Category: Parkinson's Disease: Surgical Therapy
Objective: To quantify and compare the differential effects of DBS and L-dopa on the individual kinematic components of bradykinesia.
Background: Parkinson’s disease (PD) bradykinesia is a complex of motor abnormalities. Deep brain stimulation (DBS) and L-dopa both improve bradykinesia, but their differential effects on each component remain unknown.
Method: PD patients with bilateral STN-DBS were prospectively evaluated at least three months after surgery. Clinical and kinematic analyses of finger tapping were performed under three conditions: OFF, ON-DBS (clinically optimized stimulation), and ON-medication. Bradykinesia was decomposed into amplitude, velocity, dysrhythmia, sequence effect, hesitations, and interruptions. Data were analyzed using repeated-measures ANOVA or Friedman tests, with Bonferroni-corrected post hoc comparisons.
Results: Twenty patients with PD were evaluated: mean follow-up after surgery of 7.5 (4.75-11.25) months. Both L-dopa and STN-DBS significantly improved clinical MDS-UPDRS part III finger-tapping scores compared to baseline (p < 0.001). Kinematically, neither therapy was statistically superior overall, but STN-DBS showed a significantly greater effect on amplitude, velocity, and interruptions (p < 0.05), while L-dopa only showed a greater effect on hesitations (p = 0.03), compared with the OFF baseline. Dysrhythmia and sequence effects were unaffected by either therapy. When the kinematic components corresponding to the puntuation items of MDS-UPDRS part III finger-tapping (velocity, slope of amplitude, hesitations and interruptions) were combined in a composite kinematic score, only DBS showed a significant difference compared with the OFF baseline (p < 0.001).
Conclusion: Although L-dopa and STN-DBS provide comparable clinical improvement in bradykinesia, each therapy has differential effects on specific kinematic components. STN-DBS might provide greater improvement in both individual and combined components of bradykinesia. The pathophysiological mechanisms underlying these differences may involve broader neural networks that are differentially targeted by each therapy.
References: 1. Bologna M, Espay AJ, Fasano A, Paparella G, Hallett M, Berardelli A. Redefining Bradykinesia. Mov Disord. 2023;38(4):551-557. doi:10.1002/mds.29362
2. Paparella G, De Riggi M, Cannavacciuolo A, Birreci D, Costa D, Angelini L, Alunni Fegatelli D, Fasano A, Espay AJ, Bologna M. Analyzing the ‘Bradykinesia Complex’ in Parkinson’s Disease. Mov Disord. 2026 Jan;41(1):143-155. doi: 10.1002/mds.70082.
To cite this abstract in AMA style:
D. Marín-Medina, M. Wilken, F. Wainberg, M. Merello. Differential effects of levodopa and subthalamic nucleus deep brain stimulation on the bradykinesia components in Parkinson’s Disease [abstract]. Mov Disord. 2026; 41 (suppl 1). https://www.mdsabstracts.org/abstract/differential-effects-of-levodopa-and-subthalamic-nucleus-deep-brain-stimulation-on-the-bradykinesia-components-in-parkinsons-disease/. Accessed October 1, 2026.« Back to 2026 International Congress
MDS Abstracts - https://www.mdsabstracts.org/abstract/differential-effects-of-levodopa-and-subthalamic-nucleus-deep-brain-stimulation-on-the-bradykinesia-components-in-parkinsons-disease/
