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Original research
Sweets for my sweet: modulation of the limbic system drives salience for sweet foods after deep brain stimulation in Parkinson’s disease
  1. Julia Steinhardt1,
  2. Henrike Hanssen1,2,
  3. Marcus Heldmann1,3,
  4. Alexander Neumann4,
  5. Alexander Münchau5,
  6. Peter Schramm4,
  7. Dirk Rasche6,
  8. Assel Saryyeva7,
  9. Lars Büntjen8,
  10. Jürgen Voges8,9,
  11. Volker Tronnier6,
  12. Joachim K. Krauss7,
  13. Thomas F. Münte1,3,
  14. Norbert Brüggemann1,2
  1. 1Department of Neurology, Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany
  2. 2Institute of Neurogenetics, University of Lübeck, Lübeck, Germany
  3. 3Institute of Psychology II, University of Lübeck, Lübeck, Germany
  4. 4Institute of Neuroradiology, University of Lübeck, Lübeck, Germany
  5. 5Institute of Systems Motor Science, University of Lübeck, Lübeck, Germany
  6. 6Department of Neurosurgery, University of Lübeck, Lübeck, Germany
  7. 7Department of Neurosurgery, Hannover Medical School, Hanover, Niedersachsen, Germany
  8. 8Department of Neurology and Stereotactic Neurosurgery, Otto von Guericke University Magdeburg, Magdeburg, Germany
  9. 9Leibniz Institute of Neurobiology, Magdeburg, Germany
  1. Correspondence to Dr Norbert Brüggemann, Department of Neurology, University of Lübeck, Lübeck, Germany; norbert.brueggemann{at}neuro.uni-luebeck.de

Abstract

Background An increase in body weight is observed in the majority of patients with Parkinson’s disease (PD) who undergo deep brain stimulation (DBS) of the subthalamic nucleus (STN) although the mechanisms are unclear.

Objectives To identify the stimulation-dependent effects on reward-associated and attention-associated neural networks and to determine whether these alterations in functional connectivity are associated with the local impact of DBS on different STN parcellations.

Methods We acquired functional task-related MRI data from 21 patients with PD during active and inactive STN DBS and 19 controls while performing a food viewing paradigm. Electrode placement in the STN was localised using a state-of-the-art approach. Based on the 3D model, the local impact of STN DBS was estimated.

Results STN DBS resulted in a mean improvement of motor function of 22.6%±15.5% (on medication) and an increase of body weight of ~4 kg within 2 years of stimulation. DBS of the limbic proportion of the STN was associated with body weight gain and an increased functional connectivity within the salience network and at the same time with a decreased activity within the reward-related network in the context of sweet food images.

Conclusions Our findings indicate increased selective attention for high-caloric foods and a sweet food seeking-like behaviour after DBS particularly when the limbic proportion of the STN was stimulated.

  • Parkinson's disease
  • electrical stimulation
  • limbic system
  • visual attention

Data availability statement

Data are available upon reasonable request. The data that support the findings of this study are available from the corresponding author, upon reasonable request. The MRI datasets are not publicly available because of data privacy regulations of patient data.

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Data availability statement

Data are available upon reasonable request. The data that support the findings of this study are available from the corresponding author, upon reasonable request. The MRI datasets are not publicly available because of data privacy regulations of patient data.

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Footnotes

  • JS and HH contributed equally.

  • Contributors NB, MH and HH conceived and planned the experiments. HH, AN, PS, DR, AS, LB, JV, VT, JKK, TM and NB planned and organised the experiments. JS, HH, MH, AM and NB carried out the experiments. JS, MH and NB planned the statistical analysis. JS and NB carried out the statistical analysis. All authors contributed to the interpretation of the results. JS took the lead in writing the manuscript and wrote the first draft. All authors provided critical feedback and helped shape the research, analysis and manuscript. N.B. took the full responsibility for the work and the conduction of the study, had access to the data, and controlled the decision for publication.

  • Funding This publication was supported by grants of the German Research Foundation to the Graduiertenkolleg 1957 ‘Adipocyte-Brain Crosstalk’, University of Lübeck and to the Sonderforschungsbereich 936 ‘Multi-Cite Communication in the brain’ (project C5).

  • Competing interests JKK is a consultant to Medtronic and Boston Scientific.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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