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PubMed1983

Treatment of status epilepticus in adults.

Status epilepticus is a medical emergency requiring immediate treatment. General treatment is aimed at restoring physiologic homeostasis, and drug therapy is aimed at arresting the convulsive activity and preventing its recurrence. Concurrent administration of diazepam and either phenytoin or phenobarbital will be effective in most cases. After the status epilepticus has been treated the underlying cause should be investigated and, if possible, treated.

Acid-Base Equilibrium↗
PubMed2006

Transient and permanent magnetic resonance imaging abnormalities after complex partial status epilepticus.

Epileptic seizures, especially status epilepticus can produce MRI changes. In contrast to convulsive status epilepticus (CSE), permanent parenchymal loss is not well documented with nonconvulsive status epilepticus (NCSE) and the observed MRI changes are transient. We describe a patient with non-lesional right-sided temporal lobe epilepsy with complex partial seizures and repeated episodes of untreated complex partial status epilepticus (CPSE). Diffusion-weighted MRI exhibited marked and extended signal changes within the right temporal, frontal, insular and cingulate regions. The affected areas are considered propagation pathways of temporal lobe epilepsies. After admission, the patient was treated with i.v. antiepileptic drugs. Behavioral, EEG and MRI signal changes resolved. An atrophy of the right temporal lobe not seen in the pre-status MRI examinations was observed 6 weeks after the resolution of MRI hyperintensities. Prior episodes of CPSE had been correctly treated and remained without permanent brain damage. This case report is in favour of immediate and aggressive treatment of partial NCSE in order to avoid irreversible parenchymal loss.

Adult↗
PubMed1993

Systemic effects of generalized convulsive status epilepticus.

Generalized convulsive status epilepticus (GCSE) is accompanied by a marked increase in plasma catecholamines. This produces a number of changes in general systemic physiology including hypertension, tachycardia, cardiac arrhythmias, hyperglycemia, acidosis, and hyperpyrexia. If SE is stopped quickly, these changes are self-correcting and do not produce an increased risk of neuropathology. However, if seizures continue, many of the early physiologic changes reverse, and late status epilepticus is marked by hypotension, hypoglycemia, pulmonary edema and a continued acidosis and elevation of body temperature. Prevention of serious hypoglycemia, maintenance of adequate systemic blood pressure to provide adequate cerebral perfusion, and normalizing the body temperature will minimize or prevent neuropathologic sequelae to SE of extended duration.

Arrhythmias, Cardiac↗
PubMed2000

Status epilepticus: risk factors and complications.

Status epilepticus is common and associated with significant mortality and complications. It affects approximately 50 patients per 100,000 population annually and recurs in >13%. History of epilepsy is the strongest single risk factor for generalized convulsive status epilepticus. More than 15% of patients with epilepsy have at least one episode of status epilepticus and low antiepileptic drug levels are a potentially modifiable risk factor. Other risks include young age, genetic predisposition, and acquired brain insults. Fever is a very common risk in children, as is stroke in adults. Mortality rates are 15% to 20% in adults and 3% to 15% in children. Acute complications result from hyperthermia, pulmonary edema, cardiac arrhythmias, and cardiovascular collapse. Long-term complications include epilepsy (20% to 40%), encephalopathy (6% to 15%), and focal neurologic deficits (9% to 11%). Neuronal injury leading to temporal lobe epilepsy is probably mediated by excess excitation via activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors and consequent elevated intracellular calcium that causes acute necrosis and delayed apoptotic cell death. Some forms of nonconvulsive status epilepticus may also lead to neuronal injury by this mechanism, but others may not. Based on clinical and experimental observations, complex partial status epilepticus is more likely to result in neuronal injury similar to generalized convulsive status epilepticus. Absence status epilepticus is much less likely to result in neuronal injury, and complications because it may be mediated primarily through excess inhibition. Future research strategies to prevent complications of status epilepticus include the study of new drugs (including NMDA antagonists, new drug delivery systems, and drug combinations) to stop seizure activity and prevent acute and delayed neuronal injury that leads to the development of epilepsy.

Adult↗
PubMedDate not supplied

Nonconvulsive status epilepticus: high incidence of complex partial status.

