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At least 19 recordsLinked to original sources

PubMed1999

Assessing the outcomes in patients with nonconvulsive status epilepticus: nonconvulsive status epilepticus is underdiagnosed, potentially overtreated, and confounded by comorbidity.

Nonconvulsive status epilepticus (NCSE) is characterized by behavioral or cognitive change from baseline for at least 30 minutes with EEG evidence of seizures. Categorized into complex partial status epilepticus (with lateralized seizures), and generalized nonconvulsive status epilepticus (bilateral diffuse synchronous seizures), there is debate regarding the diagnosis and morbidity of NCSE. Because EEG is needed for diagnosis, only a high index of suspicion leads to a request for the study, whereas EEG is often unavailable after hours or on weekends. Furthermore, the cognitive changes during NCSE are often incorrectly ascribed to a postictal state, intoxication, psychogenic or psychotic states, and mental retardation. Regarding categorization, present classifications address EEG features but fail to distinguish among depths of coma. Deeply comatose patients (with coma etiologies that themselves carry poor prognoses) are mixed with lightly obtunded patients with no morbidity, confusing the prognosis. Thus, a classification that subsumes depth of coma, and possibly etiology, is sorely warranted. Regarding treatment, comatose NCSE patients treated with benzodiazepines may worsen, whereas generalized nonconvulsive status epilepticus patients may suffer iatrogenically from aggressive treatment (hypotension and respiratory depression) necessitating balancing the potential neurologic morbidity of NCSE against the possible morbidity of IV antiepileptic drugs. A high index of suspicion is needed to initiate EEG studies. Better stratification of level of consciousness will be needed to distinguish among morbidity due to underlying conditions, treatment, and the effects of status epilepticus, proper.

Behavior↗

PubMed2003

Management of status epilepticus.

Status epilepticus is an increasingly recognized public health problem in the United States. Status epilepticus is associated with a high mortality rate that is largely contingent on the duration of the condition before initial treatment, the etiology of the condition, and the age of the patient. Treatment is evolving as new medications become available. Three new preparations--fosphenytoin, rectal diazepam, and parenteral valproate--have implications for the management of status epilepticus. However, randomized controlled trials show that benzodiazepines (in particular, diazepam and lorazepam) should be the initial drug therapy in patients with status epilepticus. Despite the paucity of clinical trials comparing medication regimens for acute seizures, there is broad consensus that immediate diagnosis and treatment are necessary to reduce the morbidity and mortality of this condition. Moreover, investigators have reported that status epilepticus often is not considered in patients with altered consciousness in the intensive care setting. In patients with persistent alteration of consciousness for which there is no clear etiology, physicians should be more quickly prepared to obtain electroencephalography to identify status epilepticus. Physicians should rely on a standardized protocol for management of status epilepticus to improve care for this neurologic emergency.

Anticonvulsants↗

PubMedDate not supplied

Use of midazolam in the treatment of refractory status epilepticus.

Status epilepticus is an epileptic seizure that lasts at least 30 minutes or is repeated at sufficiently brief intervals to produce a continued epileptic condition lasting a total of 30 minutes without the patient fully regaining consciousness. Various combinations of anticonvulsant agents, including benzodiazepines, phenytoin, and phenobarbital, have been used to manage this condition. However, at least 9% of patients with generalized convulsive status epilepticus do not respond to conventional first-line agents, and additional intervention is required. Refractory status epilepticus refers to sustained seizures that do not respond to initial drug therapy and persist longer than 60 minutes. Reports on the response to first- and second-line agents suggest that the incidence of refractory status epilepticus is between 2000 and 6000 cases per year in the United States. Refractory status epilepticus is a major medical and neurologic emergency that requires immediate treatment to avoid significant morbidity and mortality. The anticonvulsive agent midazolam has proved to be effective, well tolerated, and fast acting when used to treat refractory status epilepticus in both adults and children. Its pharmacodynamic effects can be seen within 1 to 5 minutes of administration, and its anticonvulsive effects are apparent as early as 5 to 15 minutes after administration. This article reviews the pharmacology of midazolam and recent clinical reports on the drug's tolerability and effectiveness in the treatment of patients with refractory status epilepticus.

Animals↗

PubMed2006

Anticonvulsant properties of hypothermia in experimental status epilepticus.

