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PubMed2006

Update on the acute management of status epilepticus in children.

PURPOSE OF REVIEW: Status epilepticus is the most common neurologic emergency in children. The understanding of its less recognizable forms, its pharmacologic management, the role of electroencephalography and the long-term morbidity and mortality as a result of status epilepticus are consistently evolving. This review frames the current understanding of several issues as they apply to acute management in the emergency department. RECENT FINDINGS: Researchers are working to define less recognizable forms of status epilepticus such as nonconvulsive, autonomic and psychogenic. Buccal and intranasal forms of midazolam are emerging as suitable alternatives to rectal diazepam in the initial treatment of status epilepticus. Valproic acid, chloral hydrate and newer-generation antiepileptics are being proposed as safe and effective alternatives to the traditional drugs used to treat status epilepticus. The role of electroencephalography in diagnosis is being elucidated. Risk factors for neurologic sequelae and mortality after status epilepticus remain an area of research with conflicting findings and no real consensus. SUMMARY: The understanding of different types of status epilepticus, the options for pharmacologic treatment, the tools for diagnosis and the morbidity and mortality of the disease are still evolving. As a result, several areas for further research remain that will help clinicians in their approach to this complex condition.

Acute Disease↗
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↗
PubMed1993

Convulsive status epilepticus in children.

Status epilepticus (SE) occurs most commonly in infancy and childhood. Children with prior neurological abnormalities are most susceptible. More than 90% of cases are convulsive and the majority are generalized. SE may occur in the setting of an acute illness, in patients with established epilepsy or as a first unprovoked seizure. The etiology can be classified as idiopathic, remote symptomatic, febrile, acute symptomatic, or associated with a progressive encephalopathy. The morbidity and mortality of status have dramatically declined in recent years. Overall mortality in recent pediatric series was 3-10%, with almost all fatalities associated with acute central nervous system insults or progressive neurologic disorders. Neurological sequelae in children with idiopathic or febrile status are rare. Neurologically normal children with SE as their first unprovoked seizure have the same risk of experiencing subsequent seizures of any type as children who present with a brief first seizure. The risk of recurrent episodes of convulsive SE approaches 50% in neurologically abnormal children but is very low in neurologically normal children. The favorable outcome of SE in children may be related to advances in therapy and to the resistance of the immature brain to damage from seizures.

Adult↗
PubMed1997

[Neurophysiology in status epilepticus].

Cases of status epilepticus (SE) require rapid diagnosis and treatment, including simultaneous, coordinated clinical and neurophysiological assessment. The EEG is the essential diagnostic support that confirms the presence of SE and allows for its differentiation from other processes, and the characterization of type and evolutionary phase, while elucidating situations such as covert SE and nonconvulsive SE whose clinical expression is scarce and diagnosis and management difficult. Finally, EEG monitoring serves to guide treatment and recognize when crises have passed, evaluate drug response and monitor the differed evolutionary control of SE.

Diagnosis, Differential↗
PubMed2002

Mitochondrial dysfunction associated with neuronal death following status epilepticus in rat.

Status epilepticus (SE) in humans and animal models results in significant cerebral damage and an increased risk of subsequent seizures, associated with a characteristic pattern of neuronal loss particularly affecting the hippocampus. Seizure related cell death is considered to be excitotoxic, but studies have been limited, concentrating on terminal events rather than initial mechanisms. We have studied the biochemical events in the first few days following SE. Self-sustaining limbic SE was induced in adult rats using perforant path stimulation, and animals were allowed to recover. Biochemical studies were performed at 16, 44 h and 8 days following SE, using spectrophotometric enzyme assays and HPLC on regional brain homogenates compared with those from sham-operated controls. Haematoxylin and eosin histology was also undertaken at each time point. Brain aconitase and alpha-ketoglutarate dehydrogenase (alphaKDH) activity were both significantly (P<0.05) reduced by approximately 20% in the first 16-44 h following status, but had returned to normal by 8 days. These enzymes are part of the tri-carboxylic acid (Krebbs) cycle in the mitochondrial matrix, and are known to be sensitive to free radical, especially peroxynitrite damage. There was a similar decrease in reduced glutathione levels. Histological studies confirmed evidence of acute neuronal damage up to 44 h, and neuronal loss by 8 days. This is the first in vivo demonstration of this pattern of mitochondrial dysfunction and loss of brain glutathione following SE. The pattern of abnormalities is consistent with reversible mechanisms being involved in excitotoxic cell damage. This, together with the timing of changes, suggests new avenues for therapeutic intervention.

Animals↗
PubMed2003

Status epilepticus: emergency management.

