scholarly journals Method for Rapid MRI Quantification of Global Cerebral Metabolic Rate of Oxygen

2015 ◽  
Vol 35 (10) ◽  
pp. 1616-1622 ◽  
Author(s):  
Suliman Barhoum ◽  
Michael C Langham ◽  
Jeremy F Magland ◽  
Zachary B Rodgers ◽  
Cheng Li ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
T Test ◽  
Quantitative Magnetic Resonance Imaging ◽  
Cerebral Metabolic Rate ◽  
Sagittal Sinus ◽  
Scan Time ◽  
Rapid Mri ◽  
Magnetic Resonance Imaging Mri ◽  
The Brain ◽  
Good Agreement

A recently reported quantitative magnetic resonance imaging (MRI) method denoted OxFlow has been shown to be able to quantify whole-brain cerebral metabolic rate of oxygen (CMRO2) by simultaneously measuring oxygen saturation ( S v O 2) in the superior sagittal sinus and cerebral blood flow (CBF) in the arteries feeding the brain in 30 seconds, which is adequate for measurement at baseline but not necessarily in response to neuronal activation. Here, we present an accelerated version of the method (referred to as F-OxFlow) that quantifies CMRO2 in 8 seconds scan time under full retention of the parent method's capabilities and compared it with its predecessor at baseline in 10 healthy subjects. Results indicate excellent agreement between both sequences, with mean bias of 2.2% ( P = 0.18, two-tailed t-test), 3.4% ( P = 0.08, two-tailed t-test), and 2.0% ( P = 0.56, two-tailed t-test) for SvO2, CBF, and CMRO2, respectively. F-OxFlow's potential to monitor dynamic changes in SvO2, CBF, and CMRO2 is illustrated in a paradigm of volitional apnea applied to five of the study subjects. The sequence captured an average increase in SvO2, CBF, and CMRO2 of 10.1 ± 2.5%, 43.2 ± 9.2%, and 7.1 ± 2.2%, respectively, in good agreement with literature values. The method may therefore be suited for monitoring alterations in CBF and SvO2 in response to neurovascular stimuli.

Delirium: Phenomenology and Diagnosis—A Neurobiologic View

1991 ◽  
Vol 3 (2) ◽  
pp. 121-134 ◽  
Author(s):  
John P. Blass ◽  
Karen A. Nolan ◽  
Ronald S. Black ◽  
Akira Kurita
Keyword(s):  
Differential Diagnosis ◽  
Metabolic Rate ◽  
Functional Impairment ◽  
Cortical Neurons ◽  
Brain Diseases ◽  
Subcortical Structures ◽  
Confusional State ◽  
Cerebral Metabolic Rate ◽  
Neuronal Metabolism ◽  
The Brain

“Delirium” is a reversible confusional state. It results from widespread but reversible interference with the function of cortical neurons, as documented by diffuse slowing on EEG and decreases in cerebral metabolic rate. Delirium can be due to impairments in neuronal metabolism, in neurotransmission (notably cholinergic), or in input from subcortical structures. Engel and Romano (1959) formulated delirium and dementia as the two poles of a spectrum of “cerebral insufficiency,” with delirium resulting from reversible functional impairment and dementia from irreversible anatomic damage. So many disorders can precipitate delirium that the differential diagnosis tests every facet of one's knowledge of medicine. With aging, both normative changes in the brain and the increasing incidence of brain diseases predispose to the development of delirium. The brain damage responsible for a dementia can sensitize to the development of a superimposed delirium.

scholarly journals New Molecular Knowledge Towards the Trigemino-Cardiac Reflex as a Cerebral Oxygen-Conserving Reflex

2010 ◽  
Vol 10 ◽  
pp. 811-817 ◽  
Author(s):  
N. Sandu ◽  
T. Spiriev ◽  
F. Lemaitre ◽  
A. Filis ◽  
B. Schaller
Keyword(s):  
Metabolic Rate ◽  
Cerebral Metabolism ◽  
Sympathetic Neurons ◽  
Small Population ◽  
Molecular Organization ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Cerebral Metabolic Rate ◽  
External Stimuli ◽  
The Brain

