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)

Status epilepticus developed in four dogs, 2 to 3 days after ligation of an extrahepatic portosystemic shunt. Pentobarbital or phenobarbital intravenously was required to control seizure activity. Two dogs treated with phenobarbital recovered. Exacerbation of hepatic encephalopathy secondary to metabolic changes after surgery may be a cause of this syndrome. A treatment protocol for status epilepticus after ligation of a portosystemic shunt is proposed.
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PMID:Status epilepticus after ligation of portosystemic shunts. 226 77

We studied nine patients with status epilepticus refractory to standard therapy. In all patients so treated, IV pentobarbital terminated seizure activity. Mortality was high (77%) in those treated, but was attributed to underlying pathology and possibly to duration of status epilepticus. Pentobarbital therapy should be initiated within 0 to 2 hours after onset of seizures, with continuous EEG monitoring in an intensive care unit.
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PMID:Pentobarbital treatment of refractory status epilepticus. 382 47

During an infusion of thiopentone to control status epilepticus secondary to hypoxic brain damage, thiopentone and pentobarbitone levels were measured in the serum and cerebrospinal fluid (CSF). Pentobarbitone was found to be present in the serum between 7.8 and 11.1% of the thiopentone levels. There was a prompt response in serum levels of thiopentone to changes in the infusion rate. The CSF thiopentone varied between 15 and 40% of the serum levels. The CSF anticonvulsant threshold for thiopentone for this patient was between 5 and 15 mg/litre.
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PMID:Plasma and cerebrospinal fluid barbiturate levels during prolonged continuous thiopentone infusion. 709 8

In this experiment, a new model of partial status epilepticus (SE) is described which is based on the antecedent development of a kindled focus. Following kindling, the amygdala was stimulated continuously for 60 min with the previous kindling stimulus (60 Hz sine wave, 50 microA peak-to-peak). This treatment provoked SE in 22 of 35 rats. Without drug intervention, rats spontaneously recovered (SR group) from the seizure between 10 and 24 h. After recovery from SE, after discharge (AD) thresholds were elevated and remained so for the 2 weeks before sacrifice. The histologies of these SR rats indicated massive gliosis and degeneration of the ipsilateral hemisphere, extending from the medial olfactory bulb, through the amygdala-pyriform cortex to the ventral hippocampus. Damage was observed frequently in the midline thalamic nuclei and hippocampal CA1 fields. Interruption of the SE with Nembutal 30 min after the stimulation offset (30 Min group) was occasionally associated with slight gliosis at the kindled electrode, whereas interruption after 4 h of SE (4 Hr group) resulted in more extensive cell loss. The AD thresholds of the 30 Min group, like those of the rats which did not develop SE (NSE group), returned to near-normal values by 2 weeks after SE; only the NSE rats exhibited generalized seizures to their AD threshold stimulus. This model of SE results in brain pathology similar to that found in other models, but has the advantage of being uncontaminated by exogenous chemicals and toxins.
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PMID:A new model of partial status epilepticus based on kindling. 713 21

We report our experience using lidocaine to determine the epileptic focus in a case of refractory status epilepticus associated with an aberrant intracranial shunt tube. Pentobarbital anesthesia rapidly suppressed convulsions. However, whenever the pentobarbital was decreased, the status epilepticus was resumed. The seizure looked primarily generalized both clinically and electroencephalographically, but EEG monitoring with intravenous administration of lidocaine demonstrated that the ictal waves began from the right anterotemporal area, where the shunt valve and tube were placed. Removal of the shunt tube and the surrounding scar tissue eliminated status epilepticus. Our result suggests the excellent efficacy of lidocaine to distinguish secondarily generalized status epilepticus from primarily generalized one.
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PMID:[A case of refractory status epilepticus associated with aberrant intracranial shunt tube: efficacy of lidocaine in the determination of the epileptic focus]. 807 95

Pentobarbital coma (PBC) is a treatment for patients with refractory status epilepticus, but there are currently few guidelines for choosing when to initiate or continue this therapy. To identify potential prognostic factors in this setting, we reviewed the course of 17 adult patients treated with a standardized protocol of PBC for refractory status epilepticus over the past 6 years. PBC was extremely effective in aborting seizures in 16 of 17 patients, but 11 of the patients developed severe hypotension that required therapy with vasopressors. Six of the patients had full recoveries or developed only minimal residual deficits following PBC, two developed severe neurologic deficits, and nine died. Survival was associated with a history of epilepsy, absence of multiorgan failure before or during PBC, age < 40 years, and absence of hypotension requiring vasopressors during PBC. Long-term follow-up in seven of eight survivors (mean, 2.9 years; range, 1 to 5 years) showed that patients' conditions remained stable after discharge from the hospital. Thus, although PBC is effective in controlling ongoing seizures, the therapy frequently leads to significant hypotension. This side effect may be especially troublesome in patients with the negative prognostic indicators identified in this study. These findings highlight the need for alternative approaches in the management of these patients.
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PMID:Prognostic factors of pentobarbital therapy for refractory generalized status epilepticus. 816 54

