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

Neuronal lesions in the brain occur in conditions associated with a reduced supply of oxygen (hypoxia and ischemia) and glucose (hypoglycemia) as well as in those associated with a pathologically enhanced neuronal activity (status epilepticus). In only two of these conditions (hypoxia and ischemia) are the lesions correlated to cellular oxygen lack, and gross energy failure is absent in one condition (status epilepticus). Although anaerobic mechanisms seem responsible for the cell injury in hypoxia and ischemia, oxidative mechanisms could operate in hypoglycemia and status epilepticus. Since the supply of oxygen has not ceased altogether in hypoxia and incomplete ischemia, and since reoxygenation/recirculation leads to a transient increase in tissue oxygen tensions, one cannot exclude the possibility that oxidative mechanisms contribute to the final damage following all types of cellular oxygen lack. We have failed to obtain evidence that peroxidative degradation of cellular constituents occurs in hypoglycemia and status epilepticus. Thus, there is neither a perturbation of the redox state of the glutathione pool of the tissue nor a measurable degradation of polyenoic phospholipid-bound fatty acids. It is emphasized that the cascade of events triggered by an accumulation of free polyenoic fatty acids, mainly arachidonic acid, may contribute to cell lesions by leading to cell edema and/or microcirculatory changes. During seizures, such an accumulation occurs even though energy failure is moderate and it may conceivably contribute to cell damage. In general, though, mechanisms of cell damage in the brain remain partly elusive.
 ...
PMID:Neuronal cell damage in the brain: possible involvement of oxidative mechanisms. 693 2

Status epilepticus was induced in rats by the GABA receptor blocking agent, bicuculline, during artificial ventilation and with closely monitored physiologic parameters. After 1 or 2 h of status epilepticus the brains were fixed by perfusion with glutaraldehyde and processed for light and electron microscopy. In the cerebral cortex two different types of changes were present, i.e., nerve cell injuries and status spongiosus. Type 1 injured neurons, mainly in the areas of most marked sponginess (layer 3), displayed progressive condensation of both karyo-and cytoplasm. In the most advanced stages the nucleus could no longer be distinguished from the cytoplasm in the light microscope, and vacuoles of apparent Golgi cisterna origin appeared in the darkly stained cytoplasm. This type of injured neurons comprised 41 and 56% of the cortical neurons after 1 or 2 h of status epilepticus, respectively. Seven to 9% of the neurons showed another type of injury (type 2). They were mainly located in the deeper cortical layers, and showed slit-formed cytoplasmic vacuoles chiefly due to swelling of the endoplasmic reticulum including the nuclear envelope. Marked sponginess of the cortex developed principally in layer 3 and it spread into deeper layers with longer duration of status epilepticus, but the outermost layers retained a compact structure. As judged by electron microscopy, the sponginess resulted mainly from swelling of astrocytes and their processes causing both perivascular and perineuronal vacuolation. The structural changes observed are considered to be caused by astrocytic and to a lesser extent intraneuronal edema related to the seizure activity. Although the exact pathogenetic mechanisms are not known, our findings indicate that hypoxia-ischemia is not a major determinant of the tissue damage observed.
 ...
PMID:Pathogenesis of brain lesions caused by experimental epilepsy. Light- and electron-microscopic changes in the rat cerebral cortex following bicuculline-induced status epilepticus. 725 31

