Contributions of PET and SPECT to the understanding of the pathophysiology of Parkinson's disease.
Identifieur interne : 003B55 ( Main/Merge ); précédent : 003B54; suivant : 003B56Contributions of PET and SPECT to the understanding of the pathophysiology of Parkinson's disease.
Auteurs : S. Thobois [France] ; S. Guillouet ; E. BroussolleSource :
- Neurophysiologie clinique = Clinical neurophysiology [ 0987-7053 ] ; 2001.
English descriptors
- KwdEn :
- Aging (metabolism), Animals, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Basal Ganglia (diagnostic imaging), Basal Ganglia (metabolism), Basal Ganglia (physiopathology), Basal Ganglia (surgery), Brain Tissue Transplantation, Cell Transplantation, Cerebrovascular Circulation, Diagnosis, Differential, Dihydroxyphenylalanine (analogs & derivatives), Dopamine Agonists (pharmacology), Dopamine Agonists (therapeutic use), Electric Stimulation Therapy, Fetal Tissue Transplantation, Forecasting, Genetic Predisposition to Disease, Humans, Iatrogenic Disease, Imagination, Ligands, Mesencephalon (cytology), Mesencephalon (embryology), Motor Activity, Nerve Degeneration (diagnostic imaging), Neurodegenerative Diseases (diagnosis), Neurons (transplantation), Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Neurotransmitter Agents (metabolism), Parkinson Disease (diagnosis), Parkinson Disease (diagnostic imaging), Parkinson Disease (epidemiology), Parkinson Disease (genetics), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Parkinson Disease, Secondary (diagnostic imaging), Parkinsonian Disorders (diagnostic imaging), Radiopharmaceuticals, Rats, Receptors, Dopamine (metabolism), Risk, Tomography, Emission-Computed, Tomography, Emission-Computed, Single-Photon, Tremor (diagnostic imaging).
- MESH :
- chemical , analogs & derivatives : Dihydroxyphenylalanine.
- chemical , metabolism : Neurotransmitter Agents, Receptors, Dopamine.
- chemical , pharmacology : Antiparkinson Agents, Dopamine Agonists, Neuroprotective Agents.
- cytology : Mesencephalon.
- diagnosis : Neurodegenerative Diseases, Parkinson Disease.
- diagnostic imaging : Basal Ganglia, Nerve Degeneration, Parkinson Disease, Parkinson Disease, Secondary, Parkinsonian Disorders, Tremor.
- embryology : Mesencephalon.
- epidemiology : Parkinson Disease.
- genetics : Parkinson Disease.
- metabolism : Aging, Basal Ganglia.
- physiopathology : Basal Ganglia, Parkinson Disease.
- surgery : Basal Ganglia.
- chemical , therapeutic use : Antiparkinson Agents, Dopamine Agonists, Neuroprotective Agents.
- therapy : Parkinson Disease.
- transplantation : Neurons.
- Animals, Brain Tissue Transplantation, Cell Transplantation, Cerebrovascular Circulation, Diagnosis, Differential, Electric Stimulation Therapy, Fetal Tissue Transplantation, Forecasting, Genetic Predisposition to Disease, Humans, Iatrogenic Disease, Imagination, Ligands, Motor Activity, Radiopharmaceuticals, Rats, Risk, Tomography, Emission-Computed, Tomography, Emission-Computed, Single-Photon.
Abstract
Positron emission tomography (PET) and single photon emission computed tomography (SPECT) provide the means to studying in vivo the neurochemical, hemodynamic or metabolic consequences of the degeneration of the nigrostriatal dopaminergic system in Parkinson's disease (PD). The extent of striatal dopaminergic denervation can be quantified with radiotracers as [18F]FDopa for PET and [123I]tropanes for SPECT. There are other radiotracers such as [11C]Dopa and meta-tyrosines as well as PET tracers for uptake sites. Striatal uptake of [18F]FDopa and [123I]tropanes is markedly decreased in PD, more in the putamen than in the caudate nucleus, and inversely correlates with the severity of motor signs and with duration of disease. PET and SPECT make possible the assessment by noninvasive means of the changes in dopamine receptor density, the effect of neuronal transplants or neuroprotective treatments in PD patients, or the nigrostriatal dopaminergic function in at-risk subjects. Activation studies using cerebral blood flow and metabolism measurements during a motor task reveal an impaired ability to activate the supplementary motor area and dorsolateral prefrontal cortex in PD. This functional disability is reversed by the use of dopaminergic medication or by surgical treatment by pallidotomy or deep brain stimulation. The differential diagnosis between PD and multiple system atrophy, progressive supranuclear palsy or corticobasal degeneration is not yet clearly established by PET and SPECT, even though these syndromes have some particular neurochemical and metabolic profiles. On the other hand, PET and SPECT are useful for distinguishing PD from Dopa-responsive dystonia, or for assessing the integrity of the nigrostriatal dopaminergic pathway in atypical cases of postural tremor or iatrogenic parkinsonian syndromes.
