scholarly journals Local Interrelationships of Cerebral Oxygen Consumption and Glucose Utilization in Normal Subjects and in Ischemic Stroke Patients: A Positron Tomography Study

1984 ◽  
Vol 4 (2) ◽  
pp. 140-149 ◽  
Author(s):  
J. C. Baron ◽  
D. Rougemont ◽  
F. Soussaline ◽  
P. Bustany ◽  
C. Crouzel ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Kinetic Method ◽  
Normal Subjects ◽  
Combined Method ◽  
Stroke Patients ◽  
Control Subjects ◽  
Cerebral Metabolic Rate ◽  
Positron Emission ◽  
Ischemic Tissue

With the use of positron emission tomography (PET) and the 15O steady-state-[18F]fluorodeoxyglucose combined method, the local interrelationships between the cerebral metabolic rate for oxygen (CMRO2) and the cerebral metabolic rate for glucose (CMRGlc) were investigated in control subjects and in stroke patients. In addition to the classic in vivo autoradiographic approach, a kinetic method was used to measure CMRGlc because it was expected to be more reliable in cerebral ischemia. In control subjects local coupling between CBF, CMRO2, and CMRGlc was confirmed, and acceptable values for the CMRO2/CMRGlc ratio were found; the latter, however, was lower in white matter than in gray. Uncoupling between CMRO2 and CMRGlc was observed in all stroke patients, suggesting that (1) enhanced anaerobic glycolysis occurred both in reperfused recent infarcts and in chronically ischemic tissue, and (2) substrates other than blood-borne glucose were being oxidized at the borders of recent infarcts. However, methodological uncertainties presently make such observations only tentative. Finally, a coupled depression of CMRO2 and CMRGlc was found in the contralateral cerebellum.

scholarly journals Cerebral Glucose and Dopa Metabolism in Movement Disorders

1987 ◽  
Vol 14 (S3) ◽  
pp. 448-451 ◽  
Author(s):  
W.R. Wayne Martin ◽  
Michael R. Hayden
Keyword(s):  
At Risk ◽  
Glucose Metabolism ◽  
Normal Subjects ◽  
Cerebral Glucose Metabolism ◽  
Nigrostriatal Pathway ◽  
Age Related ◽  
Positron Emission ◽  
Asymptomatic Individuals ◽  
Regional Cerebral Glucose Metabolism

ABSTRACT:The development of positron emission tomography (PET) has enabled us to perform in vivo measurements of certain aspects of regional cerebral function. Regional cerebral glucose metabolism may be readily quantified with [18F] fluoro-2-deoxyglucose (FDG) and presynaptic dopaminergic function may be studied with the labelled dopa analog 6-[18F] fluoro-L-dopa. We have applied a model to the analysis of 6-FD/PET data with which in vivo age-related changes in dopaminergic function may be demonstrated in normal subjects. With this technique, we have studied a series of asymptomatic MPTP-exposed subjects and have shown evidence of subclinical nigrostriatal pathway damage. Studies of regional cerebral glucose metabolism with FDG in early Huntington's disease have shown a characteristic impairment in caudate function which precedes the development of caudate atrophy. In addition, some asymptomatic individuals who are at risk for HD have caudate hypometabolism. We feel that, at the present time, PET provides information which is complementary to the clinical examination in establishing a diagnosis of HD. In the future these studies may also help in the investigation of at risk individuals

Changes in synaptic density in the subacute phase after ischemic stroke: A 11C-UCB-J PET/MR study

2021 ◽  
pp. 0271678X2110477
Author(s):  
Laura Michiels ◽  
Nathalie Mertens ◽  
Liselot Thijs ◽  
Ahmed Radwan ◽  
Stefan Sunaert ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Standardized Uptake Value ◽  
Brain Regions ◽  
Asymmetry Index ◽  
Cerebellar Hemisphere ◽  
Future Research ◽  
Stroke Patients ◽  
Synaptic Density ◽  
Positron Emission

Functional alterations after ischemic stroke have been described with Magnetic Resonance Imaging (MRI) and perfusion Positron Emission Tomography (PET), but no data on in vivo synaptic changes exist. Recently, imaging of synaptic density became available by targeting synaptic vesicle protein 2 A, a protein ubiquitously expressed in all presynaptic nerve terminals. We hypothesized that in subacute ischemic stroke loss of synaptic density can be evaluated with 11C-UCB-J PET in the ischemic tissue and that alterations in synaptic density can be present in brain regions beyond the ischemic core. We recruited ischemic stroke patients to undergo 11C-UCB-J PET/MR imaging 21 ± 8 days after stroke onset to investigate regional 11C-UCB-J SUVR (standardized uptake value ratio). There was a decrease (but residual signal) of 11C-UCB-J SUVR within the lesion of 16 stroke patients compared to 40 healthy controls (ratiolesion/controls = 0.67 ± 0.28, p = 0.00023). Moreover, 11C-UCB-J SUVR was lower in the non-lesioned tissue of the affected hemisphere compared to the unaffected hemisphere (ΔSUVR = −0.17, p = 0.0035). The contralesional cerebellar hemisphere showed a lower 11C-UCB-J SUVR compared to the ipsilesional cerebellar hemisphere (ΔSUVR = −0.14, p = 0.0048). In 8 out of 16 patients, the asymmetry index suggested crossed cerebellar diaschisis. Future research is required to longitudinally study these changes in synaptic density and their association with outcome.

scholarly journals Cortical Hypometabolism and its Recovery following Nucleus Basalis Lesions in Baboons: A PET Study

