The Precuneus Region Drives Brain Network Changes in Tremor-Dominant Parkinson's Disease: Insights from a Morphological Causal Analysis

Moxuan Zhang , Siyu Zhou , Pengda Yang , Huizhi Wang , Jinli Ding , Xiaobo Wang , Xuzhu Chen , Chaonan Zhang , Anni Wang , Yuan Gao , Qiang Liu , Yuchen Ji , Yin Jiang , Lin Shi , Chunlei Han , Zhong Yang , Tao Feng , Jianguo Zhang , Fangang Meng

MedComm ›› 2025, Vol. 6 ›› Issue (11) : e70441

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MedComm ›› 2025, Vol. 6 ›› Issue (11) : e70441 DOI: 10.1002/mco2.70441
ORIGINAL ARTICLE

The Precuneus Region Drives Brain Network Changes in Tremor-Dominant Parkinson's Disease: Insights from a Morphological Causal Analysis

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Abstract

The tremor-dominant (TD) subtype of Parkinson's disease (PD) is characterized by prominent tremor symptoms. However, the temporal and causal relationships between brain structural alterations in TD patients remain unexplored. A total of 61 TD patients and 61 matched healthy controls (HCs) were included in this study. The gray matter volume (GMV) of the bilateral precuneus (PCUN) was significantly reduced in TD patients. A structural covariance network analysis seeded with the left pallidum (PAL.L), which had the most significant differences, revealed a substantial reduction in covariance with precentral gyrus in TD patients. We performed a causal structural covariance network analysis using the TD duration as a pseudotime series. The PCUN, with the highest out-degree in the cortex, regulates numerous regions, including the supplementary motor area and the extensive temporal lobe. Machine learning was utilized to construct a model that accurately assesses the surgical prognosis based on the above cortical volume and clinical scale, with the aim of assisting in clinical deep brain stimulation (DBS) treatment. These findings suggested a progressive pattern of GMV changes extending from the PAL.L to the PCUN region and continuing to other brain regions, providing insights into the progression of TD and enhancing DBS treatment strategies.

Keywords

brain morphology / Granger causality analysis / machine learning / structural covariance networks / Tremor-dominant Parkinson's disease

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Moxuan Zhang, Siyu Zhou, Pengda Yang, Huizhi Wang, Jinli Ding, Xiaobo Wang, Xuzhu Chen, Chaonan Zhang, Anni Wang, Yuan Gao, Qiang Liu, Yuchen Ji, Yin Jiang, Lin Shi, Chunlei Han, Zhong Yang, Tao Feng, Jianguo Zhang, Fangang Meng. The Precuneus Region Drives Brain Network Changes in Tremor-Dominant Parkinson's Disease: Insights from a Morphological Causal Analysis. MedComm, 2025, 6(11): e70441 DOI:10.1002/mco2.70441

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References

[1]

B. R. Bloem, M. S. Okun, and C. Klein, “Parkinson's Disease,” Lancet 397, no. 10291 (2021): 2284-2303.

[2]

GBD 2016 Parkinson's Disease Collaborators, Global, Regional, and National Burden of Parkinson's Disease, 1990-2016: A Systematic Analysis for the Global Burden of Disease Study 2016. Lancet Neurology 2018; 17(11): 939-953.

[3]

Y. Ben-Shlomo, S. Darweesh, J. Llibre-Guerra, C. Marras, M. San Luciano, and C. Tanner, “The Epidemiology of Parkinson's Disease,” Lancet 403, no. 10423 (2024): 283-292.

[4]

M. A. Thenganatt and J. Jankovic, “Parkinson Disease Subtypes,” JAMA Neurology 71, no. 4 (2014): 499-504.

[5]

J. Jankovic, M. McDermott, J. Carter, et al., “Variable Expression of Parkinson's Disease: A Base-Line Analysis of the DATATOP Cohort. The Parkinson Study Group,” Neurology 40, no. 10 (1990): 1529-1534.

[6]

R. Durcan, L. Wiblin, R. A. Lawson, et al., “Prevalence and Duration of Non-Motor Symptoms in Prodromal Parkinson's Disease,” European Journal of Neurology 26, no. 7 (2019): 979-985.

