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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Propofol has been proposed as a sedative agent during awake craniotomies. However, there are reports of propofol suppressing spontaneous epileptiform electrocorticography (ECoG) activity during seizure surgery, while others describe propofol-induced epileptiform activity. The purpose of this study was to determine if propofol interferes with ECoG and direct cortical stimulation during awake craniotomies in children. Children scheduled for awake craniotomies for resection of epileptic foci or tumours were studied. An intravenous bolus of 1-2 mg.kg-1 followed by infusion of 100-200 microgram.kg-1.min-1 of propofol was administered to induce unconsciousness. Fentanyl (0.5 microgram.kg-1) was administered incrementally to provide analgesia. After the cortex was exposed, the propofol infusion was stopped and the patient permitted to awaken. Cortical electrodes were applied. ECoG was recorded continuously on a Grass polygraph. Motor, sensory, language, and memory testing were done throughout the procedure. The cortex was stimulated with a hand-held electrode using sequential increases in voltage to map the relevant speech and motor areas. We studied 12 children (aged 11-15 years) with intractable seizures. The raw ECoG did not reveal any prolonged beta-waves associated with propofol effect. Electroencephalogram spikes due to spontaneous activity or cortical stimulation were easily detected. Cognitive, memory and speech testing was also successful. We conclude that propofol did not interfere with intraoperative ECoG during awake craniotomies. Using this technique, we were able to fully assess motor, sensory, cognitive, speech and memory function and simultaneously avoid routine airway manipulation.
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PMID:The effect of propofol on intraoperative electrocorticography and cortical stimulation during awake craniotomies in children. 1063 6

The effects of different doses of propofol on post-electroconvulsive therapy (ECT) cognitive recovery were evaluated together with the effects on seizure duration and hemodynamic changes during ECT in 15 depressive patients. Propofol attenuated the increase in arterial blood pressure and heart rate in a dose-dependent manner compared with thiamylal. Propofol showed a clinically significant anticonvulsant effect during ECT in a dose-dependent manner. There were no significant differences among the four different induction groups in the mean recovery time from anesthesia, however, a low dose of propofol suppressed the early recovery of cognitive function. For early cognitive recovery after ECT, a deep anesthetic level is necessary when the traditional ECT apparatus is used which produces sine curve wave stimuli.
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PMID:Effects of propofol anesthesia on cognitive recovery of patients undergoing electroconvulsive therapy. 1068 46

Propofol provokes a slight hypotensive effect that could mitigate the cardiovascular response to electroconvulsive therapy (ECT). In this study we compared the effects of propofol and thiopental for ECT anesthesia in seven women (22-67 years of age). Anesthesia was induced with either thiopental or propofol, and with atropine and suxamethonium for each treatment. The first anesthesia was assigned to thiopental or propofol at random; the next anesthesia was induced with the other drug, and alternated thereafter. Systolic blood pressure, diastolic blood pressure (DBP), and heart rate (HR) were recorded before anesthesia, after anesthetic induction, and 1 and 5 min after ECT. ECT-induced increases in DBP and HR were less marked with propofol than with thiopental. Seizure durations were decreased with propofol compared with thiopental.
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PMID:Cardiovascular Response and Anesthetic Recovery in Electroconvulsive Therapy with Propofol or Thiopental. 1194 Nov 99

Ketamine, etomidate and propofol modified behavioral and electrographic correlates of kindled seizures in rats. In detail, ketamine (5 mg/kg) and propofol (15 mg/kg) significantly increased afterdischarge threshold, reduced seizure severity and shortened seizure and afterdischarge durations. Etomidate (7.5 mg/kg) was effective in terms of seizure and afterdischarge durations. Moreover, the combinations of ketamine (2.5 mg/kg) with carbamazepine (15 mg/kg) or valproate (50 mg/kg; all drugs at their subeffective doses), reduced the severity and duration of kindled seizures. The antiseizure potency of the ketamine/carbamazepine combination was comparable to that of carbamazepine alone administered at 20 mg/kg, while the effect of ketamine/valproate was comparable to the efficacy of valproate alone at 100 mg/kg. However, the combinations of ketamine with phenobarbital or diphenylhydantoin did not exert any protective action. Propofol and etomidate entirely failed to interact with conventional antiepileptics. The combinations of ketamine with carbamazepine or valproate did not induce any significant motor impairment in the chimney test or memory deficit in the passive avoidance task. A pharmacokinetic interaction, at least in plasma, can be excluded, because ketamine (2.5 mg/kg) did not affect the free plasma concentrations of carbamazepine or valproate. Results of the present study may suggest that there may be no risk of negative interactions between injectable anesthetics and antiepileptics in cases of partial epilepsy.
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PMID:Effects of etomidate, ketamine or propofol, and their combinations with conventional antiepileptic drugs on amygdala-kindled convulsions in rats. 1287 49

