Tourette syndrome is a neurodevelopmental condition marked by unwanted, repetitive motor and vocal tics, affecting roughly 0.3 to 0.9 percent of school-aged children. Its neurobiology centers on disruptions in cortico-striato-thalamo-cortical circuits, the loops that integrate motor, sensory, and emotional processing. What has long intrigued clinicians is that tics do not emerge at random: they wax and wane with internal states, often preceded by premonitory urges, uncomfortable sensations that many patients describe as an itch that can only be relieved by moving. Stress and arousal also modulate tic severity. Because these states are indexed by autonomic activity, particularly the parasympathetic variability reflected in heart rate fluctuations, researchers have long suspected that the autonomic nervous system is not merely a bystander but an active contributor to the moment-to-moment expression of tics.

The empirical record on autonomic function in Tourette syndrome, however, has been inconsistent. Some early cardiovascular studies found little evidence of baseline autonomic abnormalities, while later work identified alterations in sensory habituation, parasympathetic tone, sympathetic reactivity, and heart rate dynamics. The research team attributes these contradictions to small samples, methodological heterogeneity, and above all a reliance on group-level analyses that can mask meaningful individual variation. Moreover, previous studies typically examined autonomic function in isolation, without jointly measuring brain activity. The new study set out to close that gap by tracking how short-timescale parasympathetic variability, estimated from the pulse signal, relates to the coordination of large-scale brain networks within individual children as they simply rested in the scanner.

Methodologically, the study stands out for its depth rather than its breadth. Each of the four participants, aged 10 to 13, underwent four to six MRI sessions on a Siemens Prisma 3T scanner, yielding tens of minutes of low-motion resting-state fMRI per child, recorded concurrently with a wireless finger-clip pulse oximeter sampling at roughly 200 hertz. This precision functional mapping approach, which densely samples each individual to boost signal-to-noise ratio, allowed the researchers to define each child’s functional networks on their own terms rather than forcing them into a group template. Using the Infomap community detection algorithm applied to correlation matrices across nearly 60,000 cortical vertices, the team assigned every vertex to one of eleven canonical networks, including the default mode, salience, ventral attention/language, frontoparietal, action-mode, and the somato-cognitive action network, the last manually identified in each individual because it is absent from standard atlases.

From the pulse recordings, the team computed the root mean square of successive differences, or RMSSD, a widely used window into cardiac vagal activity, and confirmed through split-half reliability analyses that 90-second sliding windows stepped every 45 seconds offered the most stable coupling estimates. Within each window, they calculated functional connectivity between each pair of networks and paired it with the RMSSD value from the same interval. These time-resolved estimates were then fed into Bayesian linear mixed-effects models fit separately for the children with Tourette syndrome and their siblings, with heart rate and window quality as covariates, and with a circular-shift null model that scrambled the temporal alignment between heart and brain while preserving each signal’s statistical structure. Analyses were organized around two theoretically motivated sets of connections: one targeting interoception and urge awareness, the other targeting inhibitory control and action regulation.

The most striking result was a pattern of opposing coupling directions between affected and unaffected children. In the interoceptive analysis, children with Tourette syndrome showed positive associations between RMSSD and connectivity between the default mode network and the ventral attention/language network, as well as between the somato-cognitive action network and the salience network, patterns absent or reversed in their siblings. The default mode network supports internal state representation and self-referential processing, while the ventral attention network reorients attention to salient events, so a positive coupling in these children suggests that when parasympathetic variability rises, internal bodily signals become more tightly integrated with the attentional systems that could capture them, a plausible mechanism for how premonitory urges seize awareness. Conversely, at connections linking the default mode network to the somato-cognitive action network, the unaffected siblings showed positive associations while the affected children showed negative tendencies, hinting that parasympathetic tone supports integrated internal-state-to-action coordination only in the tic-free brains.

