scholarly journals Cerebral Blood Flow and Glucose Metabolism Measured With Positron Emission Tomography Are Decreased in Human Type 1 Diabetes

Diabetes ◽  
2013 ◽  
Vol 62 (8) ◽  
pp. 2898-2904 ◽  
Author(s):  
Larissa W. van Golen ◽  
Marc C. Huisman ◽  
Richard G. Ijzerman ◽  
Nikie J. Hoetjes ◽  
Lothar A. Schwarte ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Type 1 Diabetes ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Emission Tomography ◽  
Human Type ◽  
Positron Emission ◽  
Human Type 1 Diabetes

scholarly journals Positron Emission Tomography Examination of Cerebral Blood Flow and Glucose Metabolism in Young CADASIL Patients

Stroke ◽  
2004 ◽  
Vol 35 (5) ◽  
pp. 1063-1067 ◽  
Author(s):  
Susanna Tuominen ◽  
Qing Miao ◽  
Timo Kurki ◽  
Seppo Tuisku ◽  
Minna Pöyhönen ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Emission Tomography ◽  
Positron Emission ◽  
Positron Emission Tomography Examination

Positron emissie tomografie (PET) bij stemmingsstoornissen: een overzicht

1999 ◽  
Vol 11 (3) ◽  
pp. 97-102
Author(s):  
N. Van Eyken ◽  
H. D'haenen
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Mood Disorders ◽  
Resting State ◽  
Emission Tomography ◽  
Brain Glucose ◽  
Positron Emission

SummaryPositron emission tomography is one of the most important techniques of functional imaging in psychiatry. This paper gives a synopsis of the findings in mood disorders: determination of brain glucose metabolism, cerebral blood flow and receptor studies. Investigation in a resting state as well as after activation are discussed.Although findings are somewhat discrepant hypometabolism, and/or hypoperfusion, most often in frontal and limbic areas are frequently described. Further research is needed, and standardization of the methodology would be most wellcome.

Effects of Subanesthetic Ketamine on Regional Cerebral Glucose Metabolism in Humans

2004 ◽  
Vol 100 (5) ◽  
pp. 1065-1071 ◽  
Author(s):  
Jaakko W. Långsjö ◽  
Elina Salmi ◽  
Kaike K. Kaisti ◽  
Sargo Aalto ◽  
Susanna Hinkka ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Regions Of Interest ◽  
Emission Tomography ◽  
Positron Emission ◽  
Racemic Ketamine ◽  
The Mean ◽  
Parietal Cortices

Background The authors have recently shown with positron emission tomography that subanesthetic doses of racemic ketamine increase cerebral blood flow but do not affect oxygen consumption significantly. In this study, the authors wanted to assess the effects of racemic ketamine on regional glucose metabolic rate (rGMR) in similar conditions to establish whether ketamine truly induces disturbed coupling between cerebral blood flow and metabolism. Methods 18F-labeled fluorodeoxyglucose was used as a positron emission tomography tracer to quantify rGMR on 12 brain regions of interest of nine healthy male volunteers at baseline and during a 300-ng/ml ketamine target concentration level. In addition, voxel-based analysis was performed for the relative changes in rGMR using statistical parametric mapping. Results The mean +/- SD measured ketamine serum concentration was 326.4+/-86.3 ng/ml. The mean arterial pressure was slightly increased (maximally by 16.4%) during ketamine infusion (P < 0.001). Ketamine increased absolute rGMR significantly in most regions of interest studied. The greatest increases were detected in the thalamus (14.6+/-15.9%; P = 0.029) and in the frontal (13.6+/-13.1%; P = 0.011) and parietal cortices (13.1+/-11.2%; P = 0.007). Absolute rGMR was not decreased anywhere in the brain. The voxel-based analysis revealed relative rGMR increases in the frontal, temporal, and parietal cortices. Conclusions Global increases in rGMR seem to parallel ketamine-induced increases in cerebral blood flow detected in the authors' earlier study. Therefore, ketamine-induced disturbance of coupling between cerebral blood flow and metabolism is highly unlikely. The previously observed decrease in oxygen extraction fraction may be due to nonoxidative glucose metabolism during ketamine-induced increase in glutamate release.

scholarly journals Effects of Acetazolamide on Cerebral Blood Flow, Blood Volume, and Oxygen Metabolism: A Positron Emission Tomography Study with Healthy Volunteers

2001 ◽  
Vol 21 (12) ◽  
pp. 1472-1479 ◽  
Author(s):  
Hidehiko Okazawa ◽  
Hiroshi Yamauchi ◽  
Kanji Sugimoto ◽  
Hiroshi Toyoda ◽  
Yoshihiko Kishibe ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Capillary Blood ◽  
Emission Tomography ◽  
Positron Emission ◽  
Capillary Blood Volume

To evaluate changes in cerebral hemodynamics and metabolism induced by acetazolamide in healthy subjects, positron emission tomography studies for measurement of cerebral perfusion and oxygen consumption were performed. Sixteen healthy volunteers underwent positron emission tomography studies with15O-gas and water before and after intravenous administration of acetazolamide. Dynamic positron emission tomography data were acquired after bolus injection of H215O and bolus inhalation of15O2. Cerebral blood flow, metabolic rate of oxygen, and arterial-to-capillary blood volume images were calculated using the three-weighted integral method. The images of cerebral blood volume were calculated using the bolus inhalation technique of C15O. The scans for cerebral blood flow and volume and metabolic rate of oxygen after acetazolamide challenge were performed at 10, 20, and 30 minutes after drug injection. The parametric images obtained under the two conditions at baseline and after acetazolamide administration were compared. The global and regional values for cerebral blood flow and volume and arterial-to-capillary blood volume increased significantly after acetazolamide administration compared with the baseline condition, whereas no difference in metabolic rate of oxygen was observed. Acetazolamide-induced increases in both blood flow and volume in the normal brain occurred as a vasodilatory reaction of functioning vessels. The increase in arterial-to-capillary blood volume made the major contribution to the cerebral blood volume increase, indicating that the raise in cerebral blood flow during the acetazolamide challenge is closely related to arterial-to-capillary vasomotor responsiveness.

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