Seven-day postnatal rats were subjected to unilateral common carotid artery ligation, 3 h after which they were subjected to hypoxia with 8% oxygen at 37 degrees C for 2 h. Thereafter, they received multiple s.c. injection(s) of bicuculline (6 mg/kg) adequate to produce behaviorally apparent seizures lasting greater than 1 h (status epilepticus). Repeated episodes of status epilepticus at 2, 6, and 12 h of recovery from hypoxia-ischemia (HI) produced a mortality rate of 53%. Among the survivors, there was no statistically significant difference in the extent of brain damage between convulsing and non-convulsing HI controls, analyzed at 30 d of age. Histopathologic examination for acute lesions also indicated no difference in the severity of brain damage between dead and surviving rat pups subjected to status epilepticus, indicating that mortality was not related to the severity of prior HI brain damage. Those immature rats that died during status epilepticus exhibited lower blood glucose concentrations (1.75 +/- 0.35 mmol/L) compared with surviving, convulsing animals (4.25 +/- 0.51 mmol/L; p = 0.016). Glucose supplementation (0.1 mL of 50% glucose) early during status epilepticus improved survival and significantly prolonged seizure activity (90 +/- 14 min) compared with non-glucose treated, convulsing littermates (47 +/- 10 min; p = 0.02). Glucose supplementation did not increase the extent of brain damage despite improved survival and increased duration of seizure activity.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of status epilepticus on hypoxic-ischemic brain damage in the immature rat. 747 24

Neuron-specific enolase (NSE) is a sensitive marker of brain injury after stroke, global ischemia, and coma. We report changes in serum NSE (s-NSE) in 19 patients who sustained status epilepticus. s-NSE peaked within 24 to 48 hours after status epilepticus. The mean peak s-NSE level for the entire group was elevated compared with the levels for normal controls (24.87 ng/ml versus 5.36 ng/ml, p = 0.0001) and for epileptic controls (24.87 ng/ml versus 4.61 ng/ml, p = 0.0001). The mean peak s-NSE level for the 11 subjects without an acute neurologic insult (15.44 ng/ml) was also significantly increased compared with levels for normal and epileptic controls. Further, s-NSE was significantly correlated with outcome and duration. We conclude that s-NSE is a promising in vivo marker of brain injury in status epilepticus and warrants further study in larger populations.
 ...
PMID:Serum neuron-specific enolase in human status epilepticus. 864 98

To investigate whether aggravation of damage in hyperglycemic subjects is a continuous function of changes in intra- and extracellular pH during ischemia or whether there is a threshold value, preischemic plasma glucose was varied from 8.3-20.0 mM. 10 min forebrain ischemia was induced. The results showed that no animal with plasma glucose of < 13 mM developed seizures, and that all animals with glucose of > 16 mM died in status epilepticus. Half of the animals with plasma glucose in the range of 13-16 mM showed seizures and 50% of these died. In surviving animals, histological brain damage occurred in the hippocampal CA3 sector, cingulate cortex, thalamic nuclei and substantia nigra, structures normally not injured by 10 min ischemia. The data demonstrate that there is a glucose threshold of 10-13 mM, above which seizures develop and additional damage appears, and another one (> 16 mM), above which seizures are invariably fatal.
 ...
PMID:The influence of plasma glucose concentrations on ischemic brain damage is a threshold function. 782 84

Fulminant hepatic failure is a rare complication of status epilepticus. Although many of the anticonvulsants used to treat the seizures are known to have hepatotoxic properties, the exact mechanism leading to massive destruction of the liver following a prolonged seizure remains unclear. Three children are presented who developed fulminant hepatic failure following status epilepticus and subsequently died of multiple organ failure. The literature is reviewed with particular attention to the possible interaction between the anticonvulsants and the metabolic consequences of status epilepticus. We postulate that it is a combination of hypoxia and ischemia that occurs during a prolonged seizure with altered metabolism of free radicals secondary to the anticonvulsant drugs which leads to widespread hepatocyte membrane damage.
 ...
PMID:Fulminant hepatic failure associated with status epilepticus in children: three cases and a review of potential mechanisms. 793 35

We report the historical, clinical, and laboratory findings in 5 patients after crack cocaine ingestion. All patients exhibited adrenergic crisis as a result of their ingestion. Analysis of their history revealed a latency period before signs and symptoms occurred as well as a wide variation in the number of crack cocaine nuggets ingested. Signs of intoxication were hypertension, tachycardia, hyperthermia, agitation, and generalized seizure activity. Treatment included therapeutic sedation with lorazepam and adrenolysis with esmolol infusion. The majority of patients showed electrocardiographic evidence of cardiac ischemia, but not elevations in serum creatinine phosphokinase enzymes--MB fraction. One patient died of complications associated with subclinical status epilepticus. The toxicities of crack cocaine ingestion are seldom appreciated. Prompt reversal of both cardiovascular and neurological signs and symptoms with appropriate pharmacologic agents is indicated.
 ...
PMID:Adrenergic crisis from crack cocaine ingestion: report of five cases. 759 78

