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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolism of the brain was investigated in eight patients with peritumoral edema, six patients with ischemic stroke, and 28 normal controls using proton magnetic resonance (MR) spectroscopy. The MR studies were performed using a 1.5-T whole-body imaging and spectroscopy system with a 1500-msec repetition time (TR) and a 270-msec echo time (TE). The peak areas for N-acetyl-aspartate (NAA), choline-containing compounds (Cho), creatine and phosphocreatine (Cr), and lactate (Lac) were measured, and the NAA/Cr, Cho/Cr, and Lac/Cr ratios were calculated. To quantify and compare the serial spectra, relaxation effects were investigated by acquisitions at two different points (TRs or TEs) and by monoexponential fitting. The normal NAA/Cr and Cho/Cr ratios were 2.76 and 1.09, respectively. Lac could not be identified in normal brains. In ischemic stroke and peritumoral edema, significantly increased Lac/Cr and decreased NAA/Cr ratios were observed. Resolution of peritumoral edema was associated with normalized NAA/Cr ratio and disappearance of Lac. The T1 relaxation times of the metabolites were similar in normal brain and peritumoral edema, but the T2 values were significantly shortened. Serial measurements of T2 values in two patients with peritumoral edema showed gradual normalization corresponding to improvement of the edema. To absolutely quantify metabolite concentrations in edema, changes in relaxation times should be considered.
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PMID:In vivo proton magnetic resonance spectroscopy for metabolic changes of human brain edema. 752 68

Familial hemiplegic migraine (FHM) is a rare autosomal dominant disorder of unknown pathogenesis characterized by migraine and transitory hemiplegic attacks. We describe a kindred fulfilling the diagnostic criteria for FHM in which: (1) brain phosphorus magnetic resonance spectroscopy (31P-MRS) showed a reduced phosphocreatine content accompanied by high [ADP], high percentage of V/Vmax of ATP biosynthesis and decreased phosphorylation potential; (2) muscle 31P-MRS showed a reduced rate of phosphocreatine recovery after exercise; (3) blood lactate was increased after effort; (4) muscle biopsy showed, in one patient, rare ragged red fibers succinate-dehydrogenase positive and cytochrome c oxidase negative; (5) genetic analysis of muscle mitochondrial DNA did not show any of the two point mutations in the tRNA(Leu(UUR)) associated with the MELAS syndrome (Mitochondrial myopathy, Encephalopathy with Lactic Acidosis and Stroke-like episodes). The defective energy metabolism of brain and muscle found in this pedigree suggests a multisystemic disorder of mitochondrial function in this FHM pedigree.
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PMID:Abnormal brain and muscle energy metabolism shown by 31P-MRS in familial hemiplegic migraine. 760 38

Recent results have demonstrated that the spin trapping agent N-tert-butyl-alpha-phenylnitrone (PBN) reduces infarct size due to middle cerebral artery occlusion (MCAO), even when given after ischemia. The objective of the present study was to explore whether PBN influences recovery of energy metabolism. MCAO of 2-hr duration was induced in rats by an intraluminal filament technique. Brains were frozen in situ at the end of ischemia and after 1, 2, and 4 hr of recirculation. PBN was given 1 hr after recirculation. Neocortical focal and perifocal ("penumbra") areas were sampled for analyses of phosphocreatine (PCr), creatine, ATP, ADP, AMP, glycogen, glucose, and lactate. The penumbra showed a moderate-to-marked decrease and the focus showed a marked decrease in PCr and ATP concentrations, a decline in the sum of adenine nucleotides, near-depletion of glycogen, and an increase in lactate concentration after 2 hr of ischemia. Recirculation for 1 hr led to only a partial recovery of energy state, with little further improvement after 2 hr and signs of secondary deterioration after 4 hr, particularly in the focus. After 4 hr of recirculation, PBN-treated animals showed pronounced recovery of energy state, with ATP and lactate contents in both focus and penumbra approaching normal values. Although an effect of PBN on mitochondria cannot be excluded, the results suggest that PBN acts by preventing a gradual compromise of microcirculation. The results justify a reevaluation of current views on the pathophysiology of focal ischemic damage and suggest that a therapeutic window of many hours exists in stroke.
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PMID:N-tert-butyl-alpha-phenylnitrone improves recovery of brain energy state in rats following transient focal ischemia. 776 48

