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 cases of SLE with concomitant neurological syndromes are reported. In 2 cases brain stroke with right-sided hemiplegia and aphasia developed, in the remaining cases brain-stem stroke with subarachnoid haemorrhage, progressive hemiparesis and signs of intracranial hypertension, chorea, status epilepticus in terminal uraemia were observed. In one case myasthenia coexisted. Severe neurological syndromes were preceded by signs of involvement of other organs and in most cases by low-grade signs of central nervous system involvement. Treatment with corticosteroids and immunosuppressants resulted in significant improvement without complete remission. A retrospective survey of clinical material showed that modern therapeutic methods have improved the prognosis in systemic lupus erythematosus independently of central nervous system involvement.
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PMID:[Neurological syndromes in the course of systemic lupus erythematosus]. 52 35

Sudden death is defined as any death that occurs less than 24 hours after the onset of first symptoms. Strokes account for 10 to 20% of all sudden deaths. The records of all residents of Rochester, Minn., who had their first stroke during the period 1955 through 1969 were analyzed. Among 255 deaths caused by the first stroke, 52 were sudden. Twenty-six of the deaths were due to primary intracerebral hemorrhage, and 20 to primary subarachnoid hemorrhage. Only two of the sudden deaths were caused by infarction: one by pontine and cerebellar infarct and the second by a cortical infarct, which resulted in death from status epilepticus. Among the nine patients who died within 2 hours of the onset of symptoms, six had primary subarachnoid hemorrhage. Hypertension was noted in 23 of the 26 patients (88%) who died of primary intracerebral hemorrhage; 8 patients with primary intracerebral hemorrhage were on long-term oral anticoagulant therapy, and all 8 were hypertensive.
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PMID:Sudden death from stroke. 87 Oct 28

This paper describes the clinical features of two patients with chronic renal failure and uremic anaemia treated with recombinant human erythropoietin (9000 I.U. subcutaneously subdivided in 3 times weekly at the end of haemodialysis treatment) who developed seizures and status epilepticus. This treatment has unequivocal benefits but in some patients has been accompanied by elevated blood pressure leading to hypertensive encephalopathy with seizures. In fact, the correction of the anaemia results in a rise in packed cell volume with a consequent increase in blood viscosity, predisposing to increased vascular resistance and the development of hypertension.
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PMID:[Status epilepticus in chronically dialyzed patients treated with erythropoietin]. 181 73

Neuropediatric emergencies are reviewed. In particular in this topic the Authors point out the diseases in which an immediate treatment is required. Hypoxic ischemic encephalopathy, acute neonatal metabolic disease, seizures disorders and status epilepticus, meningitis, encephalitis, post viral neurological syndromes, acute hemiplegia, coma, acute endocranial hypertension are discussed with special emphasis on the possible causes and treatment.
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PMID:[Neurologic emergencies in children]. 307 30

Cerebral blood flow was sequentially determined (every 2-3 min) with helium clearance in two "vulnerable" structures: the hippocampus and the frontoparietal cortex during bicuculline (n = 11) and kainic acid (n = 9)-induced seizures in unanaesthetized, spontaneously breathing rats. Tissue partial pressures of oxygen and carbon dioxide were continuously and simultaneously evaluated in the same brain areas. All these variables were measured by mass spectrometry with a single gas sampling cannula previously implanted in each structure. The systemic variables, arterial blood pressure, arterial partial pressures of oxygen and carbon dioxide, pH, and bicarbonate concentration were also determined. Arterial and venous catheters were chronically implanted several days prior to the definitive experiments. Bicuculline induced short (about 15 min), recurrent, generalized seizures, with an abrupt rise in arterial blood pressure, an arterial metabolic acidosis and comparable blood flow increases (4-fold) in the hippocampus and the neocortex. A marked increase in tissue partial pressure of oxygen was always preceded by an increase in tissue partial pressure of carbon dioxide. After the seizures, in the 5 rats that survived, cerebral blood flow was significantly lowered; tissue partial pressure of oxygen and partial pressure of carbon dioxide also decreased, but to a lesser extent. Histological examination revealed two types of lesions: predominantly selective chromatolysis but also ischaemic cell change. Kainic acid first induced a decrease in arterial pressure and then hypertension during status epilepticus, with a return of arterial pressure towards basal levels during the recovery period (4 h after the injection). Respiratory alkalosis occurred throughout the experiment. Cerebral blood flow increased progressively to become maximal during status epilepticus. This vasodilatation was greater in the hippocampus (x 8) than in the neocortex (x 4). During recovery, cerebral blood flow tended to decrease but remained significantly elevated. In both structures, tissue partial pressure of oxygen was first lowered while tissue partial pressure of carbon dioxide was elevated; with the occurrence of the wet dog shakes, tissue partial pressure of O2 increased and tissue partial pressure of CO2 decreased. The changes in tissue gases were maximal during status epilepticus and tended to return to their basal levels thereafter, but no decrease in tissue partial pressure of O2 was observed, even 4 h after kainic acid administration. Histological analysis demonstrated ischaemic cell changes, particularly in the limbic system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Continuous determination of the cerebrovascular changes induced by bicuculline and kainic acid in unanaesthetized spontaneously breathing rats. 312 92

