|
| ||
|
|
||
Cerebral Metabolism (cerebral + metabolism)
Selected AbstractsCerebral Metabolism is Influenced by Muscle Ischaemia During Exercise in HumansEXPERIMENTAL PHYSIOLOGY, Issue 2 2003Mads K. Dalsgaard Maximal exercise reduces the cerebral metabolic ratio (O2/(glucose + 1/2lactate)) to < 4 from a resting value close to 6, and only part of this decrease is explained by the ,intent' to exercise. This study evaluated whether sensory stimulation of brain by muscle ischaemia would reduce the cerebral metabolic ratio. In 10 healthy human subjects the cerebral arterial-venous differences (a-v differences) for O2, glucose and lactate were assessed before, during and after three bouts of 10 min cycling with equal workload: (1) control exercise at light intensity, (2) exercise that elicited a high rating of perceived exertion due to a 100 mmHg thigh cuff, and (3) exercise followed by 5 min of post-exercise muscle ischaemia that increased blood pressure by , 20%. Control exercise did not significantly affect the a-v differences. However, during the recovery from exercise with thigh cuffs the cerebral metabolic ratio decreased from a resting value of 5.4 ± 0.2 to 4.0 ± 0.4 (mean ±s.e.m.. P < 0.05) as a discrete lactate efflux from the brain at rest shifted to a slight uptake. Also, following post-exercise muscle ischaemia, the cerebral metabolic ratio decreased to 4.5 ± 0.3 (P < 0.05). The results support the hypothesis that during exercise, cerebral metabolism is influenced both by the mental effort to exercise and by sensory input from skeletal muscles. [source] Clinical and imaging evidence of zolpidem effect in hypoxic encephalopathyANNALS OF NEUROLOGY, Issue 1 2007Christine Brefel-Courbon MD We conducted a randomized, double-blind, placebo-controlled, single-patient (N = 1) trial to evaluate the efficacy of zolpidem in a 48-year-old woman with an akinetic mutism. Motor and cognitive examinations and functional imaging were performed. Acute administration of zolpidem markedly improved motor performance and neuropsychological status. Cerebral metabolism (18F-fluorodeoxyglucose positron emission tomography) increased in postrolandic territories and in frontal cortex. Using the H215O positron emission tomography, we found a drug-induced activation in the anterior cingulate and orbitofrontal cortices. Zolpidem induced a transient improvement in motor and cognitive performances. This paradoxical effect could result from an activation of limbic loops modulating motivational processes. Ann Neurol 2007 [source] Dynamic study of cerebral bioenergetics and brain function using in vivo multinuclear MRS approachesCONCEPTS IN MAGNETIC RESONANCE, Issue 2 2005Wei Chen Abstract One of the greatest merits of nuclear magnetic resonance (NMR) methodology used in biomedical research and clinical settings is its capability of measuring various physiological parameters in vivo. Besides MR imaging (MRI), which has been routinely applied to obtain vital information in living organs at normal and diseased states, in vivo MR spectroscopy (MRS) provides an invaluable tool for determining metabolites, chemical reaction rates, bioenergetics, and their dynamic changes in the human and animals noninvasively. These MRS capabilities are further enhanced at high/ultrahigh magnetic fields because of significant gain in NMR detection sensitivity and improvement in the spectral resolution. Recent progress has shown that in vivo MRS holds great promise in many biomedical research areas,in particular, brain research. This article provides a broad review of (i) in vivo multinuclear MRS approaches, (ii) advanced MRS methodologies, and (iii) MRS applications for determining cerebral metabolism as well as bioenergetics at resting brain state and their dynamic changes in response to brain activation. © 2005 Wiley Periodicals, Inc. Concepts Magn Reson Part A 27A: 84-121, 2005 [source] Insights into the acute cerebral metabolic changes associated with childhood diabetesDIABETIC MEDICINE, Issue 5 2005F. J. Cameron Abstract Aims Type 1 diabetes is a prevalent chronic disease in childhood with the commonest single cause of death being cerebral oedema in the context of diabetic ketoacidosis (DKA). The nature of the alterations in cerebral metabolism that may result in vulnerability to neuronal injury remains unknown. The aim of this study