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Updated: Jan 9, 2026

Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
Published on: October 4, 2021
Cortical Sulcal Depth Alterations in Parkinson's Disease Patients With Levodopa-Induced Dyskinesia
Qianqian Si1, Caiting Gan1, Jiaxin Shi1
1Department of Neurology, The First Affiliated Hospital with Nanjing Medical University, 210029 Nanjing, Jiangsu, China.
Background:
In Parkinson's disease (PD), levodopa-induced dyskinesia (LID) represents a common motor complication of long-term dopaminergic therapy. Although levodopa remains the most effective treatment for PD, the neurological mechanisms underlying the LID remain incompletely understood. This study aimed to investigate the pattern of cortical morphological and subcortical structural alterations associated with LID in PD.
Methods:
Clinical data and T1-weighted structural brain images were obtained for 62 patients with PD, including 30 with LID and 32 without LID, along with 30 healthy controls (HCs). Regional sulcal depth (SD) and subcortical volumes were quantified to assess alterations in cortical surface morphology and subcortical structures. The study further aimed to evaluate the association between structural indicators and the severity of LID, as well as to determine their potential diagnostic ability.
Results:
PD patients with LID demonstrated reduced regional SD in the right inferior parietal and insula cortices, compared with PD patients without LID and HCs (after Bonferroni correction). The right putamen volume in both PD subtypes was lower than that of HCs (after Bonferroni correction). In particular, the level of right inferior parietal SD was negatively associated with the severity of LID (r = -0.494, p = 0.017). Receiver operating characteristic (ROC) curve analyses further revealed that the combination of cortical SD values demonstrated excellent performance in distinguishing PD-LID from PD-non-levodopa-induced dyskinesia (NLID) (area under the curve [AUC] = 0.913).
Conclusions:
Our main findings show that structural alterations associated with LID extend from the frontal to the parietal and insula cortices, suggesting that decreased cortical SD values in these regions may contribute to a better understanding of the neurological underpinnings of LID in PD.
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