Nonconvulsive status epilepticus may be subdivided into generalized (absence) status and complex partial status. The latter is regarded as a rarity, whereas the former constitutes the dominant part of the hitherto reported cases. We report 10 consecutive cases of adult patients with nonconvulsive status epilepticus, all documented by ictal electroencephalographic (EEG) recordings. Five had a complex partial status; the origin of the complex partial status appeared to be frontal in four of these patients. Three had recurrent complex partial seizures with incomplete recovery between seizures, and two had more continuous symptoms. One of the latter exhibited neither motor phenomena nor automatisms. The effect of diazepam or clonazepam was immediate in all 10 cases though transient in eight. A lasting control of the status was not achieved in six patients until i.v. phenytoin was added. The difficulties in the differentiation between complex partial status and absence status despite ictal EEG recordings are discussed, illustrated by a case with seizure discharges of a focal onset which rapidly generalized. The study indicates that complex partial status may be more common and the clinical expressions of absence status more variable than hitherto recognized.

Adult↗
PubMed1991

Severe forms of status epilepticus.

Severe forms of status epilepticus needing ventilation with or without the need for a general anaesthetic were studied among the children admitted to the paediatric department at Assir Central Hospital, Saudi Arabia. From November 1988 to April 1990, 255 children were admitted because of fits, of whom 12 (4.7%) developed severe status epilepticus and required admission to the intensive care unit for ventilation. This group was studied in detail with regard to past history, course in the hospital and outcome. Five children recovered fully, four were left with neurological disability, and three died. The need to ventilate a patient or give a general anaesthetic for status epilepticus rarely arises in ordinary clinical practice. This study demonstrates the importance of these measures to reduce the risks of permanent neurological deficit and, possibly, death in severe status epilepticus.

Adolescent↗
PubMed2003

Status epilepticus on the intensive care unit.

Status epilepticus occurs on the intensive care unit, either because the patient has been transferred with refractory status epilepticus or as an incidental finding. Management of refractory status epilepticus on the intensive care unit is necessary for adequate treatment of the physiological compromise that occurs in convulsive status epilepticus. In addition, anaesthesia is sometimes necessary for the treatment of status epilepticus, and provided that the potential benefit of anaesthesia offsets the associated morbidity, then such an approach is warranted. In certain instances of nonconvulsive status epilepticus, especially in the elderly, the risks of anaesthesia outweigh the benefits of such aggressive treatment, and thus some caution must be exercised. Status epilepticus is also under-recognised as a cause of persistent coma on the intensive care unit, though the gain from aggressive treatment in this situation is unknown. In most instances, status epilepticus in coma carries such a poor prognosis that aggressive treatment is probably justified. Myoclonic status epilepticus also occurs on the intensive care unit, usually following cardiorespiratory arrest; this does not necessarily represent an agonal event especially if the initial insult was hypoxia related.

Anesthesia, General↗
PubMedDate not supplied

[Non-convulsive status epilepticus].

DEVELOPMENT: Non-convulsive status epilepticus (NCSE) is an epileptic condition lasting more than 30 minutes in which continuous or recurrent seizure activity on the electroencephalogram (EEG) is responsible for diverse clinical symptoms including alteration of mental state, abnormal behaviour, perception disturbances or consciousness impairment. Most authors recognize two types of NCSE depending on the ictal electroencephalographic changes: generalized (absence status epilepticus) and complex partial status epilepticus (CPSE). In addition, there is also a simple form of partial status which is likely underdiagnosed because of its frequent progression to CPSE, subtle and varied symptomatology and high proportion of normal electroencephalograms (EEG). Absence status epilepticus (ASE) may occur in different clinical situations including idiopathic generalized epilepsy (typical AS), symptomatic generalized epilepsy (atypical AS), and elderly subjects without antecedents of epilepsy on chronic treatment with psychotropic drugs (de novo AS of late onset). Furthermore, CPSE is more frequent than previously mentioned. Although initially was equated with temporal lobe status epilepticus, extratemporal cases of CPSE have been well-documented, and the electroclinical characteristics of two types (I and II) of frontal CPSE have been recently described. NCSE may occur in patients with diverse clinical diagnosis such as hypoxic-anoxic encephalopathy, cancer, drugs, autoimmune disorders, Creutzfeldt-Jakob disease, chromosomal alterations, peritoneal dialysis, infections, cerebral hamartomas or head trauma. CONCLUSION: The identification of NCSE may be particularly arduous and, therefore, a high level of suspicion is essential to obtain an early diagnosis. An urgent EEG with administration of intravenous benzodiazepines is considered as the method of choice in the diagnostic evaluation of NCSE.

Anticonvulsants↗
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↗
PubMed1989

Status epilepticus after electroconvulsive therapy.

