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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of the present work was to study cerebral energy metabolism at threshold levels of hypoxia, i.e., degrees of hypoxia that abolish cerebral electrical activity, in the "normal" and in the epileptic brain. Seizures were induced by intravenous bicuculline and cerebral oxygen availability was reduced by a combination of lowered PO2 and reduced blood pressure to give a transformation of the burst suppression pattern to either one with single spikes or overt EEG flattening. Nonepileptic control animals were exposed to degrees of hypoxia that gave either a markedly depressed EEG pattern with sparse slow waves or EEG flattening. Epileptic and nonepileptic groups proved comparable in terms of calculated oxygen availability and cerebral oxygen consumption at the threshold of "transmission failure." At levels of hypoxia that markedly attenuated or completely abolished seizure discharge, the cerebral metabolic changes were more marked than in comparable nonepileptic animals. These changes comprised an imminent severe perturbation of cerebral cortical phosphorylation potential, a pronounced lactic acidosis with a precipitous redox change, and a marked accumulation of ammonia. The more labile energy balance of the epileptic brain may indicate that the "seizure state" either increases cellular energy demands in spite of the electrical silence or reduces the efficiency of ATP production at the prevailing oxygen availability. It is conceivable that energy failure elicited by complicating hypoxia can aggravate or precipitate brain cell damage in epilepsy.
J Cereb Blood Flow Metab 1985 Sep
PMID:Influence of reduced oxygen availability on cerebral metabolic changes during bicuculline-induced seizures in rats. 403 Sep 21

The purpose of this study was to investigate the possible importance of adenosine in cerebrocortical vasodilatation accompanying brain activation (epileptic seizures and direct electrical stimulation) and hypoxia (arterial hypoxia and cyanide poisoning of the brain cortex). In chloralose-anesthetized cats a circumscribed area of the brain cortex was treated with adenosine deaminase (Type III; Sigma), which potently deaminates adenosine to the nonvasoactive inosine. Cerebrocortical vascular volume and fluorescence of reduced nicotinamide adenine dinucleotide were measured in vivo by surface fluororeflectometry. The responses of small pial and intracortical vessels to brain activation and hypoxia were studied in brain cortices superfused with artificial (mock) CSF and 5 U/ml adenosine deaminase. It was found that superficially applied adenosine deaminase readily diffuses onto the brain cortex. Prolonged pretreatment of the brain cortices with 0.025 U/ml adenosine deaminase eliminated almost completely the vasodilative effect of 10(-7) mol/ml adenosine. The inhibitory effect of the enzyme on adenosine-induced cortical vasodilatation was specific, because 5 U/ml adenosine deaminase did not attenuate the vasodilative potency of 10(-8) mol/ml 2-chloroadenosine. Adenosine deaminase (5 U/ml) pretreatment of the brain cortices did not diminish the cerebrocortical vascular volume, which increased with arterial hypoxia, topical cyanide poisoning, and direct electrical stimulation. However, it slightly decreased the vasodilative effect of epileptic seizures. On the basis of these results, it seems very unlikely that adenosine is a critical factor in the control of cerebrovascular tone during arterial hypoxia and brain activation.
J Cereb Blood Flow Metab 1984 Sep
PMID:Effect of topical adenosine deaminase treatment on the functional hyperemic and hypoxic responses of cerebrocortical microcirculation. 647 59

Local cerebral blood flow (LCBF) was evaluated with the [14C]iodoantipyrine quantitative autoradiographic technique in 29 brain structures in conscious control rats and during fentanyl-induced electroencephalographic (EEG) spike and/or seizure activity and in the postseizure EEG suppression phase. During spike activity, LCBF increased in all structures; the increase reached statistical significance (p less than 0.05) in the superior colliculus, sensorimotor cortex, and pineal body (+130%, +187%, and +185% from control, respectively). With progressive development of seizure activity, LCBF significantly increased in 24 brain structures (range, +58% to +231% from control). During the postseizure EEG suppression phase, LCBF remained elevated in all structures (+80% to +390% from control). The local cerebrovascular resistance (LCVR) significantly decreased in 10 of 29 structures with the onset of spike activity (range, -24% to -64%), and remained decreased in all brain structures during seizure activity (range, -34% to -67%) and during the EEG suppression phase (range, -24% to -74%). This reduction of LCVR represents a near maximal state of cerebrovasodilation during fentanyl-induced EEG seizure or postseizure suppression activity. The global nature of the LCBF elevation indicates that factors other than local metabolic control are responsible for CBF regulation during local seizure activity.
J Cereb Blood Flow Metab 1984 Mar
PMID:Local cerebral blood flow with fentanyl-induced seizures. 669 16

