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Myocardial 123metaiodobenzylguanidine uptake in genetic Parkinson's disease

✍ Scribed by Aldo Quattrone; Antonio Bagnato; Grazia Annesi; Fabiana Novellino; Letterio Morgante; Giovanni Savettieri; Mario Zappia; Patrizia Tarantino; Innocenza Claudia Cirò Candiano; Ferdinanda Annesi; Donatella Civitelli; Francesca Emanuela Rocca; Marco D'Amelio; Giuseppe Nicoletti; Maurizio Morelli; Alfredo Petrone; Piercostanzo Loizzo; Francesca Condino

Publisher: John Wiley and Sons
Year: 2008
Tongue: English
Weight: 348 KB
Volume: 23
Category: Article
ISSN: 0885-3185
DOI: 10.1002/mds.21701

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

Myocardial ^123^Metaiodobenzylguanidine (MIBG) enables the assessment of postganglionic sympathetic cardiac innervation. MIBG uptake is decreased in nearly all patients with Parkinson's disease (PD). Our objective was to evaluate MIBG uptake in patients with genetic PD. We investigated MIBG uptake in 14 patients with PD associated with mutations in different genes (Parkin, DJ‐1, PINK1, and leucine‐rich repeat kinase 2 ‐LRRK2), in 15 patients with idiopathic PD, and 10 control subjects. The myocardial MIGB uptake was preserved in 3 of the 4 Parkin‐associated Parkinsonisms, in 1 of the 2 patients with DJ‐1 mutations, in 1 of the 2 brothers with PINK1 mutations, in 3 of the 6 unrelated patients with Gly2019Ser mutation in the LRRK2 gene, whereas it was impaired in all patients with idiopathic PD. MIBG was preserved in all control subjects. Our study shows that myocardial MIGB uptake was normal in 8 of 14 patients with genetic PD, suggesting that cardiac sympathetic denervation occurs less frequently in genetic PD than in idiopathic PD. Our findings also demonstrate that MIGB uptake has a heterogeneous pattern in genetic PD, because it was differently impaired in patients with different mutations in the same gene or with the same gene mutation. © 2007 Movement Disorder Society

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