Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study effects of catecholamines on cerebral oxygen consumption (CMRo2) and blood flow (CBF), rats maintained on 75% N2O and 25% O2 were infused i.v. with noradrenaline (2, 5, or 8 microgram.kg-1.min-1) or adrenaline (2 or 8 microgram.kg-1.min-1) for 10 min before CBF and CMRo2 were measured. In about 50% of animals infused with 2--8 microgram.kg-1.min-1 of noradrenaline, CMRo2 (and CBF) rose. However, there was no dose-dependent response, and CMRo2 did not exceed 150% of control. The effects of noradrenaline in a dose of 5 microgram.kg-1.min-1 on CMRo2 and CBF were blocked by propranolol (2.5 mg.kg-1). In animals infused with adrenaline (8 microgram.kg-1.min-1) CMRo2 was doubled and, in many, CBF rose 4- to 6-fold. It is concluded that, when given in sufficient amounts, catecholamines have pronounced effects on cerebral metabolism and blood flow, the effects of adrenaline on CMRo2 and CBF resembling those observed in status epilepticus.
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PMID:Influence of intravenously administered catecholamines on cerebral oxygen consumption and blood flow in the rat. 69 50

The value of transcranial Doppler sonography is demonstrated in two infants with an elevation of intracranial pressure (ICP). One of them suffered from hydrocephalus and ICP increased because of her VP shunt-insufficiency. In the other case status epilepticus caused brain oedema and a rise in intracranial pressure. In both cases, transcranial Doppler sonography showed a decrease in blood flow (CBF) velocity and an increase in the Pourcelot index in the middle cerebral artery. Quick or gradual reduction of the ICP led to an increase in CBF velocity and a decrease in the Pourcelot index. On the basis of experiences of the authors, transcranial Doppler sonography is a valuable method of verifying the elevation of ICP. It is suitable for measuring the effect of treatment necessitated by the elevation of ICP. The method is non-invasive, quick and it can be freely repeated. Therefore it is applicable for monitoring the dynamic of ICP.
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PMID:[Detection of increased intracranial pressure by transcranial Doppler sonography in infants]. 267 36

A spectacular spongiotic lesion, symmetrical in distribution and restricted to the pars reticulata of the substantia nigra (SNPR) has recently been described in hyperglycemic rats surviving 1-18 h after a brief period of transient ischemia. The purpose of this study was to clarify the pathogenesis of the lesion. In order to study whether the lesion was due to changes occurring during ischemia, local cerebral blood flow (l-CBF) and energy metabolites were measured in the substantia nigra (SN) and in other brain areas. Furthermore, brains were examined by light and electron microscopy immediately after ischemia and in the early recirculation period. Autoradiographic CBF measurements showed ischemia flow levels in the SN of 30-40% of control, similar in normo- and hyperglycemic rats. Thus, although ischemic, this structure had a considerable amount of residual flow. There was also a corresponding partial preservation of the adenylate energy charge. However, lactate levels were high, and in hyperglycemic subjects they rose to values previously described during status epilepticus (about 25 mumol/g). In hyperglycemic animals, neuronal alterations were consistently present in SNPR by the end of the 10-min period of ischemia. They included clumping of nuclear chromatin and subplasmalemmal clearing of the perikaryon. Some mitochondrial swelling was present in neuronal perikarya and in dendrites. The normal alignment of microtubules in the dendrites was disturbed, but there was no or only slight swelling of the dendrites. Aggregation of synaptic vesicles was a conspicuous finding in axonal terminals, which were also slightly swollen. Otherwise, the axons appeared largely spared. Microvessels looked quite intact. Similar cellular changes were observed in the early recovery period. Dendrites, however, started to swell, and their expansion finally caused the spongiotic appearance of the pars reticulata. The appearance of the dendritic lesions is strongly suggestive of transmitter-mediated ("excitotoxic") damage. However, it seems likely that the marked acidosis is injurious as well. We tentatively conclude that both mechanisms interact to give the final lesion. The results, and those previously obtained in epileptic seizures, suggest that mitochondria of SN neurons and neuronal processes are particularly prone to damage.
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PMID:Pathogenesis of substantia nigra lesions following hyperglycemic ischemia: changes in energy metabolites, cerebral blood flow, and morphology of pars reticulata in a rat model of ischemia. 336 99

