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PreprintCC BY-NC-ND 4.0arXiv

Synchronized Hearts, Desynchronized Brains: A Nonlinear Dynamics Perspective for Function and Failure

7 more authors

Abstract

Both the heart and the brain are built from electrically excitable cells, yet the emergent dynamics of these organs could not differ more. In the myocardium, a coherent traveling wave of action potentials ensures coordinated contraction; in the cerebral cortex, distributed, irregular spiking underlies efficient information processing and the generation of behavior. Here, we illuminate the principles that underlie the emergence of such distinct nonlinear dynamics using concepts from complex systems. We trace these principles across scales from ion channels and cellular action potential generation, through cellular coupling mechanisms and network architecture, to organ level dynamics and clinical phenotypes. Designed to support either synchronized waves or desynchronized information processing, the heart and the brain can thus be understood as operating on opposite sides of a synchronization phase transition. Crossing this transition implies pathological dynamics in both organs: Loss of synchrony in the heart produces arrhythmia; excess synchrony in the brain leads to epileptic seizures. We discuss how adaptation mechanisms, including plasticity, modulation, remodeling, and learning, maintain the appropriate level of (de)synchronization. Overall, we provide a unified excitable-system perspective, together with an educational notebook, to foster cross-disciplinary insights into cardiac and neural function and pathology.

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BibTeX
@misc{pellini2026synchronized,
  title = {{Synchronized Hearts, Desynchronized Brains: A Nonlinear Dynamics Perspective for Function and Failure}},
  author = {Irene Pellini and Simon Bauer and Seba Contreras and Ruben Fernández Busnadiego and Anushka Deb and Sophia Hartmann and Sayedeh Hussaini and Dörte M. Katschinski and Sarah Köster and Stephan E. Lehnart and Tobias Moser and Andreas Neef and Ulrich Parlitz and Silvio Rizzoli and Maria-Patapia Zafeiriou and Wolfram-Hubertus Zimmermann and Johannes Zierenberg and Philip Bittihn and Viola Priesemann},
  howpublished = {arXiv},
  year = {2026},
  month = nov,
  doi = {10.48550/arxiv.2611.06618},
  eprint = {2611.06618},
  archivePrefix = {arXiv},
  url = {https://arxiv.org/abs/2611.06618},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - UNPB
TI  - Synchronized Hearts, Desynchronized Brains: A Nonlinear Dynamics Perspective for Function and Failure
AU  - Irene Pellini
AU  - Simon Bauer
AU  - Seba Contreras
AU  - Ruben Fernández Busnadiego
AU  - Anushka Deb
AU  - Sophia Hartmann
AU  - Sayedeh Hussaini
AU  - Dörte M. Katschinski
AU  - Sarah Köster
AU  - Stephan E. Lehnart
AU  - Tobias Moser
AU  - Andreas Neef
AU  - Ulrich Parlitz
AU  - Silvio Rizzoli
AU  - Maria-Patapia Zafeiriou
AU  - Wolfram-Hubertus Zimmermann
AU  - Johannes Zierenberg
AU  - Philip Bittihn
AU  - Viola Priesemann
PY  - 2026
DA  - 2026/11/04
PB  - arXiv
DO  - 10.48550/arxiv.2611.06618
UR  - https://arxiv.org/abs/2611.06618
AB  - Both the heart and the brain are built from electrically excitable cells, yet the emergent dynamics of these organs could not differ more. In the myocardium, a coherent traveling wave of action potentials ensures coordinated contraction; in the cerebral cortex, distributed, irregular spiking underlies efficient information processing and the generation of behavior. Here, we illuminate the principles that underlie the emergence of such distinct nonlinear dynamics using concepts from complex systems. We trace these principles across scales from ion channels and cellular action potential generation, through cellular coupling mechanisms and network architecture, to organ level dynamics and clinical phenotypes. Designed to support either synchronized waves or desynchronized information processing, the heart and the brain can thus be understood as operating on opposite sides of a synchronization phase transition. Crossing this transition implies pathological dynamics in both organs: Loss of synchrony in the heart produces arrhythmia; excess synchrony in the brain leads to epileptic seizures. We discuss how adaptation mechanisms, including plasticity, modulation, remodeling, and learning, maintain the appropriate level of (de)synchronization. Overall, we provide a unified excitable-system perspective, together with an educational notebook, to foster cross-disciplinary insights into cardiac and neural function and pathology.
ER  -