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

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

Generalized seizures can induce both hypertension and hyperglycemia which may aggravate preexisting cerebral or medical conditions in patients. In vivo fluorescent imaging of regional cortical blood flow and brain intracellular pH (pHi) was performed in fasted New Zealand rabbits (n = 35) in which either mean arterial blood pressure (MABP) or serum glucose was the covaried factor during pentylenetetrazole induced status epilepticus under 1.5% inspired halothane. Baseline brain pHi and regional cortical blood flow were 7.02 +/- 0.02 and 51.1 +/- 1.7 ml/100 g/min, respectively. Following seizure induction, MABP increased to 105 mm Hg and brain pHi fell to 6.79 +/- 0.03 within 15 min and remained at this level for 1 h (P < 0.001). With normalization of MABP during ongoing seizures, there was no worsening in brain pHi despite a significant decrease in regional cortical blood flow. Hyperglycemia decreased pHi to 6.71 +/- 0.02 compared to 6.84 +/- 0.04 in normoglycemic animals (P < 0.001). Using pHi as a cerebral metabolic index, these data suggest that normalization of MABP does not increase metabolic injury while hyperglycemia does significantly worsen brain acidosis. Therefore, administration of glucose to patients with status epilepticus should be avoided unless there is documented hypoglycemia.
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PMID:Effect of arterial blood pressure and serum glucose on brain intracellular pH, cerebral and cortical blood flow during status epilepticus in the white New Zealand rabbit. 845 50

Cerebrospinal fluid (CSF) examinations of 212 children aged two to 24 months with idiopathic nonfebrile seizures, complex febrile seizures, or status epilepticus, who had a lumbar puncture within 24 hours of the convulsion, were reviewed to determine whether an idiopathic convulsion can result in CSF abnormalities. Children with complex febrile seizures had a median CSF white blood cell count of 1 cell/mm3 (range 0-19 cells/mm3) and a median CSF polymorphonuclear (PMN) cell count of 0 cells/mm3 (range 0-8 cells/mm3). The CSF white blood cell (WBC) count was elevated above the upper limit of normal of 5 cells/mm3 in 9.8% and the absolute number of polymorphonuclear cells was more than 0 cells/mm3 in 26.2% of the complex febrile seizure subjects. Values at the 95th percentile were calculated; a total of 8 WBC/mm,3 4 PMN/mm,3 protein of 73 mg/dl and glucose of 119 mg/dl determined the 95th percentile CSF values for the patients with complex febrile seizures. Patients with nonfebrile seizures or with status epilepticus had similar findings. We conclude that complex febrile, idiopathic nonfebrile convulsions or status epilepticus may affect CSF findings in children: CSF with > 20 WBC/mm3 or > 10 PMN/mm3 should not be attributed to seizures.
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PMID:Cerebrospinal fluid analysis in children with seizures. 853 68

In order to assess acute, short and long-term effects of seizures in the immature rat brain, we studied the metabolic, circulatory and histopathological changes induced by pentylenetetrazol (PTZ) given at postnatal day 10 (P10) or 21 (P21). Seizures were induced by repetitive subconvulsive injections of PTZ given as a first dose of 40 mg/kg followed 10 min later by 20 mg/kg. Thereafter, rats received every 10 min additional injections of PTZ 10 mg/kg until the onset of status epilepticus. Local cerebral metabolic rates for glucose (LCMRglc) were measured both during the seizures in P10 and P21 rats and in the young adult animal at P60 by means of the quantitative 2-deoxyglucose technique. Rates of local cerebral blood flow (LCBF) were determined during the seizures by the iodoantipyrine technique. Short-term histological changes were assessed by acid fuchsin and hematoxylin-eosin staining and by HSP72 immunohistochemistry. At P10, LCMRglcs uniformly increased (38-400%) over control values during seizures. At P21, metabolic increases (39-181%) occurred only in 20% of the structures while LCMRglcs decreased in most cortical, hippocampal and sensory areas as well as in mammillary body, discrete thalamic nuclei and white matter areas. At P10, LCBF rose (32-184%) in all brain structures whereas, at P21, LCBF decreased in cortical, hippocampal and sensory regions and increased in most other areas. At P60, in animals having seized at either age, significant long-term decreases in LCMRglcs were recorded in hippocampus, auditory and piriform cortex, medial geniculate body and mammillary body. In P60 animals exposed to PTZ at P10, LCMRglcs were also decreased in 3 other sensory areas. In P60 animals exposed to seizures at P21, LCMRglcs were additionally decreased in sensory regions, cortices, thalamic and hypothalamic regions. Neuronal cells were transiently stained with acid fuchsin, with a peak occurring at 24 h after the seizures. The stain was visible in all regions of cerebral cortex and hippocampus and in some thalamic and hypothalamic nuclei. This transient staining was not accompanied by cell degeneration as assessed by hematoxylin-eosin histology. No HSP72 expression could be detected 24 h after the seizures, neither at P10 nor at P21. The present study shows that the immature rat neurons undergo altered metabolic rates and local circulatory decreases in the acute phase, a change in the affinity of acid fuchsin as a short-term effect and long-term metabolic decreases. All these changes are located in the same regions, i.e., cerebral cortex, hippocampus, sensory regions as well as scattered thalamic and hypothalamic nuclei. Thus, short- and long-term metabolic changes induced by seizures can be used as an index of cell stress in the immature rat brain. Since all these changes occur in the absence of visible neuronal death, they might be related to changes in the final arborization and synaptic organization of the developing brain.
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PMID:The model of pentylenetetrazol-induced status epilepticus in the immature rat: short- and long-term effects. 898 91

