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)

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)
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PMID:Effect of status epilepticus on hypoxic-ischemic brain damage in the immature rat. 747 24

A case of radiation-induced vasculopathy of a pineal glioma was presented with haemodynamic and metabolic changes before and after radiotherapy. After radiation of 60 Gy with conventional fractionation (1.8-2.0 Gy daily, 5 days per week), regional blood flow, oxygen extraction fraction, metabolic rate of oxygen, kinetic metabolic rate of glucose and the rate constants (K2, K3) were markedly depressed (20% or greater) compared with the pre-irradiated study. 7 months after radiotherapy, the patient developed transient transient episodes of both right and left upper limb convulsion, terminating in generalized convulsion. When she developed status epilepticus, computed tomography showed extensive low density areas in the territory supplied by the right middle cerebral and the right posterior cerebral arteries. Cerebral angiography revealed diffuse stenosis at both carotid bifurcations and at the origins of the right posterior communicating and posterior cerebral arteries. Haemodynamic and metabolic depression therefore implicated radiation-induced vasculopathy in the present case.
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PMID:Case report: radiation-induced vasculopathy implicated by depressed blood flow and metabolism in a pineal glioma. 771 89

A 38-year-old man with chronic low back pain underwent myelography and was inadvertently injected with ionic contrast medium. Within minutes, he started complaining of muscle spasms in his lower extremities, followed by respiratory distress and myoclonus. Immediate intravenous treatment with fluids, antihistamines, and supplemental oxygen was started. Within 1 hour after the myelogram, he was intubated and paralyzed with a neuromuscular blocking agent. Shortly thereafter, he began receiving triple anticonvulsant therapy and a lumbar drain was inserted to allow for the evacuation of cerebrospinal fluid. Electroencephalographic monitoring, which initially showed that the patient was in status epilepticus, subsequently showed no more episodes of seizure activity. Massive rhabdomyolysis, renal failure, and metabolic derangement were prevented. He was then extubated and regained full consciousness. He was discharged on the 13th day of hospitalization with mild amnesia and some cognitive dysfunction. A review of the literature reveals descriptions of 9 of 15 patients who survived similar episodes. We conclude that prompt identification of the contrast medium error and prompt intervention are crucial to increase significantly the chances of survival. Elective paralysis, anticonvulsant therapy, and cerebrospinal fluid drainage are the recommended modes of treatment.
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PMID:Inadvertent use of ionic contrast material in myelography: case report and management guidelines. 773 26

Acetylcholine (ACh) is a powerful excitotoxic neurotransmitter in the brain. By stimulating Ca(2+)-mobilizing receptors, ACh, through G-protein(s), stimulates phospholipase C and causes the hydrolysis of a membrane phospholipid, phosphatidylinositol-4,5-bisphosphate to two second messengers, inositol-1,4,5-trisphosphate (ins-(1,4,5)-P3), and diacylglycerol. Ins-(1,4,5)-P3 is important in cholinergic neuronal stimulation, and injury. Cholinergic agonists cause tonic-clonic convulsions which may be either transient or persistent. Even short-term cholinergic convulsions may be associated with neuronal injury, especially in the basal forebrain and the hippocampus. Cholinergic-induced convulsions also elevate levels of brain Ca2+ which precede neuronal injury. Female sex and senescence increase the sensitivity of rats to cholinergic excitotoxicity. Even if cholinergic-induced brain phosphoinositide signalling is likely to trigger cholinergic excitotoxicity, several other processes may be involved in the ensuing neuronal injury. Once initiated, cholinergic convulsions cannot be stopped with cholinergic antagonists such as atropine even though they are effective when given prior to a cholinergic agonist. However, glutaminergic antagonists, and GABAergic agonists, are effective in the attenuation of ongoing cholinergic status epilepticus. Cholinergic brain stimulation may be, in fact, under a partial control of brain GABAergic tonus, but also cause the release of glutamate. Glutamate stimulates inositol lipid signalling in several neuronal cells and, therefore, underlines the significance of inositol lipid signalling in cholinergic-induced excitotoxicity. Moreover, the anatomical distribution of cholinergic brain damage correlates well with that of glutaminergic neurons. Furthermore, glutamate increases neuronal oxidative stress, i.e. it increases the levels of free intracellular calcium, the production of reactive oxygen species, and causes the depletion of neuronal glutathione. The role of excitatory amino acids as common mediators of cholinergic excitotoxicity may offer new insights into the neurotoxic consequences of cholinergic neuronal stimulation.
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PMID:Phosphoinositide second messengers in cholinergic excitotoxicity. 785 83