The second analysis sharpened the picture around action regulation. At the connection between the somato-cognitive action network and the action-mode network, which supports sustained task control and physiological regulation with documented links to the adrenal medulla, children with Tourette syndrome again showed positive RMSSD coupling where their siblings showed the opposite, negative direction. Meanwhile, the affected children displayed negative associations between RMSSD and connectivity anchored on the frontoparietal network, the brain’s top-down executive control system, with no comparable disengagement in siblings. The authors interpret this as a possible decoupling of executive control circuitry precisely when parasympathetic variability is elevated, though they caution that their correlational design cannot determine whether such coupling facilitates tic generation or its suppression. Notably, the default mode to somato-cognitive action connection, shared between both analyses as an anchor, reproduced the same reversed pattern in both, suggesting it may reflect a stable difference in brain-heart organization rather than an analytical artifact.

It is essential to underscore what these findings are and are not. With only two children per group, all credible intervals crossed zero, and the authors explicitly frame the results as directional trends and hypothesis-generating observations rather than definitive estimates. The physiological measures themselves appeared to follow familial rather than diagnostic lines: one sibling pair showed higher heart rates and lower RMSSD than the other regardless of Tourette status, indicating that shared familial or developmental factors shape baseline autonomic function. Clinical heterogeneity also complicates interpretation, since one affected child carried comorbid ADHD, generalized anxiety disorder, and obsessive-compulsive disorder, and roughly 80 percent of children with Tourette syndrome have at least one comorbid psychiatric condition. Pulse-derived RMSSD, moreover, is an estimate of vagal activity rather than an electrocardiographic measurement, respiration was not explicitly modeled, and tic events were not individually annotated during scanning, leaving open whether tic-related motion contributed to the signals.

Yet the significance of the approach may outlast the preliminary nature of its conclusions. By pairing individualized network mapping with time-resolved physiology, the study demonstrates that autonomic-neural coupling can be measured at the level of a single child and that its directional properties may carry clinically relevant information invisible to group averages. The discordant sibling design, comparing children who share genetics and environment but differ in tic expression, offers a template for isolating disorder-specific features of brain-body interaction. The authors envision future work combining precision mapping with task-based paradigms such as voluntary tic suppression, multimodal recordings including electrocardiography and respiratory monitoring, subcortical structures like the basal ganglia and thalamus, and wearable pulse devices that would track brain-heart coupling in the daily contexts where tics and premonitory urges actually unfold.

If replicated in larger family-based cohorts, the findings could reshape how clinicians think about tic disorders, positioning altered brain-heart coupling not as a uniform excess or deficit but as a reorganization of how internal bodily signals are woven into attentional and action systems. They also point toward personalized interventions: behavioral therapies, biofeedback, and neurofeedback approaches targeting internal state awareness and autonomic regulation might eventually be guided by an individual’s own coupling profile. For now, the study stands as a compelling proof of concept that in Tourette syndrome, the dialogue between heart and brain may be speaking in a different direction than in the siblings who share everything but the tics.

Subject of Research: Brain-heart coupling and autonomic influence on functional brain networks in Tourette syndrome

Article Title: Brain-heart coupling in tourette syndrome: a precision functional mapping study of discordant siblings

Article References: Ali, S. A., Demeter, D. V., Baim, A. R., Ahern, J., Ben Ahn, J. H., Chang, S. E., Koithan, E. M., Park, S., Smarr, B. L., & Greene, D. J. (2026). Brain-heart coupling in tourette syndrome: a precision functional mapping study of discordant siblings. Frontiers in Network Physiology, 6, Article 1881914. https://doi.org/10.3389/fnetp.2026.1881914

Image Credits: AI Generated

DOI: 10.3389/fnetp.2026.1881914

Keywords: Tourette syndrome, brain-heart coupling, heart rate variability, precision functional mapping, functional connectivity, autonomic nervous system, interoception, premonitory urges, resting-state fMRI, network physiology, sibling study, RMSSD