One hundred percent of anesthetized rats administered 6.6 gm/kg of ethanol IP died within 10-35 min of alcohol injection; upon autopsy of the brain all demonstrated profound subarachnoid and intracranial bleeding, clear signs of hemorrhagic stroke. Pretreatment of rats with 4 mumol/min MgCl2, but not saline, via IV administration (for 30-45 min), prevented hemorrhagic stroke in all animals so treated with 6.6 gm/kg ethanol. Administration of the stroke dose of alcohol resulted in rapid (within 3-5 min) and marked deficits in whole brain intracellular free Mg ([Mg2++]i) as observed by in vivo 31P-NMR spectroscopy. Intracellular pH (pHi) and the phosphocreatine [PCr]/[ATP] ratio also fell following a significant fall in brain [Mg2+]i). Brains of rats that exhibited strokelike events, upon death and autopsy, demonstrated continued and marked intracellular acidosis with progressive fall in the [PCr]/[ATP] ratio and elevation of inorganic phosphate (Pi) and [H+]i; these events were not accompanied by any rises in systemic arterial blood pressure. Rats pretreated with MgCl2 exhibited relatively stable brain [Mg2+]i, and essentially unchanged pHi, [PCr], [ATP], or [Pi] following alcohol administration, although such animals exhibited threefold alterations in plasma Mg2+, as measured by ion selective electrodes. These observations suggest that high alcohol ingestion can result in severe vasospasm, ischemia, and rupture of blood vessels probably as a consequence of depletion of brain [Mg2+]i, events that can be prevented by Mg2+ pretreatment.
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PMID:Role of brain [Mg2+]i in alcohol-induced hemorrhagic stroke in a rat model: a 31P-NMR in vivo study. 777 64

It is not known why alcohol ingestion poses a risk for development of hypertension, stroke and sudden death. Of all drugs, which result in body depletion of magnesium (Mg), alcohol is now known to be the most notorious cause of Mg-wasting. Recent data obtained through the use of biophysical (and noninvasive) technology suggest that alcohol may induce hypertension, stroke, and sudden death via its effects on intracellular free Mg2+ ([Mg2+]i), which in turn alter cellular and subcellular bioenergetics and promote calcium ion (Ca2+) overload. Evidence is reviewed that demonstrates that the dietary intake of Mg modulates the hypertensive actions of alcohol. Experiments with intact rats indicates that chronic ethanol ingestion results in both structural and hemodynamic alterations in the microcirculation, which, in themselves, could account for increased vascular resistance. Chronic ethanol increases the reactivity of intact microvessels to vasoconstrictors and results in decreased reactivity to vasodilators. Chronic ethanol ingestion clearly results in vascular smooth muscle cells that exhibit a progressive increase in exchangeable and cellular Ca2+ concomitant with a progressive reduction in Mg content. Use of 31P-NMR spectroscopy coupled with optical-backscatter reflectance spectroscopy revealed that acute ethanol administration to rats results in dose-dependent deficits in phosphocreatine (PCr), the [PCr]/[ATP] ratio, intracellular pH (pHi), oxyhemoglobin, and the mitochondrial level of oxidized cytochrome oxidase aa3 concomitant with a rise in brain-blood volume and inorganic phosphate. Temporal studies performed in vivo, on the intact brain, indicate that [Mg2+]i is depleted before any of the bioenergetic changes. Pretreatment of animals with Mg2+ prevents ethanol from inducing stroke and prevents all of the adverse bioenergetic changes from taking place. Use of quantitative digital imaging microscopy, and mag-fura-2, on single-cultured canine cerebral vascular smooth muscle, human endothelial, and rat astrocyte cells reveals that alcohol induces rapid concentration-dependent depletion of [Mg2+]i. These cellular deficits in [Mg2+]i seem to precipitate cellular and subcellular disturbances in cytoplasmic and mitochondrial bioenergetic pathways leading to Ca2+ overload and ischemia. A role for ethanol-induced alterations in [Mg2+]i should also be considered in the well-known behavioral actions of alcohol.
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PMID:Role of magnesium and calcium in alcohol-induced hypertension and strokes as probed by in vivo television microscopy, digital image microscopy, optical spectroscopy, 31P-NMR, spectroscopy and a unique magnesium ion-selective electrode. 784 86

