Discovering the hidden secrets of levodopa-induced dyskinesia (LID) in Parkinson’s disease (PD) requires a closer look at the mysterious basal ganglia (BG). In this study, researchers used a cutting-edge surface-based shape analysis technique to investigate structural changes in the BG that may be associated with LID. They compared two groups of PD patients: one group who developed LID within 3 years and another group who did not develop it even after 7 years of levodopa treatment. The results revealed interesting findings – the LID group displayed localized atrophy in the right globus pallidus interna (GPi), while both groups had similar volumes. Additionally, there was a significant reduction in structural connectivity between the left GPi and thalamus in the LID group. These findings indicate that the shape alterations in specific regions of the BG, particularly the GPi, are linked to LID in PD. Since the GPi is a crucial hub involved in both direct and indirect pathways of the BG, its structural changes may play a vital role in the development of LID. Further research could provide a deeper understanding of these mechanisms and potentially lead to novel treatments for LID in PD.
BackgroundDespite the clinical impact of levodopa-induced dyskinesia (LID) in Parkinson’s disease (PD), the mechanism, especially the role of basal ganglia (BG), is not fully elucidated yet. We investigated the BG structural changes related to LID in PD using a surface-based shape analysis technique.MethodsWe recruited patients with PD who developed LID within 3 years (LID group, 28 patients) and who did not develop it after 7 years (non-LID group, 35 patients) from levodopa treatment for the extreme case-control study. BG structure volumes were measured using volumetry analysis and the surface-based morphometry feature (i.e., Jacobian) from the subcortical surface vertices. We compared the volume and Jacobian of meshes in the regions between the two groups. We also performed a correlation analysis between local atrophy and the severity of LID. Additionally, we evaluated structural connectivity profiles from globus pallidus interna and externa (GPi and GPe) to other brain structures based on the group comparison.ResultsThe demographic and clinical data showed no significant difference except for disease duration, treatment duration, parkinsonism severity, and levodopa equivalent dose. The LID group had more local atrophies of vertices in the right GPi than the non-LID group, despite no difference in volumes. Furthermore, the LID group demonstrated significantly reduced structural connectivity between left GPi and thalamus.ConclusionThis is the first demonstration of distinct shape alterations of basal ganglia structures, especially GPi, related to LID in PD. Considering both direct and indirect BG pathways share the connection between GPi and thalamus, the BG pathway plays a crucial role in the development of LID.
Dr. David Lowemann, M.Sc, Ph.D., is a co-founder of the Institute for the Future of Human Potential, where he leads the charge in pioneering Self-Enhancement Science for the Success of Society. With a keen interest in exploring the untapped potential of the human mind, Dr. Lowemann has dedicated his career to pushing the boundaries of human capabilities and understanding.
Armed with a Master of Science degree and a Ph.D. in his field, Dr. Lowemann has consistently been at the forefront of research and innovation, delving into ways to optimize human performance, cognition, and overall well-being. His work at the Institute revolves around a profound commitment to harnessing cutting-edge science and technology to help individuals lead more fulfilling and intelligent lives.
Dr. Lowemann’s influence extends to the educational platform BetterSmarter.me, where he shares his insights, findings, and personal development strategies with a broader audience. His ongoing mission is shaping the way we perceive and leverage the vast capacities of the human mind, offering invaluable contributions to society’s overall success and collective well-being.