Status Epilepticus (SE) is a medical emergency and requires prompt and aggressive treatment. Stabilization of airway, breathing and circulation and expeditious termination of seizures are immediate goals. Intravenous benzodiazepines-diazepam, midazolam or lorazepam and phenytoin are the first line drugs recommended for termination of seizures. Diazepam (or midazolam), thiopental and propofol infusion are useful for control of Refractory SE (RSE). Newer drugs are being investigated for use in SE. We prefer diazepam infusion. In children the mortality from SE ranges from 3-10% and the morbidity is twice. Mortality and morbidity are highest with SE associated with CNS infections, which is the most important cause of SE in our country. The outcome depends on the underlying etiology, age, rapidity of SE and adequacy of care. Adherence to a time-framed protocol in the emergency department helps in improving the final outcome.

Anticonvulsants↗
PubMedDate not supplied

[Status epilepticus in childhood].

Status Epilepticus (SE) is defined as an epileptic seizure which is so frequently repeated or so prolonged as to create a fixed and lasting epileptic condition. SE is observed in all age groups, but its frequency increases among younger children. Etiological factors vary with age. During infancy acute encephalopathies (infectious, anoxic-ischaemic, metabolic, etc.) are prevalent, while later non progressive encephalopathies are more frequent. Cryptogenic cases are present in all age groups, but "febrile" cases are observed before two years of age. Generalized forms are rare. The most frequent SE is Unilateral non alternating, which is observed exclusively among children. The semeiological diagnosis of SE with the help of EEG monitoring can be useful, since some forms of SE have constant etiological factors and prognosis. Since the condition of SE may cause brain damage or even endanger patient's life, immediate and adequate treatment is necessary. Diazepam and Phenytoin are particularly effective for stopping the seizures. A practical scheme for treatment is presented.

Adolescent↗
PubMed1999

The effect of alpha-phenyl-N-tert-butyl nitrone on bioenergetic state in substantia nigra following flurothyl-induced status epilepticus in rats.

Status epilepticus (SE), i.e. ongoing seizures of more than 30 min duration, gives rise to bilateral pan-necrotic lesions of the substantia nigra, pars reticulata (SNPR). These are known to be preceded by an initial increase, followed by a depression of metabolic rate, and by failure of the bioenergetic state, suggesting mitochondrial dysfunction. We have previously shown that the spin trap alpha-phenyl-N-tert-butyl nitrone (PBN) prevents the lesions caused by 45 min of SE from occurring, in spite of ongoing seizure activity. In this article, we demonstrate that PBN, given 30 min before seizure induction, reduces or prevents the decrease in ATP concentration and adenylate energy charge, without significantly reducing the amount of lactate accumulated, or the decrease in intracellular pH (pHi). The results suggest that the spin trap nitrone preserves the structural and functional integrity of SNPR neurons by protecting the mitochondria against oxidative damage.

Animals↗
PubMed1990

Status epilepticus: epidemiologic considerations.

Status epilepticus (SE) will occur in 50,000 to 60,000 individuals in the United States annually: one third as the presenting symptom in patients with a 1st unprovoked seizure or with epilepsy, one third in patients with established epilepsy, and one third in individuals with no history of epilepsy. The greatest number of cases will occur in children, although the risk is equally high in the over-60 population. In patients with epilepsy, SE is more likely to occur in those with partial seizures and in those with remote symptomatic epilepsy. The presence of a preexisting neurologic abnormality is associated with an increased risk of SE in those with acute systemic insults. There is a high mortality reported, but this is related predominantly to the underlying condition. The 1 to 2% mortality attributed to SE probably reflects an overestimation of the risk. There is an increased risk of seizures and of intellectual dysfunction following the occurrence of an episode of SE, although the causal association is not clear. Individuals with epilepsy who experience an episode of SE probably have a lower likelihood of remission of epilepsy.

Brain Diseases↗
PubMed2001

Temporal and spatial patterns of DNA fragmentation following focally or systemically-evoked status epilepticus in rats.

Status epilepticus (SE) triggers neuronal degeneration comprised of both necrotic and apoptotic components. Here we determined whether internucleosomal DNA fragmentation reflects the severity of SE-induced neuronal damage. We utilized both a systemic (kainic acid) and a focally-induced model of SE in rats. DNA fragmentation was analyzed in rhinal cortex and hippocampus at various time points following SE episodes of varying durations (30-120 min). Radioactively labeled DNA fragments were analyzed by agarose gel electrophoresis and quantified by liquid scintillation counting. The spatial and temporal characteristics of the SE-evoked DNA fragmentation indicated that this marker of apoptosis appears as early as 8 h after SE and reaches peak expression at 48 h. This method permitted us to quantitatively monitor the evolution of the apoptotic component of cell death over the acute post-injury period (8-72 h). Moreover, in both models of SE, the DNA fragmentation varied directly as a linear function of the duration of SE between 30 and 120 min suggesting that this marker should be highly responsive to neuroprotective intervention.