A case of adult Reye's syndrome is described. A previously healthy 17-year-old man developed convulsions 2 days after resolution of an upper respiratory infection with parainfluenza virus type 3. During the preceding infection, he took aspirin. On admission, he was drowsy. There was no focal signs. Cranial CT scan was unremarkable. A lumbar puncture revealed an opening pressure of 180 mm H2O; the cerebrospinal fluid was acellular with normal protein level. Serum chemistry showed elevated transaminase activities and normal bilirubin level. Blood ammonia level was high; urea and citrulline levels were abnormally low. These abnormalities disappeared later, suggesting transient cysfunction of mitochondrial urea-cycle enzymes. Free and acyl carnitine levels were unremarkable. Both metabolic acidosis and ketonuria were absent. Thus, a variety of aminoacidurias and organic acidemias are unlikely. All these findings meet diagnostic criteria for Rye's syndrome proposed by the CDC of the USA. Status epilepticus was treated with intravenous infusion of thiamylal sodium. He was treated with hypertonic glucose solution and osmotic diuretic. Three months after the onset of the illness, his convulsions were controlled only with zonisamide, clonazepam, and carbamazepine. He had motor dysfunctions. This case is unique in that a patient with adult Reye's syndrome and status epilepticus favorably recovered.
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PMID:[A case of adult Reye's syndrome with favorable outcome despite status epilepticus]. 904 59

An 11-year-old girl developed signs of intracranial hypertension after status epilepticus with convulsive movements of her right upper limb. Computerized tomography revealed left hemispheric hypodensity with mass effect, attributed to vasogenic edema. Intracranial hypertension was controlled under intracranial pressure monitoring and clinical status slowly improved. The patient was aphasic and right hemiplegic when she recovered consciousness but she remarkably recovered from her neurological deficits during the following two years despite neuroradiological evolution demonstrating extensive destruction of the left cortex and white matter. Two positron emission tomography (PET) scans were performed respectively six weeks and eight months after status epilepticus, and both demonstrated profound left hemispheric hypometabolism except in the lenticular nucleus and a restricted area of motor/premotor cortex. On the other hand, glucose metabolism in the right hemisphere was heterogeneously increased on the second PET when compared with the first PET. We concluded that, in this case, clinical recovery might have implicated functional reorganization arising from the intact hemisphere.
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PMID:[Cerebral lesions following convulsive partial status epilepticus. Clinical, neuroradiologic and PET study of a case]. 919 Mar 70

Status epilepticus (SE) is one of the most common emergencies in pediatric neurology and it is associated with high mortality and morbidity. SE is more frequent in children than in adults. SE occurs in variety of settings especially in children-infections, patients with previously established epilepsy, cerebral malformations, hypoxia, hypoglucemia and head trauma- but in many cases SE can present as a first unprovoked seizures. Being better known the convulsive SE, non-convulsive SE that may present the same complications as the convulsive SE may be found in many patients. The mortality associated with SE in children is between 3 and 7%. The mortality and morbidity is estimated very high in the refractory SE. Although SE is defined as more than 30 min of continuous seizure activity, antiepileptic drug administration should be considered whenever a seizure has lasted 10 min. Initial therapeutic and etiological diagnostic have be conducted simultaneously. The commonest lines for treating SE and SE refractory are shown. The SE treatment should be managed including the ABCs of vital functions-supporting respiration, maintaining blood pressure, gaining access to circulation, electrolyte levels, renal and hepatic functioning and glucose levels- as well as a prompt administration of appropriate drugs in adequate doses. The different antiepileptic drugs that can be administered to the SE treatment are presented as well as the pharmacologic peculiarities, route of choice for drug administration, doses and risks of the traditional and the new antiepileptic drugs.
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PMID:[Status epilepticus in childhood]. 947 Apr 36

