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At least 19 recordsLinked to original sources
PubMed1978

Complex partial status epilepticus (psychomotor status).

A 20-year-old mentally retarded woman, who had a history of intractable epileptic seizures since early childhood, had prolonged episodes of confusion, decreased responsiveness and automatic behavior lasting as long as 2 days. These are believed to represent epileptic status of the complex partial (psychomotor) type because the electroencephalogram (EEG) recorded during two such periods showed continuous high amplitude, semirhythmic, 4 to 6 cycles per second (cps), spike activity over both frontotemporal regions; several interictal tracings revealed a consistent spike focus in the right anterior temporal area. Diazepam given intravenously during one such episode terminated both the abnormal behavior and the ictal discharges in the EEG.

Adult↗
PubMed1978

Drug therapy reviews: drug therapy of status epilepticus.

Drug treatment of status epilepticus is reviewed. Tonic-clonic, focal motor, complex partial and absence status epilepticus are discussed. In managing tonic-clonic status epilepticus one should: (1) maintain vital functions at all times, (2) identify and treat precipitating factors and (3) administer an intravenous loading dose of phenytoin sodium or phenobarbital sodium. Careful use of i.v. diazepam sometimes helps to achieve these objectives. Intravenous phenytoin sodium and phenobarbital sodium provide definitive, long-term control of tonic-clonic seizures but must be administered slowly and require time to reach peak brain concentrations. Intravenous diazepam appears to enter and exit from the brain rapidly and may control seizures while therapeutic brain concentrations of long-acting drugs are being achieved. Phenytoin, phenobarbital and diazepam should not be administered intramuscularly in treating status epilepticus. Treatment of focal motor and complex partial status epilepticus is similar to that of tonic-clonic status epilepticus, but i.v. diazepam is required less frequently and loading doses of phenytoin and phenobarbital sometimes can be given more slowly. Status epilepticus of the absence type is managed with i.v. acetazolamide sodium or diazepam. Paraldehyde, muscle relaxants, general anesthesia and lidocaine may be tried when conventional therapies fail.

Anesthesia, General↗
PubMed2024

Drug repurposing in status epilepticus.

The treatment of status epilepticus (SE) has changed little in the last 20 years, largely because of the high risks and costs of new drug development for SE. Moreover, SE poses specific challenges to drug development, such as patient diversity, logistical hurdles, and the need for acute treatment strategies that differ from chronic seizure prevention. This has reduced the appetite of industry to develop new drugs in this area. Drug repurposing is an attractive approach to address this unmet need. It offers significant advantages, including reduced development time, lower costs, and higher success rates, compared to novel drug development. Here I demonstrate how novel methods integrating biological knowledge and computational methods can be applied to drug repurposing in status epilepticus. Biological approaches focus on addressing mechanisms underlying drug resistance in SE (using for example ketamine, tacrolimus and safinamide) and longer-term consequences (using for example omaveloxolone, celecoxib and losartan). Additionally, artificial intelligence platforms, such as ChatGPT, can rapidly generate promising drug lists, while in silico methods can analyze gene expression changes to predict molecular targets. Combining AI and in silico approaches has identified several candidate drugs, including metformin, sirolimus and riluzole, for SE treatment. Despite the promise of repurposing, challenges remain, such as intellectual property issues and regulatory barriers. Nonetheless, drug repurposing presents a viable solution to the high costs and slow progress of traditional drug development for SE. This paper is based on a presentation made at the 9th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures, in April 2024.

Animals↗
PubMed1979

Status epilepticus in childhood: a retrospective study of initial convulsive status and subsequent epilepsies.

A retrospective study was carried out on 261 patients with various epilepsies who had undergone convulsive status epilepticus prior to the subsequent onset of epileptic seizures. 1. Convulsive status epilepticus was found more in partial epilepsy and secondary generalized epilepsy at about the same rate, and evidently less in primary generalized epilepsy. On the average, three-fourths commenced their convulsive disorders with initial status epilepticus. 2. There were free intervals of years following initial status and preceding subsequent epilepsy. The interval was evidently shorter, less than two years, in a majority of patients with secondary generalized epilepsy, whereas the interval was mostly longer, more than six years, in patients with partial epilepsy. 3. The permanent deficient sequelae resulting from initial status were most closely associated with secondary generalized epilepsy. This was also exemplified by the higher rate of atrophic change on CCT. On the contrary, such permanent sequelae were less marked in partial epilepsy especially of complex seizure. 4. It was concluded that secondary generalized epilepsy resulted in cases with more severe brain damage within a relatively shorter interval, whereas complex partial seizure resulted from less severe damage with an obviously longer interval following convulsive status epilepticus.