Status epilepticus in patients often does not respond to first-line anticonvulsants, and subsequent treatment escalation with continuous intravenous anesthetics may be associated with significant side-effects. Therefore, alternative treatment regimens are urgently needed. Hypothermia has been shown to reduce excitatory transmission and may thus serve as an interesting adjunct in the management of status epilepticus. In the current experiments, three treatment groups were compared. Animals with self-sustaining status epilepticus were treated with external cooling for 3 h, with low-dose diazepam, or with a combination of both. The effect of these regimens on epileptic activity was compared with untreated controls. Animals that underwent cooling were rewarmed, and all animals were monitored for 5 h to assess occurrence and severity of motor seizures and frequency and amplitude of spontaneous epileptic discharges. Cooling alone significantly reduced number and severity of motor seizures but did not alter epileptic discharges. Cooling in addition to low-dose diazepam significantly diminished amplitudes and frequencies of epileptic discharges, while diazepam alone had only a minor reducing effect on discharge amplitudes. However, at later stages of status epilepticus, diazepam significantly reduced motor seizures. Following rewarming, the discharge frequency tended to increase again, suggesting partial reversibility. The current experiments show that in status epilepticus hypothermia exhibits anticonvulsant effects which are most pronounced if co-administered with low-dose diazepam. The results still require confirmation in other animal models and also clinical studies are urgently needed. However, our data indicate that cooling could well become a future adjunct in the treatment of status epilepticus in patients.

Animals↗

PubMed1989

Status epilepticus.

Status epilepticus generally is considered to be a medical emergency requiring immediate intervention to prevent permanent injury to the brain. Tonic-clonic status epilepticus is a very frightening event; the inexperienced parents invariably believe that their child is dying. Emergent management is imperative for convulsive tonic-clonic (grand mal) status epilepticus, but there are nonconvulsive types of status epilepticus in which the problem is more one of correct diagnosis than emergent management. This article reviews aspects of status epilepticus, particularly the classification and treatment of the various types of status.

Anesthesia, General↗

PubMed2002

Management of status epilepticus.

Status epilepticus is a medical emergency, if not treated in time and effectively may cause significant mortality and morbidity. Medical therapy has been the mainstay of treatment but in refractory status surgical resection, multiple subpial transection, electroconvulsive therapy, caudate stimulation and acupuncture play important role. The present operational definition for adults and older children considers status as > or = 5 minutes of continuous seizure or two or more discrete seizures without regaining of full consciousness. Status epilepticus accounts for 1-8% of all hospital admissions for epilepsy. Physiological changes in generalised convulsive status epilepticus include transient or early (0-30 minutes) and late (after 30 minutes) changes. Temporal changes occur as tonic-clonic status epilepticus progresses. Management can be considered in two ways--out hospital management and inpatient management. Benzodiazepine is considered 1st line of treatment outside hospital. Emergency/inpatient management includes basic life support (0-10 minutes) and pharmacological management (10-60 minutes). Drugs used in pharmacological management are lorazepam, midazolam, propofol, phenobarbital, phenytoin, fosphenytoin, i.v. valproate, rectal diazepam, etc. The classical definition of refractory status epilepticus includes seizure that has not responded to sequential treatment of lorazepam, phenytoin or phenobarbitone or seizure continuing > 60-90 in spite of adequate treatment.

Alcohol Withdrawal Seizures↗

PubMed2005

Mechanisms underlying status epilepticus.

Status epilepticus is a state of prolonged or recurrent seizure activity that is associated with significant mortality and morbidity. At a cellular level, status epilepticus results from a failure of normal inhibitory pathways, primarily mediated by gamma-n-aminobutyric acid (GABA) acting via GABA(A) receptors. This loss of inhibitory drive allows the activation of excitatory feedback loops, leading to repetitive, synchronous firing of large groups of neurons. As seizure activity continues, there is further decline in GABAergic function. Continued excitatory input mediated primarily by glutamate leads to neuronal cell death. These alterations in inhibitory and excitatory pathways have important implications for the pharmacologic management of status epilepticus. Currently recommended agents act primarily through the GABA(A) receptor and have been shown to become less effective in status epilepticus of longer duration. Agents designed to inhibit glutamate activity show promise both in the treatment of status epilepticus and in the prevention of associated neuronal injury.

Animals↗

PubMed2006

Stimulus-sensitive burst-spiking in burst-suppression in children: implications for management of refractory status epilepticus.

Status epilepticus refractory to sequential trials of multiple medication is a rare but significant problem in children. We describe stimulus sensitivity arising during the treatment of convulsive status epilepticus in children (stimulus-sensitive burst-spiking in burst-suppression). We reviewed retrospectively clinical and EEG features in six children (three months to ten years), with status epilepticus requiring intensive care, in whom tactile, auditory and visual stimulation induced myoclonic jerks and bursts of EEG spikes. Sensitivity was not present at onset, but appeared after 24 hours as myoclonic jerks of the eyes, face and limbs, irrespective of the modality and site of stimulation. These were associated with burst-suppression in the EEG, the induced spiking forming the burst component. Various antiepileptic drugs, including GABAergic and NMDA blockers had no effect, but halogenated agents (used in two patients) abolished the sensitivity. Two children died, but the remainder returned to their previous clinical state. We conclude that stimulus sensitivity may appear in the context of refractory status epilepticus treated with high-dose barbiturates. Outcome may be more favorable than previously reported in adults, mostly in the context of post-anoxic or toxic coma. Evaluation of ventilated children in status epilepticus should include electroclinical assessment using sensory stimulation. If present, the drug regime should be reviewed and halogenated agents considered.

