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

Electrocorticographic (ECoG) and depth recordings have previously demonstrated the epileptogenic nature of surgical concentrations of the volatile anesthetic enflurane. We contrasted ECoG activity with local cerebral glucose uptake [( 14C]2-deoxyglucose autoradiography) in 23 brain structures in order to identify the epileptogenic foci. Autoradiograms were obtained from sectioned rat brain following a 30 min period of steady-state anesthesia at 1, 1.5, or 2 MAC (minimum alveolar concentration) enflurane. Pseudo-epileptiform ECoGs were obtained at 1 MAC where bursts of slow waves and sharp waves were evoked by peripheral sensory stimulation. At 1.5 MAC, the ECoG displayed frank, spontaneous epileptiform activity with large amplitude spike-wave complexes; repetitive auditory stimulation occasionally precipitated grand-mal seizures. At 2 MAC, spike complexes were less frequent and could not be repetitively driven. At 1 MAC enflurane, regional cerebral metabolism was generally depressed approximately 14% from the awake controls. However, metabolism in the dentate gyrus of the hippocampus and other subcortical structures in the limbic brain was increased. At 1.5 MAC this dichotomy in local cerebral metabolic rate was maximal; we observed increased metabolism in the hippocampus, habenula, habenulo-interpeduncular tract and interpeduncular nucleus and pineal. Metabolism in all other structures was significantly depressed (P less than 0.05) compared to awake values. At 2 MAC, metabolism was decreased in all structures. We conclude that the low seizure threshold hippocampus and related structures associated with the limbic system and its pathways are the epileptogenic foci for seizures induced with enflurane in the rat. At 1.5 MAC, epileptiform activity spreads throughout the visceral brain when seizure threshold is at a minimum.
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PMID:Local cerebral metabolism during enflurane anesthesia: identification of epileptogenic foci. 9 9

The effects of halothane, isoflurane, and enflurane on background neuronal activity and reactive capability in the central nervous system were studied in cats. The background neuronal activity was assessed by midbrain reticular cell firing, which was measured by the method of multi-unit activity, and the EEG in the cortex, amygdala, and hippocampus. The reactive capability was assessed by evoked responses in the visual neuronal pathway. All anaesthetics studied suppressed reticular cell firing in a dose-dependent manner, and the suppression by halothane (43.8 +/- 10.3% of control, mean +/- SD) was less than isoflurane (66.5 +/- 5.8%, P < 0.01) and enflurane (73.1 +/- 8.8%, P < 0.05) at 1 MAC. Spontaneous EEG spikes developed at 4.8% isoflurane and 3.6% enflurane anaesthesia. Phasic activation of reticular cell firing was associated with EEG spikes during isoflurane and enflurane anaesthesia, and the activation during enflurane anaesthesia was greater than during isoflurane anaesthesia (P < 0.01). Photic stimulation provoked EEG spikes and repetitive stimulation induced seizure activity only at 3.6% enflurane anaesthesia. Halothane and isoflurane suppressed stimulation induced responses in the visual neuronal pathway. The amplitudes of N1 in visual cortical evoked responses induced by photic stimulation were suppressed to 70.1 +/- 24.5% of control at 2.4% halothane and 39.3 +/- 27.3% at 4.8% isoflurane. Enflurane, at 3.6%, augmented the evoked response induced by photic stimulation (398.4 +/- 83.0% of control in the amplitude of N1). These results indicate that all the agents studied had suppressive actions on background neuronal activity in the order halothane < isoflurane = enflurane. The effects on reactive capability were divergent among agents, e.g., enflurane enhanced, halothane suppressed, and the actions of isoflurane were intermediate. We conclude that the anaesthetic effects on background activity and on reactive capability are divergent and that suppression of reactive capability is a factor in determining the ease of clinical application of the anaesthetics.
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PMID:The divergent actions of volatile anaesthetics on background neuronal activity and reactive capability in the central nervous system in cats. 128 11

We have studied the effects of suxamethonium 1.0 mg kg-1 i.v. on cerebral blood flow (CBF), cerebral metabolic rate (CMRO2), and the electroencephalogram (EEG) in dogs anaesthetized with halothane (1.0 MAC) following blood-brain barrier (BBB) disruption with intracarotid (i.c.) mannitol. The combination produced a transient increase in CBF, while CMRO2 did not change. These responses were similar to those produced by i.c. mannitol plus i.v. saline. Suxamethonium produced desynchronization of the EEG that persisted longer than that produced by saline. In only one of the six animals was the desynchronization sustained (90 min) beyond that found in dogs with a normal BBB. We conclude that disruption of the BBB did not enhance the cerebral stimulating effects of i.v. suxamethonium, and did not increase the likelihood of seizure activity following suxamethonium.
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PMID:Effects of suxamethonium on the cerebrum following disruption of the blood-brain barrier in dogs. 212 96

