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PubMed1985

Status epilepticus.

Convulsive status epilepticus is a life-threatening disorder. Every emergency room that treats patients with this problem should have a treatment protocol prepared in advance to allow for prompt and appropriate therapy. The recommended treatment is an intravenous infusion of 20 mg/kg of phenytoin. Lorazepam or diazepam may be used to stop a convulsion in progress. If seizures persist, the second step may be an intravenous infusion of phenobarbital. If convulsions persist beyond the first hour and have not responded to the above, a barbiturate coma should be induced.

Adult↗
PubMed2000

[Psychotropic agents may induce de novo nonconvulsive status epilepticus].

Nonconvulsive status epilepticus (NCSE) shows a prolonged state of confusion and psychosis accompanied by many different kinds of continuous epileptic discharges. NCSE may occur not only in epileptic patients but also in adults with no previous history of epilepsy. Some de novo NCSE may be caused by the administration of psychotropic agents such as antidepressants and neuroleptics and withdrawal from benzodiazepines. However, little attention has been paid to such de novo NCSE in Japan. Previous reports with respect to psychotropic drug-related NCSE were reviewed.

Adult↗
PubMed2001

Effects of benzodiazepines on triphasic waves: implications for nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (NCSE) is often diagnosed based on abolition of rhythmic sharp waves by benzodiazepines. It is possible that sharp waves resulting from metabolic (nonepileptic) encephalopathies may also respond to benzodiazepines and are potentially misdiagnosed as NCSE. The authors hypothesized that triphasic waves (TW) resulting from metabolic encephalopathy are abolished by benzodiazepines. They retrospectively identified patients with TW resulting from metabolic encephalopathy who had EEG recordings before, during, and after benzodiazepine administration. Benzodiazepines were given either because of the possibility of NCSE or for a medically indicated purpose. All patients were diagnosed definitively with a metabolic cause of encephalopathy and not NCSE. Ten patients (mean age, 59 years) met the criteria and were reviewed. TW resolved persistently in four patients and intermittently in six patients. Background activity slowed in five patients and was attenuated in five patients. Unresponsive patients did not arouse and three of five drowsy patients became less responsive. Rhythmic sharp waves resulting from metabolic encephalopathy are abolished by benzodiazepines, similar to NCSE, but without improvement in mental status. This suggests that definitive electrographic diagnosis of primary NCSE should not be based entirely on abolition of sharp waves by benzodiazepines. This also implies that gamma-aminobutyric acid neurotransmission is important in the expression of TW.

Aged↗
PubMed2003

Efficacy of topiramate in children with refractory status epilepticus.

PURPOSE: Status epilepticus (SE) is a life-threatening medical condition associated with significant morbidity and mortality that requires urgent medical intervention. Although several agents are available to treat SE, they occasionally fail to abort seizure activity. Topiramate (TPM) was anecdotally reported to be effective in adult patients with refractory SE. In this study, we evaluated the efficacy of TPM administered to children with this condition. METHODS: We retrospectively reviewed the pediatric SE database at the University of Michigan Medical Center and identified three children with refractory SE who were treated with TPM. Those children failed to respond to treatment with benzodiazepines, phenytoin, phenobarbital, midazolam, or pentobarbital. Additional treatment with TPM was administered by nasogastric tube. All patients were continuously monitored by 21-channel digital EEG machines, and the diagnosis of SE was made by a board-certified neurophysiologist. RESULTS: The ages of the three children were 4.5 months, 34 months, and 11 years. TPM was initiated at 2 mg/kg/day in two children and at 3 mg/kg/day in the third. The status was terminated in all three children within 24 h of maintenance therapy with TPM at 5-6 mg/kg/day. CONCLUSIONS: These results support the potential efficacy of TPM for children with refractory SE. Larger prospective series are needed to confirm those results.

Child↗
PubMed2006

Refractory status epilepticus.

