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

In twelve patients the EEG was recorded under isoflurane--nitrous oxide inhalation anesthesia. A quiet EEG pattern was registered, without suppressions and seizures of spike activity which are often observed under enflurane. This was the case even when end expiratory CO2 shifted to low values (3-3.6 Vol%). In one patient the induction with N2O/O2 and thiopentone, resulted in spikes and suppression bursts on the EEG. After isoflurane was added, these changes disappeared. In another patient, epileptic EEG patterns were observed prior to the induction (confirmed by the history of the patient). During isoflurane anesthesia the epileptic waves disappeared and remained absent.
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PMID:Absence of electroencephalographic excitation pattern under isoflurane anesthesia. 652 87

A total of 272 patients with epileptic seizures were examined and treated, using pneumoencephalography (PEG). In 185 cases, the cerebral fluid was insufflated with air and in 87 cases with nitrous oxide. Nitrous oxide was administered at a faster rate and in larger amounts but the patients tolerated this manipulation much easier. In the nitrous oxide group, the seizures abated in 49 patients (56.32%). In the air group, remission occurred in 45 patients (23.78%). A more prominent therapeutic effect of nitrous oxide was observed in all patients irrespective of either their age or the etiology, character and frequency of epileptic attacks or the EEG and PEG changes. Nitrous oxide is recommended for wide application for diagnostic and therapeutic purposes.
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PMID:[Comparative analysis of the therapeutic effect of endolumbar insufflation of air and nitrous oxide in patients with epileptic seizures]. 654 99

The authors investigated the value of high-dose thiopental (TH) therapy after 16-min complete global brain ischemia (GBI) in three groups of pigtailed monkeys, using a neck cuff model of GBI with 96 h intensive care postischemia (PI). Control group (n18): Normotension was restored within 2 min PI; paralysis/controlled ventilation was maintained for 48 h PI with 50% N2O/O2. Thiopental loading group (n13): Control treatment plus TH-loading with 90 mg/kg iv given from 5 to 65 min PI (mean peak TH plasma level 130 micrograms/ml). Thiopental anesthesia group (n14): Control treatment plus TH anesthesia with 90 mg/kg iv given over 12 h PI (sustained TH plasma levels of 25-35 micrograms/ml and EEG burst suppression). Norepinephrine requirement for blood pressure control PI was greater in the TH groups than in the control group (P less than 0.05). Lidocaine was needed for control of arrhythmias in the TH loading group. There was no significant difference in mortality or neurologic outcome between the groups. At 96 h PI seven of 11 animals were awake in the control group, compared with seven of 12 and six of 12 in the two TH groups. Neurologic deficit scores (NDS) for the survivors at 96 h PI were 23 +/- 6% (mean +/- SD) (n10) in the control group, compared with 25 +/- 9% (n11) and 26 +/- 12% (n10) in the two TH groups (NDS 100% = brain death, 0% = normal). Seizures PI (in 1-2 of each group) were associated with worse neurologic deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thiopental treatment after global brain ischemia in pigtailed monkeys. 669 50

In order to evaluate the possible contribution of regional insufficiency in blood flow to the development of epileptic brain damage, we have measured changes in total and regional cerebral blood flow (tCBF and rCBF) during the course of prolonged sustained seizures. We have used both a particle distribution method (radioactively labelled microspheres) and a diffusible tracer method (iodo [14C]antipyrine). Seizures were induced with bicuculline (1.2 mg/kg, i.v.) in rats with neuromuscular paralysis, mechanically ventilated with 70% N2O/30% O2, rCBF was determined in 13 brain regions after 10, 30, 60 and 120 min of seizure activity. Microsphere and iodo[14C]antipyrine methods gave identical control values for tCBF (0.88 +/- 0.02 vs 0.86 +/- 0.07 ml/g brain/min) and closely similar rCBF values. The increases in tCBF after 10 and 30 min seizure activity were less as measured with microspheres than with iodo [14C]antipyrine (2.42 +/- 0.29 vs. 4.99 +/- 0.94 and 1.79 +/- 0.18 vs 3.05 +/- 0.30 mg/g brain/min, respectively). With microspheres, rCBF values showed considerable interhemisphere variability, but did not do so with iodo [14C]antipyrine. The regional pattern of flow changed during seizures. Changes in neocortical rCBF tended to match changes in tCBF. Consistent decreases in rCBF relative to tCBF were seen in the pons-medulla and cerebellum at all seizures times. Relative increases in rCBF were seen at all seizure times in the thalamus, and at 10 and 30 min in colliculi and midbrain. In the hippocampus, rCBF was unchanged (relative to tCBF) at 10 and 30 min, but was increased at 60 and 120 min of seizure activity. Thus, regions developing epileptic brain damage in this model of status epilepticus (hippocampus, thalamus, neocortex) show increases in rCBF greater than those in regions not showing brain damage (cerebellum, brain stem).
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PMID:Regional cerebral blood flow in the rat during prolonged seizure activity. 676 47