was to analyse the magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) brain data from eight children with diabetes following acute presentation with hyperglycaemia with or without ketoacidosis, to determine the nature and timing of any alterations in cerebral structure and metabolism. Methods This study used MRI and MRS to investigate regional cerebral abnormalities in a small series of diabetic patients with and without DKA. Changes were compared with the clinical and biochemical features of the patients studied. Results Our small series of patients all demonstrated abnormal signal changes in the frontal region on fluid attenuated inversion recovery (FLAIR) MR imaging, suggestive of oedema, and spectroscopic abnormalities of increased taurine, myoinositol and glucose levels. The MR abnormalities varied in severity but did not correlate with any clinical or biochemical parameters. Conclusions These changes indicate that many diabetic children, particularly at presentation, may have alterations in cerebral metabolism with implications for the pathogenesis and treatment of the cerebral complications of DKA. In addition, our findings suggest that increased taurine may be one of the important differentiating factors in the response of the brain of diabetic children to DKA that may reflect an increase in their vulnerability to cerebral oedema compared with diabetic adults. [source] Cerebral Metabolism is Influenced by Muscle Ischaemia During Exercise in HumansEXPERIMENTAL PHYSIOLOGY, Issue 2 2003Mads K. Dalsgaard Maximal exercise reduces the cerebral metabolic ratio (O2/(glucose + 1/2lactate)) to < 4 from a resting value close to 6, and only part of this decrease is explained by the ,intent' to exercise. This study evaluated whether sensory stimulation of brain by muscle ischaemia would reduce the cerebral metabolic ratio. In 10 healthy human subjects the cerebral arterial-venous differences (a-v differences) for O2, glucose and lactate were assessed before, during and after three bouts of 10 min cycling with equal workload: (1) control exercise at light intensity, (2) exercise that elicited a high rating of perceived exertion due to a 100 mmHg thigh cuff, and (3) exercise followed by 5 min of post-exercise muscle ischaemia that increased blood pressure by , 20%. Control exercise did not significantly affect the a-v differences. However, during the recovery from exercise with thigh cuffs the cerebral metabolic ratio decreased from a resting value of 5.4 ± 0.2 to 4.0 ± 0.4 (mean ±s.e.m.. P < 0.05) as a discrete lactate efflux from the brain at rest shifted to a slight uptake. Also, following post-exercise muscle ischaemia, the cerebral metabolic ratio decreased to 4.5 ± 0.3 (P < 0.05). The results support the hypothesis that during exercise, cerebral metabolism is influenced both by the mental effort to exercise and by sensory input from skeletal muscles. [source] The functional neuroanatomy of geriatric depressionINTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, Issue 8 2009Gwenn S. Smith Abstract Objective Positron Emission Tomography (PET) studies of cerebral glucose metabolism have demonstrated sensitivity in evaluating the functional neuroanatomy of treatment response variability in depression, as well as in the early detection of functional changes associated with incipient cognitive decline. The evaluation of cerebral glucose metabolism in late life depression may have implications for understanding treatment response variability, as well as evaluating the neurobiological basis of depression in late life as a risk factor for dementia. Methods Sixteen patients with geriatric depression and 13 comparison subjects underwent resting PET studies of cerebral glucose metabolism, as well as magnetic resonance (MR) imaging scans to evaluate brain structure. Results Cerebral glucose metabolism was elevated in geriatric depressed patients relative to comparison subjects in anterior (right and left superior frontal gyrus) and posterior (precuneus, inferior parietal lobule) cortical regions. Cerebral atrophy (increased cerebrospinal fluid [CSF] and decreased grey and white matter volumes) were observed in some of these regions, as well. Regional cerebral metabolism was positively correlated with severity of depression and anxiety symptoms. Conclusions In contrast to decreased metabolism