Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study investigated the clinical and EEG characteristics of initial status epilepticus (SE) during infancy in patients with mesial temporal lobe epilepsy (MTLE). The subjects were six patients who had been brought to our emergency clinic and treated for their initial SE between 1977 and 1988, and later developed MTLE. We reviewed the medical records and laboratory findings at the time of the initial SE, and the clinical evolution up to the development of MTLE. The six patients included four females and two males. The initial SE developed at ages ranging from 7 months to 2 years and 9 months with a mean of 1 year and 2 months. These episodes were characterized by an elevated temperature of more than 38 degrees C (4/6 cases), clusters of prolonged seizures during one episode of SE (4/6 cases), long-lasting SE (120-380 min, mean 227 min, 6/6 cases), postictal prolonged loss of consciousness (median 5 h, 6/6 cases), and the presence of Todd's paralysis (3/6 cases). The lateralization of the ictal or postictal EEGs of the SE in five of the six cases was identical to that of the hippocampal atrophy later confirmed by MRI. Follow-up EEG examinations at a 6 month interval demonstrated temporal spike discharges appearing only after the onset of complex partial seizures. Two patients, who had no fever at the initial SE, were characterized by a very early appearance of epileptic EEG abnormality and a short interval between the initial SE and the development of complex partial seizures, suggesting that the SE was the first epileptic manifestation. The result of this study showed that SE progressing to MTLE tends to have complicated clinical manifestations characterized by clusters of unilateral or generalized SE followed by prolonged postictal unconsciousness, generalized clinical manifestations despite lateralized ictal EEG discharges, and the Todd's paresis in addition to the prolonged seizure duration.
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PMID:Clinical and EEG analysis of initial status epilepticus during infancy in patients with mesial temporal lobe epilepsy. 1201 66

Shire is developing DP-VPA, a prodrug of valproic acid (VPA) licensed from D-Pharm, for the potential treatment of severe forms of epilepsy, including status epilepticus, acute repetitive seizures in children and possibly manic depression and migraine [242649], [385958]; the drug is also being developed for bipolar disorder and migraine prophylaxis [385862]. By March 2000, phase I trials had been completed [359581], [373232] and in October 2000, the compound entered phase II trials for the treatment of epilepsy, bipolar disorder and migraine [385862]; these trials were ongoing in November 2001 [429470]. In October 2001, Shire initiated multicenter, multinational phase II trials of SPD-421 as add-on therapy in the treatment of complex partial seizures [425660]. In February 2002, Shire reported that it planned to make a decision regarding the future of the compound by the second half of 2002 [441819]. DP-VPA is based on D-Pharm's regulation activation of prodrugs (RAP) technology, which designs drugs to be internalized within cells and to be activated only when the tissue becomes diseased. In the case of DP-VPA, the pathological epilepsy process activates it on demand [342433]. RAP-prodrugs are composed of the active drug moiety attached via a chemical linkage to a hydrophobic molecule which allows the agent to penetrate into the cell [182806]. In October 2000, D-Pharrm received patent US-06077837 from the USPTO covering novel 'Prodrugs with enhanced penetration into cells'. This patent claims prodrugs, comprising a pharmacologically active compound covalently linked to an intracellular transporter by a bond which is preferentially cleaved by disease-associated supranormal enzyme activity [385507]. In April 2000, Lehman Brothers predicted the launch of DP-VPA during 2003 [365103]. In December 2001, Lehman Brothers suggested that the product would be approved in 2004. The analysts estimated a 25% probability of the drug reaching the market, and envisaged peak sales of $200 million [434768]. Analysts at Schroder Salomon Smith Barney predicted in March 2002, that sales for Shire of DP-VPA would reach US $9.5 million in 2005, rising to US $31 million in 2006 [449087].
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PMID:DP-VPA D-Pharm. 1213 14

Status epilepticus (SE) is a condition requiring emergency care. There are convulsive SE, non-convulsive SE including complex partial status and absence status, non-convulsive electric SE and pseudostatus epilepticus, although convulsive SE is the most common. Diagnosis of status epilepticus of complex partial seizures (CPS) and absence seizures was significantly delayed because delays in seeking medical attention were common. The seizures were generalized convulsive SE in 84% and CPS status in 16%, and the overall mortality rate was 15% in 41 SE patients of our study. EEG monitoring is important to make or exclude the diagnosis of SE. Diazepam is the first choice medication and effective in the management of SE, and lately, lorazepam, midazolam, propofol and pentobarbital etc as emergency therapy. Phenytoin is also considered first-line agent in the emergency management of SE. Repetitive transcranial magnetic stimulation (rTMS) led to a prolonged latency for seizure induction after an intraperitoneal injection of pentylenetetrazol (PTZ) and effectively prevented the development of status epilepticus of PTZ-induced convulsions in the rats. Our data suggest that rTMS has suppressive effects on the neuronal excitability in rats. These effects are anticonvulsive and suggest the possibility of therapeutic use of rTMS in the patients with refractory seizures.
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PMID:[Treatment of status epilepticus]. 1223 7