Refractory status epilepticus (RSE) is a common problem in intensive care units and emergency departments. The important risk factor predisposing patients with SE to RSE is delay in receiving treatment. Self-sustaining SE is associated with progressive, time-dependent development of pharmacoresistance. Early termination of convulsive SE by aggressive treatment is the best way to prevent RSE. RSE once develop, requires more aggressive treatment as it is associated with higher mortality and morbidity. To date, no randomized controlled trials have been done for RSE. The most experience exists with coma inducing agents like pentobarbital, midazolam and propofol. New evidence suggests for the possible role of newer AEDs.

Anticonvulsants↗
PubMed1995

Catatonia mimicking nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (NCSE) and catatonia share many clinical features and distinguishing between them on the basis of the physical examination may be difficult and even impossible. Although several reports have been made of NCSE simulating catatonia, there are no published cases of catatonia mimicking NCSE. We report a 24-year-old woman whose initial examination was notable for a fixed stare, no response to voice or command, gaze preference, tonic head posturing, constant stereotypic chewing movements, profuse foamy salivation, and dramatic response to the parenteral administration of benzodiazepines (BZDs). She was initially misdiagnosed as having NCSE. EEG, however, was normal. We believe this is the first published report of catatonia simulating NCSE. The EEg may be more useful than the clinical examination in distinguishing NCSE from catatonia.

Adult↗
PubMed1997

[Status epilepticus].

INTRODUCTION: Status epilepticus (SE) is a condition in which epileptic discharges are sufficiently prolonged or repeated so as to cause persistent changes in neurological function. DEVELOPMENT: At the present time the classification of SE seems to be incomplete and therefore provisional. However the broad subdivision into convulsive SE and non-convulsive SE is still useful in clinical practice when emergency treatment is required. The neuropathological changes are largely determined by the nature (excitory or inhibitory) and the duration of the event which originated the crisis. Tonic-clonic SE is only one of many variants of SE. However, unlike many others, it is a medical emergency which if not suitably treated may lead to permanent neurological damage. Neurone damage and death are the result of a series of parallel processes occurring at a systemic and neuronal level. Outstanding amongst the latter is the activation of a complex neurotoxic cascade. Better understanding of the physiopathological mechanisms occurring in SE would set the stage for a more logical use of treatment. CONCLUSIONS: With advances in the treatment of SE in recent years the prognosis of these patients has improved considerably. However, we should now consider the use of conventional anticonvulsant drugs alone to be insufficient, and that this should give way to polytherapy with neuroprotector agents.

Anticonvulsants↗
PubMed2005

Trafficking of GABA(A) receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus.

During status epilepticus (SE), GABAergic mechanisms fail and seizures become self-sustaining and pharmacoresistant. During lithiumpilocarpine-induced SE, our studies of postsynaptic GABA(A) receptors in dentate gyrus granule cells show a reduction in the amplitude of miniature IPSCs (mIPSCs). Anatomical studies show a reduction in the colocalization of the beta2/beta3 and gamma2 subunits of GABA(A) receptors with the presynaptic marker synaptophysin and an increase in the proportion of those subunits in the interior of dentate granule cells and other hippocampal neurons with SE. Unlike synaptic mIPSCs, the amplitude of extrasynaptic GABA(A) tonic currents is augmented during SE. Mathematical modeling suggests that the change of mIPSCs with SE reflects a decrease in the number of functional postsynaptic GABA(A) receptors. It also suggests that increases in extracellular [GABA] during SE can account for the tonic current changes and can affect postsynaptic receptor kinetics with a loss of paired-pulse inhibition. GABA exposure mimics the effects of SE on mIPSC and tonic GABA(A) current amplitudes in granule cells, consistent with the model predictions. These results provide a potential mechanism for the inhibitory loss that characterizes initiation of SE and for the pharmacoresistance to benzodiazepines, as a reduction of available functional GABA(A) postsynaptic receptors. Novel therapies for SE might be directed toward prevention or reversal of these losses.

Animals↗
PubMed2004

Differential neuroprotective effects of the NMDA receptor-associated glycine site partial agonists 1-aminocyclopropanecarboxylic acid (ACPC) and D-cycloserine in lithium-pilocarpine status epilepticus.