The brain uptake of phenobarbital during prolonged status epilepticus (3 h) was studied in paralyzed, ventilated sheep. The first 30 min of status epilepticus was characterized by systemic hypertension, increased CBF, increased peripheral vascular resistance, a fall in brain pH, and an elevation in brain lactate concentrations. Subsequently, hemodynamic factors normalized and brain acidosis persisted. Phenobarbital administered during the early phase of status epilepticus produced higher levels of brain phenobarbital concentration, which was greatest at the earliest sample time (5 min following infusion), compared to nonseizure controls. This elevation persisted for the first 3 h following the infusion. Phenobarbital administration during the established phase of status epilepticus, when systemic blood pressure, peripheral vascular resistance, and CBF had returned to preseizure values, resulted in attenuated brain phenobarbital uptake not different from controls for the first 30 min. These results are explained by disruption of the blood-brain barrier to phenobarbital during the early (hypertensive) phase of status epilepticus.
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PMID:Brain phenobarbital uptake during prolonged status epilepticus. 369 34

A cured case of superior sagittal sinus thrombosis is reported. The patient, a 26-year-old man, also displayed severe complications such as hemorrhagic infarction and status epilepticus. Although his prognosis was considered to be extremely poor, conservative treatment, with mannitol, steroid, anticonvulsants, etc. was effective, and he was discharged without any neurological deficit. This report discusses the clinical course, CT findings, angiographical findings and regional cerebral blood flow (rCBF). At first, CT showed no abnormal findings, but hemorrhagic infarction was detected on the 3rd day after the onset. Follow-up CT showed subcortical low density area, hemorrhagic infarction with perifocal brain edema, midline shift etc; the focus of hemorrhagic infarction was almost absorbed 2.5 months after the onset. Cerebral angiogram showed not only the obstruction of the superior sagittal sinus but also that of cortical veins of cerebral convexity at first. Follow-up angiogram showed the development of collateral circulations such as deep cerebral, ophthalmic and emissary veins. On CBF study, low rCBF at the bilateral parasagittal region was observed, but marked increase of rCBF was measured in the parasagittal region, especially at the site of hemorrhagic infarction after the administration of 20% mannitol. We, therefore, consider mannitol as an effective agent for the treatment of cerebral sino-venous thrombosis.
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PMID:[Administration of mannitol for severe superior sagittal sinus thrombosis]. 641 84

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.
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PMID:Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model. 646 70

The quantitative autoradiographic [14C]-iodoantipyrine technique was applied to measure the effects of a 30-min period of pentylenetetrazol (PTZ)-induced status epilepticus (SE) on local cerebral blood flow (LCBF) in rats 10 (P10), 14 (P14), 17 (P17), and 21 (P21) days after birth. The animals received repetitive, timed injections of subconvulsive doses of PTZ until SE was reached. At P10, SE induced a 32 to 184% increase in the rates of LCBF affecting all structures studied. In P14- and P17 PTZ-treated rats, LCBF values significantly increased in two-thirds of the structures belonging to all systems studied and were not changed by SE in the parietal cortex, dorsal hippocampus, and dentate gyrus. At P21, rates of LCBF were still increased in 48 of the 73 structures studied; however, LCBF values were decreased by SE in most cortical areas, the hippocampus, and the dentate gyrus. CBF and cerebral metabolic rate for glucose (CMRglc) remained coupled in both controls and PTZ-exposed rats. Our results show that changes in LCBF with seizures are age dependent. At the most immature ages, P10 and P14, both LCBF and local CMRglc (LCMRglc) values are largely increased by long-lasting seizures. At P17 and P21, the blood flow response to SE becomes more heterogeneous, with specific decreases in the hippocampus and cortex at P21. The absence of mismatch between LCBF and LCMRglc in PTZ-exposed rats at all ages may explain at least partly why the immature brain is more resistant to seizure-induced brain damage than the adult brain.
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PMID:Effects of pentylenetetrazol-induced status epilepticus on local cerebral blood flow in the developing rat. 786 Jun 61