[7]

A. S. Shalash, E. Hamid, H. Elrassas, et al., “Non-Motor Symptoms in Essential Tremor, Akinetic Rigid and Tremor-Dominant Subtypes of Parkinson's Disease,” PLoS ONE 16, no. 1 (2021): e0245918.

[8]

R. Moretti, V. Milner, P. Caruso, S. Gazzin, and R. Rumiati, “Frontal Tasks and Behavior in Rigid or Tremor-Dominant Parkinson Disease,” American Journal of Alzheimers Disease and Other Dementias 32, no. 5 (2017): 300-306.

[9]

E. J. Burton, “Cerebral Atrophy in Parkinson's Disease With and Without Dementia: A Comparison With Alzheimer's Disease, Dementia With Lewy Bodies and Controls,” Brain 127, no. 4 (2004): 791-800.

[10]

H. Wilson, F. Niccolini, C. Pellicano, and M. Politis, “Cortical Thinning Across Parkinson's Disease Stages and Clinical Correlates,” Journal of the Neurological Sciences 398 (2019): 31-38.

[11]

Z. Qing, F. Chen, J. Lu, et al., “Causal Structural Covariance Network Revealing Atrophy Progression in Alzheimer's Disease Continuum,” Human Brain Mapping 42, no. 12 (2021): 3950-3962.

[12]

Z. Zhang, W. Liao, Q. Xu, et al., “Hippocampus-Associated Causal Network of Structural Covariance Measuring Structural Damage Progression in Temporal Lobe Epilepsy,” Human Brain Mapping 38, no. 2 (2017): 753-766.

[13]

Y. Jiang, C. Luo, X. Li, et al., “Progressive Reduction in Gray Matter in Patients With Schizophrenia Assessed With MR Imaging by Using Causal Network Analysis,” Radiology 287, no. 2 (2018): 729.

[14]

J. Xu, H. Lyu, T. Li, et al., “Delineating Functional Segregations of the human Middle Temporal Gyrus With Resting-State Functional Connectivity and Coactivation Patterns,” Human Brain Mapping 40, no. 18 (2019): 5159-5171.

[15]

J. Xu, Y. Luo, K. Peng, et al., “Supplementary Motor Area Driving Changes of Structural Brain Network in Blepharospasm,” Brain 146, no. 4 (2023): 1542-1553.

[16]

A. E. Bond, B. B. Shah, D. S. Huss, et al., “Safety and Efficacy of Focused Ultrasound Thalamotomy for Patients With Medication-Refractory, Tremor-Dominant Parkinson Disease: A Randomized Clinical Trial,” JAMA Neurology 74, no. 12 (2017): 1412-1418.

[17]

A. Boutet, R. Madhavan, G. J. B. Elias, et al., “Predicting Optimal Deep Brain Stimulation Parameters for Parkinson's Disease Using Functional MRI and Machine Learning,” Nature Communications 12, no. 1 (2021): 3043.

[18]

K. Seo, I. Matunari, and T. Yamamoto, “Cerebral Cortical Thinning in Parkinson's Disease Depends on the Age of Onset,” PLoS ONE 18, no. 2 (2023): e0281987.

[19]

V. Purrer, E. Pohl, J. M. Lueckel, et al., “Artificial-Intelligence-Based MRI Brain Volumetry in Patients With Essential Tremor and Tremor-Dominant Parkinson's Disease,” Brain Communications 5, no. 6 (2023): fcad271.

[20]

J. Li, Y. Zhang, Z. Huang, et al., “Cortical and Subcortical Morphological Alterations in Motor Subtypes of Parkinson's Disease,” npj Parkinson's Disease 8, no. 1 (2022): 167.

[21]

R. Perneczky, B. C. Ghosh, L. Hughes, R. H. Carpenter, R. A. Barker, and J. B. Rowe, “Saccadic Latency in Parkinson's disease Correlates With Executive Function and Brain Atrophy, but Not Motor Severity,” Neurobiology of Disease 43, no. 1 (2011): 79-85.

[22]

E. C. S. Künstler, K. Finke, A. Günther, C. Klingner, O. Witte, and P. Bublak, “Motor-Cognitive Dual-Task Performance: Effects of a Concurrent Motor Task on Distinct Components of Visual Processing Capacity,” Psychological Research 82, no. 1 (2018): 177-185.