The trigemino-cardiac reflex (TCR) represents the most powerful of the autonomous reflexes and is a subphenomenon in the group of the so-called “oxygen-conserving reflexes”. Within seconds after the initiation of such a reflex, there is a powerful and differentiated activation of the sympathetic system with subsequent elevation in regional cerebral blood flow (CBF), with no changes in the cerebral metabolic rate of oxygen (CMRO2) or in the cerebral metabolic rate of glucose (CMRglc). Such an increase in regional CBF without a change of CMRO2or CMRglcprovides the brain with oxygen rapidly and efficiently. Features of the reflex have been discovered during skull base surgery, mediating reflex protection projects via currently undefined pathways from the rostral ventrolateral medulla oblongata to the upper brainstem and/or thalamus, which finally engage a small population of neurons in the cortex. This cortical center appears to be dedicated to transduce a neuronal signal reflexively into cerebral vasodilatation and synchronization of electrocortical activity; a fact that seems to be unique among autonomous reflexes. Sympathetic excitation is mediated by cortical-spinal projection to spinal preganglionic sympathetic neurons, whereas bradycardia is mediated via projections to cardiovagal motor medullary neurons. The integrated reflex response serves to redistribute blood from viscera to the brain in response to a challenge to cerebral metabolism, but seems also to initiate a preconditioning mechanism. Previous studies showed a great variability in the human TCR response, in special to external stimuli and individual factors. The TCR gives, therefore, not only new insights into novel therapeutic options for a range of disorders characterized by neuronal death, but also into the cortical and molecular organization of the brain.

scholarly journals 0424 Effect of Chronic Intermittent Hypoxia on Global Cerebral Metabolic Rate of Oxygen Consumption in Rats

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A162-A163
Author(s):  
J Xu ◽  
E Geng ◽  
L Brake ◽  
A Wiemken ◽  
B Keenan ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Oxygen Consumption ◽  
Sleep Apnea ◽  
Metabolic Rate ◽  
Intermittent Hypoxia ◽  
Sleep Cycle ◽  
Chronic Intermittent Hypoxia ◽  
Cerebral Metabolic Rate ◽  
Obstructive Sleep ◽  
The Brain

Abstract Introduction Patients with obstructive sleep apnea (OSA) commonly exhibit grey and white matter loss, which may be related to hypoxic damage in the brain during sleep. Our preliminary data demonstrated lower values of cerebral metabolic rate of oxygen (CMRO2) consumption in apneics versus controls. As such, reduced CMRO2 may be an important contributor to the neurologic consequences of OSA. Here we report a rodent model for chronic intermittent hypoxia (CIH) to quantify effects on CMRO2 consumption. We hypothesized that increased severity of CIH results in decreased CMRO2 levels. Methods Three groups of rats were subject to varying levels of hypoxia: sham (21% oxygen; n = 19), moderate (11% oxygen; n = 14), and severe (6% oxygen; n = 21). To deliver hypoxia, rats were exposed to three-minute cycles of oxygen between 21% and condition-specific nadir O2 for 12 hours daily during their sleep cycle. CMRO2 values were measured with MRI techniques, performed on anesthetized rats before and after 3 months exposure to CIH. Results Rats from the three hypoxia groups did not differ significantly in CMRO2 values at baseline (0 months). After 3 months of exposure to hypoxic conditions, there was a trending difference (p=0.0726) in percent change from baseline between severely hypoxic (-35.3%) and sham (+12.3%) rats. Moderately hypoxic rats demonstrated an intermediate decrease from baseline after 3 months (-19.0%). Conclusion Our findings suggest that increased severity of intermittent hypoxia yields a dose-response decrease in brain oxygen consumption. Our data add to the growing body of evidence on the relationship between obstructive sleep apnea and hypoxic damage in the brain, suggesting that CMRO2 levels may be an indicator of the neurologic consequences of OSA. Support Funded by NIH P01 HL094307

scholarly journals Glycolysis versus TCA Cycle in the Primate Brain as Measured by Combining 18F-FDG PET and 13C-NMR

2005 ◽  
Vol 25 (11) ◽  
pp. 1418-1423 ◽  
Author(s):  
Fawzi Boumezbeur ◽  
Laurent Besret ◽  
Julien Valette ◽  
Marie-Claude Gregoire ◽  
Thierry Delzescaux ◽  
...  
Keyword(s):  
Tca Cycle ◽  
Glycolytic Flux ◽  
Cerebral Metabolic Rate ◽  
Metabolic Coupling ◽  
Primate Brain ◽  
Positron Emission ◽  
The Tca Cycle ◽  
The Brain ◽  
Good Agreement ◽  
C Nmr

