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Erschienen in: Journal of Neural Transmission 4/2017

03.02.2017 | High Impact Review in Neuroscience, Neurology or Psychiatry - Review Article

Neuromelanin MRI is useful for monitoring motor complications in Parkinson’s and PARK2 disease

verfasst von: Taku Hatano, Ayami Okuzumi, Koji Kamagata, Kensuke Daida, Daisuke Taniguchi, Masaaki Hori, Hiroyo Yoshino, Shigeki Aoki, Nobutaka Hattori

Erschienen in: Journal of Neural Transmission | Ausgabe 4/2017

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Abstract

Parkinson’s disease (PD) is caused by the loss of dopaminergic neurons. Recently, specific T1-weighted magnetic resonance imaging (MRI) at 3 Tesla was reported to visualize neuromelanin (NM)-related contrast of dopaminergic neurons. Using NM-MRI, we analyzed whether disease severity and motor complications (MC) are associated with the degree of dopaminergic neuronal degeneration in the substantia nigra pars compacta (SNc) in patients with idiopathic PD (PD) and PARK2. We examined 27 individuals with PD, 11 with PARK2, and a control group of 18. A 3T MRI was used to obtain a modified NM-sensitive T1-weighted fast-spin echo sequence. The size of the SNc was determined as the number of pixels with signal intensity higher than background signal intensity +2 standard deviations. NM-MRI indicated that the T1 hyperintense area in the SNc in patients with PD and PARK2 was significantly smaller than that in control subjects. When compared with the PD group without MC, both PD with MC and PARK2 showed a markedly smaller size of NM-rich SNc area. Receiver operating characteristic curve analysis revealed a sensitivity of 86.96% and a specificity of 100% in discriminating between patients with and without MC (area under the curve = 0.98). Correlation analysis between the T1 hyperintense SNc area and l-dopa and l-dopa equivalent dose demonstrated a significant negative correlation. The association between a reducing SNc NM-rich area and MC with increasing dopaminergic medication dose suggests that NM-MRI findings might be a useful tool for monitoring the development of MC in PD and PARK2.
Literatur
Zurück zum Zitat Booth TC, Nathan M, Waldman AD, Quigley AM, Schapira AH, Buscombe J (2015) The role of functional dopamine-transporter SPECT imaging in parkinsonian syndromes, part 1. AJNR Am J Neuroradiol 36(2):229–235. doi:10.3174/ajnr.A3970 CrossRefPubMed Booth TC, Nathan M, Waldman AD, Quigley AM, Schapira AH, Buscombe J (2015) The role of functional dopamine-transporter SPECT imaging in parkinsonian syndromes, part 1. AJNR Am J Neuroradiol 36(2):229–235. doi:10.​3174/​ajnr.​A3970 CrossRefPubMed
Zurück zum Zitat Castellanos G, Fernandez-Seara MA, Lorenzo-Betancor O et al (2015) Automated neuromelanin imaging as a diagnostic biomarker for Parkinson’s disease. Mov Disord 30(7):945–952. doi:10.1002/mds.26201 CrossRefPubMed Castellanos G, Fernandez-Seara MA, Lorenzo-Betancor O et al (2015) Automated neuromelanin imaging as a diagnostic biomarker for Parkinson’s disease. Mov Disord 30(7):945–952. doi:10.​1002/​mds.​26201 CrossRefPubMed
Zurück zum Zitat Hattori N, Kitada T, Matsumine H et al (1998a) Molecular genetic analysis of a novel Parkin gene in Japanese families with autosomal recessive juvenile parkinsonism: evidence for variable homozygous deletions in the Parkin gene in affected individuals. Ann Neurol 44(6):935–941. doi:10.1002/ana.410440612 CrossRefPubMed Hattori N, Kitada T, Matsumine H et al (1998a) Molecular genetic analysis of a novel Parkin gene in Japanese families with autosomal recessive juvenile parkinsonism: evidence for variable homozygous deletions in the Parkin gene in affected individuals. Ann Neurol 44(6):935–941. doi:10.​1002/​ana.​410440612 CrossRefPubMed
Zurück zum Zitat Hattori N, Matsumine H, Asakawa S et al (1998b) Point mutations (Thr240Arg and Gln311Stop) [correction of Thr240Arg and Ala311Stop] in the Parkin gene. Biochem Biophys Res Commun 249(3):754–758CrossRefPubMed Hattori N, Matsumine H, Asakawa S et al (1998b) Point mutations (Thr240Arg and Gln311Stop) [correction of Thr240Arg and Ala311Stop] in the Parkin gene. Biochem Biophys Res Commun 249(3):754–758CrossRefPubMed
