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

We have examined the anticonvulsant properties of propofol in high doses in two experimental models of status epilepticus: generalized pentylenetetrazol (PTZ)-induced seizures and partial, cortically applied penicillin G-induced seizures. Propofol was administered either as a single bolus injection or as a bolus injection followed by an infusion for 1 h. When administered as a single bolus injection, propofol 12 mg kg-1 suppressed electrical and clinical seizures in PTZ generalized epileptic status, and an infusion of 50 mg kg-1 h-1 prevented the reappearance of electrical and clinical signs. In focal epileptic status, the single dose stopped paroxysmal activity and the associated clonic jerks for a few seconds. When the bolus dose was followed by an infusion, the firing bursts were replaced by isolated spikes, and contralateral jerks became sporadic and feeble. The greater efficacy of propofol against PTZ convulsions may be a reflection of the opposite action of the two drugs on neural membrane conductance: PTZ induces paroxysmal neural discharge by enhancing membrane conductance while propofol appears to decrease membrane conductance, thus suppressing paroxysmal discharge. There was no close relationship between blood concentration of the anaesthetic and its clinical effects, at least after a short-term infusion, as used in the present experiments. We suggest that propofol may be a potentially useful drug in status epilepticus in patients in whom benzodiazepines, barbiturates and phenytoin have failed.
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PMID:Propofol anticonvulsant activity in experimental epileptic status. 138 23

Total intravenous anaesthesia with propofol and alfentanil is an established alternative to inhalation anaesthesia for intracranial neurosurgical procedures. Its usefulness has been somewhat overshadowed by reports of seizure-like movements, both during anaesthesia and in the recovery period. These can be related to the use of either anaesthetic agent, but true epileptogenic properties still remain to be demonstrated in man. Opioid-induced rigidity is a well known phenomenon and must not be mistaken for an epileptic seizure. Myoclonic motor activity can be observed even under physiological conditions, e.g. sleep. Almost all anaesthetic agents have been found to produce "epileptic" EEG changes (spikes, polyspikes, spike-wave complexes), but in man these have never been correlated to motor reactions. Propofol's pro- or anticonvulsive action is unclear. While some groups found shortened convulsing times in patients undergoing electroconvulsive therapy with propofol instead of methohexitone, others have reported activation of epileptogenic foci in the EEGs of known epileptic patients. A synergistic effect of propofol and alfentanil in the generation of seizure-like movements cannot be excluded. Whether seizure-like movements indicate a true "epileptogenic potency" of the anaesthetic drugs or are related to other phenomena remains to be studied. Electro-encephalographic monitoring during anaesthesia as well as careful observation and documentation of motor reactions may contribute to elucidation of the problem. We report a case of seizure-like movements during propofol-alfentanil anaesthesia for an elective craniotomy. A 52-year-old patient presented with a history of headaches of increasing frequency. A CT brain scan demonstrated a tumor in the left occipital region.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A myoclonic seizure during propofol-alfentanil anesthesia?]. 149 34

We have investigated the pharmacological basis of CNS excitation that occurs in association with general anaesthesia in mice. Propofol produced sustained clonic movements during anaesthesia. Methohexitone produced intermittent non-rhythmic jerking during anaesthesia. Ethanol and pentobarbitone produced anaesthesia without associated clonic movements. Doses of all anaesthetic drugs were equipotent. Surface EEG recordings showed paroxysmal discharges consistent with interictal manifestations of cortical seizures with methohexitone or propofol, but not with ethanol or pentobarbitone. Strychnine, a glycine antagonist without effects on the cerebral cortex, and bicuculline, a GABAA antagonist with effects on the cerebral cortex, were used in doses that were equipotent-0.5 log units less than the ED10 for clonic convulsions. Strychnine potentiated both excitatory behaviour and EEG paroxysmal discharges when given with methohexitone or propofol, but not with ethanol or pentobarbitone. Bicuculline did not affect either behaviour or EEG with any of the anaesthetic drugs. Our data show that methohexitone and propofol produced CNS excitation, while pentobarbitone and ethanol did not. We propose that the pharmacological basis of this excitation may be glycine antagonism occurring in subcortical structures.
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PMID:Does glycine antagonism underlie the excitatory effects of methohexitone and propofol? 164 44

Propofol was used for 1,350 sessions of electro-convulsive therapy (ECT). After 0.5 mg of intravenous atropine, patients received 1 to 1.5 mg.kg-1 bolus of propofol over a period of 20 seconds or less. This was convenient for loss of the eye-lash reflex. A bolus of 15 to 20 mg suxamethonium was given, in non allergic patients, to prevent trauma from the seizure. The patient was hyperventilated with pure oxygen through a facial mask. The electric shock was delivered bitemporally after a dental protection had been inserted. For each patient, the following data were noted: sex, use of tricyclic antidepressant drugs, atopy, amount of administered propofol and the effective intensity of the electric shock. The 99 patients were given 16.27 +/- 14 ECT sessions. Among them 26 took antidepressant drugs and 34 were atopic. There was no difference, except for weight, between the 25 men and 74 women. The mean dose of propofol was 1.37 +/- 0.3 mg.kg-1. The dose decreased with increasing age. There was no statistical relationship between the amount of propofol and intensity of the electric shock required to set off a seizure. The use of antidepressant drugs, and atopy did not influence the required amount of propofol. Speed of injection seemed to be the determining factor for narcosis with low doses of propofol. Hyperoxia and hypocapnia induced by hyperventilating with pure oxygen seemed to facilitate occurrence and duration of seizures. Although propofol has been said to reduce the length of seizures, there is controversy concerning the ECT efficacy criteria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of propofol in 1350 anesthetized patients for electroconvulsive therapy]. 200 69