The status epilepticus (SE) induced in rats by lithium-pilocarpine (Li-pilo) shares many common features with soman-induced SE including a glutamatergic phase that is inhibited by NMDA antagonists. The present study determined whether 1-aminocyclopropanecarboxylic acid (ACPC) or D-cycloserine (DCS), both partial agonists of the strychnine-insensitive glycine site on the NMDA receptor ionophore complex, exerted anticonvulsant or neuroprotectant activity in Li-pilo SE. ACPC or DCS were administered either immediately following pilocarpine (exposure treatment) or 5 min after the onset of SE as determined by ECoG activity. SE was allowed to proceed for 3 h before termination with propofol. The rats were sacrificed 24 h following pilocarpine administration. Neither drug had an effect on the latency to seizure onset or the duration of seizure activity. ACPC administered 5 min after SE onset produced significant neuroprotection in cortical regions, amygdala and CA1 of the hippocampus. In contrast, when administered as exposure treatment ACPC enhanced the neural damage in the thalamus and CA3 of the hippocampus suggesting the neuropathology in those regions is mediated by a different subset of NMDA receptors. DCS had no neuroprotectant activity in Li-pilo SE but exacerbated neuronal damage in the thalamus. Neither drug affected the cholinergic convulsions but both had differential effects on neural damage. This suggests that the SE-induced seizure activity and subsequent neuronal damage involve independent mechanisms.

Amino Acids, Cyclic↗
PubMed2001

Short-term outcomes of children with febrile status epilepticus.

Febrile status epilepticus (SE) represents the extreme end of the complex febrile seizure spectrum. If there are significant sequelae to febrile seizures, they should be more common in this group. We have prospectively identified 180 children aged 1 month to 10 years who presented with febrile SE over a 10-year period in Bronx, New York, and Richmond, Virginia. They were compared with 244 children who presented with their first febrile seizure (not SE) in a prospective study done in the Bronx. The mean age of the children with febrile SE was 1.92 years, and of the comparison group, 1.85 years. Duration of SE was 30-59 min in 103 (58%), 60-119 min in 43 (24%), and > or =120 min in 34 (18%). Focal features were present in 64 (35%) of cases. There were no deaths and no cases of new cognitive or motor handicap. Children with febrile SE were more likely to be neurologically abnormal (20% vs. 5%; p < 0.001), to have a history of neonatal seizures (3% vs. 0; p = 0.006) and a family history of epilepsy (11% vs. 5%; p = 0.05) and less likely to have a family history of febrile seizures (15% vs. 27%; p = 0.01) than were children in the comparison group. The short-term morbidity and mortality of febrile SE are low. There are differences in the types of children who have febrile SE compared with those who experience briefer febrile seizures. Long-term follow-up of this cohort may provide insight into the relationship of prolonged febrile seizures and subsequent mesial temporal sclerosis.

Age Distribution↗
PubMed2005

Comparison of neuroprotective effects induced by alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) in lithium-pilocarpine status epilepticus.

The status epilepticus (SE) induced in rats by lithium-pilocarpine (Li-pilo) shares many common features with soman-induced SE including extensive limbic neuropathology. Reactive oxygen species are hypothesized to play a role in the SE induced neuropathology and we propose that the free radical scavengers alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) may be neuroprotective. PBN or S-PBN were administered either immediately following pilocarpine (exposure treatment) or 5 min after the onset of SE as determined by ECoG activity. SE was allowed to continue for 3 h before termination with propofol. The rats were sacrified 24 h following pilocarpine administration. S-PBN induced minor effects to reduce SE duration and improve neurological deficit 24 h following pilocarpine administration. One hundred and fifty milligrams per kilograms PBN administered 5 min after SE onset produced significant neuroprotection in the parietal, occipital, perirhinal and piriform cortices as well as the lateral amygdala. One hundred and fifty milligrams per kilograms S-PBN was neuroprotective only in the occipital and perirhinal cortex while 300 mg/kg S-PBN exacerbated cortical neuropathology. S-PBN administered 5 min after SE onset exacerbated neuropathology in thalamic regions. In contrast, PBN and S-PBN administered as exposure treatment exacerbated neuropathology in thalamic and CA3 regions. The differential neuroprotective effects of PBN and S-PBN may be the result of the poor brain penetration by S-PBN. The results suggest that free radical scavenger activity is neuroprotective in cortical regions during cholinergic convulsions. Regional variations in drug-induced neuroprotectant activity in Li-pilo SE are common and suggest multiple mechanisms of neuropathology.