The influence of age and volatile anesthetic agents on plasma concentrations and toxic effects of bupivacaine were studied in 2-day-old, 2-week-old, and 2-month-old pigs. Bupivacaine was infused at a constant rate while the pigs' ECGs and EEGs were recorded. Six pigs in each age group were lightly anesthetized with 70% N2O/30% O2 during the bupivacaine infusion, and twelve 2-day-old pigs were anesthetized with 70% N2O/30% O2 plus either 0.5 X MAC halothane or isoflurane. Two-day-old pigs were more resistant than older pigs to the toxic effects of bupivacaine despite higher plasma concentrations at all sample times. All pigs given N2O alone or N2O plus halothane had ventricular dysrhythmias, but only one pig in the N2O plus isoflurane group had a ventricular dysrhythmia. Threshold doses of bupivacaine for dysrhythmias in the N2O alone and N2O plus halothane groups did not differ. Seizures occurred in all pigs in the N2O alone group, in none of the N2O plus halothane group, and in two of the N2O plus isoflurane group. The doses required to depress cardiac index and cause asystole were less in the groups receiving halothane and isoflurane. It was concluded that N2O plus halothane and N2O plus isoflurane increase the lethality of bupivacaine while preventing early warning signs of toxicity.
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PMID:Bupivacaine toxicity in young pigs is age-dependent and is affected by volatile anesthetics. 238 52

Among the non-depolarizing neuromuscular blocking drugs, atracurium appears to be unique in its ability to produce cerebral stimulation in lightly anaesthetized animals. This effect is attributed to the atracurium metabolite, laudanosine. The following studies were performed to determine if pretreatments with the non-depolarizing neuromuscular blockers pancuronium, atracurium or vecuronium would differ in their effects on the seizure threshold of lignocaine. Adult mongrel cats were anaesthetized with 1.0 MAC halothane in oxygen and nitrogen. Ventilation, blood-gas tensions, acid-base balance and temperature were controlled. Cats received pancuronium 0.2 mg kg 1 i.v. (n = 7), atracurium 1.0 mg kg-1 i.v. (n = 7) or vecuronium 0.2 mg kg-1 i.v. (n = 7). Ten minutes after the administration of the myoneural blocker, all cats received lignocaine 4 mg kg-1 min-1 i.v. until the onset of EEG evidence of generalized seizure activity. At seizure onset, there were no statistically significant differences among the cumulative lignocaine doses or the serum lignocaine concentrations in cats pretreated with pancuronium, atracurium or vecuronium.
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PMID:Effects of atracurium, vecuronium or pancuronium pretreatment on lignocaine seizure thresholds in cats. 289 21

The effects of 0.5 and 1.0 MAC end-tidal concentrations of sevoflurane on intracranial pressure, cerebral metabolic rate for oxygen, cerebral blood flow, and the electroencephalogram were compared to those of equi-MAC concentrations of isoflurane in rabbits anesthetized with morphine-nitrous oxide. At 1.0 MAC end-tidal level, both sevoflurane and isoflurane caused a significant reduction in cerebral metabolic rate for oxygen of about 50%. Neither anesthetic caused a significant change in global cerebral blood flow or cortical cerebral blood flow during either 0.5 or 1.0 MAC administration. However, both sevoflurane and isoflurane caused small but significant increases in intracranial pressure during 0.5 MAC and 1.0 MAC administration. The electroencephalogram of animals anesthetized with 1.0 MAC of either anesthetic demonstrated a burst suppression pattern with no evidence of spike or seizure activity. The data suggest that the effects of sevoflurane on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are indistinguishable from those of equivalent concentrations of isoflurane in the rabbit.
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PMID:The effects of sevoflurane on cerebral blood flow, cerebral metabolic rate for oxygen, intracranial pressure, and the electroencephalogram are similar to those of isoflurane in the rabbit. 335 92

I653 is a new volatile anesthetic structurally similar to enflurane and isoflurane. Since enflurane can induce convulsions, whereas isoflurane progressively depresses cortical electrical activity, the authors believed it important to assess the effect of I653 on the EEG (in both the "time" and "frequency" domain). The EEG was assessed visually and quantitatively, and a new EEG parameter was introduced. The burst-suppression ratio (percentage of time the EEG was isoelectric) quantified the extent of burst suppression phenomena. Eight swine were anesthetized with I653 or isoflurane in oxygen and in random sequence, exposed to approximately 0.8, 1.2, or 1.6 MAC with normocapnea and to 1.2 MAC with hypocapnea (PETCO2 of 25 mmHg). Four animals were also anesthetized with 3.2% (1.2 MAC) enflurane in oxygen. Both I653 and isoflurane produced a dose-related depression of cortical electrical activity. At 0.8 and 1.2 MAC of either agent, occasional sharp waves occurred singly, were apparently not related to external (auditory) stimuli, and probably represented normal variation in the EEG. No electrographic or gross motor seizures occurred with either I653 or isoflurane. In contrast, all pigs given enflurane developed seizures during hypocapnea. At equipotent concentrations, I653 and isoflurane had the same effect on EEG parameters. Increasing doses of either I653 or isoflurane caused decreasing amplitude and frequency and increasing suppression. Hypocapnea during either agent slightly increased high-frequency activity, and slightly decreased burst suppression.
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PMID:I653 and isoflurane produce similar dose-related changes in the electroencephalogram of pigs. 341 10