Adolescent↗
PubMed1976

The use of sodium valproate in a case of status epilepticus.

A child in status epilepticus, who did not respond to intravenous diazepam, was treated with sodium valproate by naso-gastric tube. Subsequent clinical and encephalographic improvement appeared to be related to the sodium valproate, and its value in cases of status epilepticus is discussed.

Child↗
PubMed1978

Rectal administration of sodium valproate in status epilepticus.

Six patients suffering from status epilepticus were refractory to parenteral treatment with either diazepam, amobarbital or both, and were given sodium valproate 200 to 800 mg every 6 hours. The drug was administered rectally as 200 mg lipid-based suppositories, thereby avoiding impaired absorption, which occurs in the presence of paralytic ileus. Plasma levels of sodium valproate in all patients reached the therapeutic range within 36 hours of starting therapy. Seizures were totally controlled in five patients and a 75 percent reduction was noted in the sixth. In two patients, the route of administration was changed from rectal to an equivalent oral dose with continuing control of seizures and minimal change in plasma levels, suggesting that bioavailability is similar for the two forms of the drug. The rectal route of administration was effective in achieving systemic absorption of sodium valproate in the treatment of status epilepticus.

Adolescent↗
PubMed1979

Case report: althesin in status epilepticus.

A case of status epilepticus, resistant to conventional anti-epileptic treatment is described. Althesin rapidly abolished the epileptic activity, and control was achieved by a continuous infusion of Althesin.

Aged↗
PubMed1978

Enzyme histochemistry of the rat hippocampus during experimental status epilepticus.

EEG registered hippocampal status epilepticus (HSE) was provoked in 41 adult albino rats by intraseptal injection of ouabain, and the hippocampus was studied from 1 1/2 to 24 hr with the enzyme histochemical tests for succinic dehydrogenase (SDH), lactic dehydrogenase (LDH), thiaminopyrophosphatase (TPPase), acid phosphatase (AcPase), Mg2+ adenosine triphosphatase (Mg2++ ATPase), and with general and neurohistological stains. In a first group of animals (1 1/2 to 10 hr of HSE), a stage of general increase in enzymatic activity was detected in the pyramidal neurons (SDH, LDH, AcPase, and TPPase). Mg2+ ATPase showed a marked increase in astrocytes. In a second group (more than 10 hr of HSE), SDH was found decreased in the dendritic fields. LDH activity persisted in neuronal bodies, and AcPase and TPPase showed diffuse activity in the cytoplasm of some pyramidal neurons. In a third group (more than 18 hr of HSE), SDH activity was low. No AcPase granules were observed in some pyramidal neurons and TPPase was negative in some areas of pyramidal layer. Mg2+ ATPase reaction showed scare and retracted astroglial processes. These changes were coincident with "cellular ghosts" observed with hematoxylin-eosin techniques of the same samples in the pyramidal field and were interpreted as cellular death, attributed to relative anoxia following neuronal discharge.

Acid Phosphatase↗
PubMed1976

[Etiology and clinic of status epilepticus].

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.

Birth Injuries↗
PubMed1978

Complex partial status epilepticus: case report and proposal for diagnostic criteria.

A child had complex partial status epilepticus after resection of a craniopharyngioma. The status epilepticus was manifested by confusion and documented electroencephalographically by continuous focal seizure patterns in the right temporal region. Complex partial status epilepticus is an electroclinical syndrome of prolonged or repetitive complex partial seizures (with continuous interictal confusion) accompanied by electroencephalographic seizure patterns, which are either focal (usually temporal lobe) or secondarily generalized from a focal pacemaker.

Child, Preschool↗
PubMed1978

Adenosine and cyclic AMP in cerebral cortex of rats in hypoxia, status epilepticus and hypercapnia.

