Automatic analysis of integrated magnetic resonance and positron emission tomography images improves the accuracy of detection of focal cortical dysplasia type IIb lesions

Author(s):  
Yaoyun Lin ◽  
Jiajie Mo ◽  
Huiwen Jin ◽  
Xueliang Cao ◽  
Yang Zhao ◽  
...  
Author(s):  
Yongxiang Tang ◽  
Jie Yu ◽  
Ming Zhou ◽  
Jian Li ◽  
Tingting Long ◽  
...  

Abstract   Purpose The loss of synaptic vesicle glycoprotein 2A (SV2A) is well established as the major correlate of epileptogenesis in focal cortical dysplasia type II (FCD II), but this has not been directly tested in vivo. In this positron emission tomography (PET) study with the new tracer 18F-SynVesT-1, we evaluated SV2A abnormalities in patients with FCD II and compared the pattern to 18F-fluorodeoxyglucose (18F-FDG). Methods Sixteen patients with proven FCD II and 16 healthy controls were recruited. All FCD II patients underwent magnetic resonance imaging (MRI) and static PET imaging with both 18F-SynVesT-1 and 18F-FDG, while the controls underwent MRI and PET with only 18F-SynVesT-1. Visual assessment of PET images was undertaken. The standardized uptake values (SUVs) of 18F-SynVesT-1 were computed for regions of interest (ROIs), along with SUV ratio (SUVr) between ROI and centrum semiovale (white matter). Asymmetry indices (AIs) were analyzed between the lesion and the contralateral hemisphere for intersubject comparisons. Results Lesions in the brains of FCD II patients had significantly reduced 18F-SynVesT-1 uptake compared with contralateral regions, and brains of the controls. 18F-SynVesT-1 PET indicated low lesion uptake in 14 patients (87.5%), corresponding to hypometabolism detected by 18F-FDG PET, with higher accuracy for lesion localization than MRI (43.8%) (P < 0.05). AI analyses demonstrated that in the lesions, SUVr for each of the radiotracers were not significantly different (P > 0.05), and 18F-SynVesT-1 SUVr correlated with that of 18F-FDG across subjects (R2 = 0.41, P = 0.008). Subsequent visual ratings indicated that 18F-SynVesT-1 uptake had a more restricted pattern of reduction than 18F-FDG uptake in FCD II lesions (P < 0.05). Conclusion SV2A PET with 18F-SynVesT-1 shows a higher accuracy for the localization of FCD II lesions than MRI and a more restricted pattern of abnormality than 18F-FDG PET.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Sangwoo Kim ◽  
Youngjeon Lee ◽  
Chang-Yeop Jeon ◽  
Yeung Bae Jin ◽  
Sukhoon Oh ◽  
...  

Abstract Background Although the thalamus is known to modulate basal ganglia function related to motor control activity, the abnormal changes within the thalamus during distinct medical complications have been scarcely investigated. In order to explore the feasibility of assessing iron accumulation in the thalamus as an informative biomarker for Parkinson’s disease (PD), this study was designed to employ quantitative susceptibility mapping using a 7 T magnetic resonance imaging system in cynomolgus monkeys. A 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-injected cynomolgus monkey and a healthy control (HC) were examined by 7 T magnetic resonance imaging. Positron emission tomography with 18F-N-(3-fluoro propyl)-2ß-carboxymethoxy-3ß-(4-iodophenyl) nortropane was also employed to identify the relationship between iron deposits and dopamine depletion. All acquired values were averaged within the volume of interest of the nigrostriatal pathway. Findings Compared with the HC, the overall elevation of iron deposition within the thalamus in the Parkinson’s disease model (about 53.81% increase) was similar to that in the substantia nigra (54.81%) region. Substantial susceptibility changes were observed in the intralaminar part of the thalamus (about 70.78% increase). Additionally, we observed that in the Parkinson’s disease model, binding potential values obtained from positron emission tomography were considerably decreased in the thalamus (97.51%) and substantia nigra (92.48%). Conclusions The increased iron deposition in the thalamus showed negative correlation with dopaminergic activity in PD, supporting the idea that iron accumulation affects glutaminergic inputs and dopaminergic neurons. This investigation indicates that the remarkable susceptibility changes in the thalamus could be an initial major diagnostic biomarker for Parkinson’s disease-related motor symptoms.


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