Interrelationship between the breakdown of the blood-brain barrier (BBB) to Evans blue and elevations in the regional cerebral blood flow (rCBF) was studied in rabbits subjected to adrenaline- or metaraminol-induced systemic hypertension and also in bicuculline-induced seizures. The rCBF was assessed in small samples from various regions of the brain with the use of [3H]nicotine, and the permeability of the BBB was evaluated with an Evans blue tracer. In acute hypertension, Evans blue extravasations were observed in the occipital cortex and sometimes in the superior colliculus, i.e., the regions which also showed the highest elevations in rCBF. The breakdown of the BBB in acute hypertension was clearly related to the rate of mean arterial blood pressure rise, being much less pronounced in the metaraminol group, which showed a much slower blood pressure elevation rate. In bicuculline-induced seizures, there was no evident correlation between the amplitude of rCBF elevations and Evans blue extravasations. Preservation of BBB integrity was observed in areas showing high elevations in the rCBF.
J Cereb Blood Flow Metab 1984 Mar
PMID:Regional changes in cerebral blood flow and blood-brain barrier permeability during epileptiform seizures and in acute hypertension in rabbits. 669 17

Before, during, and after bicuculline-induced seizures, changes in microflow, local tissue PO2, and extracellular H+ and K+ activities were continuously recorded in the suprasylvian gyrus of the cat in parallel with electrical activity. Additionally, the patterns of microflow during seizures after blockade of the beta-adrenergic and cholinergic receptors and after phentolamine application were studied. With the onset of discharges, microflow increased at all sites. The maximum increase was observed when the electrical activity was the strongest. During the period of alternating silent and nonsilent phases, microflow oscillated in parallel with functional activity. When the discharges ceased, microflow decreased to a new steady-state level. Tissue hypoxia was not responsible for the increase in flow because local tissue PO2 increased after the onset of seizures. H+ activity increased after a short delay and also oscillated during the period of oscillating functional activity. After the end of discharges, H+ activity decreased. K+ activity increased immediately with the onset of discharges and mirrored the electrical activity in the further course. The pattern of microflow was not changed by blockade of alpha- and beta-adrenergic and cholinergic receptors. We conclude that besides the increase in systemic blood pressure, K+ and H+ activities could be the main factors responsible for the increase in flow during seizures.
J Cereb Blood Flow Metab 1984 Jun
PMID:Mechanisms of regulation of cerebral microflow during bicuculline-induced seizures in anaesthetized cats. 672 27

Cerebral oxygenation initially increases and later decreases in rats subjected to experimental status epilepticus. In this study, we have compared cerebral oxygen supply and vascular changes during paroxysmal events of different durations and at different time intervals to test the hypothesis that oxygen insufficiency is associated more readily with paroxysmal events of greater intensity. Continuous measurements were made of local changes in cortical blood volume, redox levels of cytochrome a, a3, cortical Po2, and systemic arterial blood pressure during recurrent seizures induced by pentylenetetrazol or bicuculline. In contrast to expectations, systemic and cerebral vascular responses and associated increases in cerebral oxygenation were better maintained during long-duration ictal episodes than during short-duration ictal bursts, interictal spikes, or evoked potentials. Short-duration paroxysmal events were often accompanied by decreases in cerebral oxygenation, whereas long-duration events were still accompanied by increases in oxygenation. Ictal bursts occurring with short interburst intervals caused a more rapid failure of vascular responsiveness than those occurring at longer intervals. These relationships of intensity and frequency of repetition of seizures to changes in vascular responses indicate progressive dissociation of the normally tight couple between neuronal activity, energy demand, and cerebral blood flow during status epilepticus.
J Cereb Blood Flow Metab 1983 Sep
PMID:Importance of vascular responses in determining cortical oxygenation during recurrent paroxysmal events of varying duration and frequency of repetition. 687 42

Local cerebral blood flow (ICBF) was measured with [14C]iodoantipyrine in conscious, unrestrained rats during electrical stimulation of the fastigial nucleus (FN). Electrode position in the FN was determined by blood pressure (MABP) responses to stimulation under anesthesia. In nine rats in which MABP responses had been variable under anesthesia, bipolar stimulation (50 Hz, 0.5 ms, 1 s on/1 s off) with currents of 30-100 microA after recovery from anesthesia produced stereotypic behavior but little effect on MABP and ICBF. In seven other conscious rats currents could be raised to 75-200 microA without inducing seizures, resulting in sustained MABP elevations during the ICBF measurement and significantly increased ICBF in the sensory-motor (+45%), parietal (+31%), and frontal cortices (+56%) and the caudate-putamen (+27%) above control values (n = 9). Glucose utilization, measured with [14C]deoxyglucose, in rats similarly stimulated was significantly increased in six structures, including some of the above, indicating increases in ICBF due to metabolic activation. Unilateral or bilateral electrolytic lesions of the FN, placed 6-7 days before ICBF measurement, had negligible effects on resting ICBF and on autoregulation in conscious rats. These results fail to support a specific role for the FN in physiological regulation of cerebral blood flow in unanesthetized rats.
J Cereb Blood Flow Metab 1995 Jan
PMID:Role of the cerebellar fastigial nucleus in the physiological regulation of cerebral blood flow. 779 31

