Relative preservation of thalamic centromedian nucleus in parkinsonian patients with dystonia
Identifieur interne : 002087 ( Main/Exploration ); précédent : 002086; suivant : 002088Relative preservation of thalamic centromedian nucleus in parkinsonian patients with dystonia
Auteurs : Linda Truong [Australie] ; Daniel Brooks [Australie] ; Fabricio Amaral [Australie] ; Jasmine M. Henderson [Australie] ; Glenda M. Halliday [Australie]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-10-30.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (therapeutic use), Atrophy, Cell Count, Disease Progression, Dystonia, Dystonia (etiology), Dystonia (pathology), Female, Human, Humans, Imaging, Three-Dimensional, Intralaminar Thalamic Nuclei (pathology), Lewy Bodies (pathology), Male, Middle Aged, Nerve Degeneration (pathology), Nervous system diseases, Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson disease, Parkinson's disease, Preservation, Thalamus, alpha-Synuclein (metabolism), centromedian‐parafascicular nuclei, dystonia, falls, thalamus.
- MESH :
- chemical , metabolism : alpha-Synuclein.
- chemical , therapeutic use : Antiparkinson Agents.
- complications : Parkinson Disease.
- drug therapy : Parkinson Disease.
- etiology : Dystonia.
- pathology : Dystonia, Intralaminar Thalamic Nuclei, Lewy Bodies, Nerve Degeneration, Parkinson Disease.
- Aged, Atrophy, Cell Count, Disease Progression, Female, Humans, Imaging, Three-Dimensional, Male, Middle Aged.
Abstract
To determine whether variable thalamic degeneration in Parkinson's disease (PD) contributes to less drug responsive clinical features. Formalin‐fixed thalami from longitudinally followed patients with PD and early dystonia (N = 6), early falls (N = 5) or no dystonia or falls (N = 6) and age‐matched controls without neuropathology (N = 10) were serially sectioned, stained, and analyzed. Neurons in the centromedian parafascicular (CM‐Pf) nucleus were quantified using the optical disector method and analysis of variance with post hoc testing used to determine variability in neurodegeneration between groups. Patients with PD were confirmed to have significant neurodegeneration in the CM‐Pf complex, with no difference in the degree of neurodegeneration between patients with PD with early falls compared with patients with no history of falls or dystonia. In contrast, patients with PD with early dystonia had significantly less neurodegeneration of the CM but not the Pf than patients without this feature. Preservation of the CM in patients with PD with early dystonia would result in a relative increase in CM activity through the direct basal ganglia pathway and increased primary motor cortex activity. Overall this data provides evidence for pathway‐specific neurodegeneration as an underlying feature of the clinical variability observed in patients with PD. © 2009 Movement Disorder Society
Url:
DOI: 10.1002/mds.22747
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-10-30">2009-10-30</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">14</biblScope><biblScope unit="page" from="2128">2128</biblScope><biblScope unit="page" to="2135">2135</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">DC1FAF06C2D506A6E4F1FA0C0F502FC710A4D28D</idno><idno type="DOI">10.1002/mds.22747</idno><idno type="ArticleID">MDS22747</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antiparkinson Agents (therapeutic use)</term><term>Atrophy</term><term>Cell Count</term><term>Disease Progression</term><term>Dystonia</term><term>Dystonia (etiology)</term><term>Dystonia (pathology)</term><term>Female</term><term>Human</term><term>Humans</term><term>Imaging, Three-Dimensional</term><term>Intralaminar Thalamic Nuclei (pathology)</term><term>Lewy Bodies (pathology)</term><term>Male</term><term>Middle Aged</term><term>Nerve Degeneration (pathology)</term><term>Nervous system diseases</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (pathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Preservation</term><term>Thalamus</term><term>alpha-Synuclein (metabolism)</term><term>centromedian‐parafascicular nuclei</term><term>dystonia</term><term>falls</term><term>thalamus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dystonia</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dystonia</term><term>Intralaminar Thalamic Nuclei</term><term>Lewy Bodies</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Atrophy</term><term>Cell Count</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Imaging, Three-Dimensional</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dystonie</term><term>Homme</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Préservation</term><term>Thalamus</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To determine whether variable thalamic degeneration in Parkinson's disease (PD) contributes to less drug responsive clinical features. Formalin‐fixed thalami from longitudinally followed patients with PD and early dystonia (N = 6), early falls (N = 5) or no dystonia or falls (N = 6) and age‐matched controls without neuropathology (N = 10) were serially sectioned, stained, and analyzed. Neurons in the centromedian parafascicular (CM‐Pf) nucleus were quantified using the optical disector method and analysis of variance with post hoc testing used to determine variability in neurodegeneration between groups. Patients with PD were confirmed to have significant neurodegeneration in the CM‐Pf complex, with no difference in the degree of neurodegeneration between patients with PD with early falls compared with patients with no history of falls or dystonia. In contrast, patients with PD with early dystonia had significantly less neurodegeneration of the CM but not the Pf than patients without this feature. Preservation of the CM in patients with PD with early dystonia would result in a relative increase in CM activity through the direct basal ganglia pathway and increased primary motor cortex activity. Overall this data provides evidence for pathway‐specific neurodegeneration as an underlying feature of the clinical variability observed in patients with PD. © 2009 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Australie</li></country><settlement><li>Sydney</li></settlement></list><tree><country name="Australie"><noRegion><name sortKey="Truong, Linda" sort="Truong, Linda" uniqKey="Truong L" first="Linda" last="Truong">Linda Truong</name></noRegion><name sortKey="Amaral, Fabricio" sort="Amaral, Fabricio" uniqKey="Amaral F" first="Fabricio" last="Amaral">Fabricio Amaral</name><name sortKey="Brooks, Daniel" sort="Brooks, Daniel" uniqKey="Brooks D" first="Daniel" last="Brooks">Daniel Brooks</name><name sortKey="Halliday, Glenda M" sort="Halliday, Glenda M" uniqKey="Halliday G" first="Glenda M." last="Halliday">Glenda M. Halliday</name><name sortKey="Henderson, Jasmine M" sort="Henderson, Jasmine M" uniqKey="Henderson J" first="Jasmine M." last="Henderson">Jasmine M. Henderson</name><name sortKey="Truong, Linda" sort="Truong, Linda" uniqKey="Truong L" first="Linda" last="Truong">Linda Truong</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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