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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The high mortality associated with status epilepticus (SE) has been hypothesized to result partially from neurologically induced changes in cardiac function. To test this hypothesis, we reviewed electrocardiograms of 60 patients presenting in status epilepticus. Sequential electrocardiograms before, during and after ictal episodes were compared to define changes from baseline studies. 58.3% of the SE patients (N = 35) exhibited significant abnormalities on electrocardiograms obtained within 24 h of status epilepticus. Specific electrocardiographic changes included arrhythmias, axis changes, conduction abnormalities and ischemic patterns. All of these abnormal ECG changes met generally accepted cardiologic standards for a high risk of myocardial dysfunction or ischemia. The association of ECG changes with mortality was statistically significant. These results indicate that a significant proportion of SE patients are at risk for cardiac dysfunction and that close monitoring of cardiac function is indicated during and after SE.
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PMID:Analysis of electrocardiographic changes in status epilepticus. 844 82

The apparent diffusion coefficient of brain water was decreased by frontal cortical electroshock, usually but not always associated with brief epileptic afterdischarge detectable at the parietal cortex. Previous studies have shown that status epilepticus causes similar larger decreases, which are largely reversible by the termination of seizure discharge with pentobarbital. Cerebral blood flow is elevated in these conditions, and biochemical energy failure does not occur. The brain water diffusion coefficient also decreases in spreading depression, without depletion of energy stores. All of these findings may be due in part to the reduction of brain extracellular space caused by cell swelling, which occurs to some degree in all three conditions. However, major biological differences between brain activation and brain ischemia and new evidence for increased cytosolic viscosity in the latter both suggest that other mechanisms deserve further investigation. Use-dependent motility of dendritic spines and other phenomena that may allow direct detection of neural activity by diffusion-weighted NMR imaging are of special interest.
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PMID:Diffusion-weighted NMR imaging changes caused by electrical activation of the brain. 873 72

Cerebrospinal fluid (CSF) concentrations of glutamate and gamma- aminobutyric acid (GABA), as estimates of levels in the extracellular compartment of brain, were determined in 7-day postnatal rats at the terminus of hypoxia-ischemia and during status epilepticus, induced with bicuculline, at 2 and 24 h of recovery. Hypoxia-ischemia was associated with increased CSF glutamate, which was not increased further during status epilepticus. In contrast, CSF GABA was increased by hypoxia-ischemia as well as by status epilepticus during recovery. CSF glutamate/GABA ratios in rat pups subjected to status epilepticus with or without prior hypoxia-ischemia were lower than control animals during recovery. The lack of any significant increase in glutamate or in the glutamate/GABA ratio during status epilepticus would preclude any neuronal injury from occurring in those immature rats sustaining seizures alone or any accentuation of brain damage in those animals subjected to prior cerebral hypoxia-ischemia.
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PMID:Cerebrospinal fluid concentrations of glutamate and GABA during perinatal cerebral hypoxia-ischemia and seizures. 883 71

Normoglycemic animals subjected to 10-20 min of transient ischemia survive without major neurological symptoms, but incur delayed neuronal damage selectively affecting vulnerable neuronal populations. If the animals are hyperglycemic before ischemia is induced, cell damage develops more rapidly, and postischemic seizures appear after a delay of 18-24 h. This study was designed to assess whether the primary insult, i.e., transient ischemia in hyperglycemic animals, triggers early epileptogenic activity which 'matures' into clinical seizures, or if the seizures arise as a result of secondary events occurring after many hours of recirculation. EEG activity during 20-24 h of postischemic recirculation was recorded from electrodes implanted in the neocortex and hippocampus of freely moving rats which had been subjected to 10 min of ischemia under normoglycemic or hyperglycemic conditions. Normoglycemic animals showed a transient postischemic reduction of EEG amplitude and frequency, and sparse and temporary epileptiform activity. In contrast, hyperglycemic animals showed a more pronounced reduction of EEG amplitude and frequency, and early appearing epileptiform activity which was sustained, and ultimately transformed into overt electrographic seizures. The EEG changes were more pronounced in the neocortex than in the hippocampus. The results thus demonstrate that the initial ischemic insult, and not the secondary damage appearing many hours after the initiation of recirculation, triggers epileptiform activity that 'matures' into status epilepticus.
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PMID:Characteristics of postischemic seizures in hyperglycemic rats. 883 68

