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Peer-reviewedCC BYImaging neuroscience (Cambridge, Mass.)

Disrupted brain network topology and structure-function coupling in non-specific low back pain.

  • Lionel Butry1
  • Frederick Junker2
  • Sam Vickery2
  • Daniel L Belavy2
  • Rebekka Döding2,3
  • Katja Ehrenbrusthoff2
  • Maia Angelova4
  • Bjoern Buehring5,6
  • Bernadette Fitzgibbon7
  • Chandan Karmakar8
  • Clint T Miller9
  • Patrick J Owen10,11
7 more authors
  • Tobias L Schulte12
  • Scott D Tagliaferri13,14
  • Guy Trudel15,16,17
  • Jessica Van Oosterwijck18,19
  • Hans-Joachim Wilke20
  • Elena K Enax-Krumova1
  • Lara Schlaffke1,21,22
22 affiliations
  1. 1Ruhr University Bochum, BG University Hospital Bergmannsheil, Department of Neurology, Bochum, Germany.
  2. 2Fachbereich Pflege-, Hebammen- und Therapiewissenschaften (PHT), Hochschule Bochum, Bochum, Germany.
  3. 3Institute of Exercise Training and Sport Informatics, German Sport University Cologne, Cologne, Germany.
  4. 4Sir Peter Rigby Digital Futures Institute, Aston University, Birmingham, United Kingdom.
  5. 5Bergisches Rheuma-Zentrum, Krankenhaus St Josef, Wuppertal, Germany.
  6. 6Ruhr University Bochum, Rheumazentrum Ruhrgebiet, Bochum, Germany.
  7. 7School of Medicine and Psychology, College of Health and Medicine, The Australian National University, Canberra, Australia.
  8. 8School of Information Technology, Deakin University, Geelong, Australia.
  9. 9Institute for Physical Activity and Nutrition (IPAN), School of Exercise and Nutrition Sciences, Deakin University, Geelong, Australia.
  10. 10Eastern Health Emergency Medicine Program, Melbourne, Australia.
  11. 11Eastern Health Clinical School, Monash University, Melbourne, Australia.
  12. 12Ruhr University Bochum, St. Josef-Hospital, Katholisches Klinikum Bochum, Department of Orthopaedics and Trauma Surgery, Bochum, Germany.
  13. 13The National Centre of Excellence in Youth Mental Health, Orygen, Parkville, Australia.
  14. 14Centre for Youth Mental Health, University of Melbourne, Melbourne, Australia.
  15. 15Bone and Joint Research Laboratory, Ottawa Hospital Research Institute, Ottawa, Canada.
  16. 16Department of Medicine, The Ottawa Hospital, Ottawa, Canada.
  17. 17Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Canada.
  18. 18Spine, Head and Pain Research Unit Ghent, Department of Rehabilitation Sciences, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium.
  19. 19Pain in Motion International Research Consortium, Brussels, Belgium.
  20. 20Institute of Orthopaedic Research and Biomechanics, Ulm University Medical Centre, Ulm, Germany.
  21. 21Department of Information Technology, FH Dortmund, University of Applied Sciences and Arts, Dortmund, Germany.
  22. 22Ruhr University Bochum, St. Josef-Hospital, University Hospital of Pediatrics and Adolescent Medicine, Bochum, Germany.
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Abstract

Central nervous system mechanisms contribute to non-specific low back pain (LBP), with widespread alterations in brain function and structure reported. It remains unclear how these alterations propagate to brain network topology and structure-function coupling. In this cross-sectional study, 282 participants with non-specific LBP (mean ± standard deviation, pain intensity 4.3 ± 1.7 [0-10 numerical rating scale]; current pain duration 54 ± 105 weeks) and 71 pain-free controls underwent resting-state functional and diffusion-weighted MRI to derive functional and structural connectomes. Subgroups were analyzed by pain status during scanning and pain duration. The main graph-theory analysis revealed that participants with non-specific LBP had lower segregation (d = 0.39-0.45, P = 0.009-0.019) in the whole-brain functional network and higher integration (d = 0.30-0.38, P = 0.005-0.027) in the functional ventral attention network. Subgroup analysis showed that participants with chronic non-specific LBP had lower segregation (d = 0.48, P = 0.002) and higher integration (d = 0.45, P = 0.004) within the structural default mode network. By modeling functional connectivity using structural communication predictors in a multivariable linear regression, we identified structure-function decoupling in participants with non-specific LBP across the whole-brain (d = 0.25-0.28, P = 0.026-0.041), ventral attention (d = 0.28-0.32, P = 0.005-0.048), and default mode network (d = 0.22-0.24, P = 0.031-0.046), alongside complex regional patterns of both decoupling and hypercoupling. Explorative partial correlation analyses associated disability, rather than pain intensity, with differences in brain network topology and structure-function decoupling. These findings advance the mechanistic understanding of the severity and persistence of non-specific LBP, showing disrupted bottom-up attentional processing and self-referential circuitry, resulting in large-scale structure-function decoupling.