[23]

R. C. Helmich, M. J. Janssen, W. J. Oyen, B. R. Bloem, and I. Toni, “Pallidal Dysfunction Drives a Cerebellothalamic Circuit Into Parkinson Tremor,” Annals of Neurology 69, no. 2 (2011): 269-281.

[24]

M. Tahmasian, L. M. Bettray, T. van Eimeren, et al., “A Systematic Review on the Applications of Resting-state fMRI in Parkinson's Disease: Does Dopamine Replacement Therapy Play a Role?,” Cortex; A Journal Devoted to the Study of the Nervous System and Behavior 73 (2015): 80-105.

[25]

X. Xu, X. Guan, T. Guo, et al., “Brain Atrophy and Reorganization of Structural Network in Parkinson's Disease With Hemiparkinsonism,” Frontiers in Human Neuroscience 12 (2018): 117.

[26]

E. Wang, Y. Jia, Y. Ya, et al., “Patterns of Sulcal Depth and Cortical Thickness in Parkinson's Disease,” Brain Imaging and Behavior 15, no. 5 (2021): 2340-2346.

[27]

R. B. Thibes, N. P. Novaes, L. T. Lucato, et al., “Altered Functional Connectivity between Precuneus and Motor Systems in Parkinson's Disease Patients,” Brain Connect 7, no. 10 (2017): 643-647.

[28]

X. Zhang, R. Li, Y. Xia, et al., “Topological Patterns of Motor Networks in Parkinson's Disease With Different Sides of Onset: A Resting-State-Informed Structural Connectome Study,” Frontiers in Aging Neuroscience 14 (2022): 1041744.

[29]

M. Mijalkov, G. Volpe, and J. B. Pereira, “Directed Brain Connectivity Identifies Widespread Functional Network Abnormalities in Parkinson's Disease,” Cerebral Cortex 32, no. 3 (2022): 593-607.

[30]

J. C. Culham, C. Cavina-Pratesi, and A. Singhal, “The Role of Parietal Cortex in Visuomotor Control: What Have We Learned From Neuroimaging?,” Neuropsychologia 44, no. 13 (2006): 2668-2684.

[31]

N. B. Dadario and M. E. Sughrue, “The Functional Role of the Precuneus,” Brain 146, no. 9 (2023): 3598-3607.

[32]

A. Potvin-Desrochers, A. Martinez-Moreno, J. Clouette, F. Parent-L'Ecuyer, H. Lajeunesse, and C. Paquette, “Upregulation of the Parietal Cortex Improves Freezing of Gait in Parkinson's Disease,” Journal of the Neurological Sciences 452 (2023): 120770.

[33]

J. M. Bronstein, M. Tagliati, R. L. Alterman, et al., “Deep Brain Stimulation for Parkinson Disease: An Expert Consensus and Review of Key Issues,” Archives of Neurology 68, no. 2 (2011): 165.

[34]

A. Horn, G. Wenzel, F. Irmen, et al., “Deep Brain Stimulation Induced Normalization of the human Functional Connectome in Parkinson's Disease,” Brain 142, no. 10 (2019): 3129-3143.

[35]

K. Liang, R.-P. Li, Y. Gao, et al., “Emotional Symptoms and Cognitive Function Outcomes of Subthalamic Stimulation in Parkinson's Disease Depend on Location of Active Contacts and the Volume of Tissue Activated,” CNS Neuroscience & Therapeutics 29, no. 8 (2023): 2355-2365.

[36]

R. B. Postuma, D. Berg, M. Stern, et al., “MDS Clinical Diagnostic Criteria for Parkinson's Disease,” Movement Disorders 30, no. 12 (2015): 1591-1601.

[37]

C. G. Goetz, B. C. Tilley, S. R. Shaftman, et al., “Movement Disorder Society-Sponsored Revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS): Scale Presentation and Clinimetric Testing Results,” Movement Disorders 23, no. 15 (2008): 2129-2170.

[38]

G. T. Stebbins, C. G. Goetz, D. J. Burn, J. Jankovic, T. K. Khoo, and B. C. Tilley, “How to Identify Tremor Dominant and Postural Instability/Gait Difficulty Groups With the Movement Disorder Society Unified Parkinson's disease Rating Scale: Comparison With the unified Parkinson's Disease Rating Scale,” Movement Disorders 28, no. 5 (2013): 668-670.

