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Editorial commentary
Filling in the missing puzzle piece between cardiac MIBG scintigraphy findings and Parkinson's disease pathology
  1. Hirohisa Watanabe1,
  2. Gen Sobue1,2
  1. 1Nagoya University, Brain and Mind Research Center, Nagoya, Japan
  2. 2Nagoya University Graduate School of Medicine, Nagoya, Japan
  1. Correspondence to Dr Hirohisa Watanabe, Nagoya University, Brain and Mind Research Center, Showa-ku, Nagoya 466-8550, Japan; nabe{at}med.nagoya-u.ac.jp

https://doi.org/10.1136/jnnp-2015-310862

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    123I-meta-iodobenzylguanidine (MIBG) cardiac scintigraphy can be used to assess the pathophysiology of postganglionic presynaptic cardiac sympathetic nerve endings and is the most frequently used imaging agent to assess cardiac sympathetic innervation. In 1994, Hakusui et al1 were the first to report reduced cardiac MIBG and preserved thallium accumulation in Parkinson's disease (PD). Subsequently, many studies confirmed the usefulness of 123I-MIBG cardiac scintigraphy for investigating early sympathetic involvement in PD and for differentiating PD from neurodegenerative parkinsonism including multiple system atrophy (MSA), progressive supranuclear palsy, and corticobasal degeneration together with vascular parkinsonism and essential tremor.

    With respect to the pathophysiology involved in reduced MIBG uptake in …

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    Footnotes

    • Contributors GS was responsible for manuscript preparation, including review and critique.

    • Competing interests None declared.

    • Provenance and peer review Commissioned; internally peer reviewed.

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