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Cite

BibTeXRIS
BibTeX
@article{butry2026disrupted,
  title = {{Disrupted brain network topology and structure-function coupling in non-specific low back pain.}},
  author = {Lionel Butry and Frederick Junker and Sam Vickery and Daniel L Belavy and Rebekka Döding and Katja Ehrenbrusthoff and Maia Angelova and Bjoern Buehring and Bernadette Fitzgibbon and Chandan Karmakar and Clint T Miller and Patrick J Owen and Tobias L Schulte and Scott D Tagliaferri and Guy Trudel and Jessica Van Oosterwijck and Hans-Joachim Wilke and Elena K Enax-Krumova and Lara Schlaffke},
  journal = {Imaging neuroscience (Cambridge, Mass.)},
  year = {2026},
  month = oct,
  doi = {10.1162/imag.a.1412},
  url = {https://europepmc.org/article/MED/42948267},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Disrupted brain network topology and structure-function coupling in non-specific low back pain.
AU  - Lionel Butry
AU  - Frederick Junker
AU  - Sam Vickery
AU  - Daniel L Belavy
AU  - Rebekka Döding
AU  - Katja Ehrenbrusthoff
AU  - Maia Angelova
AU  - Bjoern Buehring
AU  - Bernadette Fitzgibbon
AU  - Chandan Karmakar
AU  - Clint T Miller
AU  - Patrick J Owen
AU  - Tobias L Schulte
AU  - Scott D Tagliaferri
AU  - Guy Trudel
AU  - Jessica Van Oosterwijck
AU  - Hans-Joachim Wilke
AU  - Elena K Enax-Krumova
AU  - Lara Schlaffke
PY  - 2026
DA  - 2026/10/26
JO  - Imaging neuroscience (Cambridge, Mass.)
DO  - 10.1162/imag.a.1412
UR  - https://europepmc.org/article/MED/42948267
AB  - Central nervous system mechanisms contribute to non-specific low back pain (LBP), with widespread alterations in brain function and structure reported. It remains unclear how these alterations propagate to brain network topology and structure-function coupling. In this cross-sectional study, 282 participants with non-specific LBP (mean ± standard deviation, pain intensity 4.3 ± 1.7 [0-10 numerical rating scale]; current pain duration 54 ± 105 weeks) and 71 pain-free controls underwent resting-state functional and diffusion-weighted MRI to derive functional and structural connectomes. Subgroups were analyzed by pain status during scanning and pain duration. The main graph-theory analysis revealed that participants with non-specific LBP had lower segregation (d = 0.39-0.45, P = 0.009-0.019) in the whole-brain functional network and higher integration (d = 0.30-0.38, P = 0.005-0.027) in the functional ventral attention network. Subgroup analysis showed that participants with chronic non-specific LBP had lower segregation (d = 0.48, P = 0.002) and higher integration (d = 0.45, P = 0.004) within the structural default mode network. By modeling functional connectivity using structural communication predictors in a multivariable linear regression, we identified structure-function decoupling in participants with non-specific LBP across the whole-brain (d = 0.25-0.28, P = 0.026-0.041), ventral attention (d = 0.28-0.32, P = 0.005-0.048), and default mode network (d = 0.22-0.24, P = 0.031-0.046), alongside complex regional patterns of both decoupling and hypercoupling. Explorative partial correlation analyses associated disability, rather than pain intensity, with differences in brain network topology and structure-function decoupling. These findings advance the mechanistic understanding of the severity and persistence of non-specific LBP, showing disrupted bottom-up attentional processing and self-referential circuitry, resulting in large-scale structure-function decoupling.
SN  - 2837-6056
ER  -