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PET Measurement of Cardiac and Nigrostriatal Denervation in Parkinsonian Syndromes

¹ Division of Nuclear Medicine, Department of Radiology, University of Michigan, Ann Arbor, Michigan; ² Department of Biostatistics, University of Michigan, Ann Arbor, Michigan; and ³ Department of Neurology, University of Michigan, Ann Arbor, Michigan

Correspondence: For correspondence or reprints contact: David M. Raffel, PhD, Division of Nuclear Medicine, Department of Radiology, University of Michigan Medical School, 3480 Kresge III Bldg., Ann Arbor, MI 48109-0552. E-mail: raffel{at}umich.edu

Scintigraphic imaging with ¹²³I-metaiodobenzylguanidine (¹²³I-MIBG) has demonstrated extensive losses of cardiac sympathetic neurons in idiopathic Parkinson's disease (IPD). In contrast, normal cardiac innervation has been observed in ¹²³I-MIBG studies of multiple-system atrophy (MSA) and progressive supranuclear palsy (PSP). Consequently, it has been hypothesized that cardiac denervation can be used to differentiate IPD from MSA and PSP. We sought to test this hypothesis by mapping the distribution of cardiac sympathetic neurons in patients with IPD, MSA, and PSP by using PET and ¹¹C-meta-hydroxyephedrine (¹¹C-HED). Also, the relationship between cardiac denervation and nigrostriatal denervation was investigated by measuring striatal presynaptic monoaminergic nerve density with PET and ¹¹C-dihydrotetrabenazine (¹¹C-DTBZ). Methods: ¹¹C-HED and ¹¹C-DTBZ scans were obtained for patients with IPD (n = 9), MSA (n = 10), and PSP (n = 8) and for age-matched control subjects (n = 10). Global and regional measurements of ¹¹C-HED retention were obtained to assess the extent of cardiac sympathetic denervation. ¹¹C-DTBZ binding was measured in the caudate nucleus, anterior putamen, and posterior putamen. Results: As expected, extensive cardiac denervation was observed in several of the patients with IPD. However, substantial cardiac denervation was also seen in some patients with MSA and PSP. ¹¹C-DTBZ studies demonstrated striatal denervation in all patients with IPD and in most patients with MSA and PSP. No correlation was found between cardiac ¹¹C-HED retention and striatal ¹¹C-DTBZ binding. Conclusion: Cardiac sympathetic denervation was found to occur not only in IPD but also in other movement disorders, such as MSA and PSP. This finding implies that scintigraphic detection of cardiac sympathetic denervation cannot be used independently to discriminate IPD from other movement disorders, such as MSA and PSP. Cardiac sympathetic denervation was not correlated with striatal denervation, suggesting that the pathophysiologic processes underlying cardiac denervation and striatal denervation occur independently in patients with parkinsonian syndromes. These findings provide novel information about central and peripheral denervation in patients with neurodegenerative disorders.

Key Words: Parkinson's disease • multiple-system atrophy • progressive supranuclear palsy • PET • meta-hydroxyephedrine • dihydrotetrabenazine

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