Nonconvulsive status epilepticus (NCSE) is much more common than is generally appreciated. It is certainly underdiagnosed, but its presentation is protean. Diagnostic criteria and treatment are controversial. Absence status is characterized by confusion or diminished responsiveness, with occasional blinking or twitching, lasting hours to days, with generalized spike and slow wave discharges on the EEG. Complex partial status consists of prolonged or repetitive complex partial seizures (with a presumed focal onset) and produces an "epileptic twilight state" with fluctuating lack of responsiveness or confusion. There is a clear overlapping of syndromes. Other confused, stuporous, or comatose patients with rapid, rhythmic, epileptiform discharges on the EEG may have "electrographic" status and should be considered in the same diagnostic category. NCSE typically occurs following supposedly controlled convulsions or other seizures, but with persistent neurologic dysfunction despite apparently adequate treatment. Confusion in the elderly or among emergency room patients is also a typical setting. The diagnosis of NCSE usually involves an abnormal mental status with diminished responsiveness, a supportive EEG, and often a response to anticonvulsant medication. All patients have clinical neurologic deficits, but the EEG findings and response to seizure medication are variable and are more controversial criteria. The response to drugs can be delayed for up to days. Experimental models and pathologic studies showing neuronal damage from status epilepticus pertain primarily to generalized convulsive status. Most morbidity from NCSE appears due to the underlying illness rather than to the NCSE itself. Some cases of prolonged NCSE or those with concomitant systemic illness, focal lesions, or very rapid epileptiform discharges may suffer more long-lasting damage. Although clinical studies show little evidence of permanent neurologic injury, the prolonged memory dysfunction in several cases and the similarities to convulsive status suggest that NCSE should be treated expeditiously. The diagnosis is important to make because NCSE impairs the patient's health significantly, and it is often a treatable and completely reversible condition.
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PMID:Presentation, evaluation, and treatment of nonconvulsive status epilepticus. 1260 61

There is a growing number of publications in the recent literature reporting the incidence of non-convulsive status epilepticus in the elderly, including both absence epilepsy and partial epileptic seizures. Absence status epilepticus creates a diagnostic problem because of its clinical features: confusion ranging from slight disorientation to stupor. Duration of such states may vary from one hour to a few weeks, with fluctuations and epileptic features in EEG recording (a typical pattern of spikes-slow waves, 3 Hz frequency, symmetrical and synchronical) that disappear after an intravenous injection of benzodiazepines. Absence status epilepticus can be evoked by toxic, metabolic or pharmacological factors as well as by convulsive epileptic seizures. Besides absence epileptic states of middle-cerebral origin there is a rising concern about absence status resulting from simple or complex partial seizures. Generalized non-convulsive status epilepticus following either simple partial or simple complex seizures is characterized by the presence of various focal signs associated with confusion, stupor or coma. The latter may be masking the clinical picture of an underlying cerebral pathology (e.g. brain tumor, hemorrhage, etc.), and epileptic changes can be seen in EEG recording only. Absence status epilepticus can occur in various forms of brain pathology, including stroke, brain tumors, traumatic lesions and other conditions, as well as in systemic diseases affecting the central nervous system function. Therefore, the authors emphasize the importance of electroencephalography in severely ill and unconscious patients, as well as the role of proper anti-epileptic treatment, as this may improve the outcome.
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PMID:["De novo" non-convulsive status epilepticus in adults and in the elderly]. 1459 57

Acute pathologic neurologic laughter has been described as an ictal phenomenon in epilepsy, as a result of electrical brain stimulation to the cortex and to deep brain structures, in brain tumors, and in stroke. We report what is, to our knowledge, the first report of a case of postictal pathologic laughter. Previously diagnosed with medically refractory complex partial seizures, our patient was admitted to the hospital with phenytoin toxicity. During video-EEG monitoring she experienced multiple brief absence seizures as well as a prolonged episode of absence status epilepticus. Immediately following cessation of the seizure she began to laugh. Her laughter was mirthful and infectious. This lasted several minutes and was followed immediately by several minutes of crying and then a return to normal. We propose that diffuse cortical inhibition led to release of subcortical structures involved in emotional expression. Possible neural substrates of laughter are discussed.
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PMID:Postictal laughter following absence status epilepticus. 1469 18

