Imaging characteristics of brain 18F-FDG PET/CT of 26 Alzheimer’s Disease patients in National Hospital of Geriatrics

Du Duc Chien1, Pham Thang1, Mai Trong Khoa2, Tran Dinh Ha2, Nguyen Thi Thanh Binh1, Nguyen Thanh Binh1, Nguyen Trong Hung1, Ho Thi Kim Thanh1, Tran Hai Binh3, Nguyen Thi The3,
1 Central Geriatric Hospital
2 Nuclear Medicine and Cancer Center Tumor - Bach Mai Hospital
3 Nuclear Medicine and Oncology Center - Bach Mai Hospital

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Abstract

SUMMARY


Purpose: Applying the brain PET/CT imaging technic in order to define imaging characteristics of cerebral glucose metabolism using 18F-FDG in studying dementia caused by Alzheimer’s Disease in the National Hospital of Geriatrics.
Methods: From 2014 to 2015, 26 demential patients with
clinically definite diagnosis of Alzheimer’s disease were selected from the National Geriatric Hospital and undergone brain 18F-FDG PET/CT scans at the Center of Nuclear Medicine and Oncology - Bach Mai Hospital.
Results: Mean age of Alzheimer’s disease patients is 66.3 ±
8.2 years old and mainly aging over 60 years old (76.7%). Female patients are dominant (female/male ratio is 1.9). 80.8% patients having low scholary - under - graduating and 65% patients living in urban areas. Main risk factors of Alzheimer’s disease patients present in different frequencies as diabetes (23.1%), hypertriglyceride (50%), hypercholesteremia (57,7%), arterosclerosis (29.2%) and
cardiopathy (33.3%). Most of Alzheimer’s disease patients examined at moderate to severe stage (84.6%) and MMSE mean at 13,50±6,24. Brain 18F-FDG PET/CT imaging on 26 Alzheimer’s disease patients shows a glucose hypometabolism in medial temporo-hippocampal
area in 96.2% of cases on left side, meanwhile 92.3% of cases having a hypometabolism in right medial temporo-hippocampal area as well as in bilateral posterior cingulate gyrus. Hypometabolism in temporo - parietal area rates 76.9% on right side and 86.5% on left side. Cerebral metabolism in occipital lobes principally reserved and
partially affected only in 15.4% of cases on right side and 11.5% on left side. Hypometabolism extending to bilateral frontal lobe in a half of cases. Brain glucose metabolism partially reserved at primary moto - sensory cortices, occipital, frontal and cerebellar lobes, as well as in anterior cingulate gyrus. High reservation of glucose metabolism
at basal ganglias in Alzheimer disease (96.2%). Visualisation of glucose hypometabolic Alzheimer like patterns in 92.3% of cases in which 84.6% on both sides and only 2 cases presenting unilaterally on left side (dominant hemisphere). Alzheimer’s disease grading by 18F-FDG PET/CT is correspondent to clinical staging which is not realy high but statistically significant.
Conclusion: Glucose metabolism characteristic imaging in 18F-FDG PET/ CT brain scans is specifically and anatomically regional with high rate in medial
temporo - hippocampal, posterior temporal, temporo parietal and posterior cingulate areas. Frontal lobes and a part of occipital lobes affected in late stage. Principally,
metabolism reserved moderately in cerebellum, occipital lobes, as well as in the
primary moto-sensory cortices, especially well reserved at basal ganglias. 18F-FDG PET/CT imaging characteristics in this study are well correspondent to glucose metabolic patterns in Alzheimer’s disease. With high diagnostic value and important role confirmed in medial literature in discriminative diagnosis of Alzheimer’s disease from other demential forms, as well as in pre-clinical diagnostic ability, brain 18F-FDG PET/CT scan can be considered as a safe and valuable imaging technic in Alzheimer’s Disease studying and clinical practice in particular as well as in dementia in general.