The glycolytic flux (cerebral metabolic rate of glucose CMRglc) and the TCA cycle flux ( VTCA) were measured in the same monkeys by 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) and 13C NMR spectroscopy, respectively. Registration of nuclear magnetic resonance (NMR) and PET data were used for comparison of CMRglc and VTCA in the exact same area of the brain. Both fluxes were in good agreement with literature values (CMR glc 0.23 ± 0.03 μmol/g min, VTCA = 0.53 ± 0.13 μmol/gmin). The resulting [ CMRglc/VTCA] ratio was 0.46 ± 0.12 ( n = 5, mean ± s.d.), not significantly different from the 0.5 expected when glucose is the sole fuel that is completely oxidized. Our results provide a cross-validation of both techniques. Comparison of CMRglc with VTCA is in agreement with a metabolic coupling between the TCA cycle and glycolysis under normal physiologic conditions.

scholarly journals MRI-based methods for quantification of the cerebral metabolic rate of oxygen

2016 ◽  
Vol 36 (7) ◽  
pp. 1165-1185 ◽  
Author(s):  
Zachary B Rodgers ◽  
John A Detre ◽  
Felix W Wehrli
Keyword(s):  
Magnetic Resonance ◽  
Metabolic Rate ◽  
Energy Requirements ◽  
Clinical Tool ◽  
Mri Contrast ◽  
Cerebral Metabolic Rate ◽  
Positron Emission ◽  
Obstructive Sleep ◽  
Contrast Mechanism ◽  
Magnetic Resonance Imaging Mri

The brain depends almost entirely on oxidative metabolism to meet its significant energy requirements. As such, the cerebral metabolic rate of oxygen (CMRO2) represents a key measure of brain function. Quantification of CMRO2 has helped elucidate brain functional physiology and holds potential as a clinical tool for evaluating neurological disorders including stroke, brain tumors, Alzheimer’s disease, and obstructive sleep apnea. In recent years, a variety of magnetic resonance imaging (MRI)-based CMRO2 quantification methods have emerged. Unlike positron emission tomography – the current “gold standard” for measurement and mapping of CMRO2 – MRI is non-invasive, relatively inexpensive, and ubiquitously available in modern medical centers. All MRI-based CMRO2 methods are based on modeling the effect of paramagnetic deoxyhemoglobin on the magnetic resonance signal. The various methods can be classified in terms of the MRI contrast mechanism used to quantify CMRO2: T2*, T2′, T2, or magnetic susceptibility. This review article provides an overview of MRI-based CMRO2 quantification techniques. After a brief historical discussion motivating the need for improved CMRO2 methodology, current state-of-the-art MRI-based methods are critically appraised in terms of their respective tradeoffs between spatial resolution, temporal resolution, and robustness, all of critical importance given the spatially heterogeneous and temporally dynamic nature of brain energy requirements.

Systemic and cerebral effects of prostacyclin-induced arterial hypotension in the dog

1984 ◽  
Vol 60 (6) ◽  
pp. 1201-1206 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
Julie J. Olin ◽  
James A. Sprowell
Keyword(s):  
Blood Flow ◽  
Average Rate ◽  
Recovery Period ◽  
Content Type ◽  
Cerebral Metabolic Rate ◽  
Sagittal Sinus ◽  
Arterial Blood ◽  
Intraoperative Hypotension ◽  
Before And After ◽  
The Brain