Zurück zum Zitat Kempster PA, Williams DR, Selikhova M, Holton J, Revesz T, Lees AJ (2007) Patterns of levodopa response in Parkinson’s disease: a clinico-pathological study. Brain 130(Pt 8):2123–2128. doi:10.1093/brain/awm142 CrossRefPubMed Kempster PA, Williams DR, Selikhova M, Holton J, Revesz T, Lees AJ (2007) Patterns of levodopa response in Parkinson’s disease: a clinico-pathological study. Brain 130(Pt 8):2123–2128. doi:10.​1093/​brain/​awm142 CrossRefPubMed
Zurück zum Zitat Kempster PA, O’Sullivan SS, Holton JL, Revesz T, Lees AJ (2010) Relationships between age and late progression of Parkinson’s disease: a clinico-pathological study. Brain 133(Pt 6):1755–1762. doi:10.1093/brain/awq059 CrossRefPubMed Kempster PA, O’Sullivan SS, Holton JL, Revesz T, Lees AJ (2010) Relationships between age and late progression of Parkinson’s disease: a clinico-pathological study. Brain 133(Pt 6):1755–1762. doi:10.​1093/​brain/​awq059 CrossRefPubMed
Zurück zum Zitat Olanow WC, Kieburtz K, Rascol O et al (2013) Factors predictive of the development of Levodopa-induced dyskinesia and wearing-off in Parkinson’s disease. Mov Disord 28(8):1064–1071. doi:10.1002/mds.25364 CrossRef Olanow WC, Kieburtz K, Rascol O et al (2013) Factors predictive of the development of Levodopa-induced dyskinesia and wearing-off in Parkinson’s disease. Mov Disord 28(8):1064–1071. doi:10.​1002/​mds.​25364 CrossRef
Zurück zum Zitat PD-MED collaborative group (2014) Long-term effectiveness of dopamine agonists and monoamine oxidase B inhibitors compared with levodopa as initial treatment for Parkinson’s disease (PD MED): a large, open-label, pragmatic randomised trial. Lancet 384(9949):1196–1205. doi:10.1016/S0140-6736(14)60683-8 CrossRef PD-MED collaborative group (2014) Long-term effectiveness of dopamine agonists and monoamine oxidase B inhibitors compared with levodopa as initial treatment for Parkinson’s disease (PD MED): a large, open-label, pragmatic randomised trial. Lancet 384(9949):1196–1205. doi:10.​1016/​S0140-6736(14)60683-8 CrossRef
Zurück zum Zitat Reimao S, Pita Lobo P, Neutel D et al (2015) Substantia nigra neuromelanin magnetic resonance imaging in de novo Parkinson’s disease patients. Eur J Neurol 22(3):540–546. doi:10.1111/ene.12613 CrossRefPubMed Reimao S, Pita Lobo P, Neutel D et al (2015) Substantia nigra neuromelanin magnetic resonance imaging in de novo Parkinson’s disease patients. Eur J Neurol 22(3):540–546. doi:10.​1111/​ene.​12613 CrossRefPubMed
Zurück zum Zitat Schwarz ST, Rittman T, Gontu V, Morgan PS, Bajaj N, Auer DP (2011) T1-weighted MRI shows stage-dependent substantia nigra signal loss in Parkinson’s disease. Mov Disord 26(9):1633–1638. doi:10.1002/mds.23722 CrossRefPubMed Schwarz ST, Rittman T, Gontu V, Morgan PS, Bajaj N, Auer DP (2011) T1-weighted MRI shows stage-dependent substantia nigra signal loss in Parkinson’s disease. Mov Disord 26(9):1633–1638. doi:10.​1002/​mds.​23722 CrossRefPubMed
Zurück zum Zitat Tomlinson CL, Stowe R, Patel S, Rick C, Gray R, Clarke CE (2010) Systematic review of levodopa dose equivalency reporting in Parkinson’s disease. Mov Disord 25(15):2649–2653. doi:10.1002/mds.23429 CrossRefPubMed Tomlinson CL, Stowe R, Patel S, Rick C, Gray R, Clarke CE (2010) Systematic review of levodopa dose equivalency reporting in Parkinson’s disease. Mov Disord 25(15):2649–2653. doi:10.​1002/​mds.​23429 CrossRefPubMed
Metadaten
Titel
Neuromelanin MRI is useful for monitoring motor complications in Parkinson’s and PARK2 disease
verfasst von
Taku Hatano
Ayami Okuzumi
Koji Kamagata
Kensuke Daida
Daisuke Taniguchi
Masaaki Hori
Hiroyo Yoshino
Shigeki Aoki
Nobutaka Hattori
Publikationsdatum
03.02.2017
Verlag
Springer Vienna
Erschienen in
Journal of Neural Transmission / Ausgabe 4/2017
Print ISSN: 0300-9564
Elektronische ISSN: 1435-1463
DOI
https://doi.org/10.1007/s00702-017-1688-9

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