The occurrence of physiological cell death has been known for decades, but interest in the subject was renewed in 1972 when Kerr, Wyllie and Currie described in detail the ultrastructural changes characteristic of dying cells and coined the term apoptosis to describe the process. Cells display a wide variety of morphological changes when dying during development or following a toxic insult. A binary classification scheme suggests that physiologically appropriate death is due to apoptosis and that pathological mechanisms involve necrosis. However, recent studies indicate a potential involvement of apoptotic cell death in ischemia, status epilepticus and HIV-1 infection.
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PMID:Apoptotic features of selective neuronal death in ischemia, epilepsy and gp 120 toxicity. 905 57

Increased glutamate-receptor-mediated Ca++ influx is considered an important factor underlying delayed neurodegeneration following ischemia or seizures. Until recently, the NMDA receptor was the only glutamate receptor known to be Ca(++)-permeable. It is now well established that glutamate receptors of the AMPA type, encoded by a gene family designated GluR1-GluR4, exist in both Ca(++)-permeable and Ca(++)-impermeable forms, depending on their subunit composition and degree of RNA editing. Recombinant channels assembled without GluR2 are permeable to Ca++; channels assembled with (edited) GluR2 are Ca(++)-impermeable. AMPA receptors in most adult neurons are hetero-oligomers containing GluR2 subunits, but some neurons have GluR2-less, Ca(++)-permeable receptors. The "GluR2 hypothesis" predicts that a relative reduction in the expression of GluR2 results in enhanced Ca++ influx through newly synthesized AMPA receptors, thereby increasing neurotoxicity of endogenous glutamate. Recent observations indicate reduction in GluR2 expression and predict formation of Ca(++)-permeable AMPA receptors following global ischemia and kainate-induced status epilepticus; these changes are likely to be a major factor contributing to the delayed neurodegeneration that follows these pathological events. The delayed neurodegeneration appears to be primarily apoptotic. Thus, there are at least three strategies for neuroprotection: block of formation of GluR2-less receptors, which may be possible at several levels; block of the GluR2-less receptors themselves; and block of the subsequent apoptosis.
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PMID:The GluR2 hypothesis: Ca(++)-permeable AMPA receptors in delayed neurodegeneration. 924 66

The etiology of sudden death in patients with epilepsy remains unclear. Previous studies in a well-established sheep model of status epilepticus showed that more than one-third of the unsedated animals died within 5 minutes of seizure onset due to hypoventilation. The relative contributions of airway obstruction and central hypoventilation could not be determined because airway flow and respiratory effort were not monitored. In this study, status epilepticus was induced in unsedated sheep with tracheostomies monitored by electrocardiography, electroencephalography, arterial line, serial blood gases, and airway flowmeter. All 8 animals demonstrated central apnea and hypoventilation, which resulted in the death of 1 and contributed to the death of another. A third animal died of acute heart failure within 2 minutes of seizure onset, accompanied by a large septal myocardial hemorrhage, contraction bands, and signs of global cardiac ischemia. More subtle contraction bands, subendocardial hemorrhage, and signs of acute myocardial ischemia were seen in other animals as well, none of which died of cardiac causes. Malignant arrhythmia was not seen in any of the sheep. Central hypoventilation and apnea accompany generalized status epilepticus and may be an important cause of sudden death in epileptics. Acute cardiac failure may also be a cause of epileptic sudden death.
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PMID:Central apnea and acute cardiac ischemia in a sheep model of epileptic sudden death. 938 70