✓ Prostacyclin has strong vasodilating and antiplatelet properties. This study was performed to investigate its potential for producing profound intraoperative hypotension. Five dogs were anesthetized with morphine, nitrous oxide, and oxygen, paralyzed with pancuronium, and ventilated to a PaCO2 of 40 torr. Mean arterial blood pressure (MABP) was lowered to 40 mm Hg with an intravenous infusion of prostacyclin in 0.05 M Tris buffer (average rate of infusion 3 ± 1 µg/kg/min). Blood flow was determined using the radioactive microsphere technique. Measurements were made before and after 20, 40, and 60 minutes of hypotension; and after a 40-minute recovery period. Infusion of prostacyclin reduced MABP 63% while increasing heart rate 51%. Tachyarrhythmias occurred in all dogs, and cardiac index decreased 18%. Myocardial blood flow decreased an average of 29%, cerebral blood flow decreased 30%, cerebellar blood flow decreased 18%, and blood flow in the brain stem and spinal cord was unchanged. Cerebral metabolic rate of oxygen, determined by measuring the oxygen content of the sagittal sinus, was unchanged. Hypotension was easily induced and maintained using prostacyclin, without apparent tachyphylaxis. However, the cardiac changes caused by this drug are more severe than those accompanying hypotension induced by most other agents, and may represent a serious contraindication to its clinical use.

scholarly journals Error Sensitivity of Fluorodeoxyglucose Method for Measurement of Cerebral Metabolic Rate of Glucose

1981 ◽  
Vol 1 (4) ◽  
pp. 391-401 ◽  
Author(s):  
Sung-Cheng Huang ◽  
Michael E. Phelps ◽  
Edward J. Hoffman ◽  
David E. Kuhl
Keyword(s):  
Metabolic Rate ◽  
Rate Constants ◽  
Normal Values ◽  
Weighted Average ◽  
Control Group ◽  
Kinetic Measurements ◽  
Normal Value ◽  
Cerebral Metabolic Rate ◽  
Scan Time ◽  
Metabolic Conditions

The fluorodeoxyglucose (FDG) method for the measurement of local cerebral metabolic rate of glucose (LCMRGlc) employs typical values of the FDG transport rate constants that have been obtained by kinetic measurements on an appropriate control group. Discrepancies between the true values of the rate constants in tissue and the typical values used in the operational equation of the FDG method will introduce error in the estimate of LCMRGlc. Computer simulations were used to evaluate the accuracy of the FDG method in cases where (1) the tissue LCMRGlc deviates greatly from the normal values (e.g., stroke) or (2) the tissue LCMRGlc changes during the experiment (e.g., epileptic seizure). The effects of the magnitude and duration of metabolic changes were studied. The rsults indicate that if tissue LCMRGlc differs greatly from the normal value, the error in the estimated LCMRGlc at a scan time of 60 min is less than 20% of the difference between the true and normal values. In the non-steady-state cases, the estimated LCMRGlc was found to be a weighted average of the metabolic rates during the experiments, with the weightings approximately proportional to the plasma FDG concentration at the corresponding times. For example, if LCMRGlc in tissue was 5 times the normal values for the first 10 min but then returned to normal state, the LCMRGlc measured by the FDG method at a scan time of 60 min would be about only 2–3 times the normal value. The results of this study provide a better understanding of the accuracy of the FDG method under various tissue metabolic conditions and is useful for interpreting metabolic values obtained with the FDG method.

scholarly journals Hyperammonaemia depresses glucose consumption throughout the brain

1991 ◽  
Vol 277 (3) ◽  
pp. 693-696 ◽  
Author(s):  
J Jessy ◽  
M R DeJoseph ◽  
R A Hawkins
Keyword(s):  
Hepatic Encephalopathy ◽  
Metabolic Rate ◽  
Brain Function ◽  
Inverse Correlation ◽  
Glucose Consumption ◽  
Brain Structures ◽  
High Plasma ◽  
Plasma Ammonia ◽  
Cerebral Metabolic Rate ◽  
The Brain

Recent studies showed that hyperammonaemia caused many of the metabolic changes in portacaval-shunted rats, a model of hepatic encephalopathy. These changes included a depression in the cerebral metabolic rate of glucose (CMRGlc), an indication of decreased brain function. 2. The purpose of the present experiments was to determine whether the depression of CMRGlc caused by ammonia is confined to certain brain structures, or whether the depression is an overall decrease in all structures, such as occurs in portacaval-shunted rats. To accomplish this objective, rats were made hyperammonaemic by giving them intraperitoneal injections of 40 units of urease/kg body wt. every 12 h; control rats received 0.154 m-NaCl. CMRGlc was measured 48 h after the first injection, by using quantitative autoradiography with [6-14C]glucose as a tracer. 3. The experimental rats had high plasma ammonia concentrations (control 70 nmol/ml, experimental 610 nmol/ml) and brain glutamine levels (control 5.4 mumol/ml). Hyperammonaemia decreased CMRGlc throughout the brain by an average of 19%. CMRGlc showed an inverse correlation with plasma ammonia, but a stronger correlation with the brain glutamine content. 4. Hyperammonaemia led to a decrease in CMRGlc throughout the brain that was indistinguishable from the pattern seen in portacaval-shunted rats. This is taken as further evidence that the cerebral depression found in portacaval-shunted rats is a consequence of hyperammonaemia. The observation that depression of CMRGlc correlated more closely with brain glutamine content than with plasma ammonia suggests that metabolism of ammonia is an important step in the pathological sequence.