PubMed: 11817273
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 001229
- to stream PubMed, to step Curation: 001188
- to stream PubMed, to step Checkpoint: 001188
- to stream Ncbi, to step Merge: 000222
- to stream Ncbi, to step Curation: 000222
- to stream Ncbi, to step Checkpoint: 000222
Links to Exploration step
pubmed:11817273Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Contributions of PET and SPECT to the understanding of the pathophysiology of Parkinson's disease.</title><author><name sortKey="Thobois, S" sort="Thobois, S" uniqKey="Thobois S" first="S" last="Thobois">S. Thobois</name><affiliation wicri:level="3"><nlm:affiliation>CERMEP et service de neurologie D, hôpital neurologique Pierre-Wertheimer, 59, boulevard Pinel, Lyon, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CERMEP et service de neurologie D, hôpital neurologique Pierre-Wertheimer, 59, boulevard Pinel, Lyon</wicri:regionArea><placeName><region type="region">Auvergne-Rhône-Alpes</region><region type="old region">Rhône-Alpes</region><settlement type="city">Lyon</settlement></placeName></affiliation></author><author><name sortKey="Guillouet, S" sort="Guillouet, S" uniqKey="Guillouet S" first="S" last="Guillouet">S. Guillouet</name></author><author><name sortKey="Broussolle, E" sort="Broussolle, E" uniqKey="Broussolle E" first="E" last="Broussolle">E. Broussolle</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2001">2001</date><idno type="RBID">pubmed:11817273</idno><idno type="pmid">11817273</idno><idno type="wicri:Area/PubMed/Corpus">001229</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001229</idno><idno type="wicri:Area/PubMed/Curation">001188</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001188</idno><idno type="wicri:Area/PubMed/Checkpoint">001188</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001188</idno><idno type="wicri:Area/Ncbi/Merge">000222</idno><idno type="wicri:Area/Ncbi/Curation">000222</idno><idno type="wicri:Area/Ncbi/Checkpoint">000222</idno><idno type="wicri:doubleKey">0987-7053:2001:Thobois S:contributions:of:pet</idno><idno type="wicri:Area/Main/Merge">003B55</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Contributions of PET and SPECT to the understanding of the pathophysiology of Parkinson's disease.</title><author><name sortKey="Thobois, S" sort="Thobois, S" uniqKey="Thobois S" first="S" last="Thobois">S. Thobois</name><affiliation wicri:level="3"><nlm:affiliation>CERMEP et service de neurologie D, hôpital neurologique Pierre-Wertheimer, 59, boulevard Pinel, Lyon, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>CERMEP et service de neurologie D, hôpital neurologique Pierre-Wertheimer, 59, boulevard Pinel, Lyon</wicri:regionArea><placeName><region type="region">Auvergne-Rhône-Alpes</region><region type="old region">Rhône-Alpes</region><settlement type="city">Lyon</settlement></placeName></affiliation></author><author><name sortKey="Guillouet, S" sort="Guillouet, S" uniqKey="Guillouet S" first="S" last="Guillouet">S. Guillouet</name></author><author><name sortKey="Broussolle, E" sort="Broussolle, E" uniqKey="Broussolle E" first="E" last="Broussolle">E. Broussolle</name></author></analytic><series><title level="j">Neurophysiologie clinique = Clinical neurophysiology</title><idno type="ISSN">0987-7053</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aging (metabolism)</term><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Basal Ganglia (diagnostic imaging)</term><term>Basal Ganglia (metabolism)</term><term>Basal Ganglia (physiopathology)</term><term>Basal Ganglia (surgery)</term><term>Brain Tissue Transplantation</term><term>Cell Transplantation</term><term>Cerebrovascular Circulation</term><term>Diagnosis, Differential</term><term>Dihydroxyphenylalanine (analogs & derivatives)</term><term>Dopamine Agonists (pharmacology)</term><term>Dopamine Agonists (therapeutic use)</term><term>Electric Stimulation Therapy</term><term>Fetal Tissue Transplantation</term><term>Forecasting</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Iatrogenic Disease</term><term>Imagination</term><term>Ligands</term><term>Mesencephalon (cytology)</term><term>Mesencephalon (embryology)</term><term>Motor Activity</term><term>Nerve Degeneration (diagnostic imaging)</term><term>Neurodegenerative Diseases (diagnosis)</term><term>Neurons (transplantation)</term><term>Neuroprotective Agents (pharmacology)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Neurotransmitter Agents (metabolism)</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (epidemiology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Parkinson Disease, Secondary (diagnostic imaging)</term><term>Parkinsonian Disorders (diagnostic imaging)</term><term>Radiopharmaceuticals</term><term>Rats</term><term>Receptors, Dopamine (metabolism)</term><term>Risk</term><term>Tomography, Emission-Computed</term><term>Tomography, Emission-Computed, Single-Photon</term><term>Tremor (diagnostic imaging)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Dihydroxyphenylalanine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Neurotransmitter Agents</term><term>Receptors, Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agonists</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Mesencephalon</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Basal Ganglia</term><term>Nerve Degeneration</term><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term><term>Parkinsonian Disorders</term><term>Tremor</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Mesencephalon</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Aging</term><term>Basal Ganglia</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Basal Ganglia</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Dopamine Agonists</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="transplantation" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Brain Tissue Transplantation</term><term>Cell Transplantation</term><term>Cerebrovascular Circulation</term><term>Diagnosis, Differential</term><term>Electric Stimulation Therapy</term><term>Fetal Tissue Transplantation</term><term>Forecasting</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Iatrogenic Disease</term><term>Imagination</term><term>Ligands</term><term>Motor Activity</term><term>Radiopharmaceuticals</term><term>Rats</term><term>Risk</term><term>Tomography, Emission-Computed</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Positron emission tomography (PET) and single photon emission computed tomography (SPECT) provide the means to studying in vivo the neurochemical, hemodynamic or metabolic consequences of the degeneration of the nigrostriatal dopaminergic system in Parkinson's disease (PD). The extent of striatal dopaminergic denervation can be quantified with radiotracers as [18F]FDopa for PET and [123I]tropanes for SPECT. There are other radiotracers such as [11C]Dopa and meta-tyrosines as well as PET tracers for uptake sites. Striatal uptake of [18F]FDopa and [123I]tropanes is markedly decreased in PD, more in the putamen than in the caudate nucleus, and inversely correlates with the severity of motor signs and with duration of disease. PET and SPECT make possible the assessment by noninvasive means of the changes in dopamine receptor density, the effect of neuronal transplants or neuroprotective treatments in PD patients, or the nigrostriatal dopaminergic function in at-risk subjects. Activation studies using cerebral blood flow and metabolism measurements during a motor task reveal an impaired ability to activate the supplementary motor area and dorsolateral prefrontal cortex in PD. This functional disability is reversed by the use of dopaminergic medication or by surgical treatment by pallidotomy or deep brain stimulation. The differential diagnosis between PD and multiple system atrophy, progressive supranuclear palsy or corticobasal degeneration is not yet clearly established by PET and SPECT, even though these syndromes have some particular neurochemical and metabolic profiles. On the other hand, PET and SPECT are useful for distinguishing PD from Dopa-responsive dystonia, or for assessing the integrity of the nigrostriatal dopaminergic pathway in atypical cases of postural tremor or iatrogenic parkinsonian syndromes.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Main/Merge
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003B55 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Merge/biblio.hfd -nk 003B55 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonFranceV1
|flux= Main
|étape= Merge
|type= RBID
|clé= pubmed:11817273
|texte= Contributions of PET and SPECT to the understanding of the pathophysiology of Parkinson's disease.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Merge/RBID.i -Sk "pubmed:11817273" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Merge/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonFranceV1
| This area was generated with Dilib version V0.6.29. |  |