Short-term effects of subthalamic deep brain stimulation on clinical symptoms and biomarkers of neurodegeneration in Parkinson's disease

  1. Sanmartino, Florencia
  2. Rashid-López, Raúl
  3. Cruz-Gómez, Álvaro J.
  4. Lozano-Soto, Elena
  5. Cano-Cano, Fátima
  6. López-Sosa, Fernando
  7. Riqué, Jesús
  8. Espinosa-Rosso, Raúl
  9. González-Rosa, Javier J.
Revista:
Brain Stimulation

ISSN: 1935-861X

Any de publicació: 2023

Volum: 16

Número: 1

Pàgines: 304

Tipus: Article

DOI: 10.1016/J.BRS.2023.01.551 GOOGLE SCHOLAR lock_openAccés obert editor

Altres publicacions en: Brain Stimulation

Resum

Background and objectives: Here we investigated the possible changes in clinical and, neurocognitive status as well as in the regional magnetic resonance imaging (MRI) and blood markers of neurodegeneration and neuroaxonal injury induced after 1-year of deep brain stimulation of the subthalamic nucleus (STN-DBS) in patients with Parkinson disease (PD).Methods: Nine PD patients were assessed at baseline (before DBS electrodes implantation) and at 1-year after continuous STN-DBS treatment by a full clinical evaluation, a comprehensive neurocognitive assessment, a serum neurofilament light (sNfL) levels testing, and structural brain MRI measures.Results: Compared with the baseline, motor function, aspects of activities of daily living, and motor complications improved by bilateral STN-DBS treatment after short-term follow-up. No major changes in global or specific cognitive and neuropsychiatric functioning were observed, while at the group level, we identified a decrease in sNfL levels over time that was linked to improvement in motor complications. After multiple comparison corrections, a clear ventricular enlargement as well as decreased GM volume in specific orbitofrontal, inferior parietal, and cerebellar regions, including an increased GM volume of thalamic subnuclei, were also noticed at 1-year of follow-up.Conclusions: These findings emphasize the robust motor and non-motor clinical benefits of short-term bilateral STN stimulation in PD, supporting the notion of STN-DBS as an effective treatment. Importantly, the notable decrease of sNfL levels could represent a transient neuroprotective effect of the DBS probably caused by a dopaminergic-mediated “regulation” of STN stimulation. Nevertheless, the brain structural integrity changes observed after 1-year treatment suggest some type of neurodegenerative processes or structural changes and reorganization of key brain regions that might contribute to both clinical functional recovery and potential side effects in PD patients after STN-DBS. Taken together, these results emphasize emergent directions for neurodegeneration related-DBS biomarkers research.