scholarly journals Superior sagittal sinus and transverse sagittal sinus thrombus secondary to occult meningioma

2017 ◽  
Vol 5 (10) ◽  
pp. 4619
Author(s):  
Anaz Bin Azeez ◽  
Prashant Kashyap ◽  
Dhaval Dhave ◽  
Shameer Hakkim ◽  
Nikhil Sam Varghese ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Superior Sagittal Sinus ◽  
Sinus Thrombosis ◽  
Transverse Sinus ◽  
Cerebral Venous Sinus Thrombosis ◽  
Cerebral Veins ◽  
Sagittal Sinus ◽  
Magnetic Resonance Imaging Mri ◽  
The Brain ◽  
Transverse Sinuses

The superior sagittal sinus is the largest of the venous sinuses. It receives blood from the frontal, parietal, and occipital superior cerebral veins and the diploic veins, which communicate with the meningeal veins. The superior sagittal sinus drains into the transverse sinuses. Central nervous system tumors like meningioma, glomus tumor, and meduloblastoma, often directly compress the veins and sinuses of the brain. Major sites of the occlusion include superior sagittal sinus (SSS) and transverse sinus. Initial days cerebral venous sinus thrombosis (CVST) was diagnosed only on autopsy. Since the advent of modern investigative modalities like magnetic resonance Imaging (MRI), Computerised Tomography Angiography (CTA) and Magnetic Resonance Venography (MRV), more and more cases are being diagnosed confidently.

scholarly journals High Temporal Resolution MRI Quantification of Global Cerebral Metabolic Rate of Oxygen Consumption in Response to Apneic Challenge

2013 ◽  
Vol 33 (10) ◽  
pp. 1514-1522 ◽  
Author(s):  
Zachary B Rodgers ◽  
Varsha Jain ◽  
Erin K Englund ◽  
Michael C Langham ◽  
Felix W Wehrli
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Metabolic Rate ◽  
Temporal Resolution ◽  
Healthy Adults ◽  
High Temporal Resolution ◽  
View Sharing ◽  
Cerebral Metabolic Rate ◽  
Sagittal Sinus ◽  
Rate Of Oxygen Consumption

We present a technique for quantifying global cerebral metabolic rate of oxygen consumption (CMRO2) in absolute physiologic units at 3-second temporal resolution and apply the technique to quantify the dynamic CMRO2 response to volitional apnea. Temporal resolution of 3 seconds was achieved via a combination of view sharing and superior sagittal sinus-based estimation of total cerebral blood flow (tCBF) rather than tCBF measurement in the neck arteries. These modifications were first validated in three healthy adults and demonstrated to produce minimal errors in image-derived blood flow and venous oxygen saturation (SvO2) values. The technique was then applied in 10 healthy adults during an apnea paradigm of three repeated 30-second breath-holds. Subject-averaged baseline tCBF, arteriovenous oxygen difference (AVO2D), and CMRO2 were 48.6±7.0 mL/100 g per minute, 29.4 ± 3.4%HbO2, and 125.1±11.4 μmol/100 g per minute, respectively. Subject-averaged maximum changes in tCBF and AVO2D were 43.5±9.4% and − 32.1±5.7%, respectively, resulting in a small (6.0±3.5%) but statistically significant ( P = 0.00044, two-tailed t-test) increase in average end-apneic CMRO2. This method could be used to investigate neurometabolic-hemodynamic relationships in normal physiology, to better define the biophysical origins of the BOLD signal, and to quantify neurometabolic responsiveness in diseases of altered neurovascular reactivity.

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