The substantia nigra pars reticularis (SNPR) of rats is highly susceptible to both seizure- and ischaemia-mediated damage. Hyperglycaemic exacerbation of brain damage similar to that observed after global brain ischaemia may also occur in rats with status epilepticus. We tested the hypotheses that hyperglycaemia exacerbates seizure-induced SNPR damage in rats and that SNPR lesions develop rapidly post-seizure. Halothane-anaesthetized, paralysed, and mechanically ventilated rats were prepared for haemodynamic and EEG monitoring. Halothane was discontinued, and mechanical ventilation on 30% oxygen/70% nitrous oxide was continued for 1 h. Three treatment groups (20 rats each) were studied: (1) control, lactated Ringer's solution; (2) equiosmolar control, 40% mannitol; and (3) hyperglycaemia, 50% dextrose. Infusions were started 5 min before seizures were induced with flurothyl 3% administered for either 45 (n = 10) or 75 (n = 10) min. Immediately after seizures, half of the animals underwent cerebral perfusion-fixation with formalin and half were allowed to recover for 2 h post-seizure and then perfused. Brain histology was assessed by light microscopy and scored 0-5 (0 = no damage) for the percentage of eosinophilic neurons and vacuolation in the SNPR. Glucose administration decreased the severity of SNPR damage in rats subjected to 75 min of seizures and 2 h recovery (pathology scores: control, eosinophilic neurons = 3.6, vacuolation = 4.0; hyperglycaemia, eosinophilic neurons = 3.0, vacuolation = 2.75; p < 0.05). SNPR damage was worse after 2 h of recovery (pathology scores: 0 h recovery, eosinophilic neurons = 0.9, vacuolation = 0.1; 2 h recovery, eosinophilic neurons = 3.9, vacuolation = 3.8; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substantia nigra damage after fluorothyl-induced seizures in rats worsens after post-seizure recovery: no exacerbation with hyperglycaemia. 790 8

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

Cerebral air embolism occurred in a patient undergoing posterior fossa surgery performed in the sitting position for acoustic neuroma removal. The patient experienced two episodes of venous air embolism, as evidenced by precordial Doppler, end-tidal carbon dioxide reduction, and oxygen desaturation. In both cases, air was aspirated from the central venous catheter; during the second episode there was arterial hypotension and electrocardiogram changes, and air bubbles were visualized in the cerebellar arteries. The patient did not regain consciousness after surgery and developed early tonic-clonic convulsions and electroencephalogram status epilepticus, which was treated with barbiturate coma. Intracardiac septal defects were not detected by transesophageal echocardiography, and computerized tomography of the brain demonstrated multifocal discrete ischemic areas in the cerebral hemispheres. The patient died 6 days after surgery without having regained consciousness. This case appears to represent the occurrence of transpulmonary passage of venous air embolism.
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PMID:Cerebral ischemia after venous air embolism in the absence of intracardiac defects. 871 84

We report a 83 year-old woman with dementia. She was apparently well until December of 1993 when she was 81-year-old. At that time, she was operated or her cataract. Her post operative course was uneventful, however, shortly after her operation, she had an onset of memory loss and abnormal behavior. She showed a fluctuating course in her mental disturbance. In 1995, her dementia worsened with nocturnal agitation. She was admitted to our service on June 12, 1995. She was alert and her blood pressure was 140/100 mmHg. She showed recent memory loss and disorientation to time. Motor wise, she was unable to stand unsupported. Her gait with support showed small steps and a wide base. She was bradykinetic and ataxic in her finger-to-nose and heel-to-knee test, however, no rigidity or tremor was noted. Her MRI showed T2-high signal lesions in both medial thalamic areas, in the right occipital lobe, and in the bilateral cerebral white matters as well as in the basal ganglia. She was discharged for out-patient follow up on July 3, 1995. Four days after the discharge, she showed declining responses to stimuli and she developed dyspnea on July 14, 1995. She was admitted again on the same day. Her body temperature was 38.5 degrees C and moist rales were heard in the left lung field. She appeared drowsy and no verbal response was obtained; no apparent motor palsy was noted. Blood count showed leukocytosis (14,300/ml). Blood gas analysis under 61 of oxygen inhalation through a mask was as follows: pH 7.460, PCO2 39.6 mmHg, PO2 67 mmHg, and HCO3-28.5 mEq/l. Two days after admission, she developed a convulsion in her left arm and she became unconscious. Her EEG showed periodically recurring lateralized epileptic discharges on the right fronto-central areas. Her subsequent course was complicated by status epilepticus and respiratory distress. She died on July 26, 1995. She was discussed in a neurological CPC. The chief discussant arrived at a conclusion that she suffered from multi-infarct dementia. Bilateral thalamic infarctions were considered to have played a significant role in her dementia. Post-mortem examination revealed subcortical leukoencephalopathy of Binswanger's type and cerebral infarctions in the thalamic and basal ganglia regions and in the right occipital lobe. In addition, she showed isolated angitis of the central nervous system involving mainly in the small arteries located in the superficial areas of the brain and the spinal cord. This patient was interesting in that despite relatively mild leukoaraiosis in MRI, post-mortem examination revealed profound pathologic changes in the subcortical white matters. In addition, she showed the isolated angitis of the CNS. The cause and the clinical correlates of her angitis were unclear.
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PMID:[A 83 year-old woman with dementia, gait disturbance, and convulsion]. 904 33