1987 ◽  
Vol 7 (6) ◽  
pp. 812-817 ◽  
Author(s):  
Motohiro Kiyosawa ◽  
Sabina Pappata ◽  
Danielle Duverger ◽  
Danielle Riche ◽  
Henri Cambon ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Metabolic Rate ◽  
Nucleus Basalis ◽  
Emission Tomography ◽  
Metabolic Effects ◽  
Metabolic Depression ◽  
Cerebral Metabolic Rate ◽  
Positron Emission ◽  
Adaptive Mechanisms ◽  
Nucleus Basalis Lesions

The cerebral metabolic rate for glucose was measured serially with positron emission tomography and [18F]fluorodeoxyglucose in five baboons with stereotactic electrocoagulation of the left nucleus basalis of Meynert (NbM). Four days after lesion, a significant metabolic depression was present in the ipsilateral cerebral cortex, most marked in the frontotemporal region, and which recovered progressively within 6–13 weeks. These data demonstrate that adaptive mechanisms efficiently compensate for the cortical metabolic effects of NbM-lesion-induced cholinergic deafferentation. Moreover, unilateral NbM lesions also induced a transient reduction in contralateral cortical metabolic rate, the mechanisms of which are discussed. Explanation of these effects of cholinergic deafferentation in the primate could further our understanding of the metabolic deficits observed in dementia of the Alzheimer's type.

Magnetic resonance cerebral metabolic rate of oxygen utilization in hyperacute stroke patients

2003 ◽  
Vol 53 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Jin-Moo Lee ◽  
Katie D. Vo ◽  
Hongyu An ◽  
Azim Celik ◽  
Yueh Lee ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Metabolic Rate ◽  
Oxygen Utilization ◽  
Stroke Patients ◽  
Hyperacute Stroke ◽  
Cerebral Metabolic Rate

scholarly journals Computed Tomography and Positron Emission Transaxial Tomography Evaluations of Normal Aging and Alzheimer's Disease

1983 ◽  
Vol 3 (3) ◽  
pp. 391-394 ◽  
Author(s):  
Mony J. de Leon ◽  
Steven H. Ferris ◽  
Ajax E. George ◽  
Barry Reisberg ◽  
David R. Christman ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Senile Dementia ◽  
Normal Subjects ◽  
Normal Aging ◽  
Biochemical Changes ◽  
Positron Emission ◽  
Glucose Metabolic Rate ◽  
Brain Changes ◽  
In Vivo Diagnosis

Young normal subjects, old normal subjects, and patients with senile dementia of the Alzheimer's type (SDAT) were studied with both computed tomography (CT) and positron emission transaxial tomography (PETT). Increases in ventricular size with both aging and disease were measured. Regional glucose metabolic rate was not affected by age, but was markedly reduced in SDAT patients. These data indicate that in normal aging, structural brain changes may be more salient than biochemical changes. Although both structural and biochemical changes occur in SDAT, the biochemical changes are more marked. The results suggest that PETT is potentially more useful than CT in the in vivo diagnosis of SDAT.

scholarly journals Repeat Positron Emission Tomographic Studies in Transient Middle Cerebral Artery Occlusion in Cats: Residual Perfusion and Efficacy of Postischemic Reperfusion

1997 ◽  
Vol 17 (4) ◽  
pp. 388-400 ◽  
Author(s):  
Wolf-Dieter Heiss ◽  
Rudolf Graf ◽  
Jan Löttgen ◽  
Kouichi Ohta ◽  
Toshiaki Fujita ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Cerebral Metabolic Rate ◽  
Positron Emission ◽  
Reperfusion Period ◽  
Ischemic Episode ◽  
Cerebral Artery Occlusion

The wider clinical acceptance of thrombolytic therapy for ischemic stroke has focused more attention on experimental models of reversible focal ischemia. Such models enable the study of the effect of ischemia of various durations and of reperfusion on the development of infarctions. We used high-resolution positron emission tomography (PET) to assess cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral metabolic rate of glucose (CMRglc) before, during, and up to 24 h after middle cerebral artery occlusion (MCAO) in cats. After determination of resting values, the MCA was occluded by a transorbital device. The MCA was reopened after 30 min in five, after 60 min in 11, and after 120 min in two cats. Whereas all cats survived 30-min MCAO, six died after 60-min and one after 120-min MCAO during 6–20 h of reperfusion. In those cats surviving the first day, infarct size was determined on serial histologic sections. The arterial occlusion immediately reduced CBF in the MCA territory to <40% of control, while CMRO2 was less affected, causing an increase in OEF. Whereas in the cats surviving 24 h of reperfusion after 60- and 120-min MCAO, OEF remained elevated throughout the ischemic episode, the initial OEF increase had already disappeared during the later period of ischemia in those cats that died during the reperfusion period. After 30-min MCAO, the reperfusion period was characterized by a transient reactive hyperemia and fast normalization of CBF, CMRO2, and CMRglc, and no or only small infarcts in the deep nuclei were found in histology. After 60- and 120-min MCAO, the extent of hyperperfusion was related to the severity of ischemia, decreased CMRO2 and CMRglc persisted, and cortical/subcortical infarcts of varying sizes developed. A clear difference was found in the flow/metabolic pattern between surviving and dying cats: In cats dying during the observation period, extended postischemic hyperperfusion accompanied large defects in CMRO2 and CMRglc, large infarcts developed, and intracranial pressure increased fatally. In those surviving the day after MCAO, increased OEF persisted over the ischemic episode, postischemic hyperperfusion was less severe and shorter, and the perfusional and metabolic defects as well as the final infarcts were smaller. These results stress the importance of the severity of ischemia for the further course after reperfusion and help to explain the diverging outcome after thrombolysis, where a relation between the residual flow and the effectiveness of reperfusion was also observed.

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