Status epilepticus is a rare complication of ECT. We describe a patient who suffered a prolonged seizure which required termination with intravenous diazepam. The status epilepticus was not accompanied by motor movements, and the diagnosis was made only because of simultaneous EEG monitoring. The incidence of status epilepticus after ECT may be underestimated.

Acetaminophen↗
PubMed2003

Unilateral cortical necrosis following status epilepticus with hypoglycemia.

Isolated status epilepticus or severe hypoglycemia rarely causes irreversible focal neurologic deficits in children. We describe three children who presented with status epilepticus and prolonged hypoglycemia resulting in hemiplegia due to unilateral hemispheric damage. The non-vascular cortical topography of the lesions is consistent with selective neuronal necrosis, confirmed by histopathology in one patient. This suggests increased neuronal vulnerability to necrosis secondary to energy failure resulting from combination of hypoglycemia and status epilepticus.

Brain Damage, Chronic↗
PubMedDate not supplied

Levetiracetam in porphyric status epilepticus: a case report.

Status epilepticus in patients with acute intermittent porphyria (AIP) are difficult to treat. In this report the author describes a patient with AIP and status epilepticus who was successfully treated with a combination of intravenous magnesium and levetiracetam. This case and the limited experience reported in the literature show that it is probably safe to administer levetiracetam in patients with AIP; however, its role in the treatment of status epilepticus deserves further evaluation.

Anticonvulsants↗
PubMed1995

Subclinical status epilepticus following ECT.

Subclinical status epilepticus is a rare complication of electroconvulsive therapy (ECT). We describe the case of a 70-year-old man with psychotic depression who developed prolonged subclinical status epilepticus following an initial ECT treatment; he subsequently received a course of ECT without complications. It is important to consider status epilepticus in the differential diagnosis of patients who do not regain consciousness following ECT, even in the absence of overt motor seizure activity. The development of this complication does not preclude the future use of ECT; in fact, ECT has been repeated successfully in individuals who developed this complication, including this case. Identification of potential risk factors, appropriate preventive measures, and early intervention are important in the management of this complication. The literature is reviewed and appropriate preventive and treatment measures are discussed.

Aged↗
PubMed2006

The use of levetiracetam in refractory status epilepticus.

Six patients with status epilepticus (SE) of various etiologies refractory to at least two antiepileptic drugs (AEDs) had complete cessation of their seizures following administration of oral levetiracetam (LEV). Seizure types included convulsive, focal, and nonconvulsive status epilepticus. Effective doses of levetiracetam ranged from 500 to 3000 mg/day, achieving seizure control within 12-96 h. No significant adverse events were noted. Adjunctive levetiracetam should be considered for patients with status epilepticus unresponsive to initial therapy.

Adolescent↗
PubMed1995

[Use of intravenous midazolam in status epilepticus in children].

BACKGROUND: Status epilepticus is usually treated by benzodiazepines such as diazepam or clonazepam in association with phenytoin and phenobarbital. Midazolam (MDZ) is a recently developed short-elimination half-life benzodiazepine. CASE REPORTS: Four children, aged 3 days to 4 years, were hospitalized in the pediatric intensive care unit for life-threatening illness and developed status epilepticus. They were given an i.v. bolus dose of 300 to 500 micrograms/kg of MDZ immediately followed by a continuous i.v. infusion at the dose of 100 to 300 micrograms/kg/h. All seizures stopped within 1 hour after the bolus dose administration. No acute adverse events of MDZ were noted. Withdrawal symptoms in one patient were controlled by progressive reduction of MDZ doses. Neurologic sequelae were noted in three children, secondary to their primitive illness. CONCLUSIONS: High doses of MDZ are effective for treating refractory status epilepticus; optimal dosage and duration of treatment remains to be determined.

Anti-Anxiety Agents↗
PubMed2001

The prehospital treatment of status epilepticus (PHTSE) study: design and methodology.

Status epilepticus is a neurological emergency that is typically first encountered and managed in the prehospital environment. Although aggressive pharmacological treatment of status epilepticus is well established in the emergency department and hospital settings, the relative risks and benefits of active therapy for status epilepticus in the prehospital setting are not known. The Prehospital Treatment of Status Epilepticus (PHTSE) study is a prospective, randomized, double-blind, placebo-controlled study designed to address the following aims: (1) to determine whether administration of benzodiazepines by paramedics is an effective and safe means of treating status epilepticus in the prehospital setting and whether this therapy influences longer-term patient outcome, (2) to determine whether lorazepam is superior to diazepam for the treatment of status epilepticus in the prehospital setting, and (3) to determine whether control of status epilepticus prior to arrival to the emergency department influences patient disposition. The initial phase of the PHTSE study began in January 1994 and was completed in February 1999 after the successful enrollment of 205 patients into the three treatment arms. In this paper, we describe the rationale for the conceptualization of the study and details of the study design and methodology, and emphasize some aspects of study implementation that are unique to research involving the emergency medical system.

