No relevant midbrain atrophy in Parkinson's disease

dc.contributor.authorElina Mäkinen
dc.contributor.authorJuho Joutsa
dc.contributor.authorJuuso Isotalo
dc.contributor.authorValtteri Kaasinen
dc.contributor.organizationfi=PET-keskus|en=Turku PET Centre|
dc.contributor.organizationfi=kliininen laitos|en=Department of Clinical Medicine|
dc.contributor.organizationfi=kliiniset neurotieteet|en=Clinical Neurosciences|
dc.contributor.organizationfi=lääketieteellinen tiedekunta|en=Faculty of Medicine|
dc.contributor.organizationfi=tyks, vsshp|en=tyks, varha|
dc.contributor.organization-code1.2.246.10.2458963.20.61334543354
dc.contributor.organization-code1.2.246.10.2458963.20.74845969893
dc.contributor.organization-code2607000
dc.contributor.organization-code2609810
dc.converis.publication-id17528612
dc.converis.urlhttps://research.utu.fi/converis/portal/Publication/17528612
dc.date.accessioned2022-10-28T14:29:05Z
dc.date.available2022-10-28T14:29:05Z
dc.description.abstract<p>Aims of the study - To investigate whether significant midbrain atrophy is present in Parkinson's disease (PD), and if so, whether it can be used as a marker of striatal dopaminergic degeneration. Methods - In total, 150 PD patients and 155 controls were scanned with both brain dopamine transporter (DAT) [I-123]FP-CIT SPECT and 1.5T MRI. Midbrain atrophy was measured from sagittal MRIs using the midbrain-to-pons ratios. Both striatal region-of-interest-based (Brass) and striatal and extrastriatal voxel-by-voxel-based DAT binding (SPM8) were investigated in relation to midbrain atrophy. Results - The midbrain-to-pons ratios in PD patients were slightly lower than those in the controls (mean 0.59 vs 0.61, P < 0.05). The ratios did not significantly correlate with striatal or extrastriatal [I-123] FP-CIT uptake in controls or patients with PD. Conclusions - Mild midbrain atrophy is present in PD and can be detected with MRI. However, the midbrain atrophy in PD is not associated with the level of striatal dopaminergic dysfunction, and midbrain measurements therefore cannot be used as a clinically useful predictor of dopamine function.<br /></p>
dc.format.pagerange378
dc.format.pagerange381
dc.identifier.jour-issn0001-6314
dc.identifier.olddbid188543
dc.identifier.oldhandle10024/171637
dc.identifier.urihttps://www.utupub.fi/handle/11111/53572
dc.identifier.urnURN:NBN:fi-fe2021042715802
dc.language.isoen
dc.okm.affiliatedauthorMyller, Elina
dc.okm.affiliatedauthorJoutsa, Juho
dc.okm.affiliatedauthorIsotalo, Juuso
dc.okm.affiliatedauthorKaasinen, Valtteri
dc.okm.affiliatedauthorDataimport, tyks, vsshp
dc.okm.discipline3124 Neurology and psychiatryen_GB
dc.okm.discipline3124 Neurologia ja psykiatriafi_FI
dc.okm.internationalcopublicationnot an international co-publication
dc.okm.internationalityInternational publication
dc.okm.typeA1 ScientificArticle
dc.publisherWILEY-BLACKWELL
dc.publisher.countryUnited Statesen_GB
dc.publisher.countryYhdysvallat (USA)fi_FI
dc.publisher.country-codeUS
dc.relation.doi10.1111/ane.12551
dc.relation.ispartofjournalActa Neurologica Scandinavica
dc.relation.issue5
dc.relation.volume134
dc.source.identifierhttps://www.utupub.fi/handle/10024/171637
dc.titleNo relevant midbrain atrophy in Parkinson's disease
dc.year.issued2016

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