[6-14C]Glucose is the tracer sometimes recommended to assay cerebral glucose utilization (CMRglc) during transient or brief functional activations, but when used to study visual stimulation and seizures in other laboratories, it underestimated CMRglc. The metabolic fate of [6-14C]glucose during functional activation of cerebral metabolism is not known, and increased labeling of diffusible metabolites might explain underestimation of CMRglc and also reveal trafficking of metabolites. In the current studies cerebral cortex in conscious rats was unilaterally activated metabolically by KCl application, and CMRglc was determined in activated and contralateral control cortex with [6-14C]glucose or 2-[14C]deoxy-glucose ([14C]DG) over a 5- to 7-min interval. Local 14C concentrations were determined by quantitative autoradiography. Labeled precursor and products were measured bilaterally in paired cortical samples from funnel-frozen brains. Left-right differences in 14C contents were small with [6-14C]glucose but strikingly obvious in [14C]DG autoradiographs. CMRglc determined with [6-14C]glucose was slightly increased in activated cortex but 40-80% below values obtained with [14C]DG. [14C]Lactate was a major metabolite of [6-14C]glucose in activated but not control cortex and increased proportionately with unlabeled lactate. These results demonstrate significant loss of labeled products of [6-14C]glucose from metabolically activated brain tissue and indicate that [14C]DG is the preferred tracer even during brief functional activations of brain.
J Cereb Blood Flow Metab 1995 Jan
PMID:Labeling of metabolic pools by [6-14C]glucose during K(+)-induced stimulation of glucose utilization in rat brain. 779 43

Susceptibility to audiogenic seizures (AGS) was investigated in Sprague-Dawley rats subjected to cardiac arrest cerebral ischemia (CACI), produced by compression of the major cardiac vessels. The onset of AGS was regularly observed 1 day after CACI of > 5 min duration. The duration of postischemic susceptibility to AGS was directly related to the density of cerebral ischemia, with 50% of more severely ischemic animals still showing AGS susceptibility 8 weeks after CACI. Lesioning of the inferior colliculi (IC) abolished the onset of AGS; no such effect was observed after lesioning the medial geniculate (MG). Glutamic acid decarboxylase (GAD) immunochemistry revealed approximately 50% loss of GAD-positive neurons in the IC, which was similar in animals with various durations of AGS susceptibility. Otherwise, there was a conspicuous sprouting of gamma-aminobutyric acid (GABA)-ergic terminals in the ventral thalamic nuclei, which peaked approximately 1 month after the CACI. Evaluation of GABA-A inhibitory function in the hippocampus by the paired pulse stimulation revealed changes indicating loss of GABA-A inhibition coinciding with the onset of AGS, and its return in animals tested 2 months after CACI. Our observations suggest a potential role of GABA-ergic dysfunction in the postischemic development of AGS.
J Cereb Blood Flow Metab 1995 Mar
PMID:Development of susceptibility to audiogenic seizures following cardiac arrest cerebral ischemia in rats. 786 Jun 59

The quantitative autoradiographic [14C]iodoantipyrine technique was applied to the measurement of rates of local cerebral blood flow (LCBF) during audiogenic seizures in Wistar AS rats belonging to a genetic strain selected at the Centre de Neurochimie (Strasbourg, France) for their sensitivity to sound. Seizures were elicited in native rats never exposed to sound (single audiogenic seizures) or in rats previously exposed to 10-40 seizure-inducing sound stimulations until generalization of the seizure to forebrain areas (referred to as "kindled animals"). During single audiogenic seizures, rates of LCBF increased over control values in all areas but the genu of the corpus callosum. The highest increases in LCBF (180-388%) were recorded in the inferior and superior colliculus, reticular formation, monoaminergic cell groupings, especially the substantia nigra, posterior vegetative nuclei, and many thalamic and hypothalamic regions. The lowest increases were seen in forebrain limbic regions and cortical areas. In kindled animals, LCBF rates increased over control levels in 67 areas of the 75 studied. LCBF increases were generally of a lower amplitude in kindled than in naive rats. Differences between the two groups of seizing rats were located mostly in brain-stem regions, mainly the inferior colliculus, reticular formation, substantia nigra, and posterior vegetative nuclei. Conversely, rates of LCBF were similar in forebrain areas of naive and kindled animals. In conclusion, the present data show that there is a good correlation between the structures known to be involved in the expression of audiogenic seizures (inferior colliculus, reticular formation, substantia nigra mainly) and the large increase in LCBF during single audiogenic seizures, while rates of LCBF increase to a lesser extent in forebrain areas not involved in this type of seizures. The circulatory adaptation to kindled seizures is rather a decreased response in brain-stem regions and no change in the forebrain, although the kindling process induces a generalization of the seizure from brain-stem to anterior regions.
J Cereb Blood Flow Metab 1995 Mar
PMID:Mapping of cerebral blood flow changes during audiogenic seizures in Wistar rats: effect of kindling. 786 Jun 60


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