Nigral degeneration and striatal dopaminergic dysfunction in idiopathic and parkin‐linked Parkinson's disease
Identifieur interne : 003317 ( Main/Exploration ); précédent : 003316; suivant : 003318Nigral degeneration and striatal dopaminergic dysfunction in idiopathic and parkin‐linked Parkinson's disease
Auteurs : Michele T. M. Hu [Royaume-Uni] ; Christoph Scherfler [Royaume-Uni] ; Naheed L. Khan [Royaume-Uni] ; Jo V. Hajnal [Royaume-Uni] ; Andrew Lees (neurologue) [Royaume-Uni] ; Niall Quinn [Royaume-Uni] ; Nicholas W. Wood [Royaume-Uni] ; David J. Brooks [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2006-03.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adult, Caudate Nucleus (metabolism), Caudate Nucleus (pathology), Corpus Striatum (metabolism), Corpus Striatum (physiopathology), Degeneration, Dopamine (metabolism), Dysfunction, Emission tomography, Female, Fluorodeoxyglucose F18 (diagnostic use), Fluorodeoxyglucose F18 (pharmacokinetics), Humans, Idiopathic, Magnetic Resonance Imaging, Male, Middle Aged, Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Nervous system diseases, Nuclear magnetic resonance imaging, Parkin, Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson Disease (radionuclide imaging), Parkinson disease, Parkinson's disease, Point Mutation (genetics), Positron emission tomography, Positron-Emission Tomography, Putamen (metabolism), Putamen (pathology), Radiopharmaceuticals (diagnostic use), Radiopharmaceuticals (pharmacokinetics), Substantia Nigra (metabolism), Substantia Nigra (pathology), Ubiquitin-Protein Ligases (genetics), magnetic resonance imaging, nigral degeneration, parkin, positron emission tomography.
- MESH :
- chemical , diagnostic use : Fluorodeoxyglucose F18, Radiopharmaceuticals.
- chemical , genetics : Ubiquitin-Protein Ligases.
- chemical , metabolism : Dopamine.
- genetics : Parkinson Disease, Point Mutation.
- metabolism : Caudate Nucleus, Corpus Striatum, Nerve Degeneration, Putamen, Substantia Nigra.
- pathology : Caudate Nucleus, Nerve Degeneration, Parkinson Disease, Putamen, Substantia Nigra.
- chemical , pharmacokinetics : Fluorodeoxyglucose F18, Radiopharmaceuticals.
- physiopathology : Corpus Striatum.
- radionuclide imaging : Parkinson Disease.
- Adult, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography.
Abstract
We have used MR segmented inversion recovery ratio imaging (SIRRIM) of the substantia nigra pars compacta to detect and correlate nigral signal change in idiopathic Parkinson's disease (PD) and parkin patients with striatal 18F‐dopa uptake. Nine PD patients, nine parkin patients, and eight control subjects were studied with a combination of MR inversion recovery sequences sensitive to nigral cell loss. Blinded independent observer rating and quantified nigral signal analysis were performed on all subjects. Striatal regions of interest were defined on T1‐weighted MRI coregistered to 18F‐dopa positron emission tomography. On blinded observer rating of the SIRRIM dorsal and ventral nigral images, 25% (2/8) of control subjects, 44% (4/9) of PD patients, and 67% (6/9) of parkin patients were classified as abnormal. Quantified total nigral signal intensities were reduced to a greater extent in the parkin compared to PD patients. There was a greater predilection for signal reduction in the ventral nigral slice of the PD compared to the parkin patient group, who showed a more uniform involvement. All PD and parkin patients were discriminated from controls on the basis of caudate and putamen 18F‐dopa Ki reductions. Our results suggest that MR segmented inversion recovery ratio imaging shows poor sensitivity for discriminating parkin and idiopathic PD patients from normal controls. Where nigral signal abnormalities were seen, parkin patients manifested generalized nigral cell loss with widespread striatal dopamine terminal dysfunction compared with the lateral nigral targeting seen in PD and selective loss of putamen 18F‐dopa uptake. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20702
Affiliations:
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M." last="Hu">Michele T. M. Hu</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Clinical Sciences Centre, Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Robert Steiner MR Unit, Imperial College School of Medicine, Hammersmith Hospital, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Scherfler, Christoph" sort="Scherfler, Christoph" uniqKey="Scherfler C" first="Christoph" last="Scherfler">Christoph Scherfler</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Clinical Sciences Centre, Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Khan, Naheed L" sort="Khan, Naheed L" uniqKey="Khan N" first="Naheed L." last="Khan">Naheed L. Khan</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Molecular Pathogenesis, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Hajnal, Jo V" sort="Hajnal, Jo V" uniqKey="Hajnal J" first="Jo V." last="Hajnal">Jo V. Hajnal</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Robert Steiner MR Unit, Imperial College School of Medicine, Hammersmith Hospital, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><orgName>National Hospital for Neurology and Neurosurgery</orgName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><orgName>National Hospital for Neurology and Neurosurgery</orgName></affiliation></author><author><name sortKey="Quinn, Niall" sort="Quinn, Niall" uniqKey="Quinn N" first="Niall" last="Quinn">Niall Quinn</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Wood, Nicholas W" sort="Wood, Nicholas W" uniqKey="Wood N" first="Nicholas W." last="Wood">Nicholas W. Wood</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Molecular Pathogenesis, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>MRC Clinical Sciences Centre, Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>National Hospital for Neurology and