Calcium plays a prominent role in the neuronal degeneration which accompanies stroke and there has been much conjecture about the possible source of this Ca2+. The transmembrane Ca2+ transporting processes are considered likely candidates for the ischemia-induced rise in intracellular Ca2+. In the present paper we have monitored metabolism in the cerebral cortex in vitro before, during and after aglycaemic hypoxia using 31P and 1H NMR spectroscopy. We used the recovery of cellular metabolites phosphocreatine, ATP, lactate, glutamate and N-acetyl aspartate determined by NMR as an indicator of cell damage caused by hypoxia. Phosphocreatine concentration recovered to only approximately 58% of its control level following 15 min of aglycaemic hypoxia in the presence of 1.2 mM Ca2+. The ratios of phosphocreatine/ATP, lactate/N-acetyl aspartate and glutamate/N-acetyl aspartate did not differ at 1 h of recovery from the prehypoxia levels showing that the hypoxia resistant cells were metabolically viable. In the absence of external Ca2+, phosphocreatine recovery improved to approximately 80%. Ten mM Mg2+ or 25 microM diltiazem in the presence of 1.2 mM Ca2+ improved recovery of phosphocreatine to approximately 85%. Two other antagonists of L-type voltage-gated Ca(2+)-channels, verapamil and nifedipine, did not protect the cerebral cortex from hypoxic damage. N-methyl-D-aspartate (100 microM) applied during hypoxia with 1.2 mM Ca2+ did not augment the loss of phosphocreatine indicating that the cellular damage was not potentiated by the drug, even when 30 mM K+ was present. The presence of N-methyl-D-aspartate did not weaken the protective effect of diltiazem. Blockade of N-methyl-D-aspartate or non-N-methyl-D-aspartate channels did not alleviate cellular damage caused by hypoxic insult. The present results suggest that the immediate, Ca(2+)-mediated neuronal damage in the cerebral cortex may be mediated by Ca2+ influx through L-type voltage-gated Ca(2+)-channels.
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PMID:Calcium-mediated damage following hypoxia in cerebral cortex ex vivo studied by NMR spectroscopy. Evidence for direct involvement of voltage-gated Ca(2+)-channels. 790 49

We investigated 22 patients with migraine without aura, all drug-free and in headache-free periods, by means of 31P-magnetic resonance spectroscopy (MRS) of brain and muscle. Brain 31P-MRS showed significantly low phosphocreatine, increased adenosine diphosphate, and decreased phosphorylation potential. There was a slow rate of phosphocreatine recovery after exercise in the muscle of 12 of 22 patients. Energy metabolism is abnormal in migraine without aura, as previously demonstrated in patients with migraine stroke and migraine with aura.
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PMID:31P-magnetic resonance spectroscopy in migraine without aura. 816 22