Adult↗
PubMed1999

Acute cellular alterations in the hippocampus after status epilepticus.

The critical, fundamental mechanisms that determine the emergence of status epilepticus from a single seizure and the prolonged duration of status epilepticus are uncertain. However, several general concepts of the pathophysiology of status epilepticus have emerged: (a) the hippocampus is consistently activated during status epilepticus; (b) loss of GABA-mediated inhibitory synaptic transmission in the hippocampus is critical for emergence of status epilepticus; and, finally (c) glutamatergic excitatory synaptic transmission is important in sustaining status epilepticus. This review focuses on the alteration of GABAergic inhibition in the hippocampus that occurs during the prolonged seizures of status epilepticus. If reduction in GABAergic inhibition leads to development of status epilepticus, enhancement of GABAergic inhibition would be expected to interrupt status epilepticus. Benzodiazepines and barbiturates are both used in the treatment of status epilepticus and both drugs enhance GABA(A) receptor-mediated inhibition. However, patients often become refractory to benzodiazepines when seizures are prolonged, and barbiturates are often then used for these refractory cases of status epilepticus. Recent evidence suggests the presence of multiple GABA(A) receptor isoforms in the hippocampus with different sensitivity to benzodiazepines but similar sensitivity to barbiturates, thus explaining why the two drug classes might have different clinical effects. In addition, rapid functional plasticity of GABA(A) receptors has been demonstrated to occur during status epilepticus in rats. During status epilepticus, there was a substantial reduction of diazepam potency for termination of the seizures. The loss of sensitivity of the animals to diazepam during status epilepticus was accompanied by an alteration in the functional properties of hippocampal dentate granule cell GABA(A) receptors. Dentate granule cell GABA(A) receptor currents from rats undergoing status epilepticus had reduced sensitivity to diazepam and zinc but normal sensitivity to GABA and pentobarbital. Therefore, the prolonged seizures of status epilepticus rapidly altered the functional properties of hippocampal dentate granule cell GABA(A) receptors, possibly explaining why benzodiazepines and barbiturates may not be equally effective during treatment of the prolonged seizures of status epilepticus. A comprehensive understanding of the cellular and molecular events leading to the development, maintenance, and cytotoxicity of status epilepticus should permit development of more effective treatment strategies and reduction in the mortality and morbidity of status epilepticus.

Animals↗
PubMed1999

Basic mechanisms of status epilepticus.

This chapter reviews two main aspects of the basic mechanisms of status epilepticus--acute factors, which are important in inducing status epilepticus in an in vitro brain slice model of status epilepticus, and the acute and chronic epileptogenic consequences of status epilepticus. Status epilepticus is difficult to produce in vitro in normal extracellular medium. This suggests that seizure-terminating mechanisms are normally quite robust. To produce long- duration, self-sustained epileptic discharges in vitro, we have found it necessary to include reciprocally connected entorhinal cortex with our hippocampal slices. Doing so closes the normal excitatory limbic loop in the brain. We found incorporation of the full loop in our brain-slice preparations necessary to bring about epileptic discharges of long duration that fit the definition of status epilepticus. Reentrant activation from distant sites may be necessary for maintenance of status epilepticus-like activity of long duration. Similar requirements may exist for generalized tonic-clonic status epilepticus discharges, but as yet no data support or refute this hypothesis. There are both acute and chronic consequences of an episode of status epilepticus. Acute consequences are alterations in membrane potential and membrane properties of hippocampal pyramidal cells accompanied by alterations in neurotransmitter-activated conductances and receptor expression. Some of these acute alterations in receptor and transmembrane iongradient associated with status epilepticus may be critically involved in the development of drug resistance during the late stages of status epilepticus. Long-term consequences of status epilepticus in the limbic system include alterations in patterns of expression of neurotransmitter receptors and in the function of excitatory and inhibitory synapses, cell loss, and circuit rearrangements within the limbic system. An episode of status epilepticus that involves the limbic system clearly elicits brain damage, at least among adult animals. This brain damage can contribute to the development of epilepsy, or a condition of recurrent, spontaneous seizures. Conversely, development of an epileptic condition enhances the susceptibility of the limbic system to trigger status epilepticus discharges.

Animals↗