observed in normal aging and neurodegenerative conditions such as Alzheimer's disease, cortical glucose metabolism was increased in geriatric depressed patients relative to demographically matched controls, particularly in brain regions in which cerebral atrophy was observed, which may represent a compensatory response. Copyright © 2009 John Wiley & Sons, Ltd. [source] 1H magnetic resonance spectroscopy in human hydrocephalusJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 3 2003Kees P.J. Braun MD Abstract Purpose To evaluate cerebral metabolism in clinical hydrocephalus with 1H magnetic resonance spectroscopy (MRS). Materials and Methods In 24 children and adults with progressive, arrested, or normal pressure hydrocephalus, long-echo time 1H MR spectra were acquired from periventricular white matter and intraventricular cerebrospinal fluid (CSF). Metabolite ratios, and the presence of lactate, were compared with 38 age-matched controls. Results Metabolite ratios of patients were within the 95% confidence interval (CI) of controls. A small lactate resonance was detected in 20% of control and hydrocephalic subjects. Lactate was consistently visible in CSF spectra, though lactate concentrations were normal. The CSF lactate T2 was long in comparison with the known intracellular metabolite T2 relaxation times. In three neonates with hydrocephalus and spina bifida, 3-hydroxybutyrate was detected in CSF in vivo. Conclusion Within the limits of the present methods, 1H MRS could not detect cerebral metabolic abnormalities in human hydrocephalus and provided no additional diagnostic information. The long T2 of lactate in CSF explains its high visibility. Hence, the detection of lactate in spectra acquired from voxels that contain CSF does not necessarily imply cerebral ischemia. J. Magn. Reson. Imaging 2003;17:291,299. © 2003 Wiley-Liss, Inc. [source] In vivo quantitative proton MRSI study of brain development from childhood to adolescence,JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2002Alena Horská PhD Abstract Purpose To quantify regional variations in metabolite levels in the developing brain using quantitative proton MR spectroscopic imaging (MRSI). Materials and Methods Fifteen healthy subjects three to 19 years old were examined by in vivo multislice proton MRSI. Concentrations of N-acetyl aspartate (NAA), total choline (Cho), total creatine (Cr), and peak area ratios were determined in selected frontal and parietal gray and white matter regions, basal ganglia, and thalamus. Results In cortical gray matter regions, the ratio of NAA/Cho increased to a maximum at 10 years and decreased thereafter (P = 0.010). In contrast, in white matter, average ratios NAA/Cho increased linearly with age (P = 0.045). In individual brain regions, age-related changes in NAA/Cho were found in the putamen (P = 0.044). No significant age-related changes in NAA, Cho, Cr, or other metabolite ratios could be determined. Conclusion Consistent with recent studies using other structural and functional neuroimaging techniques, our data suggest that small but significant changes occur in regional cerebral metabolism during childhood and adolescence. Non-linear age related changes of NAA/Cho in frontal and parietal areas, resembling previously reported age related changes in rates of glucose utilization and cortical volumes, may be associated with dendritic and synaptic development and regression. Linear age-related changes of NAA/Cho in white matter are also in agreement with age-related increases in white matter volumes, and may reflect progressive increases in axonal diameter and myelination. J. Magn. Reson. Imaging 2002;15:137,143. Published 2002 Wiley-Liss, Inc. [source] Astrocyte metabolism is disturbed in the early development of experimental hydrocephalusJOURNAL OF NEUROCHEMISTRY, Issue 1 2003Daniel Kondziella Abstract The proper diagnosis of the arrested or the progressive form of hydrocephalus has a critical impact on treatment, but remains difficult. The assessment of early changes in cerebral metabolism might help in the development of adequate non-invasive diagnostic tools. This study examined the alterations in label incorporation in neurotransmitter amino acids and other compounds in kaolin-induced progressive hydrocephalus in rats by means of magnetic resonance spectroscopy (MRS) combined