Animals↗
PubMedDate not supplied

Midazolam treatment of acute and refractory status epilepticus.

Generalized convulsive status epilepticus (GCSE) is a medical emergency requiring prompt resolution. Acute treatment is often delayed by difficulty in obtaining intravenous (i.v.) access. Refractory GCSE is often difficult to treat, and traditional therapy with barbiturates induces hypotension and respiratory depression and prolongs recovery. Midazolam is particularly useful for treating acute GCSE because it has an imidazole ring that is open at low pH, allowing it to be dissolved in aqueous solution for intramuscular injection, but closed at physiologic pH, increasing lipophilicity and rendering good intramuscular absorption, brain penetration, and fast onset of action. When given intramuscularly as a 0.2 mg/kg bolus, it has efficacy at least equal to that of i.v. diazepam, is well tolerated, induces little respiratory compromise, and has a shorter latency to onset of action. Therefore, it should be considered for the treatment of acute GCSE when i.v. access is problematic. For refractory GCSE, continuous i.v. midazolam infusion at 0.1-0.6 mg/kg/hr after a 0.2 mg/kg i.v. bolus is effective and has advantages over traditional therapies because it induces less hypotension and cardiorespiratory depression and can be easily titrated. Further prospective studies are needed to define the role of continuous i.v. midazolam compared to other contemporary therapies.

Acute Disease↗
PubMed2001

Treatment of status epilepticus in children.

Status epilepticus (SE) is a condition characterised by frequent and prolonged epileptic seizures which frequently develop in the immature brain. Fever, metabolic disorders and subtherapeutic concentrations of antiepileptic drugs are the most common factors precipitating SE in children. Progressive neuronal damage occurs if convulsive SE persists for more than 30 minutes, with neurological, epileptic and cognitive sequelae. Unfortunately, the immature brain is more predisposed to SE and its sequelae than the mature brain. SE may be categorised as convulsive, nonconvulsive or neonatal according to its responsiveness to antiepileptic drugs. Regardless of category, the main objective in the treatment of SE is to abort the seizures and treat the inciting condition. Treatment includes: (i) monitoring of hydration, electrolyte balance, and cardiocirculatory and pulmonary functions; and (ii) rapid intravenous administration of specific antiepileptic drugs. Benzodiazepines (usually diazepam, lorazepam or midazolam) are the most effective agents for the initial treatment of convulsive and nonconvulsive SE. In particular, midazolam infusion is an effective and well tolerated therapeutic approach for the management of childhood SE, including refractory SE. Phenytoin remains an excellent agent because of its long duration of action, but it is not active in nonconvulsive SE. Fosphenytoin, a phenytoin prodrug, represents a significant advance in the treatment of children with convulsive SE. Intravenous phenytoin and intramuscular phenobarbital (phenobarbitone) are generally used in neonatal SE; other agents are rarely used.

Anti-Anxiety Agents↗
PubMed1997

[Status epilepticus in childhood].

Status epilepticus (SE) is one of the most common emergencies in pediatric neurology and it is associated with high mortality and morbidity. SE is more frequent in children than in adults. SE occurs in variety of settings especially in children-infections, patients with previously established epilepsy, cerebral malformations, hypoxia, hypoglucemia and head trauma- but in many cases SE can present as a first unprovoked seizures. Being better known the convulsive SE, non-convulsive SE that may present the same complications as the convulsive SE may be found in many patients. The mortality associated with SE in children is between 3 and 7%. The mortality and morbidity is estimated very high in the refractory SE. Although SE is defined as more than 30 min of continuous seizure activity, antiepileptic drug administration should be considered whenever a seizure has lasted 10 min. Initial therapeutic and etiological diagnostic have be conducted simultaneously. The commonest lines for treating SE and SE refractory are shown. The SE treatment should be managed including the ABCs of vital functions-supporting respiration, maintaining blood pressure, gaining access to circulation, electrolyte levels, renal and hepatic functioning and glucose levels- as well as a prompt administration of appropriate drugs in adequate doses. The different antiepileptic drugs that can be administered to the SE treatment are presented as well as the pharmacologic peculiarities, route of choice for drug administration, doses and risks of the traditional and the new antiepileptic drugs.

Anticonvulsants↗
PubMed1999

Status epilepticus: an overview of the clinical problem.