Based on experimental data from animal studies different theories regarding the size of an epileptic focus have been postulated which range from single pacemaker cells to extended neuronal networks. We report a case which gives further information about the size of a human epileptic focus which can trigger manifest epileptic seizures. We report a 22-year-old man with medically refractory temporal lobe epilepsy. This patient suffered from brief complex partial seizures and frequent epigastric auras. To differentiate a mesiotemporal from a temporolateral seizure origin the patient was implanted with a 10 contact depth electrode from a posterior approach into the right hippocampus, and additional temporobasal/temporolateral subdural strip electrodes. Depth recordings revealed an electrographic status with continuous rhythmic sharp wave activity (1 Hz), the field of which was confined to a diameter of less than 1 cm in the anterior hippocampus, whereas temporobasal subdural strip electrodes did not display this activity. Periodically, spread of this activity occurred to the amygdala, to the posterior part of the hippocampus, and less often to the temporobasal cortex. Most seizure patterns remained subclinical, few of them became symptomatic as partial seizures. This case demonstrates that a hippocampal epileptic focus causing electrographic focal status epilepticus may be limited to a volume of less than 1 cm in diameter. This observation is discussed with regard to implantation strategies and to possible superselective resective or modulatory approaches in the treatment of such limited epileptogenic areas.
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PMID:How large must an epileptic focus be to cause an electrographic status epilepticus--a case report. 1535 69

In order to investigate epilepsy, that is one of the most common neurological disorders, in the last decades different animal models have been proposed. Prevention, diagnosis, treatment and basic knowledge have been improved by the mean of these models. Numerous animal models have been developed in epilepsy research, both for generalized and for simple/complex partial seizures. Animal models for generalized seizures include sensory (light, noise, movement, etc) or electrical stimulations and genetic models. Models for focal seizures include topical or systemic application of pro-convulsive compounds or electrical stimulation. Baboons, mice, rats, rabbits, and Fayoumi chicken have been extensively used in this regard. Since 1983, when magnetic resonance spectroscopy was used to evaluate for the first time in vivo alterations induced by status epilepticus in rabbit, an increasing interest for the neuroimaging perspective has led to new insights in the study of epileptic disorders. In the early 1990s experimental studies provided evidence for the feasibility of magnetic resonance imaging analysis and detection of tissue damage in kainic acid-induced epilepsy in rat. In the following years a wealth of data has been obtained by the mean of functional MRI and/or by diffusion-weighted images. The studies reported in the literature of the last decades indicate in vivo magnetic resonance of epilepsy model as valuable and extremely informative tool.
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PMID:In vivo MRI in different models of experimental epilepsy. 1547 52

In several studies the efficacy and tolerability of levetiracetam (LEV) have been demonstrated. We report two patients who developed nonconvulsive status epilepticus on treatment with LEV. Both patients never experienced status epilepticus before. One patient had a symptomatic epilepsy with complex partial seizures following radiotherapy of astrocytoma in 1985; the second patient had complex partial seizures due to mesial temporal sclerosis. Both patients received LEV 2000 mg/day. We postulate a correlation between occurrence of nonconvulsive status and treatment with LEV. This has not been described before apart from a single report of mentally retarded patients with status epilepticus on high dosages of LEV.
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PMID:Nonconvulsive status epilepticus on treatment with levetiracetam. 1587 54

The electroclinical features of two Thai women with ring chromosome 20 and nonconvulsive status epilepticus (NCSE) were studied. Both have also had generalized tonic-clonic seizures and complex partial seizures of varying frequencies since adolescence. Their intellectual functions were normal. Twenty-four-hour video/EEG telemetry recorded during the NCSE showed fluctuating consciousness between overt unresponsiveness and normal awareness. The EEG consisted of long-lasting generalized rhythmic 3-5 Hz sharp or slow waves with a few spikes, lasting several days. Despite the continuous discharges, the patients had relatively subtle clinical episodes of seizures, during which they were sometimes responsive to verbal stimuli. Intravenous antiepileptic drugs (AED) had little effect on the rhythmic EEG. No lesion in their MRIs contributed to NCSE. Ring chromosome 20 was found in 20% of female karyotype in both patients [46,XX,r(20) (p13 q13)/46,XX] but were negative in four healthy siblings. Oral AEDs decreased more than 75% of the overt CPS episodes in both patients at 22 and 26 months of follow-up but had no effect on the natural history of electrical NCSE. The patients' daily activities were minimally affected by the ongoing electrical discharges. These are the first two cases reported of ring chromosome 20 with NCSE in Thailand. Our patients present a rather benign and pharmacologically responsive course probably because of the low percentage of r(20) mosaicism. The electroclinical correlations in our cases raise the possibility that the mechanism of continuous rhythmic waves in this syndrome may be unrelated to epilepsy. Assessing the severity of this syndrome using both clinical seizures and EEG is crucial.
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PMID:Ring chromosome 20 with nonconvulsive status epilepticus: electroclinical correlation of a rare epileptic syndrome. 1612 50


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