with the administration of [1- 13C]glucose and [1,2- 13C]acetate. Some 2, 4 and 6 weeks after kaolin injection into the cisterna magna, cerebrum, brainstem and cerebellum were dissected. Interestingly, labelling of most amino acids derived from [1- 13C]glucose showed no alterations, whereas labelling from [1,2- 13C]acetate was affected. Two weeks after induction of hydrocephalus the taurine concentration was decreased, whereas the concentration of [1,2- 13C]lactate was increased in the cerebrum and that of [1,2- 13C]GABA in the brainstem. Furthermore, labelling from [1,2- 13C]acetate was significantly decreased in [4,5- 13C]glutamate, [1,2- 13C]glutamate and [1,2- 13C]GABA in cerebrum from 4 weeks after hydrocephalus induction. The concentration of N -acetylaspartate, a neuronal marker, was unchanged. However, labelling of the acetyl group from [1- 13C]glucose was decreased in cerebellum and brainstem at 6 weeks after the induction of hydrocephalus. As glucose is metabolized predominately by neurones, whereas acetate is exclusively taken up by astrocytes, these results indicate that mostly astrocytic, and only later neuronal, metabolism is disturbed in the kaolin model of hydrocephalus. If verified in patients using in vivo MRS, impaired astrocyte metabolism might serve as an early indication for operative treatment. [source] Alterations in cerebral metabolism by the neurotoxin kainic acid studied by 13C MRSJOURNAL OF NEUROCHEMISTRY, Issue 2002E. Olstad Kainic acid is a potent agonist at the kainate subclass of ionotropic glutamate receptors, and functional kainate receptors have not only been demonstrated on neurons but also on glial cells in culture. Kainic acid injections are used to induce limbic seizures in rodents. When combined with injections of [1-13C]glucose and [1,2-13C]acetate followed by analyses of forebrain extracts using 13C magnetic resonance spectroscopy (MRS) and HPLC information about glial neuronal interaction can be obtained. Using kainic acid treatment and 24 h later injection of 13C label a significant increase in label derived from [1,2-13C]acetate was observed in glutamine and glutamate. Label derived from [1-13C]glucose was unchanged in most metabolites, however, a decrease was observed in [2-13C]GABA. It should be noted that only astrocytes are able to utilize acetate as a substrate, whereas acetyl CoA derived from glucose is metabolized predominantly in the neuronal tricarboxylic acid cycle. These results indicate that turnover of metabolites was increased predominantly in astrocytes whereas glutamatergic neurons were not affected. However, GABAergic neurons showed decreased GABA labelling, possibly due to reduced GABA release 24 h after kainic acid injection. Taken together with results obtained 2 weeks after kainic acid injection, it can be suggested that increased astrocytic activity one day after epileptic seizures results, subsequently, in an increased amino acid turnover in neurons. Cell culture work was also performed, results will be presented at the meeting. [source] Remifentanil and the brainACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2008V. FODALE Background and aim: Remifentanil is an ultra-short-acting opioid, increasingly used today in neuroanesthesia and neurointensive care. Its characteristics make remifentanil a potentially ideal agent, but previous data have cast a shadow on this opioid, supporting potentially toxic effects on the ischemic brain. The aim of the present concise review is to survey available up-to-date information on the effects of remifentanil on the central nervous system. Method: A MEDLINE search within the past seven years for available up-to-date information on remifentanil and brain was performed. Results: Concise up-to-date information on the effects of remifentanil on the central nervous system was reported, with a particular emphasis on the following topics: cerebral metabolism, electroencephalogram, electrocorticography, motor-evoked potentials, regional cerebral blood flow, cerebral blood flow velocity, arterial hypotension and hypertension, intracranial pressure, cerebral perfusion pressure, cerebral autoregulation, cerebrovascular CO2 reactivity, cerebrospinal fluid, painful stimulation, analgesia and hyperalgesia, neuroprotection, neurotoxicity and hypothermia. Conclusion: The knowledge of the influence