Status epilepticus has been recognized since antiquity. The terms état de mal and "status epilepticus" are derived from the slang used by epilepsy patients housed in Salpêtrière and Bicêtre hospitals in Paris during the 1800s. The definition of status epilepticus has been evolving, and is still not precise. In 1903-04 it was described as a development of epilepsy in which seizures are so frequent that "coma and exhaustion are continuous between seizures." In 1964 the International League Against Epilepsy adopted the definition "a seizure [that] persists for a sufficient length of time or is repeated frequently enough to produce a fixed and enduring epileptic condition." 30 min has been the most common specified duration of seizures for the diagnosis of status epilepticus, although a duration of 10 or 20 min has been suggested as well. However, a new set of definitions for generalized, convulsive status epilepticus in adults has been proposed and includes an operational definition (specifying a seizure duration of a least 5 min) and a mechanistic definition. In the future, laboratory tests will provide the means for detecting and defining the critical factors that distinguish a single epileptic seizure from status epilepticus. Recent epidemiological studies suggest status epilepticus occurs in 100,000 to 150,000 people in the US each year, and is associated with substantial morbidity and mortality. Etiology, duration of the seizures, and the patient's age seem to be important determinants of the outcome in status epilepticus.

Adult↗
PubMed2006

Nonconvulsive status epilepticus and neurodevelopmental delay.

Nonconvulsive status epilepticus is characterized by continuous or near continuous epileptiform discharges on electroencephalography without overt motor or sensory phenomena. It is a symptomatic condition related to a disease such as epileptic encephalopathy or a metabolic disorder. Children with isolated nonconvulsive status epilepticus rarely present with global neurodevelopmental delay. This report describes an 18-month-old male who presented with global neurodevelopmental delay and decreased alertness in whom electrical status epilepticus during sleep, which is a form of nonconvulsive status epilepticus, was determined. Metabolic investigations and cranial magnetic resonance imaging were normal. He began to achieve developmental milestones after treatment with valproic acid. Although rare, pediatric neurologists and pediatricians must be aware of this condition in making the differential diagnosis of global neurodevelopmental delay and decreased alertness.

Anticonvulsants↗
PubMed2003

[Status epilepticus].

The review defines status epilepticus and discusses treatment options for convulsive and nonconvulsive status epilepticus. The drug of choice in Norway is diazepam intravenously (0.25 mg/kg), followed by phosphenytoin or sodium valproate intravenously and barbiturate narcosis. Other treatment options are discussed. Underlying causes must be addressed for therapeutic intervention. Given early treatment, the prognosis is generally good.

Adult↗
PubMed1983

Status epilepticus: frequency, etiology, and neurological sequelae.

Status epilepticus is associated with high mortality and is a predictor of poor neurological outcome; yet the contribution of prolonged seizures to mortality and the causal sequence for neurological damage remain unclear. Many cases of status epilepticus are precipitated by illnesses that themselves are associated with increased mortality and morbidity. In studies of children, status epilepticus appears to be no better a predictor of an adverse outcome than is any seizure disorder starting at a similar age. Status epilepticus is a condition in which fast and definitive medical intervention is warranted. Random assignment to treatment groups is difficult. Evaluation of the effect of duration of seizures is also difficult, because those patients responding promptly to treatment may be quite a different population than those not responding. The study of cases of "nonconvulsive" status may provide information regarding the effect of these continuing ictal brain discharges, which can be evaluated without the confounding effects of concomitant metabolic (e.g., anoxic, pH, electrolyte) disturbances that accompany most cases of generalized status epilepticus. It is possible that appropriately designed prospective studies of status epilepticus and/or case-control studies will assist in evaluating the contribution of a prolonged seizure per se over and above that associated with preexisting or concurrent illness.

Adolescent↗
PubMed1998

Electroencephalographic and histological characteristics of a model of limbic status epilepticus permitting direct control over seizure duration.

Status epilepticus is a neurological emergency associated with substantial morbidity and mortality. Experimental and clinical investigations suggest that prolonged seizure activity is associated with injury to vulnerable neurons. Compounds with neuroprotective properties may minimize such injury. Existing methods of inducing experimental status epilepticus result in seizure activity of variable duration and neuronal injury of variable degree. To minimize such variability, status epilepticus may be stopped with anticonvulsants, but this limits the ability to screen for independent neuroprotective properties. We have developed a simple and reliable non-pharmacological model of limbic status epilepticus in which the duration of status epilepticus is under direct experimental control. Status epilepticus is induced by continuous, unilateral hippocampal stimulation. Using this model, the degree of hippocampal pyramidal cell injury varies in direct proportion to status epilepticus duration across a range of 15-140 min. A progressive sequence of EEG changes unfolds with increasing status epilepticus duration, resembling that seen in other models. This model may serve as a reference against which the effects of potential neuroprotective compounds can be studied.

Animals↗