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References

TÀI LIỆU THAM KHẢO
1. Nguyễn Duy Bắc (2010). Nghiên cứu đặc điểm hình thái tổn thương não trên bệnh nhân Alzheimer và động vật thực nghiệm”, Luận án tiến sỹ Y học, Hà Nội
2. Feldman HH (2007), Atlas of Alzheimer’s disease, Informa Health care, CRC Press, Florida, USA
3. Foster NL, et al (1988), ”Cerebral hypometabolism in progressive supranuclear palsy studied with positron emission tomography”, Ann Neurol, 24(3), pp. 399-406
4. Foster NL, et al (2007), ”FDG-PET improves accuracy in distinguishing frontotemporal dementia and Alzheimer’s disease”, Brain, 130 (Pt 10), pp. 2616-2635
5. Herholz K, Salmon E, Perani D, et al (2002), “Discrimination between Alzheimer dementia and controls by automated analysis of multicenter FDG PET”, Neuroimage, 17: 302–316
6. Hoffman JM W-BK, Hanson M, et al (2000), ”FDG PET imaging in patients with pathologically verified dementia”, J Nucl Med, 41pp. 1920-1928
7. Karttunen K, Karppi P., et al (2011), ”Neuropsychiatric symptoms and quality of life in patients with very mild and mild Alzheimer’s disease”,
Int J Geriatr Psychiatry, 26(5), pp. 473-482
8. Mai Trong Khoa (2012), Atlas PET/CT một số bệnh ung thư ở người Việt Nam, Nhà xuất bản Y học, Hà Nội
9. Trần Viết Lực (2011). Nghiên cứu một số yếu tố nguy cơ của sa sút trí tuệ ở bệnh nhân mắc bệnh Alzheimer, Luận án tiến sỹ y học, Đại học Y Hà Nội
10. Mata M, et al (1980), ”Activity-dependent energy
metabolism in rat posterior pituitary primarily reflects
sodium pump activity”, J Neurochem, 34(1), pp. 213-215
11. Meguro K, et al (1999), “ Neocortical and
hippocampal glucose hypometabolism following
neurotoxic lesions of the entorhinal and perirhinal cortices
in the nonhuman primate as shown by PET: implications
for Alzheimer’s disease”, Brain 122, pp. 1519–1531
12. Minoshima S, Frey KA, Foster NL, et al (1995)
“ Preserved pontine glucose metabolism in Alzheimer’s
disease: a reference region for functional brain
analysis”, J Comput Assist Tomogr, 19, pp. 541–547
13. Minoshima S GB, Berent S, et al (1997),
“Metabolic reduction in the posterior cingulate cortex in
very early Alzheimer’s disease”, Ann Neurol, 42pp. 85–94
14. Perry G. AJ, Kinosita J., et al (2006),
“Alzheimer’s disease: A century of scientific and clinical
reseach. “ IOS Press, pp. 29-447
15. Plassman B.L., Langa K.M., et al (2007),
“Prevalence of Dementia in the United States:
The Aging, Demographics and Memory Study”,
Neuroepidemiology, 29(1-2), pp. 125-132
16. Silverman DH et al (2001), “Positron emission
tomography in evaluation of dementia: Regional brain
metabolism and long-term outcome”, JAMA, 286(17),
pp. 2120-2127
17. Phạm Thắng và cộng sự (2010). Hợp tác nghiên
cứu một số yếu tố nguy cơ của hội chứng sa sút trí tuệ ở
người cao tuổi và đề xuất biện pháp can thiệp dự phòng,
Báo cáo nghiệm thu đề tài cấp nhà nước, Hà Nội
18. Phạm Thắng và Nguyễn Thanh Bình (2010).
Nghiên cứu một số đặc điểm lâm sàng và trắc nghiệm
thần kinh tâm lý của bệnh Alzheimer, Tạp chí nghiên
cứu Y học, 68(3), 91-96
19. Phạm Thắng., Tạ Thành Văn., Dư Đức Chiến
và cs: Bệnh Alzheimer và các thể sa sút trí tuệ khác.
Nhà xuất bản Y học, Hà Nội 2010:3-335
20. UNPD (2011). Già hóa dân số và người cao
tuổi Việt Nam: Thực trạng, dự báo và một số khuyến
nghị chính sách, Hà Nội
21. Nguyễn Kim Việt (2008), “Nghiên cứu đặc
điểm sa sút trí tuệ tại cộng đồng “, Tạp chí Y Học Thực
Hành, 10pp. 16-19
22. WHO (2003), The World Health Report 2003 -
Shaping the future, World Health Organization, Geneva,
Switzerland