We conducted an extended clinical evaluation of localized proton magnetic resonance spectroscopy (MRS) of the brain, performed on various brain diseases using short stimulated echo times. Pathologies studied were mainly multiple sclerosis, stroke, leukoaraiosis, AIDS-related leukoencephalopathies and glial tumors. Other miscellaneous pathologies were also studied. Magnetic resonance examination of the brain was conducted on a Siemens Magnetom SP63 (equipped with a 1.5 T magnet). Localized proton MRS was performed on a routine basis immediately after imaging, using the STEAM (stimulated echo acquisition mode) with a short echo time (20 ms) combined with a CHESS (chemical shift selective excitation) sequence. One or two VOI (8 ml) were examined. Data on 125 spectra were processed by principal component analysis (PCA) and conventional variance analysis. The following metabolite resonances were studied: inositol-glycine, taurine-scyllo-inositol, choline derivatives, phosphocreatine-creatine, aspartate, glutamine glutamate, N-acetylaspartate, acetate and lactate. PCA demonstrates that the different metabolic variables are independent. The analysis of groups of spectra clearly demonstrates that the metabolic profiles detected by localized MRS in various pathologies (i) differ significantly from controls, and (ii) allow a metabolic discrimination between groups of pathologies. Results of PCA are confirmed by variance analysis. Strokes are characterized by an increase in lactate concentration and leukoaraiosis by a decrease in inositol-glycine resonance. AIDS-related leukodystrophies are characterized by increases in lactate and choline concentrations. Reduction in N-acetylaspartate which is observed in most pathologies is not significant in the small lesions of white matter. Lactate has often been found in MS plaques, but no variation in the choline/phosphocreatine ratio was observed. GABA was tentatively assigned in the spectrum of a patient with epilepsy under sodium valproate treatment. This study illustrates the clinical feasibility of the technique, the value of a multiparametric data analysis in the definition of the pertinent variables characterizing the metabolic impairment, and the impact of localized proton MR spectroscopy of the brain in the assessment of cerebral suffering.
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PMID:A multiparametric data analysis showing the potential of localized proton MR spectroscopy of the brain in the metabolic characterization of neurological diseases. 822 60

We used 31P magnetic resonance spectroscopy (MRS) to investigate changes in brain intracellular [Mg2+] following human focal cerebral ischemia. Mean brain pMg (where pMg = -log[Mg2+]) was significantly lower in the ischemic focus of all stroke patients (pMg = 3.34 +/- 0.28, n = 45, p < 0.01) when compared with normal controls (pMg = 3.50 +/- 0.08, n = 25). Ischemic brain pMg was also significantly reduced when the pH of the stroke region was acidotic (pH < 6.90, pMg = 3.07 +/- 0.44, n = 11, p < 0.01) and when the phosphocreatine index (PCrI = PCr/[PCr+Pi (inorganic phosphate)]) was reduced (PCrI < 0.47, pMg = 3.12 +/- 0.42, n = 13, p < 0.01). Mean brain pMg was significantly reduced at days 0 to 1 (acute) poststroke (pMg = 3.32 +/- 0.28, n = 26, p < 0.01) and at days 2 to 3 (subacute) poststroke (pMg = 3.38 +/- 0.28, n = 21, p = 0.03). There was also a significant (p < 0.01) correlation between decreased pMg and increased relative signal intensity of Pi (normalized by total phosphate signal, Pi/TP) for all stroke groups studied. During the temporal evolution of stroke, pH returned to normal levels by days 2 to 3, and pMg returned to normal by days 4 to 10 (subacute). PCrI and Pi/TP returned toward normal levels after 10 days (chronic), at a time when ischemic brain pH had become significantly alkalotic (pH = 7.10 +/- 0.24, n = 15, p < 0.01). Elevation of ischemic brain [Mg2+] is temporally linked to the acidotic phase of human stroke as well as the breakdown of energy metabolism. These acute changes in [Mg2+] may contribute to, or be a marker for, cellular injury.
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PMID:Acute elevation and recovery of intracellular [Mg2+] following human focal cerebral ischemia. 835 Oct 15

Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
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PMID:Ventricular remodeling after myocardial infarction. Experimental and clinical studies. 835 28


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