The incidence of postoperative convulsive seizure was compared retrospectively during either isoflurane or sevoflurane anesthesia in patients after craniotomy. Overall, 5 of a total of 125 patients suffered convulsive seizures after craniotomy: 2 (4%) of 45 patients with isoflurane anesthesia and 3 (4%) of 80 patients with sevoflurane anesthesia. No significant differences were observed between these two groups. The duration of anesthesia and duration of the MAC.h were similar between these two groups. The occurrence of postoperative convulsive seizure was not related with the inhalational anesthetic agents, the underlying disorders and patient characteristics. It is suggested that either isoflurane or sevoflurane anesthesia in neurosurgical patients may have no specific relationship with the postoperative convulsive seizures.
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PMID:[Convulsive seizure after craniotomy--comparison of isoflurane anesthesia and sevoflurane anesthesia]. 747 16

The effect of enflurane on somatosensory evoked potentials (SEP) was investigated in nine gynecological patients under nitrous oxide-enflurane anesthesia. SEPs were obtained from electrodes placed on the scalp C4 and earlobes by median nerve stimulation contralateral to the recording site. SEPs taken in a control study without enflurane consisted of six components; P12, N17, P23, N31, P50, and N65. Components N17, P23, N31, and P50, thought to be specific SEP responses, showed a dose-dependent increase in latencies under enflurane while P12, the initial SEP components, did not show any significant changes throughout the experiment. The longer the latency for a given response component, the greater was the increase in latency seen under enflurane anesthesia. On the other hand, N65, assumed to be a nonspecific SEP response, was completely lost with inhalation of 0.5 MAC or more of enflurane. However, the peak-to-peak amplitude between P23 and N31 was enhanced dose-dependently with enflurane up to 1.5 MAC. These results suggest that, at clinically effective doses, enflurane may inhibit nonspecific projection pathways while enhancing the primary cortical sensory area, and this enhancement may be responsible for provoking convulsive seizures under enflurane anesthesia.
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PMID:[Effect of enflurane on human somatosensory evoked potentials: differences between specific and nonspecific responses]. 851 38

Sevoflurane may be an interesting substance for paediatric anaesthesia due to its combination of a very low blood-gas partition coefficient and non-pungency. This review discusses the status of sevoflurane in paediatric anaesthesia on the basis of studies published so far. The blood-gas partition coefficient of sevoflurane in children is 0.66, and hence markedly lower than those of isoflurane (1.25) and halothane (2.26) [15]. Induction of anaesthesia with sevoflurane/N2O is slightly shorter compared to halothane/N2O (Table 1) [4]. During induction of anaesthesia, sevoflurane/O2 is more often associated with excitement (35%) than sevoflurane/N2O (5%) and halothane/N2O (5%) [25]. Seizure-like movements in one case [1] and electrically generalised but clinically silent seizure activity in two cases [12] may raise the question of seizure-inducing effects of sevoflurane. However, up to now there is no clinical evidence of epileptogenic effects of sevoflurane. The MAC50 in neonates and infants 1-6 months of age is 3.3 vol% [14]; in infants 6-12 months and children 1-12 years of age it is 2.5 vol.% [14]. Sixty per cent N2O decreases the MAC50 of sevoflurane and desflurane by only 20%-25% [3, 14]. In contrast, 60% N2O decreases the MAC50 of halothane in children by 60% [16]. Thus, the MAC-reducing effect of N2O in children appears to be attenuated in the presence of less soluble inhalation anaesthetics. Sevoflurane has a similar low incidence of airway irritation as halothane and provides a smooth induction (Fig. 2) [4]. Haemodynamics during sevoflurane anaesthesia may be somewhat more stable compared to halothane. Serum fluoride levels increase rapidly when sevoflurane is administered, but decrease shortly after discontinuation [4]. Mean maximum levels reported are about 20 mumol/l and are of no concern for renal function. A study with mivacurium indicates more pronounced muscle relaxation by sevoflurane compared to halothane [9]. Sevoflurane may induce malignant hyperthermia. Emergence from sevoflurane anaesthesia is significantly more rapid than after halothane anaesthesia (Table 1); however, it is associated with more restlessness and agitation, probably due to the earlier perception of pain [4]. The incidence of postoperative nausea and vomiting after sevoflurane anaesthesia is comparable to that after halothane (Table 2). Sevoflurane may be a user-friendly alternative to halothane and is more preferred by children than halothane [32]. The status of sevoflurane in paediatric anaesthesia will depend on several factors: its own benefit/risk-ratio, a possible re-evaluation of the known risks of halothane and the financial limitations of the hospitals.
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PMID:[Sevoflurane in pediatric anesthesia]. 877 99


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