Barbiturates are widely used as neuroprotective agents during status epilepticus and during surgical procedures that cause cerebral ischemia. The efficacy of this practice is unproved, however, and while barbiturates may counter neuronal excitotoxicity, they can also inhibit mitochondrial ATP production. Since glutamate uptake is energetically costly, mitochondrial inhibition could impair glutamate uptake. To examine this possibility, glutamate uptake was measured in primary rat astrocyte cultures in the presence of several barbiturates. Different barbiturates had differing effects on glutamate uptake at normal glucose concentrations, but all potentiated inhibition of glutamate uptake during glucose deprivation. Thiamylal and thiopental were the most potent barbiturates examined, with 0.3 mM causing approximately 40% reduction in glutamate uptake rates. Barbiturates also potentiated ATP depletion during glucose deprivation, supporting mitochondrial inhibition as the mechanism of these effects. These findings suggest that barbiturates can, under some conditions, impair glutamate uptake at concentrations relevant to their clinical use.
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PMID:Barbiturates impair astrocyte glutamate uptake. 981 16

Status epilepticus remains a life-threatening condition associated with a high mortality. In order to understand the pathophysiological mechanisms underlying sustained seizures, the identification of structures involved in seizure activity allowing to define epileptic networks may be important. Thus, local cerebral metabolic rate for glucose (LCMR(glc)) was measured in a rat model of self-sustaining status epilepticus (SSSE) induced by a brief intermittent perforant path stimulation of 30 min, using the quantitative [(14)C]2-deoxyglucose autoradiographic technique. SSSE induced a generalized bilateral increase in LCMR(glcs) affecting 27 of the 42 structures studied. Largest metabolic increases (>250%) were recorded in the hippocampus, amygdala, entorhinal and piriform cortices, and lateral septum. Marked metabolic activation was also seen in basal ganglia areas such as the substantia nigra, globus pallidus and accumbens nucleus. LCMR(glcs) in brainstem, some midbrain structures, and in the neocortex were not affected by SSSE. In conclusion, a brief stimulation of the hippocampus induced a reproducible limbic SSSE in 100% of the rats, characterized by the metabolic activation of limbic and extralimbic structures, known to be involved in this type of seizures. Therefore, this new model allowing the development of a well-defined SSSE, appears to be particularly suitable for further studies on the mechanisms involved in status epilepticus.
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PMID:Self-sustaining status epilepticus after a brief electrical stimulation of the perforant path: a 2-deoxyglucose study. 1044 23

We have recently characterized the histopathological changes in an experimental model of mesial temporal lobe epilepsy (MTLE) induced by the intrahippocampal injection of low dose of kainate in mice. Although cerebral metabolism and blood flow are extensively studied and used in human MTLE to locate the regions involved in seizures before surgery, this exploration is only performed once the disease has fully developed. Therefore, in the present study, we followed the temporal evolution of intrahippocampal kainate-induced metabolic changes in mice from kainate injection to 120 days later by the quantitative autoradiographic [14C]2-deoxyglucose (2DG) technique. At day 0 (late phase of status epilepticus (SE)) and 15 days after kainate, i.e., during the period of ongoing neuropathological changes, glucose utilization was decreased bilaterally in all parts of the cerebral cortex, and ipsilaterally in the thalamus. In the hippocampus, CA1 metabolic activity was depressed at day 0 and increased at day 15 while CA3 glucose utilization was increased at both day 0 and 15. By day 30, there were almost no pyramidal cells left in the two hippocampal regions. At day 120, ipsilateral decreases persisted in the entorhinal cortex, anterior and ventromedian thalamus, and metabolic increases were recorded bilaterally in the central amygdala, anterior hypothalamus and mamillary body. At all times after kainate, a normo-, hypo- or hypermetabolic level was recorded in the dentate gyrus. The present study shows that the process of hippocampal sclerosis involves bilateral cortical reactivity and the participation of some limbic forebrain and motor structures. When hippocampal sclerosis has fully developed, hypometabolism is limited to regions directly connected to the damaged hippocampus and most likely involved in the new hyperexcitable circuit of limbic seizures.
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PMID:Mapping of the progressive metabolic changes occurring during the development of hippocampal sclerosis in a model of mesial temporal lobe epilepsy. 1067 50


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