Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease.
Identifieur interne : 002365 ( Ncbi/Checkpoint ); précédent : 002364; suivant : 002366Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease.
Auteurs : Kathrin Reetz [Allemagne] ; Christian Gaser ; Christine Klein ; Johannes Hagenah ; Christian Büchel ; Stefan Gottschalk ; Peter P. Pramstaller ; Hartwig R. Siebner ; Ferdinand BinkofskiSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
English descriptors
- KwdEn :
- Adult, Aged, Basal Ganglia (pathology), Caudate Nucleus (pathology), DNA Mutational Analysis, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Organ Size, Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinsonian Disorders (genetics), Parkinsonian Disorders (pathology), Putamen (pathology), Sequence Deletion, Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , genetics : Ubiquitin-Protein Ligases.
- genetics : Parkinson Disease, Parkinsonian Disorders.
- pathology : Basal Ganglia, Caudate Nucleus, Parkinson Disease, Parkinsonian Disorders, Putamen.
- Adult, Aged, DNA Mutational Analysis, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Organ Size, Sequence Deletion.
Abstract
A bilateral compensatory increase of basal ganglia (BG) gray matter value (GMV) was recently demonstrated in asymptomatic Parkin mutation carriers, who likely have an increased risk to develop Parkinson's disease (PD). We hypothesized BG morphological changes in symptomatic Parkin mutation carriers (sPARKIN-MC) and idiopathic PD patients (iPD) after the occurrence of PD symptoms, reflecting the breakdown of compensatory mechanisms. Nine sPARKIN-MC, 14 iPD, and 24 controls were studied clinically and with voxel-based morphometry. Analysis of variance revealed mainly BG decrease of GMV in sPARKIN-MC and to a lesser extent in iPD. However, a slight increase in GMV was also found in the right globus pallidus externus in sPARKIN-MC and in the right putamen in iPD. This may reflect a structural correlate of functional compensation that can only partially be maintained when nigrostriatal neurodegeneration becomes manifest. Simple regression analyses with the UPDRS-III and disease duration score revealed a distinct more bilateral linear decrease of BG GMV in sPARKIN-MC than in iPD that may correspond to previous findings showing a symmetric reduction in putaminal (18)F-DOPA-uptake and bilateral manifestation of symptoms in sPARKIN-MC. In symptomatic PD, BG are subject to a progressive atrophy, which gradually increases with disease severity and duration.
DOI: 10.1002/mds.22333
PubMed: 18823048
Affiliations:
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Pramstaller</name></author><author><name sortKey="Siebner, Hartwig R" sort="Siebner, Hartwig R" uniqKey="Siebner H" first="Hartwig R" last="Siebner">Hartwig R. 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Pramstaller</name></author><author><name sortKey="Siebner, Hartwig R" sort="Siebner, Hartwig R" uniqKey="Siebner H" first="Hartwig R" last="Siebner">Hartwig R. Siebner</name></author><author><name sortKey="Binkofski, Ferdinand" sort="Binkofski, Ferdinand" uniqKey="Binkofski F" first="Ferdinand" last="Binkofski">Ferdinand Binkofski</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Basal Ganglia (pathology)</term><term>Caudate Nucleus (pathology)</term><term>DNA Mutational Analysis</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Organ Size</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinsonian Disorders (genetics)</term><term>Parkinsonian Disorders (pathology)</term><term>Putamen (pathology)</term><term>Sequence Deletion</term><term>Ubiquitin-Protein Ligases (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Caudate Nucleus</term><term>Parkinson Disease</term><term>Parkinsonian Disorders</term><term>Putamen</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>DNA Mutational Analysis</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Organ Size</term><term>Sequence Deletion</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A bilateral compensatory increase of basal ganglia (BG) gray matter value (GMV) was recently demonstrated in asymptomatic Parkin mutation carriers, who likely have an increased risk to develop Parkinson's disease (PD). We hypothesized BG morphological changes in symptomatic Parkin mutation carriers (sPARKIN-MC) and idiopathic PD patients (iPD) after the occurrence of PD symptoms, reflecting the breakdown of compensatory mechanisms. Nine sPARKIN-MC, 14 iPD, and 24 controls were studied clinically and with voxel-based morphometry. Analysis of variance revealed mainly BG decrease of GMV in sPARKIN-MC and to a lesser extent in iPD. However, a slight increase in GMV was also found in the right globus pallidus externus in sPARKIN-MC and in the right putamen in iPD. This may reflect a structural correlate of functional compensation that can only partially be maintained when nigrostriatal neurodegeneration becomes manifest. Simple regression analyses with the UPDRS-III and disease duration score revealed a distinct more bilateral linear decrease of BG GMV in sPARKIN-MC than in iPD that may correspond to previous findings showing a symmetric reduction in putaminal (18)F-DOPA-uptake and bilateral manifestation of symptoms in sPARKIN-MC. In symptomatic PD, BG are subject to a progressive atrophy, which gradually increases with disease severity and duration.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="Binkofski, Ferdinand" sort="Binkofski, Ferdinand" uniqKey="Binkofski F" first="Ferdinand" last="Binkofski">Ferdinand Binkofski</name><name sortKey="Buchel, Christian" sort="Buchel, Christian" uniqKey="Buchel C" first="Christian" last="Büchel">Christian Büchel</name><name sortKey="Gaser, Christian" sort="Gaser, Christian" uniqKey="Gaser C" first="Christian" last="Gaser">Christian Gaser</name><name sortKey="Gottschalk, Stefan" sort="Gottschalk, Stefan" uniqKey="Gottschalk S" first="Stefan" last="Gottschalk">Stefan Gottschalk</name><name sortKey="Hagenah, Johannes" sort="Hagenah, Johannes" uniqKey="Hagenah J" first="Johannes" last="Hagenah">Johannes Hagenah</name><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><name sortKey="Pramstaller, Peter P" sort="Pramstaller, Peter P" uniqKey="Pramstaller P" first="Peter P" last="Pramstaller">Peter P. Pramstaller</name><name sortKey="Siebner, Hartwig R" sort="Siebner, Hartwig R" uniqKey="Siebner H" first="Hartwig R" last="Siebner">Hartwig R. Siebner</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Reetz, Kathrin" sort="Reetz, Kathrin" uniqKey="Reetz K" first="Kathrin" last="Reetz">Kathrin Reetz</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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