Electroconvulsive therapy is an effective treatment for severe and medication-resistant depression. There have been no reports describing how a volatile anaesthetic affects haemodynamic responses, seizure duration, and recovery characteristics during electroconvulsive therapy. We carried out a repeated-measure crossover study to compare the effects on haemodynamic responses, seizure duration, and recovery characteristics of the following types of anaesthesia in electroconvulsive therapy: propofol alone, sevoflurane alone, and propofol combined with sevoflurane. We recruited 50 patients requiring electroconvulsive therapy for depression. For anaesthesia induction, 1.5 mg/kg propofol (condition P), 5% sevoflurane in oxygen following a vital capacity rapid inhalation induction (condition S), or 1.5 mg/kg propofol followed by 5% sevoflurane in oxygen (condition PS) was administered. Succinylcholine 1.5 mg/kg was then given. Electrical stimulation was administered after fasciculation. Measurements were obtained before anaesthesia induction (baseline), prior to succinylcholine administration, prior to electroconvulsive therapy, and at the peak after electroconvulsive therapy. After electroconvulsive therapy, peak heart rate and peak mean arterial pressure were highest in condition S. Whereas recovery time was longest in condition PS, motor seizure duration was significantly shorter than in either condition P or S. Electroencephalographic seizure duration was significantly shorter in condition PS than in condition P and significantly shorter in condition S than in condition P. Sevoflurane anaesthesia alone is most disadvantageous in terms of haemodynamics. Propofol-sevoflurane anaesthesia is advantageous in terms of haemodynamics, but disadvantageous in terms of seizure duration and recovery time. Propofol alone is most advantageous in terms of seizure duration.
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PMID:Propofol alone, sevoflurane alone, and combined propofol-sevoflurane anaesthesia in electroconvulsive therapy. 1297 63

Propofol was reported to exhibit an antiepileptic activity. This study was performed to investigate the effect of propofol on evoked and spontaneous seizure-like activity induced by the convulsant veratridine. Studies were performed on rat brain slices using conventional electrophysiological intracellular techniques. The alteration of sodium channel function by veratridine (0.3 microM) induced an evoked and spontaneous seizure-like activity in the hippocampal CA1 pyramidal neurons. Therapeutic concentrations of propofol (10 microM) were ineffective in inhibiting veratridine-induced seizure-like activity. However, higher concentrations (50-100 microM, n=6) inhibited both evoked and spontaneous bursting, induced by veratridine. The inhibitory effect of propofol (100 microM) was associated with membrane hyperpolarization [after veratridine, -66+/-0.71 mV (mean+/-S.E.M.), and after propofol, -77+/-2.15 mV] and with an increase in input resistance [after veratridine (37.8+/-1.2 MOmega) and after propofol (43+/-1.3 MOmega)]. The drug also produced an increase in current threshold. Results from this study are valuable in solving critical questions regarding the antiepileptic activity of propofol and strengthen the validity of the veratridine model in testing for potential antiepileptic drugs.
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PMID:Propofol exhibits antiepileptic activity in hippocampal pyramidal neurons. 1500 71

