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)

Alumina cream epileptic focus was established in the right sensorimotor cortex in 20 split-brain cats (partial or complete). EEG and behavioral observations were made in a period ranging from 24 to 836 days. Four types of EEG changes after alumina cream injection were differentiated. These types could be related to the direct effects of brain damage and to development of epilepsy. Spikes and sharp waves and paroxysmal discharges (focal and multifocal) were observed in about 60% of the cats. Clinical seizures developed in about the same percentage of the animals. These values are below those reported for cats with intact interhemispheric commissures. Diphenylhydantoin (DPH) was given orally in a daily dose of up to 15 mg/kg body weight in 9 animals with developed epileptic EEG activity. Five of them had epileptic seizures. DPH was introduced not earlier than 1.5 months after intracortical alumina cream injection. The plasma level of DPH varied between 7-20 mug/ml. This dose produced chronic symptoms of intoxication. Neither EEG changes nor clinical seizures were entirely controlled by this drug. Additional doses of Relanium (diazepam), and phenobarbital were necessary to stop generalized seizures or status epilepticus.
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PMID:EEG and clinical studies of the development of alumina cream epileptic focus in split-brain cats. 97 16

In the presented study we examined 110 patients who suffered from status epilepticus. Total 148 status were analysed with regard to etiology, releasing factors, course and treatment. Causes stressed were head injury with brain damage and intracranial space occupying, especially in the frontal region. Head injury with opened dura mater showed more tendency for development of status than closed ones. In a quarter of all cases origin couldn't be found. All these, with exception of one case, developed intercurrently. Isolated or initial always was consequence of brain lesion, the origin of which was or has been detected. No trend with reference to distribution of age in the particular forms of status were found out. In a third part of all a releasing factor could be discovered. Most the question in these cases was failure in medicamental treatment. We couldn't draw one's interferences about pathogenesis from etiology, age of patient, place in course and form of status. About in a quarter of all status we found defective neurological sequels, in 12% also psychical disturbances. 16 patients died during the period of observation, but only 2 within 24 hours, all together 8 in the first 14 days in deap coma. Immediately cause of death were above all complications of the heart, circulation of blood and respiration tract. In the most cases the treatment consisted in a mixture of anticonvulsive medicaments. The predominant rate of status epilepticus could be inhibited within 24 hours, only 20 lasted a longer time.
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PMID:[Etiology and clinic of status epilepticus]. 98 84

Serum anticonvulsant determinations made possible the identification of an unusual cause of status epilepticus and assisted with appropriate therapy in an epileptic patient with second-degree burns. The seizures were associated with a serum phenytoin concentration of 3.5 mug per milliliter. This suboptimal concentration of drug developed despite continuation of the patient's customary oral dose of phenytoin led to the conclusion that the unexpected decrement in serum anticonvulsant concentration was related to an experiment in absorption of that drug, possibly caused by the concurrent administration of oral oxacillin.
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PMID:Use of phenytoin serum levels in a case of status epilepticus. 98 31

A single, 2-hour episode of status epilepticus induced by flurothyl (1,500 mul) in 4-day-old rats irreversibly curtailed brain weight and brain DNA. Status epilepticus inhibited DNA synthesis but did not increase DNA breakdown and produced no histologic lesions. Rats with status epilepticus showed delayed behavioral milestones and reduced seizure thresholds several weeks after status. After milder convulsions (flurothyl 750 mul, bicuculline), brain DNA was curtailed at 7 days but returned to normal at 30 days. These results suggest that, in the immature brain, epileptic seizures too mild to cause cell necrosis can inhibit DNA synthesis and permanently curtail brain DNA content. This may account for the great vulnerability of the immature brain to epileptic seizures.
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PMID:Effects of neonatal status epilepticus on rat brain development. 98 88

