Abstract
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Objectives: Multiple system atrophy (MSA) is a parkinsonism-plus syndrome, presenting with autonomic dysfunction, parkinsonism, and cerebellar dysfunction, is difficult to differentiate from Parkinson’s disease (PD), particularly early in the course of disease. This study evaluated whether Tc-99m TRODAT-1 binding to the dopamine transporter of striatum differentiates MSA from PD, and further differentiates parkinsonism subtype (MSA-P) from cerebellar subtype (MSA-C) of MSA.
Methods: Tc-99m TRODAT-1 single-photon emission computed tomographic (SPECT) fused with brain MRI scans were acquired in 34 MSA patients, and disease-duration matched 14 PD patients. After excluding patients taking selective serotonin reuptake inhibitors, data of 43 patients (31 MSA, 12 PD) were analyzed for serotonin transporter bindings. Regions of interest (ROIs) were placed manually on 5 adjacent transversal slices containing the most intense striatal dopamine transporter (DAT) and extra-striatal serotonin transporter bindings, which represent a “punch biopsy” in order to reduce effects of volume averaging. Specific uptake ratio (SUR) and absolute value of asymmetric index (ASI) were calculated by the following equations: SUR=(ROI-Reference Region)/Reference Region, while using occipital cortex as reference region, and ASI=(2×[left UR-right UR]/[left UR+right UR])×100. Student’s t tests were used to compare MSA and PD patients, and between MSA-P and MSA-C groups. Clinical assessments of Hoeh and Yahr staging (H&Y) and Unified Parkinson’s Disease Rating Scale Part III (UPDRS III) were also performed.
Results: All available demographic data were summarized in Table 1. Patients with MSA (either MSA-P or MSA-C) were older and having more severe motor symptoms compared to those with PD. Mean SURs for each of ROIs of striatum and extrastriatum and mean ASIs were calculated along with the standard deviations and are illustrated in Table 2 and Table 3. All mean SURs were not significantly different in MSA and PD patients, except right caudate nucleus (95% CI, -0.58--0.07, P=0.014). As for striatal DAT and extrastriatal serotonin transporter bindings in subtypes of MSA, right caudate (95% CI, 0.06-0.58, P=0.016) and right putamen (95% CI, 0.08-0.85, P=0.020) were statistically significant. More asymmetric caudate bindings were found in the PD group than in MSA group (70.0 vs. 56.9, P=0.674 by t test). Among MSA group, the ASI index is markedly higher in patients with MSA-P than in MSA-C subgroups (66.1 vs 43.8, P=0.180). All ASIs in putamen were not significantly different in PD and MSA patients, and between MSA subgroups.
Conclusions: Striatal Tc-99m TRODAT-1 binding is significantly lower in patients with MSA than in those with PD. Among MSA group, the uptake is lower in MSA-P group than MSA-C group. The trend of asymmetric nigrostriatal damage was more obvious in PD than in MSA, and among MSA group, more asymmetry in MSA-P than in MSA-C patients, especially in caudate. This finding may assist clinicians for early differential diagnosis of patients with parkinsonism and provide a clue for the pathophysiology of PD and MSA.
Table 1. Available Population Characteristics
Table 2. Different Groups in Tc-99m TRODAT-1 Binding
Table 3. Asymmetric Index in Different Patient Groups
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