Contracted thalamic shape is associated with early development of levodopa-induced dyskinesia in Parkinson’s disease

Levodopa-induced dyskinesia (LID), a long-term motor complication in Parkinson’s disease (PD), is attributable to both presynaptic and postsynaptic mechanisms. However, no studies have evaluated the baseline structural changes associated with LID at a subcortical level in PD. A total of 116 right-ha...

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Published in:Scientific reports Vol. 12; no. 1; p. 12631
Main Authors: Yoo, Han Soo, Lee, Eun-Chong, Chung, Seok Jong, Ye, Byoung Seok, Sohn, Young H., Seong, Joon-Kyung, Lee, Phil Hyu
Format: Journal Article
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Published: London Nature Publishing Group UK 25-07-2022
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Abstract Levodopa-induced dyskinesia (LID), a long-term motor complication in Parkinson’s disease (PD), is attributable to both presynaptic and postsynaptic mechanisms. However, no studies have evaluated the baseline structural changes associated with LID at a subcortical level in PD. A total of 116 right-handed PD patients were recruited and based on the LID latency of 5 years, we classified patients into those vulnerable to LID (PD-vLID, n = 49) and those resistant to LID (PD-rLID, n = 67). After adjusting for covariates including dopamine transporter (DAT) availability of the posterior putamen, we compared the subcortical shape between the groups and investigated its association with the onset of LID. The PD-vLID group had lower DAT availability in the posterior putamen, higher parkinsonian motor deficits, and faster increment in levodopa equivalent dose than the PD-rLID group. The PD-vLID group had significant inward deformation in the right thalamus compared to the PD-rLID group. Inward deformation in the thalamus was associated with an earlier onset of LID at baseline. This study suggests that independent of presynaptic dopamine depletion, the thalamus is a major neural substrate for LID and that a contracted thalamic shape at baseline is closely associated with an early development of LID.
AbstractList Levodopa-induced dyskinesia (LID), a long-term motor complication in Parkinson’s disease (PD), is attributable to both presynaptic and postsynaptic mechanisms. However, no studies have evaluated the baseline structural changes associated with LID at a subcortical level in PD. A total of 116 right-handed PD patients were recruited and based on the LID latency of 5 years, we classified patients into those vulnerable to LID (PD-vLID, n = 49) and those resistant to LID (PD-rLID, n = 67). After adjusting for covariates including dopamine transporter (DAT) availability of the posterior putamen, we compared the subcortical shape between the groups and investigated its association with the onset of LID. The PD-vLID group had lower DAT availability in the posterior putamen, higher parkinsonian motor deficits, and faster increment in levodopa equivalent dose than the PD-rLID group. The PD-vLID group had significant inward deformation in the right thalamus compared to the PD-rLID group. Inward deformation in the thalamus was associated with an earlier onset of LID at baseline. This study suggests that independent of presynaptic dopamine depletion, the thalamus is a major neural substrate for LID and that a contracted thalamic shape at baseline is closely associated with an early development of LID.
Abstract Levodopa-induced dyskinesia (LID), a long-term motor complication in Parkinson’s disease (PD), is attributable to both presynaptic and postsynaptic mechanisms. However, no studies have evaluated the baseline structural changes associated with LID at a subcortical level in PD. A total of 116 right-handed PD patients were recruited and based on the LID latency of 5 years, we classified patients into those vulnerable to LID (PD-vLID, n = 49) and those resistant to LID (PD-rLID, n = 67). After adjusting for covariates including dopamine transporter (DAT) availability of the posterior putamen, we compared the subcortical shape between the groups and investigated its association with the onset of LID. The PD-vLID group had lower DAT availability in the posterior putamen, higher parkinsonian motor deficits, and faster increment in levodopa equivalent dose than the PD-rLID group. The PD-vLID group had significant inward deformation in the right thalamus compared to the PD-rLID group. Inward deformation in the thalamus was associated with an earlier onset of LID at baseline. This study suggests that independent of presynaptic dopamine depletion, the thalamus is a major neural substrate for LID and that a contracted thalamic shape at baseline is closely associated with an early development of LID.
Levodopa-induced dyskinesia (LID), a long-term motor complication in Parkinson’s disease (PD), is attributable to both presynaptic and postsynaptic mechanisms. However, no studies have evaluated the baseline structural changes associated with LID at a subcortical level in PD. A total of 116 right-handed PD patients were recruited and based on the LID latency of 5 years, we classified patients into those vulnerable to LID (PD-vLID, n = 49) and those resistant to LID (PD-rLID, n = 67). After adjusting for covariates including dopamine transporter (DAT) availability of the posterior putamen, we compared the subcortical shape between the groups and investigated its association with the onset of LID. The PD-vLID group had lower DAT availability in the posterior putamen, higher parkinsonian motor deficits, and faster increment in levodopa equivalent dose than the PD-rLID group. The PD-vLID group had significant inward deformation in the right thalamus compared to the PD-rLID group. Inward deformation in the thalamus was associated with an earlier onset of LID at baseline. This study suggests that independent of presynaptic dopamine depletion, the thalamus is a major neural substrate for LID and that a contracted thalamic shape at baseline is closely associated with an early development of LID.
ArticleNumber 12631
Author Seong, Joon-Kyung
Sohn, Young H.
Lee, Eun-Chong
Chung, Seok Jong
Ye, Byoung Seok
Lee, Phil Hyu
Yoo, Han Soo
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SSID ssj0000529419
Score 2.423524
Snippet Levodopa-induced dyskinesia (LID), a long-term motor complication in Parkinson’s disease (PD), is attributable to both presynaptic and postsynaptic mechanisms....
Abstract Levodopa-induced dyskinesia (LID), a long-term motor complication in Parkinson’s disease (PD), is attributable to both presynaptic and postsynaptic...
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proquest
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SourceType Open Website
Open Access Repository
Aggregation Database
Publisher
StartPage 12631
SubjectTerms 631/378
692/617
Basal ganglia
Central nervous system diseases
Deformation
Dopamine
Dopamine transporter
Dyskinesia
Handedness
Humanities and Social Sciences
Latency
Levodopa
Movement disorders
multidisciplinary
Neurodegenerative diseases
Parkinson's disease
Putamen
Science
Science (multidisciplinary)
Thalamus
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Title Contracted thalamic shape is associated with early development of levodopa-induced dyskinesia in Parkinson’s disease
URI https://link.springer.com/article/10.1038/s41598-022-16747-6
https://www.proquest.com/docview/2694138693
https://search.proquest.com/docview/2694962556
https://pubmed.ncbi.nlm.nih.gov/PMC9314442
https://doaj.org/article/942aa2249ae74a72afbe56cdaead7eaf
Volume 12
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