The possible roles for nitric oxide produced by neurons in epileptic conditions have been investigated from two different aspects: microcirculation and delayed damage. Our aim was to determine whether the selective inhibition of neuronal (type 1) nitric oxide synthase by 7-nitroindazole, during seizures induced by systemic kainate, modifies hippocampal blood flow and oxygen supply and influences the subsequent hippocampal damage. Experiments were performed in conscious Wistar rats whose electroencephalogram was recorded. 7-Nitroindazole (25 mg/kg, i.p.) or its vehicle was injected 30 min before kainate administration (10 mg/kg, i.p.) and then twice at 1-h intervals. Kainate triggered typical limbic seizures evolving into status epilepticus, identified by uninterrupted electroencephalographic spike activity. The seizures were stopped by diazepam (5 mg/kg, i.p.) after 1 h of status epilepticus. Three types of experiments were performed in vehicle- and 7-nitroindazole-treated rats. (1) Hippocampal nitric oxide synthase activity was measured under basal conditions, at 1 h after the onset of the status epilepticus and at 24 h after its termination (n = 4-6 per group). (2) Hippocampal blood flow and tissue partial pressure of oxygen were measured simultaneously by mass spectrometry for the whole duration of the experiment, while systemic variables and body temperature were monitored (n = 6 per group). (3) Hippocampal damage was revealed by Cresyl Violet staining and evaluated with a lesion score seven days after status epilepticus (n = 12 per group). Hippocampal nitric oxide synthase activity was not significantly modified during status epilepticus or the following day in vehicle-treated rats. In contrast, it was inhibited by 57% in 7-nitroindazole-treated rats, both in basal conditions and after 1 h of status epilepticus, but was not different from its basal level 24 h later. 7-Nitroindazole significantly decreased basal hippocampal blood flow and tissue partial pressure in oxygen by 30% and 35%, respectively without affecting any systemic or thermal variable. During status epilepticus, 7-nitroindazole significantly reduced the increase in hippocampal blood flow by 70% and prevented any increase in the tissue partial pressure of oxygen. Seven days later, the hippocampal damage in the CA1 and CA3 layers was significantly less in 7-nitroindazole-treated rats than in vehicle-treated rats. These results indicate that the inhibition of neuronal nitric oxide synthase by 7-nitroindazole protects neurons from seizure-induced toxicity despite reducing blood flow and oxygen supply to the hippocampus.
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PMID:Inhibition of neuronal (type 1) nitric oxide synthase prevents hyperaemia and hippocampal lesions resulting from kainate-induced seizures. 957 84

The mechanisms by which neurons die after stroke and status epilepticus and related neuropathological conditions are unclear, but may involve voltage-dependent Na+ channels, glutamate receptors, and nitric oxide (NO.). These questions were investigated using an in vitro primary cell culture model in which hippocampal pyramidal neurons undergo a gradual and delayed neurodegeneration induced by enhanced excitatory neurotransmission. When cells were treated with Mg2+-free, glycine-supplemented medium for a brief period (15 min) and examined 24 h later, approximately 30-40% of the neurons had died. Cell death could be inhibited by blockers of voltage-sensitive Na+ channels and by N-methyl-D-aspartate receptor antagonists. Application of either the endogenous antioxidant melatonin (EC50: 19.2+/-2.8 microM) or the NO. synthase inhibitor Nomega-nitro-L-arginine after, but not during, Mg2+-free exposure protected against delayed neuronal death; significant neuroprotection was observed when the addition was delayed for up to 4 h. This operational time window suggests that an enduring production of NO. and reactive oxygen species from neuronal sources is responsible for delayed cell death. A role for reactive oxygen species in this injury process was strengthened by the finding that, whereas neurons cocultured with astroglia were more resistant to killing, agents capable of lowering intracellular glutathione negated this protection. Because secretion levels of melatonin are decreased with aging, reductions in this pineal hormone may place neurons at a heightened risk for damage by excitatory synaptic transmission.
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PMID:Melatonin prevents the delayed death of hippocampal neurons induced by enhanced excitatory neurotransmission and the nitridergic pathway. 961 51


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