Our previous studies on cerebral metabolic activity in genetic absence epilepsy rats from Strasbourg (GAERS) were in favor of decreased functional activity during absences and normal or increased interictal activity. To ascertain that hypothesis, in the present study we performed continuous measurements of CBF in both children with typical absence epilepsy and GAERS, using Doppler ultrasonography and laser-Doppler flowmetry, respectively. CBF fluctuations during absences were recorded in four children between 5 and 6 years of age and 16 adult GAERS. In both children and animals, CBF measured in the middle cerebral artery and cortical capillaries, respectively, significantly decreased by a median value of 20-24% under basal levels during spontaneous absences. In GAERS, CBF levels were continuously decreased during haloperidol-induced absence status epilepticus, while they were not affected by ethosuximide. Conversely, convulsive seizures induced in rats either by kainate or picrotoxin led to a 175-664% increase in CBF levels. In conclusion, the present data show that during spontaneous absences, CBF decreases under basal levels in both cortical capillaries (GAERS) and the middle cerebral artery (children). Moreover, these fluctuations occur in vessels with normal vascular reactivity, are not mediated by changes in PO2, PCO2, or arterial blood pressure, and represent rather a response to reduced metabolic demand.
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PMID:Absence seizures induce a decrease in cerebral blood flow: human and animal data. 853 May 47

Two patients with status epilepticus due to specific conditions were examined using MRI and stable Xe/CT CBF. [Case 1] A 30-year-old woman developed a grand mal seizure during delivery. She was comatose, and MRI revealed abnormal high intensity areas bilateral basal ganglia, compatible with eclampsia. Regional CBF was decreased in bilateral occipital lobes and right basal ganglia. Six days after onset. Regional gray matter flow was increased, especially in the thalami and basal ganglia. [Case 2] The patient is a 31-year-old male diagnosed with temporal lobe epilepsy since 10 years. At the onset, he had a prolonged right hemiconvulsion followed by generalized tonic-clonic convulsion. MRI 13 days after onset showed left hemispheric edematous swelling of gray matter. Stable Xe/CT 3 weeks after onset demonstrated increased cortical CBF corresponding to edematous area. The results suggested that regional CBF decreased immediately after status epilepticus and then increased for 1-3 weeks in the interictal period. We speculate that the energy debt incurred during prolonged seizure causes relative ischemic condition in the neurons, with the increase in CBF resulting from accelerated energy production for a long period.
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PMID:Regional cerebral blood flow after status epilepticus. 1075 Mar 44

Angiogenesis and blood-brain-barrier (BBB) damage have been proposed to contribute to epileptogenesis and/or ictogenesis in experimental and human epilepsy. We tested a hypothesis that after brain injury angiogenesis occurs in the most damaged hippocampal areas with the highest need of tissue repair, and associates with formation of epileptogenic neuronal networks. We induced status epilepticus (SE) with pilocarpine in adult rats, and investigated endothelial cell proliferation (BrdU and rat endothelial cell antigen-1 (RECA-1) double-labeling), vessel length (unbiased stereology), thrombocyte aggregation (thrombocyte immunostaining), neurodegeneration (Nissl staining), neurogenesis (doublecortin (DCX) immunohistochemistry), and mossy fiber sprouting (Timm staining) in the hippocampus at different time points post-SE. As functional measures we determined BBB leakage (quantified immunoglobulin G (IgG) immunostaining), and hippocampal blood volume (CBV) and flow (CBF) in vivo (magnetic resonance imaging, MRI). The total length of hippocampal blood vessels was decreased by 17% at 2 d after status epilepticus (SE) induced by pilocarpine in adult rats (P<0.05 as compared to controls) which was not accompanied by alterations in hippocampal blood volume (BV) and flow (BF). Number of proliferating endothelial cells peaked at 4 d post-SE and correlated with an increase in vessel length (r=0.900, P<0.05). Vessels length had recovered to control level or even higher at 2 wk post-SE, angiogenesis being most prominent in the CA3 (128% as compared to that in controls, P<0.05), and was associated with increased BV (178% as compared to that in controls, P<0.05). Enlargement of vessel diameter in the hippocampal fissure was associated with thrombocyte aggregation in distal capillaries. BBB was most leaky during the first 4 d post-SE and increased IgG extravasation was observed for 60 d. Our data show that magnitude of endothelial cell proliferation is not associated with severity of acute post-SE neurodegeneration or formation of abnormal neuronal network. This encourages identification of molecular targets that initiate and maintain specific aspects of tissue reorganization, including preservation and proliferation of endothelial cells to reduce the risk of epileptogenesis and enhance recovery after brain injury.
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PMID:Vascular changes in epilepsy: functional consequences and association with network plasticity in pilocarpine-induced experimental epilepsy. 2000 12


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