1Department of Neurology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangdong 510630, China 2Department of Neurosurgery, the First Affiliated Hospital of Sun Yat-Sen University, Guangdong 510080, China 3Department of Neurosurgery, the University of Texas Medical School at Houston, Houston, TX 77030, USA 4Department of Radiology and Nuclear Medicine, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510630, China 5The State Key Laboratory of Medical Genetics, Central South University, Changsha, Hunan 410078, China
This study explored the association between cerebral metabolic rates of glucose (CMRGlc) and the severity of Vascular Parkinsonism (VP) and Parkinson’s disease (PD). A cross-sectional study was performed to compare CMRGlc in normal subjects vs. VP and PD patients. Twelve normal subjects, 22 VP, and 11 PD patients were evaluated with the H&Y and MMSE, and underwent 18F-FDG measurements. Pearson’s correlations were used to identify potential associations between the severity of VP/PD and CMRGlc. A pronounced reduction of CMRGlc in the frontal lobe and caudate putamen was detected in patients with VP and PD when compared with normal subjects. The VP patients displayed a slight CMRGlc decrease in the caudate putamen and frontal lobe in comparison with PD patients. These decreases in CMRGlc in the frontal lobe and caudate putamen were significantly correlated with the VP patients’ H&Y, UPDRS II, UPDRS III, MMSE, cardiovascular, and attention/memory scores. Similarly, significant correlations were observed in patients with PD. This is the first clinical study finding strong evidence for an association between low cerebral glucose metabolism and the severity of VP and PD. Our findings suggest that these changes in glucose metabolism in the frontal lobe and caudate putamen may underlie the pathophysiological mechanisms of VP and PD. As the scramble to find imaging biomarkers or predictors of the disease intensifies, a better understanding of the roles of cerebral glucose metabolism may give us insight into the pathogenesis of VP and PD.
Table 1 Demographic, motor, and non-motor parameters of patients with VP and PD.
Figure 1. MRI Imaging scans for VP and PD patients and normal subjects. (A) Normal subjects, (B) PD patients, (C) VP patients. The extent of white matter hyperintensities and multiple infarctions in the basal ganglia in the VP patients are shown in T2-weighted and FLAIR images. Arrows indicate the infarction.
Figure 2. Measurements of CMRGlc in various brain regions in VP, PD, and normal subjects. Significant relative hypometabolism in patients with VP and PD was detected in the frontal lobe and caudate putamen compared to normal subjects (A and B). The images are horizontal brain sections. The changes in glucose metabolism are indicated by high (red) to low (blue) tracer uptake or binding in the scale.
frontal lobe /cerebellum
VP vs. normal
PD vs. normal
PD vs VP
Table 2 The difference in CMRGlc in the frontal lobes and caudate putamen between normal subjects vs. VP and PD patients (Mean ± SD).
Disease duration (years)
Daily L-dopa dosage (mg)
Table 3 Spearman’s rank correlation coefficient (rs) between CMRGlc and clinical parameters in VP patients.
Disease duration (years)
Daily L-dopa dosage (mg)
Table 4 Spearman’s rank correlation coefficient (rs) between CMRGlc and clinical parameters in PD patients.
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