To determine the importance of intracranial hypertension in central nervous system acute infections, we studied intracranial pressure (ICP) in 27 patients, aged 45 days to 13 years. Fourteen had meningitis and 13 had encephalitis; all were in deep coma with a Glasgow Coma Scale 7 or less. Intracranial hypertension defined by a mean ICP above 15 mm Hg was observed in 12 patients with meningitis (86%) and in 9 with encephalitis (69%). Patients with meningitis exhibited a very early and severe intracranial hypertension. A striking difference is noted between survivors and non-survivors who had a very high maximal ICP with a severe reduction in cerebral perfusion pressure. Intracranial hypertension occurred in all patients with acute primitive encephalitis but only in 3/7 patients with post-infectious encephalitis. ICP monitoring seems to be important in the comatose forms of bacterial meningitis in the early period, herpes encephalitis and postinfectious encephalitis with severe status epilepticus.
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PMID:[Intracranial pressure in comatose meningitis and encephalitis in children]. 318 25

To determinate the importance of intracranial hypertension in central nervous system (CNS) acute infections, we studied intracranial pressure (ICP) in 27 patients, age 45 days to 13 years. Fourteen had meningitis and 13 had encephalitis; all were in deep coma with Glasgow Coma Scale 7 or less. Intracranial hypertension defined by a mean ICP above 15 mmHg, was observed in 12 patients with meningitis (86%) and in 9 with encephalitis (69%). Patients with meningitis exhibited a sudden and severe intracranial hypertension. A striking difference was noted between survivors and non survivors who had a very high maximal ICP with a severe reduction of cerebral perfusion pressure (CPP). Intracranial hypertension occurred in all patients with acute primary encephalitis but in only 3/7 patients with post-infectious encephalitis. ICP monitoring seems to be important in the comatose forms of: (1) bacterial meningitis in the early period (2) herpes encephalitis (3) post-infectious encephalitis with severe status epilepticus.
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PMID:Intracranial pressure in childhood central nervous system infections. 322 Oct 7

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

To test whether status epilepticus alters regional blood-brain barrier (BBB) permeability to water when systemic hypertension is avoided, and whether central noradrenergic innervation contributes to the regulation of BBB in this setting, Wistar rats with unilateral 6-hydroxydopamine lesion of the nucleus locus coeruleus (LC) were subjected to 8 min of bicuculline-induced status epilepticus while ventilated with 100% oxygen; arterial normotension was preserved by withdrawal of arterial blood as required. Regional cerebral blood flow and permeability-times-surface-area product (PS) for water were measured by a double-label modification of the Kety integral strategy, with [14C]butanol and [3H]water, respectively. In normocapnic control rats, regional cerebral blood flow (rCBF) was 1.92 +/- 0.57 ml/g/min and water extraction fraction was 0.81 +/- 0.08 (S.D.). Values in control rats breathing 100% oxygen were similar. During status epilepticus, rCBF increased two- to three-fold; water extraction fraction declined, but there were no significant side-to-side differences for either rCBF or regional PS product for water in LC-lesioned animals despite an 81% reduction of cortical norepinephrine content on the lesioned side. The PS product for water increased by 42% during status epilepticus, but the flow vs PS-product relationship did not depart from that predicted on the basis of data in control rats. Thus, when systemic hypertension is prevented, brief status epilepticus does not induce abnormal BBB permeability to water, and unilateral LC lesion fails to influence either rCBF or the cerebrovascular PS product for water.
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PMID:Regional blood-brain barrier permeability to water and cerebral blood flow during status epilepticus: insensitivity to norepinephrine depletion. 400 9

The effects of prolonged bicuculline-induced seizures on cerebral blood flow and metabolism were determined in paralyzed, mechanically ventilated neonatal dogs. Transient changes occurring early in the course of status epilepticus included significant arterial hypertension, hypocarbia, elevation of plasma norepinephrine levels, and decline in brain glucose concentration. Cerebral blood flow remained elevated throughout the 45 minutes of seizure. Determination of cerebral metabolite values by in vivo phosphorus 31 nuclear magnetic resonance spectroscopy and by in vitro enzymatic analysis of frozen brain samples showed significant decreases in the level of phosphocreatine and relatively less change in ATP values. Progressive intracellular acidosis occurred, coincident with elevation of brain lactate concentrations. We conclude that the physiological and metabolic alterations that occur during prolonged seizures are not uniform, but change with time. Any hypothesis advanced to explain the mechanism of neuronal injury during prolonged seizures must take into account these temporally related changes.
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PMID:31P NMR study of cerebral metabolism during prolonged seizures in the neonatal dog. 403 47


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