Animals↗
PubMed2001

Diagnosis and treatment of nonconvulsive status epilepticus.

Nonconvulsive status epilepticus (SE) is not uncommon and comprises at least one-third of all cases of SE. However, nonconvulsive SE consists of very different syndromes, a common feature being the difficulty in making the diagnosis. In this review, nonconvulsive SE is divided into typical absence SE, complex partial SE, nonconvulsive SE in patients with learning difficulties (including electrical SE during sleep, atypical absence SE and tonic SE), and nonconvulsive SE in coma. These conditions have different prognoses and treatments. The diagnosis of these conditions is critically dependent on EEG. When the EEG demonstrates typical ictal patterns, the diagnosis is usually straightforward. However, in many circumstances the EEG has to be differentiated from encephalopathic patterns, and this differentiation can prove troublesome, although the clinical and electrographic response to treatment can prove helpful. Nonconvulsive SE in patients with learning difficulties possibly provides the greatest diagnostic difficulty; the clinical presentation can be subtle resulting in the diagnosis being frequently missed. Whether the neuronal damage that occurs in convulsive SE and in animal models of limbic SE also occurs in nonconvulsive SE in humans is still a matter of debate. There are critical differences between the animal models and the human condition. Indeed, the prognosis of nonconvulsive SE is usually dependent on the underlying aetiology rather than the persistence of electrographic discharges. Because of these doubts, a more conservative approach to the treatment of particular types of nonconvulsive SE (those with a better prognosis) has been taken in this article. Thus, in most instances, oral benzodiazepines for the treatment of typical absence SE and complex partial SE are recommended. In some circumstances intravenous medication is necessary, but in neither condition is anaesthetic coma recommended. This contrasts with nonconvulsive SE in coma in which a more aggressive approach is suggested. Until there are more relevant animal models, and controlled trials of conservative versus more aggressive treatment, treatment regimens for nonconvulsive SE will remain largely speculative.

Anticonvulsants↗
PubMed2001

Time trends in incidence, mortality, and case-fatality after first episode of status epilepticus.

PURPOSE: Status epilepticus (SE) is a medical emergency associated with a high mortality. Clinical series have suggested that mortality after SE has decreased. No studies have systematically examined trends in incidence, mortality, and case fatality after SE in a well-defined population. METHODS: All first episodes of SE receiving medical attention between January 1, 1935, and December 31, 1984, were ascertained through the Rochester Epidemiology Project Records-Linkage System and followed up until death or study termination (February 1, 1996). We calculated incidence rates in the 50-year period (1935-1984), while we considered mortality and case-fatality in the last 30-year period (1955-1984). RESULTS: Incidence of SE increased over time to 18.1/100,000 (1975 through 1984). The increase was related to an increased incidence in the elderly and to the advent of myoclonic SE after cardiac arrest, a condition not seen in the early decades. In the last decade, approximately 16% of the incidence was due to myoclonic SE. The mortality rates increased from 3.6 per year in the decade 1955-1965 to 4.0/100,000 per year between 1975 and 1984. The 30-day case-fatality (CF) was unchanged, although a trend toward improvement was shown after excluding myoclonic SE. CONCLUSIONS: Incidence and mortality rates of SE have increased in the last 30 years. Case fatality remained the same. The increased incidence and mortality are due to the occurrence in the last decade of myoclonic SE after cardiac arrest. The mortality in the elderly was twice that of the youngest age group, across all study periods. Changes in the age and cause distribution of SE over time are responsible for the stable survivorship. There is improvement in survivorship in the last decade when myoclonic SE is excluded.

