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  • One side effect: two networks? Lateral and posteromedial stimulation spreads induce dysarthria in subthalamic deep brain stimulation for Parkinson’s disease

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Movement disorders
Original research
One side effect: two networks? Lateral and posteromedial stimulation spreads induce dysarthria in subthalamic deep brain stimulation for Parkinson’s disease
  1. Hannah Jergas1,
  2. Jan Niklas Petry-Schmelzer1,
  3. Jonathan H Hannemann1,
  4. Tabea Thies1,2,
  5. Joshua N Strelow1,3,
  6. Ilona Rubi-Fessen4,5,
  7. Jana Quinting5,
  8. Juan Carlos Baldermann1,6,
  9. Doris Mücke2,
  10. Gereon R Fink1,7,
  11. Veerle Visser-Vandewalle3,
  12. Till A Dembek1,
  13. Michael T Barbe1
  1. 1Department of Neurology, University Hospital Cologne, Cologne, Germany
  2. 2iFL Phonetics, University of Cologne, Cologne, Germany
  3. 3Department of Stereotactic and Functional Neurosurgery, University Hospital Cologne, Cologne, Germany
  4. 4RehaNova Neurological Rehabilitation Clinic, Cologne, Germany
  5. 5Department of Special Education and Rehabilitation, University of Cologne, Koln, Germany
  6. 6Department of Psychiatry, University of Cologne, Cologne, Nordrhein-Westfalen, Germany
  7. 7Cognitive Neuroscience Section, Institute of Neuroscience and Medicine (INM-3), Research Centre Jülich, Jülich, Germany
  1. Correspondence to Jan Niklas Petry-Schmelzer; jan.petry-schmelzer{at}uk-koeln.de

Abstract

Background Stimulation-induced dysarthria (SID) is a troublesome and potentially therapy-limiting side effect of deep brain stimulation of the subthalamic nucleus (STN-DBS) in patients with Parkinson’s disease (PD). To date, the origin of SID, and especially whether there is an involvement of cerebellar pathways as well as the pyramidal tract, remains a matter of debate. Therefore, this study aims to shed light on structural networks associated with SID and to derive a data-driven model to predict SID in patients with PD and STN-DBS.

Methods Randomised, double-blinded monopolar reviews determining SID thresholds were conducted in 25 patients with PD and STN-DBS. A fibre-based mapping approach, implementing the calculation of fibr-wise ORs for SID, was employed to identify the distributional pattern of SID in the STN’s vicinity. The ability of the data-driven model to classify stimulation volumes as ‘causing SID’ or ‘not causing SID’ was validated by calculating receiver operating characteristics (ROC) in an independent out-of-sample cohort comprising 14 patients with PD and STN-DBS.

Results Local fibre-based stimulation maps showed an involvement of fibres running lateral and posteromedial to the STN in the pathogenesis of SID, independent of the investigated hemisphere. ROC analysis in the independent out-of-sample cohort resulted in a good fit of the data-driven model for both hemispheres (area under the curve (AUC)left=0.88, AUCright=0.88).

Conclusions This study reveals an involvement of both, cerebello-thalamic fibres, as well as the pyramidal tract, in the pathogenesis of SID in STN-DBS. The results may impact future postoperative programming strategies to avoid SID in patients with PD and STN-DBS

Trial registration number DRKS00023221; German Clinical Trials Register (DRKS) Number.

  • MOTOR CONTROL
  • MOVEMENT DISORDERS
  • NEUROSURGERY
  • PARKINSON'S DISEASE
  • SPEECH, ARTICULATION

https://doi.org/10.1136/jnnp-2024-333434

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    Footnotes

    • HJ and JNP-S contributed equally.

    • Contributors HJ, JNP-S, TT, MTB and TAD are responsible for conceptualisation and methodology. HJ, JNP-S, TT, JHH and JNS are responsible for data collection and curation. HJ, JNP-S and TAD are responsible for formal analysis. HJ and JNP-S provided the first draft of the manuscript and revised the final submission; all authors contributed to discussions on data analysis and interpretation, revised the manuscript and approved the final version. The corresponding author (JNP-S) is responsible for the overall content as guarantor for the article.

    • Funding JPS was funded by the Cologne Clinician Scientist Program (CCSP)/Faculty of Medicine/University of Cologne. Funded by the German Research Foundation (DFG, FI 773/15-1). JHH was supported by the Koeln Fortune Program/Faculty of Medicine, University of Cologne.

    • Competing interests None declared.

    • 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.