predict stimulus detection (P = 0.82). (b) Alpha power before stimulus onset did not discriminate between hits and misses. Left, topographical map of the mean 1.5 s, 8–12 Hz power with parieto-occipital alpha power averaged over hits and misses. Black crosses indicate sensors with large alpha power. Right, bar graph of the mean alpha power at the sensors marked by crosses on the map separately in hits and misses (P = 0.94). (c) Neural responses evoked by the warning cue were similar in hits and misses. Left, root mean square (RMS) average across all magnetometers in hits and misses. Middle, topographical map of the most prominent peak of the event-related field (ERF) around 150 ms averaged across subjects and conditions. Black crosses indicate sensors with large responses. Right, bar graph of magnetic field amplitude separately in hits and misses over the sensors showing the largest outgoing positive field (P = 0.12) or largest ingoing negative field (P = 0.11). Error bars represent the s.e.m.

  6. Mean interbeat interval variability.
    Supplementary Fig. 1: Mean interbeat interval variability.

    Data are presented from the interbeat interval during which the warning signal appeared on the screen until interbeat intervals after response delivery. Interbeat interval variability decreased after stimulus onset (* p<0.05), but did not differ between hits and misses (Greenhouse-Geisser corrected 2-way ANOVA with factors Consciousness and Time, main effect of Time F2.0,32.0=11.7, p=2.10—4; main effect of Consciousness F1,16=0.9, p=0.36; interaction F2.39,38.24=2.0, p=0.13). Error bars represent s.e.m.

  7. Neural responses to hearbeats in subjects with fast or slow heart rate.
    Supplementary Fig. 2: Neural responses to hearbeats in subjects with fast or slow heart rate.

    Mean time course across the cluster in hits and misses, in subjects with (a) short (n=9, mean IBI 730 ms) or (b) long (n=8, mean IBI 886 ms) interbeat intervals (IBI). Neural responses to heartbeats within the cluster significantly differed between hits and misses in both groups (short IBI group, t8=3.76, p=0.006; long IBI group, t7=3.19, p=0.015). Longer IBIs did not delay the effect, indicating that the effect corresponds to a differential response to the preceding heartbeat rather than a preparation of the next heartbeat. Error bars represent s.e.m.

  8. T-locked electrocardiogram, grand-average across subjects.
    Supplementary Fig. 3: T-locked electrocardiogram, grand-average across subjects.

    Top, vertical derivation. Bottom, horizontal derivation. We did not find any significant difference between hits and misses.

  9. Influence of cardiac artefact correction using independent component analysis (ICA) on prestimulus heartbeat-evoked responses.
    Supplementary Fig. 4: Influence of cardiac artefact correction using independent component analysis (ICA) on prestimulus heartbeat-evoked responses.

    (a) Topographical map of the difference between prestimulus heartbeat-evoked responses in hits and misses, grand-averaged across 17 subjects, in the 135—171 ms time window, after ICA correction, on magnetometer signals. The topography of the difference was not affected by ICA correction. (b) T-locked magnetic fields at the sensor indicated in white in A, before (top) and after (bottom) ICA correction. The R and T waves could barely be observed on ICA corrected data, but the significant difference between hits and misses in the 135—171 ms time window (shaded area) was preserved. The overall shift toward more negative values in ICA-corrected data is due to data mean-centering by ICA. (c) Amplitude of the prestimulus heartbeat-evoked response, averaged across the cluster separately in hits and misses, and during a separate resting session with eyes open, after ICA correction. The heart-evoked response in the 135—171 ms cluster significantly differed between hits and misses (paired t-test, t16= 4.81, p=2.10—4). It was larger in hits than during rest (paired t-test, t16=3.46, p=0.003) and smaller in misses than during rest (paired t-test, t16=2.39, p=0.03). Because ICA extracts from MEG data the shape of each participant's heartbeat, this analysis further shows that the effect is not dependent on subject-specific heartbeat morphology. Error bars represent s.e.m.

  10. Distribution of respiration phase in hits and misses at stimulus onset.
    Supplementary Fig. 5: Distribution of respiration phase in hits and misses at stimulus onset.

    Each point represents a subject and a condition. No preferential phase emerged (Raighley test for non-uniformity of circular data), neither in hits (p=0.81) nor in misses (p=0.67).

  11. Prestimulus peripheral blood pressure in hits and misses.
    Supplementary Fig. 6: Prestimulus peripheral blood pressure in hits and misses.

    Blood pressure (arbitrary units) was computed over those heartbeats used to compute the heartbeat-evoked neural activity. (a) Time course of pressure, separately in hits and misses. (b) Difference between systolic and diastolic pressure, separately in hits and misses. No significant difference between hits and misses could be found in systolic, diastolic, nor difference between systolic and diastolic pressure. Error bars represent s.e.m.

  12. Peripheral blood pressure throughout a trial.
    Supplementary Fig. 7: Peripheral blood pressure throughout a trial.

    The difference between systolic and diastolic pressure in arbitrary units was measured on the heartbeat preceding warning onset, preceding stimulus onset, preceding response, as well as the first (R+1) and second (R+2) heartbeats following response. Blood pressure evolved in the course of a trial, but did not differ between hits and misses (Greenhouse-Geisser corrected 2-way ANOVA with factors Consciousness and Time, main effect of Time F2.27,22.71=4,15, p=0.025; main effect of Consciousness F1,10=2.14, p=0.17; interaction F1.85,18.54=1.52, p=0.25; paired t-test between hits and misses before stimulus onset: t10=1.50, p=0.16). Error bars represent standard errors of the mean.