of remifentanil on brain functions is crucial before routine use in neuroanesthesia to improve anesthesia performance and patient safety as well as outcome. [source] Impaired decision making following 49 h of sleep deprivationJOURNAL OF SLEEP RESEARCH, Issue 1 2006WILLIAM D. S. KILLGORE Summary Sleep deprivation reduces regional cerebral metabolism within the prefrontal cortex, the brain region most responsible for higher-order cognitive processes, including judgment and decision making. Accordingly, we hypothesized that two nights of sleep loss would impair decision making quality and lead to increased risk-taking behavior on the Iowa Gambling Task (IGT), which mimics real-world decision making under conditions of uncertainty. Thirty-four healthy participants completed the IGT at rested baseline and again following 49.5 h of sleep deprivation. At baseline, volunteers performed in a manner similar to that seen in most samples of healthy normal individuals, rapidly learning to avoid high-risk decks and selecting more frequently from advantageous low-risk decks as the game progressed. After sleep loss, however, volunteers showed a strikingly different pattern of performance. Relative to rested baseline, sleep-deprived individuals tended to choose more frequently from risky decks as the game progressed, a pattern similar to, though less severe than, previously published reports of patients with lesions to the ventromedial prefrontal cortex. Although risky decision making was not related to participant age when tested at rested baseline, age was negatively correlated with advantageous decision making on the IGT, when tested following sleep deprivation (i.e. older subjects made more risky choices). These findings suggest that cognitive functions known to be mediated by the ventromedial prefrontal cortex, including decision making under conditions of uncertainty, may be particularly vulnerable to sleep loss and that this vulnerability may become more pronounced with increased age. [source] In vivo 13C magnetic resonance spectroscopy of human brain on a clinical 3 T scanner using [2- 13C]glucose infusion and low-power stochastic decouplingMAGNETIC RESONANCE IN MEDICINE, Issue 3 2009Shizhe Li Abstract This study presents the detection of [2- 13C]glucose metabolism in the carboxylic/amide region in the human brain, and demonstrates that the cerebral metabolism of [2- 13C]glucose can be studied in human subjects in the presence of severe hardware constraints of widely available 3 T clinical scanners and with low-power stochastic decoupling. In the carboxylic/amide region of human brain, the primary products of 13C label incorporation from [2- 13C]glucose into glutamate, glutamine, aspartate, ,-aminobutyric acid, and N-acetylaspartate were detected. Unlike the commonly used alkanyl region where lipid signals spread over a broad frequency range, the carboxylic carbon signal of lipids was found to be confined to a narrow range centered at 172.5 ppm and present no spectral interference in the absence of lipid suppression. Comparison using phantoms shows that stochastic decoupling is far superior to the commonly used WALTZ sequence at very low decoupling power at 3 T. It was found that glutamine C1 and C5 can be decoupled using stochastic decoupling at 2.2 W, although glutamine protons span a frequency range of ,700 Hz. Detailed specific absorption rate analysis was also performed using finite difference time domain numerical simulation. Magn Reson Med, 2009. © 2009 Wiley-Liss, Inc. [source] Coupling of theta activity and glucose metabolism in the human rostral anterior cingulate cortex: An EEG/PET study of normal and depressed subjectsPSYCHOPHYSIOLOGY, Issue 6 2003Diego A. Pizzagalli Abstract In rodents, theta rhythm has been linked to the hippocampal formation, as well as other regions, including the anterior cingulate cortex (ACC). To test the role of the ACC in theta rhythm, concurrent measurements of brain electrical activity (EEG) and glucose metabolism (PET) were performed in 29 subjects at baseline. EEG data were analyzed with a source localization technique that enabled voxelwise correlations of EEG and PET data. For theta, but not other bands, the rostral ACC (Brodmann areas 24/32) was the largest cluster with positive correlations between current density and glucose metabolism. Positive