Age Distribution↗
PubMed1993

Pathophysiological mechanisms of brain damage from status epilepticus.

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.

Animals↗
PubMed1992

Mechanisms in the development of limbic status epilepticus and hippocampal neuron loss: an experimental study in a model of status epilepticus induced by kindling-like electrical stimulation of the deep prepyriform cortex in rats.

A new model of status epilepticus (SE), which was induced by intermittent electrical stimulation (20 Hz for 20 sec every min for 180 min) of the deep prepyriform cortex, has been developed in the conscious rat. SE was induced in 9 of 16 rats in the drug-free group. The number of stimulation trains required to induce SE in this status subgroup was 125.6 +/- 12.7 (mean +/- SEM) and the mean duration of self-sustained seizure activity (SSSA) occurring after cessation of the stimulation session was 295.4 +/- 111.4 min. Some animals showed secondary generalized seizures. Significant cell loss was observed in the hippocampal CA3 pyramidal cell layer ipsilateral to the stimulation site and bilateral CA1 areas in the status subgroup compared with the group subjected to sham operation. In addition, there was a significant negative correlation between the duration of SSSA subsequent to the stimulation session and the total number of intact pyramidal neurons observed in the bilateral CA1 and ipsilateral CA3 subfields of the status subgroup. There were significant differences between the status and non-status subgroups with respect to the number of afterdischarges (ADs) and the total AD duration during the stimulation session. Pretreatment with phenobarbital (30 mg/kg) prevented the development of SE and hippocampal cell loss completely. Pretreatment with MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist (0.25 or 1 mg/kg), also prevented hippocampal cell loss, although it did not block SE generation completely, which suggests dissociation of the mechanisms underlying the development of SE and hippocampal damage. These results indicate that prolonged SSSA actually causes hippocampal damage and it is critically dependent upon NMDA receptor participation.

Animals↗
PubMedDate not supplied

[Intramuscular midazolam in the initial treatment of status epilepticus].

INTRODUCTION: The status epilepticus a serious complication of the epileptic syndrome with high rates of morbidity and mortality. Treatment is aimed to a fast control of the crisis. AIM: To evaluate the efficacy and security of intramuscular (IM) midazolam in the initial treatment of status epilepticus. PATIENTS AND METHODS: A prospective open clinical trial that included 43 status epilepticus in 38 adult patients. All of the cases received an initial dose of 15 mg IM of midazolam, with a simultaneous oral dose of phenytoin (15 to 20 mg/kg) or carbamazepine (15 mg/kg). If there was immediate control of the seizure but recurrence occurred during the next hours, 15 mg im of midazolam every 8 hours were given, for 24 hours. If there was immediate failure intravenous (IV) midazolam was given. RESULTS: 36 of the 43 status epilepticus were controlled: 30 with only one dose, 3 required additional IM doses, and 3 needed administration of IV midazolam, no patient had neither cardiovascular, respiratory or local complications. The only adverse effect was drowsiness in a variable grade. CONCLUSIONS: The use of IM midazolam is suggested as the initial treatment in status epilepticus in adults, especially in a low complexity setting, due to its effectiveness, quick action and security.

Adolescent↗
PubMed1992

[Clinical symptoms and therapy of status epilepticus].

The term "status epilepticus" was first coined in 1824 by Calmeil as this condition had such a poor prognosis. Although still commonly misused today, from the beginning this term actually included all kinds of epileptic seizures, since there are as many types of status epileptici as there are seizure types. Status epileptici are usually triggered by a combination of factors including sleep deprivation, alcohol withdrawal, failure to take medication regularly and fever. In status epilepticus epileptic seizures and EEG discharges initially appear to be no different from isolated seizures. The longer the status epilepticus continues, however, the more atypical the seizures and EEG discharges become. Usually status epilepticus ends gradually. Irreversible damage or fatalities may occur especially in infants or under certain conditions (e.g. long status duration, protracted interval between seizure onset and medical treatment and symptomatic etiology). In most cases benzodiazepines and diphenylhydantoine are the preferred drugs used for treatment.

Anti-Anxiety Agents↗