Using ventilated rats maintained on N2O-O2 (70:30, vol/vol) we induced continuous seizures with i.v. bicuculline and analysed free fatty acids (FFA) in cerebral cortex, hippocampus, and cerebellum after seizures durations of 1-120 min. In the cerebral cortex, peak FFA concentrations were observed after 5 min, with a threefold increase in total FFA content. The values then remained unchanged for the next 15-20 min, but decreased thereafter. At 60 and 120 min, total FFA contents were only moderately increased above control. In the initial period, arachidonic acid increased about 10-fold and stearic acid 2- to 3-fold, with little change in palmitic acid and linoleic acid concentrations. At all times, the docosahexenoic acid concentration was markedly increased. Following its massive accumulation at 1 min, arachidonic acid gradually decreased in concentration. Pretreatment of animals with indomethacin did not alter this behaviour. After 20 and 120 min of seizure activity, changes in total and individual FFA concentrations in the hippocampus were similar to those observed in the cerebral cortex. The cerebellum behaved differently. Thus, at 20 min the only significant change was a 5- to 10-fold increase in arachidonic acid concentration and, after 120 min, total and individual FFA concentrations were similar to control values. Furthermore, since the control values for arachidonic acid were much lower in the cerebellum, the 20-min values were only about 20% of those observed in the cerebral cortex and the hippocampus.
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PMID:The influence of bicuculline-induced seizures on free fatty acid concentrations in cerebral cortex, hippocampus, and cerebellum. 709 86

The purpose of this study was to measure changes in local cerebral blood flow (1-CBF) during generalized seizures, and to study whether or not formation of prostaglandins or related substances contributes to the increased flow rates. Seizures were induced in ventilated rats maintained on 70% N2O and 30% O2 by the i.v. injection of the GABA receptor blocker bicuculline (1.2 mg . kg-1). Formation of prostaglandins was inhibited by the administration of the fatty acid cyclo-oxygenase inhibitor indomethacin (10 mg . kg-1). Local CBF in 21 defined brain structures was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. After 20 min of continuous seizure activity 1-CBF increased 1.5--5-fold, the smallest increases (less than 200% of control) being observed in frontal and auditory cortex and in the caudoputamen, and the largest (greater than 400% of control) in substantia nigra, thalamus, visual cortex, lateral geniculate and hypothalamus. In general, the largest increases in 1-CBF occurred in sensory and limbic systems (and hypothalamus) while motor systems showed a pronounced variability. In the majority of structures examined indomethacin failed to modify the CBF response during seizures. Although this result suggests that seizures, in contrast to hypercapnia, lead to an increased CBF by other mechanisms than those related to prostaglandin formation, some structures (nucleus ruber, cerebellum, and superior colliculus) showed a clearly reduced 1-CBF in indomethacin-treated animals.
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PMID:Local cerebral blood flow in the brain during bicuculline-induced seizures and the modulating influence of inhibition of prostaglandin synthesis. 728 97

The course of ischemic increase of extracellular potassium concentration ([K+]e) was studied in rat cerebral cortex with potassium selective microelectrodes and correlated to the preischemic functional and metabolic state. Complete cerebral ischemia was induced in artificially ventilated rats by cardiac arrest. Seven different functional states including conditions with cerebral hypermetabolism (seizures, amphetamine intoxication, hyperthermia) and hypometabolism (barbiturate anesthesia, hypothermia) were chosen in order to cover a wide range of cerebral metabolic rates (CMRO2 : 28.7--2.4 ml O2/(100 g)/min). The ischemic increase of [K+]e was delayed in conditions with low CMRO2 and accelerated in conditions with high CMRO2; the time interval to the terminal steep rise in extracellular potassium concentration varied within the extremes of 35 +/- 5 and 365 +/- 12 sec (means +/- S.E.M.), the control state (N2O-analgesia) being 116 +/- 5 sec. In groups with high CMRO2 electrocortical activity ceased within 15 sec and in groups with low CMRO2 within 22 sec. The rates of the ischemic [K+]e increase, measured as rate of change in the potassium electrode potential (mV/sec), remained high in conditions with high preischemic CMRO2 and low in conditions with low CMRO2, indicating a remaining influence of the preischemic metabolism on membrane ion permeability. These results support previous metabolic data indicating that the rate of consumption of high energy phosphates during ischemia mirrors the preischemic cerebral metabolic rate. Phenobarbital anesthesia did not change the initial rate of [K+]e increase but reduced the rate of [K+]e increase later during ischemia, suggesting a special effect of barbiturates on partly depolarized membranes.
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PMID:The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate. 740 19