Results from experiments performed with permanent non-neuronal cell lines suggest that endoplasmic reticulum (ER) calcium homeostasis plays a key role in the control of protein synthesis (PS). It has been concluded that disturbances in ER calcium homeostasis may contribute to the suppression of PS triggered by a severe metabolic stress (W. Paschen, Med. Hypoth., 47 (1996) 283-288). To elucidate how an emptying of ER calcium stores of these cells would effect PS and ribosomal aggregation of non-transformed fully differentiated cells, experiments were run on primary neuronal cell cultures. ER calcium stores were depleted by treating cells with thapsigargin (TG, a selective, irreversible inhibitor of ER Ca(2+)-ATPase), cyclopiazonic acid (CPA, a reversible inhibitor of ER Ca(2+)-ATPase), or caffeine (an agonist of ER ryanodine receptor). Changes in intracellular calcium activity were evaluated by fluorescence microscopy using fura-2-loaded cells. Protein synthesis was determined by measuring the incorporation of [3H]leucine into proteins. The degree of aggregation of ribosomes was evaluated by electron microscopy. TG induced a permanent inhibition of PS to about 10% of control which was only partially reversed within 2 h of recovery. CPA caused about 70% inhibition of PS, and PS recovered completely 60 min after treatment. Caffeine produced an inhibition of PS to about 50% of control. Loading cells with the calcium chelator BAPTA-AM (33.3 microM) alone suppressed PS without reversing TG- or caffeine-induced inhibition of PS, indicating that the suppression of PS was caused by a depletion of ER calcium stores and not by an increase in cytosolic calcium activity. TG-treatment of cells induced a complete disaggregation of polysomes which was not reversed within the 4 h recovery period following TG-treatment. After caffeine treatment of cells, we observed a heterogenous pattern of ribosomal aggregation: in some neurons ribosomes were almost completely aggregated while in other cells a significant portion of polyribosomes were disaggregated. The results indicate that a depletion of neuronal ER calcium stores disturbs protein synthesis in a similar way to the effects of transient forms of metabolic stress (ischemia, hypoglycemia or status epilepticus), thus implying that a disturbance in ER calcium homeostasis may contribute to the pathological process of stress-induced cell injury.
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PMID:Relation of neuronal endoplasmic reticulum calcium homeostasis to ribosomal aggregation and protein synthesis: implications for stress-induced suppression of protein synthesis. 943 27

Neuron-specific enolase (NSE) is a sensitive marker of brain damage in stroke, global ischemia, and coma. Serum NSE is also correlated with the duration and outcome of status epilepticus (SE). CSF-NSE levels have not been previously reported in SE. We report the CSF concentrations of NSE in 11 patients with cryptogenic/remote symptomatic SE. CSF obtained within 24 hours of SE showed increased concentrations of NSE in 9 of 11 patients. The mean CSF-NSE for the group was elevated compared with the levels for normal control subjects (30.8 +/- 18.33 versus 10.76 +/- 3.08 ng/mL; p = 0.002). Further, CSF-NSE levels were elevated compared with simultaneous serum levels in the same group of patients (p = 0.01). In addition, the CSF/serum albumin ratio (QAlb), a measure of the integrity of the blood-brain barrier, was increased in SE patients compared with control individuals (33.4 versus 4.79 x 10(-3); p = 0.0001). An increase of QAlb correlated with CSF-NSE (rs = 0.66, p = 0.04) and serum NSE levels (rs = 0.83, p = 0.004). CSF-NSE is a promising in vivo marker for brain injury after SE.
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PMID:Status epilepticus increases CSF levels of neuron-specific enolase and alters the blood-brain barrier. 959 92

Kainic acid (KA)-induced status epilepticus (SE) in adult rats results in extensive neuronal damage throughout the limbic system and the loss of selectively vulnerable neuronal populations, particularly CA3 neurons. We investigated the effects of a short episode of seizure activity on neuronal death elicited by a subsequent prolonged SE episode. A short episode of seizure activity was produced by sub-cutaneous (s.c.) injection of KA followed after 1 h by pentobarbital administration. Twenty-four hours later, KA was administered again, and animals were sacrificed 3 days later. Neuronal damage was estimated by visual analysis of neuronal density. Our results show that a short episode of seizure activity did not produce neuronal damage but almost completely protected vulnerable neurons from KA-induced neuronal damage. These results extend to epileptic tolerance the notion of tolerance previously described in the case of ischemia.
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PMID:A short episode of seizure activity protects from status epilepticus-induced neuronal damage in rat brain. 981 46


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