1. The authors examined the anticonvulsant effects of MK-801 on the pilocarpine-induced seizure model. Intraperitoneal injection of pilocarpine (400 mg/kg) induced tonic and clonic seizure. Scopolamine (10 mg/kg) and pentobarbital (5 mg/kg) prevented development of pilocarpine-induced behavioral seizure but MK-801 (0.5 mg/kg) did not. 2. An electrical seizure measured with hippocampal EEG appeared in the pilocarpine-treated group. Scopolamine and pentobarbital blocked the pilocarpine-induced electrographic seizure, MK-801 treatment augmented the electrographic seizure induced by pilocarpine. 3. Brain damage was assessed by examining the hippocampus microscopically. Pilocarpine produced neuronal death in the hippocampus, which showed pyknotic changes. Pentobarbital, scopolamine and MK-801 protected the brain damage by pilocarpine, though in the MK-801-treated group, the pyramidal cells of hippocampus appeared darker than normal. In all treatments, granule cells of the dentate gyrus were not affected. 4. These results indicate that status epilepticus induced by pilocarpine is initiated by cholinergic overstimulation and propagated by glutamatergic transmission, the elevation of which may cause brain damage through an excitatory NMDA receptor-mediated mechanism.
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PMID:MK-801 augments pilocarpine-induced electrographic seizure but protects against brain damage in rats. 906 77

To report a case in which triphasic waves developed during pentobarbital treatment. Pentobarbital coma is indicated in status epilepticus, refractory to other anticonvulsants, and in certain neurologic conditions in order to decrease brain metabolism. At high doses of pentobarbital, the EEG shows a typical burst-suppression pattern, while at low doses, diffuse slowing. Triphasic waves have not been reported in association with pentobarbital. A 54-year-old female underwent surgery for giant ophthalmic aneurysm clipping. Due to tearing and bleeding of the carotid artery, a clamp was placed, an external-internal carotid artery bypass was done, and the patient was started on pentobarbital. The patient remained comatose, the EEG showed a burst-suppression pattern, and the pentobarbital level was 30.5 micrograms/dl. One week later, the patient was still comatose, the EEG showed generalized triphasic waves with anterior predominance, and the pentobarbital level was 11 micrograms/dl. One day later, the patient was awake, and the EEG was normalized. The patient made a complete recovery. Triphasic waves may be seen in patients on pentobarbital. It is important to recognize this finding in patients on pentobarbital due to status epilepticus. This pattern should not be misinterpreted as 'electrical' status epilepticus.
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PMID:Atypical triphasic waves associated with the use of pentobarbital. 912 72

Pentobarbital and propofol are used for the treatment of refractory status epilepticus or elevated intracranial pressure, typically with continuous EEG monitoring. We report a series of patients who developed generalized periodic discharges related to anesthetic withdrawal (GRAWs), different from previous seizure activity. At times, this pattern was misinterpreted as recurrent seizure activity, leading to reinstitution of drug-induced coma, but resolved spontaneously without additional treatment.We identified five patients who developed GRAWs during pentobarbital or propofol withdrawal. Two patients received pentobarbital for increased intracranial pressure. One patient received pentobarbital and propofol for encephalopathy accompanied by a rhythmic EEG pattern erroneously thought to be ictal. Two patients received pentobarbital for refractory partial status epilepticus. In all cases, anesthetic agents were withdrawn after 24 to 48 hours of burst suppression on EEG. We analyzed the course of GRAWs on EEG and the associated clinical outcomes.All five patients developed GRAWs, consisting of periodic 1 to 4 Hz generalized periodic discharge, not previously seen on EEG. In all cases, the pattern eventually resolved spontaneously, over 12 to 120 hours. However, in three cases, the pattern was initially thought to represent ictal activity, and drug-induced coma was reinitiated. The pattern recurred during repeated anesthetic withdrawal, was then recognized as nonictal, and then resolved without further treatment. In all cases but one, the patients exhibited improvement to near-baseline mentation.Generalized periodic discharges related to anesthetic withdrawal may occur de novo after pentobarbital or propofol withdrawal. They should resolve spontaneously without treatment and without recurrence of clinical seizure activity. However, GRAWs are not likely to represent status epilepticus and should not prompt resumption of drug-induced coma, unless there is reappearance of original electrographic seizure activity.
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PMID:De novo generalized periodic discharges related to anesthetic withdrawal resolve spontaneously. 2488