[39]

C. G. Goetz, W. Poewe, O. Rascol, et al., “Movement Disorder Society Task Force Report on the Hoehn and Yahr Staging Scale: Status and Recommendations,” Movement Disorders 19, no. 9 (2004): 1020-1028.

[40]

L. M. Kopf, A. H. G. Rohl, T. Nagao, et al., “Voice Handicap Index in Parkinson's Patients: Subthalamic versus Globus Pallidus Deep Brain Stimulation,” Journal of Clinical Neuroscience 98 (2022): 83-88.

[41]

R. M. Voss and J. M. Das, “Mental Status Examination,” StatPearls (StatPearls Publishing LLC, 2024).

[42]

J. M. Kang, Y.-S. Cho, S. Park, et al., “Montreal Cognitive Assessment Reflects Cognitive Reserve,” BMC Geriatrics 18, no. 1 (2018): 261.

[43]

M. Hamilton, “The Assessment of Anxiety States by Rating,” British Journal of Medical Psychology 32, no. 1 (1959): 50-55.

[44]

M. Hamilton, “A Rating Scale for Depression,” Journal of Neurology, Neurosurgery, and Psychiatry 23, no. 1 (1960): 56-62.

[45]

G. Saranza and A. E. Lang, “Levodopa Challenge Test: Indications, Protocol, and Guide,” Journal of Neurology 268, no. 9 (2021): 3135-3143.

[46]

H. Zhai, W. Fan, Y. Xiao, et al., “Voxel-Based Morphometry of Grey Matter Structures in Parkinson's Disease With Wearing-Off,” Brain Imaging and Behavior 17, no. 6 (2023): 725-737.

[47]

P.-L. Lee, K.-H. Chou, C.-H. Lu, et al., “Extraction of Large-Scale Structural Covariance Networks From Grey Matter Volume for Parkinson's Disease Classification,” European Radiology 28, no. 8 (2018): 3296-3305.

[48]

J. Binnewies, L. Nawijn, M.-J. van Tol, N. J. A. van der Wee, D. J. Veltman, and B. Penninx, “Associations Between Depression, Lifestyle and Brain Structure: A Longitudinal MRI Study,” Neuroimage 231 (2021): 117834.

[49]

C. Vriend, P. S. W. Boedhoe, S. Rutten, H. W. Berendse, Y. D. van der Werf, and O. A. van den Heuvel, “A Smaller Amygdala Is Associated With Anxiety in Parkinson's disease: A Combined FreeSurfer-VBM Study,” Journal of Neurology, Neurosurgery, and Psychiatry 87, no. 5 (2016): 493-500.

[50]

M. P. van den Heuvel and H. E. Hulshoff Pol, “Exploring the Brain Network: A Review on Resting-State fMRI Functional Connectivity,” European Neuropsychopharmacology 20, no. 8 (2010): 519-534.

[51]

V. D. Calhoun, R. Miller, G. Pearlson, and T. Adali, “The Chronnectome: Time-Varying Connectivity Networks as the Next Frontier in fMRI Data Discovery,” Neuron 84, no. 2 (2014): 262-274.

[52]

E. B. Erhardt, S. Rachakonda, E. J. Bedrick, E. A. Allen, T. Adali, and V. D. Calhoun, “Comparison of Multi-Subject ICA Methods for Analysis of fMRI Data,” Human Brain Mapping 32, no. 12 (2011): 2075-2095.

[53]

Y. Du, G. D. Pearlson, Q. Yu, et al., “Interaction Among Subsystems Within Default Mode Network Diminished in Schizophrenia Patients: A Dynamic Connectivity Approach,” Schizophrenia Research 170, no. 1 (2016): 55-65.

[54]

A. Brovelli, M. Ding, A. Ledberg, Y. Chen, R. Nakamura, and S. L. Bressler, “Beta Oscillations in a Large-Scale Sensorimotor Cortical Network: Directional Influences Revealed by Granger Causality,” PNAS 101, no. 26 (2004): 9849-9854.

[55]

S. F. Oliveria, R. L. Rodriguez, D. Bowers, et al., “Safety and Efficacy of Dual-Lead Thalamic Deep Brain Stimulation for Patients With Treatment-Refractory Multiple Sclerosis Tremor: A Single-Centre, Randomised, Single-Blind, Pilot Trial,” Lancet Neurology 16, no. 9 (2017): 691-700.

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