Analysis of glucose metabolism of 18F-FDG in major depression patients using PET imaging: Correlation of salivary cortisol and α-amylase

2016 ◽  
Vol 629 ◽  
pp. 52-57 ◽  
Author(s):  
Kai Wei ◽  
Hong-li Xue ◽  
Yi-hui Guan ◽  
Chuan-tao Zuo ◽  
Jing-jie Ge ◽  
...  
2020 ◽  
Vol 21 (18) ◽  
pp. 6523
Author(s):  
Maria Vittoria Mattoli ◽  
Giorgio Treglia ◽  
Maria Lucia Calcagni ◽  
Annunziato Mangiola ◽  
Carmelo Anile ◽  
...  

Idiopathic normal pressure hydrocephalus (iNPH) is the only form of dementia that can be cured by surgery. Its diagnosis relies on clinical and radiological criteria. Identifying patients who can benefit from surgery is challenging, as other neurological diseases can be concomitant or mimic iNPH. We performed a systematic review on the role of positron emission tomography (PET) in iNPH. We retrieved 35 papers evaluating four main functional aspects with different PET radiotracers: (1) PET with amyloid tracers, revealing Alzheimer’s disease (AD) pathology in 20–57% of suspected iNPH patients, could be useful in predictions of surgical outcome. (2) PET with radiolabeled water as perfusion tracer showed a global decreased cerebral blood flow (CBF) and regional reduction of CBF in basal ganglia in iNPH; preoperative perfusion parameters could predict surgical outcome. (3) PET with 2-Deoxy-2-[18F]fluoroglucose ([18F]FDG ) showed a global reduction of glucose metabolism without a specific cortical pattern and a hypometabolism in basal ganglia; [18F]FDG PET may identify a coexisting neurodegenerative disease, helping in patient selection for surgery; postsurgery increase in glucose metabolism was associated with clinical improvement. (4) Dopaminergic PET imaging showed a postsynaptic D2 receptor reduction and striatal upregulation of D2 receptor after treatment, associated with clinical improvement. Overall, PET imaging could be a useful tool in iNPH diagnoses and treatment response.


2013 ◽  
Vol 106 ◽  
pp. S107
Author(s):  
A. Roszak ◽  
B. Urbanski ◽  
E. Burchardt ◽  
J. Kazmierska ◽  
Z. Warenczak-Florczak ◽  
...  

Neuroscience ◽  
2019 ◽  
Vol 417 ◽  
pp. 35-44 ◽  
Author(s):  
Jingjing Su ◽  
Qi Huang ◽  
Shuhua Ren ◽  
Fang Xie ◽  
Yu Zhai ◽  
...  

2017 ◽  
Vol 40 (3) ◽  
pp. 875-882 ◽  
Author(s):  
Jingsong Wu ◽  
Bingbing Lin ◽  
Weilin Liu ◽  
Jia Huang ◽  
Guanhao Shang ◽  
...  

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.


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