Volume 6, Issue 4, July 2018, Page: 94-98
Relationship Between Cerebral Glucose Metabolic Disorder and Malignant Tumor Type
Siwen Wei, Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, P. R. China
Zhiheng Dong, Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, P. R. China
Ruilian Ma, Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, P. R. China
Sha Li, Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, P. R. China
Rui Cheng, Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, P. R. China
Received: Aug. 9, 2018;       Published: Aug. 13, 2018
DOI: 10.11648/j.ajcem.20180604.12      View  376      Downloads  30
Abstract
Aim: To study whether cerebral glucose metabolic disorder in malignant tumor patients without cerebral diseases is related to the site of tumor by using the 18F-deoxyglucose (FDG) PET/CT brain imaging technology. Methods: 22 patients with primary liver cancer and 20 patients with pancreatic cancer were subjected to general physical examinations by 18F-FDG positron emission tomography (PET). A statistical parametric mapping (SPM) software was adopted to analyze the information about cerebral resting glucose metabolism retrospectively, and to compare with the 22 healthy subjects with matched ages and genders. Results: Both the primary liver cancer and pancreatic cancer patients underwent metabolic reduction in both sides of the frontal and temporal areas, but the range and voxel involved in the latter were more extensive than those in the former, especially in the prefrontal cortex. The elevated metabolic areas in pancreatic cancer, which were much wider than those in liver cancer, were mainly located on both sides of the hippocampus, parahippocampal gyrus, amygdala, anterior cingulate cortex and posterior cingulate cortex, and extensively increased glucose metabolism was discerned in cerebellum. The areas of the latter were mainly distributed in the posterior cingulate cortex. Conclusion: Wide areas of glucose metabolic disorder existed in the patients with malignant tumors without cerebral metastasis, the distribution of which is related to the tumor type.
Keywords
Cerebral Metabolism, 18F-deoxyglucose, Positron Emission Tomography, Psychiatric Oncology
To cite this article
Siwen Wei, Zhiheng Dong, Ruilian Ma, Sha Li, Rui Cheng, Relationship Between Cerebral Glucose Metabolic Disorder and Malignant Tumor Type, American Journal of Clinical and Experimental Medicine. Vol. 6, No. 4, 2018, pp. 94-98. doi: 10.11648/j.ajcem.20180604.12
Reference
[1]
Betul O, Ipek M. Brain tumor presenting with psychiatric symptoms. J Neuropsychiatry Clin Neurosci 2011;23:43-44.
[2]
Ni JM, Lin MF, Liu JJ, Huang G. [Regional brain metabolism changes in the body malignant tumor patients without brain metastasis]. Chin J Med Imaging Technol 2010;26:2175-2177.
[3]
Gulyás B, Halldin C. New PET radiopharmaceuticals beyond FDG for brain tumor imaging. Q J Nucl Med Mol Imaging 2012;56:173-190.
[4]
Ozeki Y, Abe Y, Kita H, Tamura K, Sakata I, Ishida J, Machida K. A case of primary lung cancer lesion demonstrated by F-18 FDG positron emission tomography/computed tomography (PET/CT) one year after the detection of metastatic brain tumor. Oncol Lett 2011;2:621-623.
[5]
Vermetten E, Lanius RA. Biological and clinical framework for posttraumatic stress disorder. Handb Clin Neurol 2012;10:291-342.
[6]
Javidi H, Yadollahie M. Post-traumatic Stress Disorder. Int J Occup Environ Med 2012;3:2-9.
[7]
Fujita Y, Yamamoto S, Morinobu S. Novel therapeutic approach for the treatment of post-traumatic stress disorder (PTSD): facilitating fear extinction. Nihon Shinkei Seishin Yakurigaku Zasshi 2012;32:195-201.
[8]
Acheson DT, Gresack JE, Risbrough VB. Hippocampal dysfunction effects on context memory: possible etiology for posttraumatic stress disorder. Neuropharmacology 2012;62:674-685.
[9]
Inagaki M, Yoshikawa E, Kobayakawa M, Matsuoka Y, Sugawara Y, Nakano T, Akizuki N, Fujimori M, Akechi T, Kinoshita T, Furuse J, Murakami K, Uchitomi Y. Regional cerebral glucose metabolism in patients with secondary depressive episodes after fatalpancreatic cancer diagnosis. J Affect Disord 2007;99:231-236.
[10]
Puskás T, Henits I. Diffusion-weighted MR imaging; the significance of ADC and perfusion values in the differential diagnosis of pancreatic adenocarcinoma and mass forming pancreatitis. Orv Hetil 2012;153:1191-1196.
[11]
Drevets WC. Functional anatomical abnormalities in limbic and prefrontal cortical structures in major depression. Prog Brain Res 2000;126:413-431.
[12]
Bench CJ, Friston KJ, Brown RG, Scott LC, Frackowiak RS, Dolan RJ. The anatomy of melancholia--focal abnormalities of cerebral blood flow in major depression. Psychol Med 1992;22:607-615.
[13]
Shah PJ, Glabus MF, Goodwin GM, Ebmeier KP. Chronic, treatment-resistant depression and right fronto-striatal atrophy. Br J Psychiatry 2002;5:430-440.
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