Propofol has been used to treat convulsions, while the drug is known to induce convulsions. We described a case of generalized convulsions during brain tumor resection under propofol anesthesia. A 24-year-old man was scheduled to undergo brain tumor resection. He had no history of epilepsy. Anesthesia was induced and maintained with propofol and fentanyl. During the craniotomy, the patient developed generalized convulsions. Diazepam, thiamylal, and phenytoin were given intravenously and the seizure activity resolved. Generalized convulsions recurred three times during the operation. Postoperative course was uneventful. On the 16 th postoperative day, the patient underwent ventriculoperitoneal shunt under general anesthesia using sevoflurane, nitrous oxide and oxygen. Convulsions were not noted intra- and postoperatively. Because convulsions did not occur during sevoflurane anesthesia and the patient had no history of epilepsy, propofol may have induced a generalized convulsions on the first operation.
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PMID:[Refractory generalized convulsions in a patient undergoing brain tumor resection during propofol anesthesia]. 1524 47

Propofol is used for the treatment of refractory status epilepticus. When given as a long-term infusion propofol may cause a rare but frequently fatal complication, the propofol infusion syndrome. The hallmarks are metabolic acidosis, lipemia, rhabdomyolysis and myocardial failure. Propofol infusion syndrome is caused by impaired fatty acid oxidation. Beside anticonvulsants the ketogenic diet, a high-fat, low-carbohydrate, adequate-protein diet, is an effective treatment for difficult-to-control seizures. We report a 10-year-old boy with catastrophic epilepsy, who developed fatal propofol infusion syndrome when a ketogenic diet was initiated. Substances like propofol which impair fatty acid oxidation may pose an increased risk if combined with ketogenic diet.
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PMID:Fatal propofol infusion syndrome in association with ketogenic diet. 1532 67

Among drugs used for the anesthesia of electroconvulsive therapy (ECT), propofol reduces seizure duration to a greater degree than etomidate. The perceived difference between the 2 anesthetics is smaller in patients with schizophrenia than in patients who suffer depression. In this study, propofol and etomidate were compared during the ECT of patients with schizophrenia, on the basis of their impact on seizure activity and on seizure-induced hemodynamic reactions. Schizophrenics (n = 34) who were treated with ECT participated in this randomized crossover study. Propofol (1 mg/kg) and etomidate (0.2 mg/kg) were used alternately. The 2 drugs were compared on the basis of EEG- and EMG-registered seizure duration, mean arterial pressure (MAP), pulse frequency, energy index, and postictal suppression. We also analyzed the number of necessary restimulations. In case of anesthesia with etomidate, both EEG- (61.29 +/- 22.4 s, 47.9 +/- 21.3 s P = 0.014) and EMG- (46.3 +/- 23.8 s, 33.6 +/- 15.9 s P = 0.006) registered seizure durations were significantly longer than in case of propofol. When using propofol, the increase in MAP was significantly lower than when etomidate was used (8.1 +/- 10.2 mm Hg, 18.3 +/- 11.2 mm Hg, P = 0.001). There were no significant differences found in the postseizure increase in pulse frequency, in postictal suppression, or in the energy index, nor did the numbers of necessary restimulations differ significantly. Propofol was found to reduce seizure duration to a significantly greater extent than etomidate. At the same time, in electrophysiological parameters that show a correlation with clinical efficacy, there was no significant difference found between the 2 anesthetics. However, the seizure-induced increase in MAP was reduced by propofol to a significantly greater degree than by etomidate.
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PMID:Etomidate versus propofol for electroconvulsive therapy in patients with schizophrenia. 1559 55

Postictal delirium is an acute confusional state occurring during the immediate postictal phase in patients receiving electroconvulsive therapy that is characterized by motor agitation, disorientation, clouded consciousness, repetitive stereotyped movements, and poor response to commands. A schizophrenic patient with severe and recurrent postictal delirium is described. The possible role of the clozapine-electroconvulsive therapy combination in the occurrence of postictal delirium is discussed. Several management strategies were tried, with various degrees of success. Propofol proved to be effective in preventing agitation when used as induction agent or when administered at seizure end. However, propofol could not prevent a delirious state when only administered after the first signs of motor restlessness had emerged.
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PMID:Propofol in the management of postictal delirium with clozapine-electroconvulsive therapy combination. 1559 60


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