The hsp70 gene is induced by denatured protein in injured cells and is an extremely sensitive and reliable marker of cells injured by ischemia, seizures, and toxins. Normal brains have little detectable hsp70 mRNA or HSP70 protein. After status epilepticus produced by systemic injections of kainic acid, however, HSP70 protein is induced in neurons but not glia in brain regions known to be injured by kainic acid. Global and focal ischemia also induce the hsp70 gene in brain. The induction of HSP70 protein in hippocampus following increasing durations of global ischemia correlates with the regional and cellular vulnerability to ischemia: CA1 neurons express HSP70 after the briefest periods of ischemia followed by CA4, CA3, dentate granule neurons, glia, and lastly, endothelial cells. Moreover, as the severity of ischemia worsens, a transcriptional and/or translational blockade of the hsp70 gene occurs in the same order so that moderate degrees of ischemia induce HSP70 in CA3 neurons and dentate granule neurons but not necrotic CA1 neurons, and severe ischemia induces HSP70 in capillary endothelial cells of hippocampus but not in any infarcted neurons or glia throughout the hippocampus. Brief periods of focal ischemia induce HSP70 primarily in neurons, suggesting that even focal ischemia can produce selective neuronal injury without infarction. In some instances, HSP70 immunoreactive astrocytes surround the HSP70 immunostained neurons. Focal ischemia that produces infarction induces HSP70 primarily in endothelial cells of cerebral blood vessels in the regions of infarction and in neurons and astrocytes on the perimeter or the penumbral area of infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:HSP70 heat shock gene regulation during ischemia. 824 24

As with other methods long used in intensive care units (ICU) and operating rooms (OR), the goal of neuroscience ICU continuous EEG (NICU-CEEG) and evoked potential (NICU-EP) monitoring is to extend our powers of observation to detect abnormalities at a reversible stage. EEG is an appropriate monitoring tool because it is linked to cerebral metabolism, is sensitive to ischemia and hypoxemia, correlates with cerebral topography, detects neuronal dysfunction at a reversible stage, and is the best method for detecting seizure activity. When applied systematically, it can impact medical decision-making in 81% of monitored patients. It is useful in monitoring precarious cerebral perfusion at the bedside, and it has revealed that nonconvulsive seizures, undetectable otherwise, occur in 34% of NICU patients. In convulsive status epilepticus, NICU-CEEG can help avoid undertreatment and overtreatment. In comatose patients, it can provide useful prognostic information as well as detect potentially treatable causes. Traditional impediments to its application are yielding to technological advances and educational efforts. Real-time digitized EEG in particular has been a major advance. Within limits, somatosensory evoked potential monitoring (ICU-SEP) is useful in the prognosis of coma, but it is less helpful in monitoring focal cerebral ischemia. Brainstem auditory evoked potential monitoring has a relatively restricted role in the NICU but is helpful in distinguishing structural from nonstructural causes of coma and can supplement ICU-SEP in predicting outcome.
 ...
PMID:Continuous EEG and evoked potential monitoring in the neuroscience intensive care unit. 830 43

Diffusion-weighted (DW) imaging has been used to record changes associated with status epilepticus (SE) in rat brain. It was found that the apparent diffusion coefficient (ADC) of water in brain decreased 14-18% during SE, and it fell a further 20-22% when the animals were sacrificed. The transverse decay time constant T2* showed corresponding reductions, but no significant changes were seen in relaxation times T1 or T2 values. Changes in ADC in status epilepticus are similar to those seen in stroke and ischemia but occur under very different conditions of blood flow and metabolism.
 ...
PMID:Changes in water diffusion and relaxation properties of rat cerebrum during status epilepticus. 836 5


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>