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Author information

Affiliations

  1. Cognitive Neuroscience Laboratory, Institut National de la Santé et de la Recherche Médicale (INSERM)–École Normale Supérieure (ENS), Paris, France.

    • Hyeong-Dong Park,
    • Stéphanie Correia &
    • Catherine Tallon-Baudry
  2. Cenir, Centre National de la Recherche Scientifique (CNRS)–Université Pierre-et-Marie-Curie (UPMC)-INSERM, Paris, France.

    • Antoine Ducorps

Contributions

H.-D.P. and C.T.-B. designed the experiment. H.-D.P. and S.C. acquired the data. H.-D.P., A.D. and C.T.-B. analyzed the data. H.-D.P. and C.T.-B. wrote the paper.

Competing financial interests

The authors declare no competing financial interests.

Corresponding author

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Supplementary information

Supplementary Figures

  1. Supplementary Figure 1: Mean interbeat interval variability. (73 KB)

    Data are presented from the interbeat interval during which the warning signal appeared on the screen until interbeat intervals after response delivery. Interbeat interval variability decreased after stimulus onset (* p<0.05), but did not differ between hits and misses (Greenhouse-Geisser corrected 2-way ANOVA with factors Consciousness and Time, main effect of Time F2.0,32.0=11.7, p=2.10—4; main effect of Consciousness F1,16=0.9, p=0.36; interaction F2.39,38.24=2.0, p=0.13). Error bars represent s.e.m.

  2. Supplementary Figure 2: Neural responses to hearbeats in subjects with fast or slow heart rate. (75 KB)

    Mean time course across the cluster in hits and misses, in subjects with (a) short (n=9, mean IBI 730 ms) or (b) long (n=8, mean IBI 886 ms) interbeat intervals (IBI). Neural responses to heartbeats within the cluster significantly differed between hits and misses in both groups (short IBI group, t8=3.76, p=0.006; long IBI group, t7=3.19, p=0.015). Longer IBIs did not delay the effect, indicating that the effect corresponds to a differential response to the preceding heartbeat rather than a preparation of the next heartbeat. Error bars represent s.e.m.

  3. Supplementary Figure 3: T-locked electrocardiogram, grand-average across subjects. (54 KB)

    Top, vertical derivation. Bottom, horizontal derivation. We did not find any significant difference between hits and misses.

  4. Supplementary Figure 4: Influence of cardiac artefact correction using independent component analysis (ICA) on prestimulus heartbeat-evoked responses. (74 KB)

    (a) Topographical map of the difference between prestimulus heartbeat-evoked responses in hits and misses, grand-averaged across 17 subjects, in the 135—171 ms time window, after ICA correction, on magnetometer signals. The topography of the difference was not affected by ICA correction. (b) T-locked magnetic fields at the sensor indicated in white in A, before (top) and after (bottom) ICA correction. The R and T waves could barely be observed on ICA corrected data, but the significant difference between hits and misses in the 135—171 ms time window (shaded area) was preserved. The overall shift toward more negative values in ICA-corrected data is due to data mean-centering by ICA. (c) Amplitude of the prestimulus heartbeat-evoked response, averaged across the cluster separately in hits and misses, and during a separate resting session with eyes open, after ICA correction. The heart-evoked response in the 135—171 ms cluster significantly differed between hits and misses (paired t-test, t16= 4.81, p=2.10—4). It was larger in hits than during rest (paired t-test, t16=3.46, p=0.003) and smaller in misses than during rest (paired t-test, t16=2.39, p=0.03). Because ICA extracts from MEG data the shape of each participant's heartbeat, this analysis further shows that the effect is not dependent on subject-specific heartbeat morphology. Error bars represent s.e.m.

  5. Supplementary Figure 5: Distribution of respiration phase in hits and misses at stimulus onset. (31 KB)

    Each point represents a subject and a condition. No preferential phase emerged (Raighley test for non-uniformity of circular data), neither in hits (p=0.81) nor in misses (p=0.67).

  6. Supplementary Figure 6: Prestimulus peripheral blood pressure in hits and misses. (62 KB)

    Blood pressure (arbitrary units) was computed over those heartbeats used to compute the heartbeat-evoked neural activity. (a) Time course of pressure, separately in hits and misses. (b) Difference between systolic and diastolic pressure, separately in hits and misses. No significant difference between hits and misses could be found in systolic, diastolic, nor difference between systolic and diastolic pressure. Error bars represent s.e.m.

  7. Supplementary Figure 7: Peripheral blood pressure throughout a trial. (56 KB)

    The difference between systolic and diastolic pressure in arbitrary units was measured on the heartbeat preceding warning onset, preceding stimulus onset, preceding response, as well as the first (R+1) and second (R+2) heartbeats following response. Blood pressure evolved in the course of a trial, but did not differ between hits and misses (Greenhouse-Geisser corrected 2-way ANOVA with factors Consciousness and Time, main effect of Time F2.27,22.71=4,15, p=0.025; main effect of Consciousness F1,10=2.14, p=0.17; interaction F1.85,18.54=1.52, p=0.25; paired t-test between hits and misses before stimulus onset: t10=1.50, p=0.16). Error bars represent standard errors of the mean.

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    Supplementary Figures 1–7 and Supplementary Tables 1–3

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