Propofol is a new anesthetic induction agent that reduces electroconvulsive therapy (ECT) seizure duration. To indirectly investigate the effect of propofol on ECT-induced acute central neurotransmitter changes, we studied neuroendocrine responses in 25 primary depressed subjects treated with ECT under either propofol or thiopentone anesthesia. Blood samples were taken prior to ECT, and then at regular intervals for 2 hr. Only the prolactin response correlated significantly with seizure duration (r = 0.52, p less than 0.01). Subjects given propofol had significantly reduced adrenocorticotropin (ACTH) (p less than 0.01) and cortisol (p less than 0.05) responses compared to thiopentone, which were independent of seizure duration. There was a trend towards a reduction in the prolactin response with propofol compared to thiopentone, but this was dependent upon the diminished seizure duration. The results indicate that propofol affects endocrine responses to ECT by two distinct mechanisms: decreasing prolactin by reducing the seizure duration and decreasing ACTH and cortisol by another process, possibly via a reduction in central noradrenergic activation.
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PMID:Effect of the anesthetic agent propofol on hormonal responses to ECT. 164 24

Propofol and thiopentone were compared as anaesthetic agents for electroconvulsive therapy in 31 patients on four occasions in a repeated measure crossover study. Discomfort on injection was significantly more common with propofol (51.6% of anaesthetics) compared to thiopentone (1.6% of anaesthetics). The duration of seizure was shorter with propofol in both treatments but there was significant drug-time interaction. Propofol gave a milder tonus and clonus during seizure when both treatments were considered together. The increase in systolic and diastolic arterial pressures and heart rate after treatment were significantly higher with thiopentone. Apnoea was significantly longer with propofol. The times to sitting up unaided and opening the eyes on command were the same for both drugs. The ability to walk 10 m 20 minutes after anaesthesia was significantly better with propofol (p less than 0.0001).
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PMID:Comparison of propofol and thiopentone as anaesthetic agents for electroconvulsive therapy. 240 70

Propofol was compared to methohexitone for induction of anaesthesia for electroconvulsive therapy. Seizures were significantly shorter after the use of propofol, in respect of both visible seizures and duration of cerebral electrical seizure activity. This suggests the possibility that additional treatments may be needed for the same clinical effect in psychiatric illness when propofol is used as the induction agent. Propofol was more effective than methohexitone at obtunding the hypertensive response to electroconvulsive therapy without causing significant hypotension.
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PMID:Comparison of propofol and methohexitone as anaesthetic agents for electroconvulsive therapy. 326 46

We studied the safety and efficacy of intravenous propofol in the out-of-hospital treatment of convulsive status epilepticus (SE) in 8 patients (age 29-70 years), 4 of them with posttraumatic epilepsy. Four patients had no history of seizures. Convulsions ceased promptly after patients received a bolus of 100-200 mg propofol administered before hospital admission by staff of a mobile intensive care unit (ICU). The median duration of coma was 3 h 15 min (range 2-41 h), and the median duration of hospital treatment was 3 1/2 days (range 12 h to 23 days). Only 1 patient was admitted to the hospital's ICU. No adverse effects was observed except for a transient decrease in systolic blood pressure (SBP). Propofol may be a useful drug for the prehospital treatment of recurrent seizures not responding to intravenous diazepam (DZP).
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PMID:Propofol in prehospital treatment of convulsive status epilepticus. 748 3

Tonic-clonic seizure activity is a recognized complication of amoxapine overdose. Refractory drug-induced status epilepticus is associated with significant morbidity and mortality. Standard regimens for controlling status epilepticus may be ineffective for aborting drug-induced seizures. The authors report the case of a 30-year-old woman who presented with an amoxapine overdose that deteriorated into status epilepticus refractory to conventional therapy. Propofol given by intravenous bolus and maintenance infusion successfully halted the patient's seizure activity. This case suggests that propofol may be effective as an anticonvulsant in refractory drug-induced status epilepticus.
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PMID:Successful treatment of amoxapine-induced refractory status epilepticus with propofol (diprivan) 880 82

Propofol (i.v. and i.p.) exhibited anticonvulsant activity in three models of seizure in the mouse, induced by bicuculline, kainic acid and N-methyl-DL-aspartic acid (NMDLA). Morphine, pethidine and fentanyl, which showed a biphasic dose-response relationship with respect to seizure modulation, abolished the anticonvulsant activity of propofol to exhibit their own intrinsic activity in proconvulsant doses. This occurred with very low doses of fentanyl and pethidine (15 micrograms kg-1 and 0.5 mg kg-1, respectively) in the NMDLA model. Thus it appears that propofol has anticonvulsant activity only when a convulsion is elicited directly; it does not prevent the actions of compounds that lower seizure threshold to convulsant stimuli. The anticonvulsant doses of morphine and fentanyl did not summate with the anticonvulsant activity of propofol. However, there was some evidence of summation of anticonvulsant activity between pethidine and propofol in the NMDLA model.
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PMID:Interactions between opioid drugs and propofol in laboratory models of seizures. 771 78


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