The influence of hypercapnia, hypoxia and status epilepticus on cerebral cortex concentrations of adenosine, adenine nucleotides and cyclic AMP was studied on lightly anaesthetized (70% N2O) and artificially ventilated rats. Neither hypercapnia (arterial PCO2 about 80 and about 300 mmHg) nor hypoxia (minimal values of 19 mmHg) altered tissue concentrations of AMP, cyclic AMP or adenosine. Bicuculline-induced status epilepticus was accompanied by increased concentrations of cyclic AMP but adenosine concentration did not change. Experiments with ischemia, and those in which tissue hypoxia was exaggerated by unilateral carotid artery ligation, showed that tissue adenosine concentrations were elevated only when AMP concentration rose. It is concluded that the marked increase in cerebral blood flow which occurs in hypoxia and status epilepticus is unrelated to changes in tissue adenosine concentration and that the increase in cyclic AMP during neuronal hyperactivity is triggered by other mechanisms than adenosine accumulation.

Adenine Nucleotides↗
PubMed1976

Effects of neonatal status epilepticus on rat brain development.

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.

Animals↗
PubMed1976

Modern concepts of status epilepticus.

Among 60 cases of status epilepticus, there were 45 cases of convulsive status and 15 cases of nonconvulsive or confusional status. In 37 cases, status was due to an identifiable cause. The most frequent etiologic factors were vascular (nine cases), traumatic (seven cases), and metabolic (five cases). Four patients with metabolic encephalopathy had focal status. While the possibility of expanding lesions should be investigated in every case of convulsive status, a complete metabolic screening is also necessary. Non-convulsive status was represented by two cases of psychomotor status and 13 cases of absence status. Clinically, these cases were characterized by various impairments of intellectual functioning and confusion. Diagnosis was determined by characteristic changes in the electroencephalogram. Aggressive treatment is indicated by one or more of the major anticonvulsants, supplemented by adequate oxygenation and maintenance of biochemical homeostasis.

Adolescent↗
PubMed1977

[Status epilepticus in Lennox-Gastaut syndrome; therapeutic aspects].

Therapeutic aspects of convulsive and non convulsive status epilepticus observed in fourteen patients with Lennox-Gastaut syndrome were studied. A temporal relationship between the status epilepticus onset and the beginning of treatment with chlonazepam and diphenylhydantoin was observed; these drugs withdrawal was followed by suppression of symptoms. The possibility of treating status epilepticus by altering the orally administered therapy and leaving parenteral therapy for such cases with progressive impairment of consciousness and/or neuvoregetative disorders was indicated.

Anticonvulsants↗
PubMed1979

The use of althesin in drug-resistent status epilepticus.

The properties of Althesin (anticonvulsant activity, depression of oxygen consumption, lowering of ICP, rapid excretion) led us to use this steroid combination to treat 11 patients in status epilepticus resistant to the standard drugs (benzodiazepines and barbiturates). The administration of Althesin by slow intravenous injection was ineffective in 2 of the 3 patients thus treated. The doses used (2--10 ml) were probably too small. One only administration of a 10% solution of Althesin in 10% fructose by intravenous drip (the rate was calculated so as to obtain the burst suppression stage at the EEG) stopped status epilepticus in 7 of the 9 patients thus treated. In this group the doses used varied from 25 to 50 ml. The 2 patients in whom it was necessary to repeat Althesin administration and combine it with other drugs had both been operated on for severe brain injuries involving marked cerebral edema. In spite of the very small number of cases, the definitive arrest of status epilepticus obtained in 8 out of 11 patients first treated with other drugs is encouraging: Althesin probably may be regarded as an adjunct in the treatment of status epilepticus.

Adolescent↗
PubMed1977

Mesial temporal haemorrhage, consequence of status epilepticus.

A 52 year old woman developed a severe encephalopathy with status epilepticus of six days duration in the terminal course of an acute hepatitis associated with hyperammonaemia and hyperventilation. Acute haemorrhagic lesions were observed in the brain, involving symmetrically both amygdala and cornu Ammonis. The sequential occurrence of these lesions with status epilepticus are discussed in the light of data from the literature.

Amygdala↗
PubMed1978

Myoglobinuria and renal failure after status epilepticus.

Acute renal failure developed in a 28-year-old man after status epilepticus. Myoglobinuria was contributed to by convulsions, trauma and coma during status epilepticus, the three mechanisms responsible for this condition.

Acute Kidney Injury↗