Anesthetics, Inhalation↗

PubMed2003

New management strategies in the treatment of status epilepticus.

Status epilepticus is a neurologic emergency associated with high mortality and long-term disability. Recent advances in our understanding of the pathophysiological mechanisms involved in the initiation and perpetuation of seizure activity have revealed that status epilepticus is a dynamic and evolving process. Alterations at the cellular level parallel physiological, physical, and electrical changes at the bedside. Loss of cerebral autoregulation and neuronal damage begin after 30 minutes of continuous seizure activity. This understanding has led to changes in treatments of status epilepticus, which must be multidisciplinary and occur simultaneously in many different areas. The goals of pharmacological therapy are to terminate seizures early and prevent recurrence. Two recent large clinical studies have shown the benefit of early administration of benzodiazepines to control status epilepticus. Pharmacological algorithms designed to focus medical management have trended toward earlier and more aggressive treatment. The hope is that continued exploration into the basic mechanisms involved in status epilepticus and future controlled clinical trials defining optimal medical management will produce further advances.

Anticonvulsants↗

PubMed2002

Characterization of pharmacoresistance to benzodiazepines in the rat Li-pilocarpine model of status epilepticus.

Status epilepticus is usually initially treated with a benzodiazepine such as diazepam. During prolonged seizures, however, patients often lose their sensitivity to benzodiazepines, thus developing pharmacoresistant seizures. In rats, administration of LiCl followed 20-24 h later by pilocarpine induces a continuous, self-sustained, and reproducible form of status epilepticus that can be terminated with diazepam when it is administered soon after the pilocarpine injection. However, when administered after a 45 min delay, diazepam is less effective. Previous findings have suggested that the development of pharmacoresistance is related to the stage of status epilepticus. In the present study, we characterized the seizure stage-dependence of diazepam pharmacoresistance. Following administration of different doses of diazepam at varying time intervals after specific behaviorally- and electrographically-defined seizure stages, stage-, time-, and dose-dependent pharmacoresistance to diazepam developed. We also studied two other antiepileptic drugs commonly used in the treatment of status epilepticus, phenobarbital and phenytoin. Consistent with previous studies, our results indicated a similar relationship between stage, time and dose for phenobarbital, but not for phenytoin. Our data are consistent with rapid modulation of GABA(A) receptors during status epilepticus that may result in pharmacoresistance to antiepileptic drugs that enhance GABA(A) receptor-mediated inhibition.

Animals↗

PubMed2004

The management of status epilepticus.

Status epilepticus is a major medical emergency associated with significant morbidity and mortality. Status epilepticus is best defined as a continuous, generalized, convulsive seizure lasting > 5 min, or two or more seizures during which the patient does not return to baseline consciousness. Lorazepam in a dose of 0.1 mg/kg is the drug of first choice for terminating status epilepticus. Patients who continue to have clinical or EEG evidence of seizure activity after treatment with lorazepam should be considered to have refractory status epileptics and should be treated with a continuous infusion of propofol or midazolam. This article reviews current information regarding the management of status epilepticus in adults.

Anticonvulsants↗

PubMed2001

Status epilepticus.

Status epilepticus is a medical emergency that requires rapid and vigorous treatment to prevent neuronal damage and systemic complications. Failure to diagnose and treat status epilepticus accurately and effectively results in significant morbidity and mortality. Cerebral metabolic decompensation occurs after approximately 30 min of uncontrolled convulsive activity, and the window for treatment is therefore limited. Therapy should proceed simultaneously on four fronts: termination of seizures; prevention of seizure recurrence once status is controlled; management of precipitating causes of status epilepticus; management of the complications. This article reviews current opinions about the classification, aetiology and pathophysiology of adult generalised convulsive status epilepticus and details practical management strategies for treatment of this life-threatening condition.

Adult↗

PubMed1981

Pathogenesis of brain lesions caused by experimental epilepsy. Light- and electron-microscopic changes in the rat cerebral cortex following bicuculline-induced status epilepticus.