Neurons synthesize NO, which may act as a retrograde messenger, involved in either potentiating or depressing neuronal excitability. NO may also play a role in the cerebral vasodilatory response to increased neuronal activity (i.e., seizures). In this study, two questions were asked: (1) is NO an endogenous anticonvulsant or proconvulsant substance? and (2) is the cerebral blood flow (CBF) increase accompanying bicuculline (BC)-induced seizures mediated by NO? The experiments were performed in 300-400-g Wistar rats anesthetized with 0.6% halothane and 70% N2O/30% O2. CBF was measured using the intracarotid 133Xe clearance method or laser-Doppler flowmetry. EEG activity was recorded. Chronic treatment (4 days) with nitro-L-arginine (L-NA), a potent NO synthase (NOS) inhibitor (400 mg/kg total), suppressed brain NOS by > 97% and prolonged seizure duration from 6 +/- 1 (saline-treated controls) to 12 +/- 2 min. In the L-NA-treated group, the CBF increase was sustained as long as seizure activity remained, indicating that CBF was still tightly coupled to seizure activity. Interestingly, the supposed inactive enantiomer of L-NA, D-NA, also showed an inhibition of brain NOS activity, ranging from 87 to 100%. The duration of seizures in this group (average 8 +/- 2 min) corresponded directly to the magnitude of reduction in NOS activity (r = 0.83, P < 0.05). Specifically, the D-NA results indicated that NOS inhibition had to exceed 95% before any effect on seizure duration could be seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitric oxide (NO) is an endogenous anticonvulsant but not a mediator of the increase in cerebral blood flow accompanying bicuculline-induced seizures in rats. 753 May 79

Exposure to nitrous oxide produces handling induced convulsions following withdrawal in mice. Since strain differences in responsiveness to the antinociceptive potency of N2O have been found, we examined whether there were differences in susceptibility to N2O withdrawal seizures. Significant differences were found between mouse strains, varying between 100% and 0% of mice exhibiting withdrawal seizures. There was a lack of correlation between the sensitivity of the mouse strains to N2O-induced analgesia and N2O withdrawal seizures, suggesting different mechanisms of action.
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PMID:Strain-dependent variability in nitrous oxide withdrawal seizure frequency. 765 19

Hypothesizing that propofol's pro and anticonvulsant effects might be dose dependent, we determined the effect of 25, 50, and 100% of a previously determined anesthetic dose of propofol for rats on the amount of lidocaine required to induce seizures. Lidocaine was infused at 2.5 mg kg-1 min-1 into animals that were receiving either (a) 70% N2O balance O2 (n = 10), control group, (b) 2 mg kg-1 bolus followed by 12 mg kg-1 h-1 propofol infusion with 70% N2O (n = 10), group 2, (c) 4 mg kg-1 followed by 24 mg kg-1 h-1 propofol with 70% N2O (n = 20), group 3, (d) 8 mg kg-1 followed by 48 mg kg-1 h-1 propofol with 70% N2O (n = 10), group 4, or (e) 8 mg kg-1 followed by 48 mg kg-1 h-1 propofol without N2O (n = 10), group 5. Temperature PaCO2, and pH were maintained within normal limits until disturbed by seizure activity or lidocaine toxicity. The plasma concentration of lidocaine required to induce electroencephalographically (EEG) detected seizures was 8.7 +/- 0.7 micrograms ml-1 in control animals, 16 +/- 1.7 micrograms ml-1 in group 2, and 32 +/- 4 micrograms ml-1 in 13 animals from group 3 that experienced a seizure (p < 0.01). Seizures did not occur in seven of 20 group 3 rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Propofol prevents or elevates the threshold for lidocaine-induced seizures in rats. 800 Jan 99


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