Neurosurgery, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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="2006-03">2006-03</date><biblScope unit="vol">21</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="299">299</biblScope><biblScope unit="page" to="305">305</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">997EBD3D49E2F59E6FBB2F996F8CE9F09FC7F534</idno><idno type="DOI">10.1002/mds.20702</idno><idno type="ArticleID">MDS20702</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Caudate Nucleus (metabolism)</term><term>Caudate Nucleus (pathology)</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (physiopathology)</term><term>Degeneration</term><term>Dopamine (metabolism)</term><term>Dysfunction</term><term>Emission tomography</term><term>Female</term><term>Fluorodeoxyglucose F18 (diagnostic use)</term><term>Fluorodeoxyglucose F18 (pharmacokinetics)</term><term>Humans</term><term>Idiopathic</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Nervous system diseases</term><term>Nuclear magnetic resonance imaging</term><term>Parkin</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Point Mutation (genetics)</term><term>Positron emission tomography</term><term>Positron-Emission Tomography</term><term>Putamen (metabolism)</term><term>Putamen (pathology)</term><term>Radiopharmaceuticals (diagnostic use)</term><term>Radiopharmaceuticals (pharmacokinetics)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Ubiquitin-Protein Ligases (genetics)</term><term>magnetic resonance imaging</term><term>nigral degeneration</term><term>parkin</term><term>positron emission tomography</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Fluorodeoxyglucose F18</term><term>Radiopharmaceuticals</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term><term>Point Mutation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Nerve Degeneration</term><term>Putamen</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Caudate Nucleus</term><term>Nerve Degeneration</term><term>Parkinson Disease</term><term>Putamen</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Fluorodeoxyglucose F18</term><term>Radiopharmaceuticals</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dégénérescence</term><term>Idiopathique</term><term>Imagerie RMN</term><term>Parkine</term><term>Parkinson maladie</term><term>Système nerveux pathologie</term><term>Tomographie émission positon</term><term>Tomoscintigraphie</term><term>Trouble fonctionnel</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We have used MR segmented inversion recovery ratio imaging (SIRRIM) of the substantia nigra pars compacta to detect and correlate nigral signal change in idiopathic Parkinson's disease (PD) and parkin patients with striatal 18F‐dopa uptake. Nine PD patients, nine parkin patients, and eight control subjects were studied with a combination of MR inversion recovery sequences sensitive to nigral cell loss. Blinded independent observer rating and quantified nigral signal analysis were performed on all subjects. Striatal regions of interest were defined on T1‐weighted MRI coregistered to 18F‐dopa positron emission tomography. On blinded observer rating of the SIRRIM dorsal and ventral nigral images, 25% (2/8) of control subjects, 44% (4/9) of PD patients, and 67% (6/9) of parkin patients were classified as abnormal. Quantified total nigral signal intensities were reduced to a greater extent in the parkin compared to PD patients. There was a greater predilection for signal reduction in the ventral nigral slice of the PD compared to the parkin patient group, who showed a more uniform involvement. All PD and parkin patients were discriminated from controls on the basis of caudate and putamen 18F‐dopa Ki reductions. Our results suggest that MR segmented inversion recovery ratio imaging shows poor sensitivity for discriminating parkin and idiopathic PD patients from normal controls. Where nigral signal abnormalities were seen, parkin patients manifested generalized nigral cell loss with widespread striatal dopamine terminal dysfunction compared with the lateral nigral targeting seen in PD and selective loss of putamen 18F‐dopa uptake. © 2005 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement><orgName><li>National Hospital for Neurology and Neurosurgery</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Hu, Michele T M" sort="Hu, Michele T M" uniqKey="Hu M" first="Michele T. M." last="Hu">Michele T. M. Hu</name></region><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name><name sortKey="Hajnal, Jo V" sort="Hajnal, Jo V" uniqKey="Hajnal J" first="Jo V." last="Hajnal">Jo V. Hajnal</name><name sortKey="Hu, Michele T M" sort="Hu, Michele T M" uniqKey="Hu M" first="Michele T. M." last="Hu">Michele T. M. Hu</name><name sortKey="Hu, Michele T M" sort="Hu, Michele T M" uniqKey="Hu M" first="Michele T. M." last="Hu">Michele T. M. Hu</name><name sortKey="Khan, Naheed L" sort="Khan, Naheed L" uniqKey="Khan N" first="Naheed L." last="Khan">Naheed L. Khan</name><name sortKey="Khan, Naheed L" sort="Khan, Naheed L" uniqKey="Khan N" first="Naheed L." last="Khan">Naheed L. Khan</name><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew Lees (neurologue)</name><name sortKey="Quinn, Niall" sort="Quinn, Niall" uniqKey="Quinn N" first="Niall" last="Quinn">Niall Quinn</name><name sortKey="Quinn, Niall" sort="Quinn, Niall" uniqKey="Quinn N" first="Niall" last="Quinn">Niall Quinn</name><name sortKey="Scherfler, Christoph" sort="Scherfler, Christoph" uniqKey="Scherfler C" first="Christoph" last="Scherfler">Christoph Scherfler</name><name sortKey="Wood, Nicholas W" sort="Wood, Nicholas W" uniqKey="Wood N" first="Nicholas W." last="Wood">Nicholas W. Wood</name><name sortKey="Wood, Nicholas W" sort="Wood, Nicholas W" uniqKey="Wood N" first="Nicholas W." last="Wood">Nicholas W. Wood</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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