Status epilepticus was induced in rats by the GABA receptor blocking agent, bicuculline, during artificial ventilation and with closely monitored physiologic parameters. After 1 or 2 h of status epilepticus the brains were fixed by perfusion with glutaraldehyde and processed for light and electron microscopy. In the cerebral cortex two different types of changes were present, i.e., nerve cell injuries and status spongiosus. Type 1 injured neurons, mainly in the areas of most marked sponginess (layer 3), displayed progressive condensation of both karyo-and cytoplasm. In the most advanced stages the nucleus could no longer be distinguished from the cytoplasm in the light microscope, and vacuoles of apparent Golgi cisterna origin appeared in the darkly stained cytoplasm. This type of injured neurons comprised 41 and 56% of the cortical neurons after 1 or 2 h of status epilepticus, respectively. Seven to 9% of the neurons showed another type of injury (type 2). They were mainly located in the deeper cortical layers, and showed slit-formed cytoplasmic vacuoles chiefly due to swelling of the endoplasmic reticulum including the nuclear envelope. Marked sponginess of the cortex developed principally in layer 3 and it spread into deeper layers with longer duration of status epilepticus, but the outermost layers retained a compact structure. As judged by electron microscopy, the sponginess resulted mainly from swelling of astrocytes and their processes causing both perivascular and perineuronal vacuolation. The structural changes observed are considered to be caused by astrocytic and to a lesser extent intraneuronal edema related to the seizure activity. Although the exact pathogenetic mechanisms are not known, our findings indicate that hypoxia-ischemia is not a major determinant of the tissue damage observed.

Animals↗

PubMed1988

Decreased calmodulin kinase activity after status epilepticus.

Status epilepticus was induced in paralyzed, ventilated rats using bicuculline and was maintained for 50 to 120 minutes. Cerebral cortex, hippocampus, and cerebellum were assayed for calmodulin kinase II activity in vitro using [gamma-32P]ATP and polyacrylamide gel electrophoresis. Seizures resulted in a 3.2 fold decrease in calmodulin kinase activity in crude synaptic membranes of cortex and in a 8.2 fold decrease in hippocampal membranes. Cytosolic calmodulin kinase activity was slightly increased in rats in status epilepticus but statistical significance was not reached. Status epilepticus did not affect calcium/calmodulin-dependent kinase activity in cerebellar membranes or cytosol. These data suggest that intense firing associated with continuous seizure activity decreases calmodulin kinase activity in cortical and hippocampal synaptic membranes, which may result in altered neuronal excitability.

Animals↗

PubMed1998

The epidemiology and management of status epilepticus.

Status epilepticus refers to a prolonged seizure state, usually taken as lasting 30 min or longer. This review considers recent studies of the epidemiology of status epilepticus; these have confirmed the high incidence and the high associated mortality and morbidity. Advances in the management of status epilepticus are also reviewed but despite these advances there is still a lack of good comparative studies on which to base treatment regimens.

Anesthetics↗

PubMed1999

Intravenous valproate treatment of generalized nonconvulsive status epilepticus.

Status Epilepticus (SE) is a medical emergency warranting prompt treatment with rapidly-acting antiepileptic drugs. For immediate effect, benzodiazepines are the drugs of choice, but may result in morbidity due to respiratory suppression and hypotension. Nonconvulsive status epilepticus usually does not have significant neurological sequelae, and there is little evidence that generalized nonconvulsive status epilepticus (GNSE) causes lasting neurologic deficits. The risk versus benefit of potentially morbid medications must, therefore, be weighed against the "adverse effects" of GNSE. A patient with frequent episodes of GNSE lasting 4-48 hours had previously been treated with benzodiazepines, but required admission for consequent somnolence. Following intravenous valproate given during EEG monitoring, GNSE broke after 30 minutes. The confused patient returned to a normal cognition and returned home without sequelae. Intravenous valproate may provide an effective treatment alternative to benzodiazepines in GNSE without their associated morbidity.

Adult↗

PubMed1998

Disseminated intravascular coagulation and status epilepticus.

Status epilepticus has been associated with disseminated intravascular coagulation (DIC), but little is known regarding the pathogenesis of this uncommon association. We describe a 41-year-old woman with status epilepticus resulting in death in whom laboratory data demonstrated profound activation of the coagulation and fibrinolytic systems; autopsy findings were consistent with DIC. The occurrence of DIC in status epilepticus may be related to widespread endothelial damage secondary to seizure-induced hyperpyrexia. Body temperature should be closely monitored in patients with prolonged seizures.

Adult↗

PubMedDate not supplied

Status epilepticus.

Status epilepticus is a life-threatening cerebral event. Within 1-2 minutes of seizure onset, massive recurrent cerebral discharges cause autonomic and endocrine dysfunction and loss of normal brain homeostasis. Intracerebral abnormalities become progressively worse and self-perpetuating the longer seizures continue. Seizures lasting 90 minutes or more may cause irreversible injury to selectively vulnerable neurons in the brain and permanent impairment of neurologic function. In addition, status epilepticus is associated with cumulative anoxia that affects almost every major organ system of the body and leads to progressive organ failure. To prevent permanent neurologic injury, the treatment of status epilepticus must be prompt, aggressive, and rational. Stop the seizures, restore homeostasis, perform a thorough diagnostic evaluation to determine the cause of status, and treat definitively.

Animals↗