論文

査読有り 筆頭著者 責任著者
2005年4月

Metaiodobenzylguanidine (MIBG) scintigraphy at various parts of the body in Parkinson's disease and multiple system atrophy

AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
  • H Matsui
  • ,
  • F Udaka
  • ,
  • M Oda
  • ,
  • T Kubori
  • ,
  • K Nishinaka
  • ,
  • M Kameyama

119
1
開始ページ
56
終了ページ
60
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.autneu.2005.03.003
出版者・発行元
ELSEVIER SCIENCE BV

We compared MIBG uptake at various parts of the body in controls and patients with Parkinson's disease and multiple system atrophy. In the heart, MIBG uptake in Parkinson's disease (early H/N4: 1.668 0.325, late HIM: 1.500 ± 0.402) was less than that in multiple system atrophy (early H/M: 2.395 ± 0.186, late H/M: 2.530 ± 0.391) and controls (early H/M: 2.635 ± 0.508, late H/M: 2.575 ± 0.635) (early: P < 0.0001, late: P < 0.0001). There were no significant differences in uptake by the lung, thyroid, or liver in the three groups. Only on early images, uptake in the shoulder in multiple system atrophy (early S/M: 0.473 ± 0.78) and Parkinson's disease (early S/M: 0.470 ± 0.710) was decreased compared to that in controls (early SIM: 0.560 ± 0.118) (P = 0.0252). MIBG is reported to be taken up in the terminal part of sympathetic nerves and demonstrates sympathetic nerve activity, especially on late images. The cause of differences between the heart and other parts of the body remains unknown. We consider the following possibilities: (a) differences in the sympathetic nervous system between Parkinson's disease and multiple system atrophy are more subtle in organs other than the heart; (b) the cause of MIBG uptake reduction by the heart in Parkinson's disease involves factors in addition to sympathetic nervous system damage; and (c) MIBG uptake by organs other than the heart involves not only the sympathetic nervous system but also non-neuronal components. In conclusion, MIBG uptake by organs other than the heart cannot differentiate Parkinson's disease from multiple system atrophy at present. © 2005 Elsevier B.V. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.autneu.2005.03.003
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/15893708
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000229551400007&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.autneu.2005.03.003
  • ISSN : 1566-0702
  • PubMed ID : 15893708
  • Web of Science ID : WOS:000229551400007

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