The role of glucose metabolism in alleviating the complications of status epilepticus (SE) was investigated in developing rats. Pretreatment with glucose reduced mortality from SE by 90% in rats under 1 week of age, 80% in 10-day-old rats, 50% in 15- to 20-day-olds, and not at all in adults. In 4-day-old animals, brain DNA synthesis during seizures, and in survivors, brain weight, DNA, RNA, protein, and cholesterol contents at 7 days of age were reduced less in glucose-treated than in saline-treated littermates. In the saline group, seizures caused a progressive fall in brain glucose level but no fall in blood glucose level, suggesting that glucose transport from blood to brain could not keep pace with glycolytic demands. In glucose-treated rats, blood and brain glucose concentrations remained elevated throughout the convulsive period. There was no reduction of brain adenosine triphosphate levels in either group. Thus, the protection by glucose appears to be related to its roles as a carbon source rather than an energy source. It is concluded that in immature animals, depletion of brain glucose can occur in the absence of hypoglycemia, and may be an important and potentially treatable complication of status epilepticus.
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PMID:Status epilepticus in immature rats. Protective effects of glucose on survival and brain development. 99 45

Two cases of traumatic aneurysm of peripheral cerebral artery were reported. Case 1. A 6-year-old girl was severely injured on her head by automobile accident. Plain skull films showed depressed fracture in the left frontal region. Left common carotid angiogram 25 days after the injury revealed small aneurysm of a cortical branch of the anterior cerebral artery. Cranioplasty and removal of the aneurysm was performed. Postoperative course of this patient was uneventful. Case 2. A 4-year-old girl fell downstaris and struck her left temporal region. On admission, she was unconscious and plain skull films showed multiple linear fractures. No aneurysm was demonstrated in the right common carotid angiogram immediately after the head trauma. Since her general condition gradually improved, she discharged 23 days after the head trauma. 63 days after the injury, she developed sudden onset of severe headache, vomiting, and status epilepticus. Right common carotid angiogram showed a large aneurysm arising from a branch of right pericallosal artery at the free edge of the falx. Parent artery of the aneurysm was clipped. Postoperatively, the patient made uneventful recovery. 60 reported cases of traumatic aneurysm of peripheral cerebral artery were reviewed and analyzed in etiology, diagnosis, clinical course, treatment and pathogenesis.
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PMID:[Traumatic aneurysm of the peripheral cerebral artery]. 103 73

Chlormethiazole (Heminevrin) was successful in controlling fits in seven out of nine episodes of intractable status epilepticus. It was administered as a constant intravenous injection at rates of up to 0.7g/h. No serious side effects were encountered, and the drug deserves wider recognition as a useful therapeutic agent in the management of status epilepticus.
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PMID:Chlormethiazole in treatment of status epilepticus. 113 33

Acute administration of taurine produced a transient loss of susceptibility to photically induced seizures in photosensitive baboons, but failed to affect kindled amygdaloid convulsions in baboons, rats, and cats. In addition, it was totally ineffective in changing the course of spontaneous status epilepticus in kindled cats. These results suggest that a taurine-deficiency model of epilepsy applies only to certain types of seizure-generating conditions, apparently excluding kindled amygdaloid convulsions.
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PMID:Effects of taurine on kindled amygdaloid seizures in rats, cats, and photosensitive baboons. 114 10

The absorption of phenytoin was studied in man. It is concluded that phenytoin absorbed from the intestine is recirculated via the bile, so that blood levels do not accurately reflect absorption. Phenytoin is loosely bound to serum proteins and is found in red cells in concentrations similar to those in plasma. It is rapidly lost from the blood stream after intravenous administration, which is an important factor to be considered in the treatment of status epilepticus.
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PMID:Studies in man of phenytoin absorption and its implications. 115 2

Despite the use of barbiturates, phenytoin sodium and diazepam given intravenously, status epilepticus continued in the three cases described until chlormethizaole (Heminevrin) was administered, when rapid resolution of the status occurred.
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PMID:Chlormethiazole in status epilepticus--three cases. 115 2


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