[18F]FDG mouse brain PET imaging: absolute quantification of regional cerebral glucose utilization as compared with 2-[14C]DG autoradiography

2004 ◽  
Vol 1265 ◽  
pp. 255-261 ◽  
Author(s):  
Hiroshi Toyama ◽  
Masanori Ichise ◽  
Jeih-San Liow ◽  
Kendra J Modell ◽  
Douglass C Vines ◽  
...  
Author(s):  
Tao Sun ◽  
Yaping Wu ◽  
Yan Bai ◽  
Zhenguo Wang ◽  
Chushu Shen ◽  
...  

Abstract As a non-invasive imaging tool, Positron Emission Tomography (PET) plays an important role in brain science and disease research. Dynamic acquisition is one way of brain PET imaging. Its wide application in clinical research has often been hindered by practical challenges, such as patient involuntary movement, which could degrade both image quality and the accuracy of the quantification. This is even more obvious in scans of patients with neurodegeneration or mental disorders. Conventional motion compensation methods were either based on images or raw measured data, were shown to be able to reduce the effect of motion on the image quality. As for a dynamic PET scan, motion compensation can be challenging as tracer kinetics and relatively high noise can be present in dynamic frames. In this work, we propose an image-based inter-frame motion compensation approach specifically designed for dynamic brain PET imaging. Our method has an iterative implementation that only requires reconstructed images, based on which the inter-frame subject movement can be estimated and compensated. The method utilized tracer-specific kinetic modelling and can deal with simple and complex movement patterns. The synthesized phantom study showed that the proposed method can compensate for the simulated motion in scans with 18F-FDG, 18F-Fallypride and 18F-AV45. Fifteen dynamic 18F-FDG patient scans with motion artifacts were also processed. The quality of the recovered image was superior to the one of the non-corrected images and the corrected images with other image-based methods. The proposed method enables retrospective image quality control for dynamic brain PET imaging, hence facilitates the applications of dynamic PET in clinics and research.


2021 ◽  
Vol 40 (1) ◽  
pp. 81-92
Author(s):  
Xiaoxi Pan ◽  
Trong-Le Phan ◽  
Mouloud Adel ◽  
Caroline Fossati ◽  
Thierry Gaidon ◽  
...  
Keyword(s):  

2018 ◽  
Vol 15 (13) ◽  
pp. 1267-1275 ◽  
Author(s):  
F.E. Reesink ◽  
D. Vállez García ◽  
C.A. Sánchez-Catasús ◽  
D.E. Peretti ◽  
A.T. Willemsen ◽  
...  

Background: We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging - Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging. Methods: 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias. Results: To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment. Conclusion: This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation.


1990 ◽  
Vol 23 (2) ◽  
pp. 129-140 ◽  
Author(s):  
ito Kiyomi ◽  
Sawada Yasufumi ◽  
Ishizuka Hitoshi ◽  
Sugiyama Yuichi ◽  
Suzuki Hiroshi ◽  
...  

2021 ◽  
Vol 96-97 ◽  
pp. S71-S72
Author(s):  
Tatsiana Auchynnikava ◽  
Xiang-Guo Li ◽  
Heidi Liljenbäck ◽  
Anne Roivainen ◽  
Anu Airaksinen

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