correlations were also found in right fronto-temporal regions. In control but not depressed subjects, theta within ACC and prefrontal/orbitofrontal regions was positively correlated. The results reveal a link between theta and cerebral metabolism in the ACC as well as disruption of functional connectivity within frontocingulate pathways in depression. [source] Brain involvement in rheumatoid arthritis: A magnetic resonance spectroscopy studyARTHRITIS & RHEUMATISM, Issue 11 2009Bart J. Emmer Objective Tumor necrosis factor , was recently implicated as an important mediator of communication between the peripheral and cerebral immune systems in an animal model of chronic inflammation. The purpose of this study was to examine by proton magnetic resonance spectroscopy (1H-MRS) the influence of inflammation on cerebral metabolism in patients with rheumatoid arthritis (RA). Methods Single-voxel 1H-MRS of the centrum semiovale was performed on 35 RA patients (6 men and 29 women; mean ± SD age 51.8 ± 14.6 years) and 28 healthy age- and sex-matched control subjects (9 men and 19 women; mean ± SD age 50.2 ± 10.4 years). None of the study subjects had any neurologic signs or symptoms. Clinical markers of disease activity were correlated with the 1H-MRS findings. Results Patients with active RA, as reflected by an elevated erythrocyte sedimentation rate (ESR), had a significantly higher ratio of choline to creatine and a significantly lower ratio of N -acetylaspartate to choline than did patients with inactive RA, as reflected by a normal ESR. Moreover, the ratios of choline to creatine and NAA to choline were significantly correlated with the ESR after correction for age, sex, smoking status, handedness, alcohol consumption, medication use, and disease duration. Medication use had no additional effect on these associations. Conclusion Our data show that systemic inflammation in RA is associated with metabolic changes in the brain. [source] Consequential Apoptosis in the Cerebellum Following Injury to the Developing Rat ForebrainBRAIN PATHOLOGY, Issue 3 2006Deanna L. Taylor In focal brain lesions, alterations in blood flow and cerebral metabolism can be detected in brain areas remote from the primary injury. The cellular consequences of this phenomenon, originally termed diaschisis, are not fully understood. Here, we report that in two distinct models of forebrain injury, neuronal death in the cerebellum, a site distant to the primary injury, results as consequence of neuronal loss in the forebrain. Fourteen-day-old rats were subjected to unilateral forebrain injury, achieved by either hypoxia-ischemia (right carotid artery ligation and hypoxia) or direct needle injury to brain tissue. At defined times after injury, the presence of apoptosis was investigated by cell morphology, in situ end labeling, electron microscopy and poly-ADP-ribose polymerase (PARP) cleavage. Injury to the rat forebrain following hypoxia-ischemia increased apoptosis in the internal granular and Purkinje cell layers of the cerebellum, a site distant to that of the primary injury. The number of apoptotic cells in the cerebellum was significantly related to cell death in the hippocampus. Similarly, direct needle injury to the forebrain resulted in extensive apoptotic cell death in the cerebellum. These results emphasize the intimate relationship between defined neuronal populations in relatively distant brain areas and suggest a cellular basis for diaschisis. [source] Rowing, the ultimate challenge to the human body , implications for physiological variablesCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2009Stefanos Volianitis Summary Clinical diagnoses depend on a variety of physiological variables but the full range of these variables is seldom known. With the load placed on the human body during competitive rowing, the physiological range for several variables is illustrated. The extreme work produced during rowing is explained by the seated position and the associated ability to increase venous return and, thus, cardiac output. This review highlights experimental work on Olympic rowing that presents a unique challenge to the human capacities, including cerebral metabolism, to unprecedented limits, and provides a unique opportunity to reveal the extreme range of many physiological variables. [source] | |||||||||||||||||||||||||