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

The protective effects of pentobarbitone, hydroxydione and diazepam against acute and chronic toxicity of high-pressure oxygen (HPO) were studied in rats. During exposure to hyperbaric oxygen body temperature was measured and ECG as well as EMG tracings from the diaphragm were obtained. Long term observations of animals after the exposure to HPO were conducted. Pentobarbitone and hydroxydione reduced the manifestations of acute toxicity but increased those of chronic toxicity. Diazepam reduced the manifestations of acute toxicity and seemed to counteract those of chronic toxicity. Lowering of body temperature of the animals which occurred during exposure to HPO was probably connected with manifestations of chronic toxicity. Observation of the cardiorespiratory functions suggested a possible connection between their disturbances and an onset of seizures and development of oxygen-induced paralysis.
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PMID:The protective action of certain anaesthetics and tranquilizers against the effects of hyperbaric oxygen. 1 48

Procaine HCl and diphenylhydantoin (DPH) increased the duration and propagation of epileptiform afterdischarges (ADs) produced by electrical stimulation of the amygdala in rats. Procaine and DPH also increased the rate of seizure development (kindling) produced by repeated stimulation of the amygdala. Procaine and to a limited extentDPH would themselves act as convulsants in well kindled subjects. Diazepam, on the other hand, retarded or blocked amygdaloid kindling. Diazepam trigered a high frequency (20-30 c/sec) rhtthm in the amygdala, hippocampus and preoptic area. None of these drugs had any significant effect on potentials evoked in secondary limbic sites by single electrical pulses applied to the amygdala. Also, none of these drugs had any effect on recruiting or post-tetanic potentiation (PTP) in secondary sites produced by amygdala stimulation and none of the drugs had any effect on amygdaloid AD thresholds. The effects of these drugs on the responses evoked by anterior neocortex stimulation were quite different. Diazepam had no effect on any of the characteristics of the discharge or convulsion even at twice the dose levels used for the amygdala group. Procaine and DPH, however, blocked not only the eonvulsion but the AD as well. Eighty percent of the procaine- and DPH-treated rats failed to respond with neocortical AD even at current levels as high as 2000 muA. The few cortically stimulated subjects that did respond with an AD showed a subcortical rather than a neocortical seizure response. DPH had no effect on recruiting or PTP of the transcallosal response. Both procaine and DPH produced a weak but significant increase in the amplitude of the transcallosal evoked potential, while diazepam produce a weak decrement in that response.
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PMID:Effects of procaine hydrochloride, diazepam, and diphenylhydantoin on seizure development in cortical and subcortical structures in rats. 4 16

With systemic (60-150 mg/kg) and topical application, Aldactone exhibited strong convulsant action on the cat cerebral cortex. The most common abnormal interictal features of the surface ECoG pattern were sequences of fast waves and slow negative waves associated with positive sharp waves, negative field potentials and burst-like neuronal activation in the extracellular microelectrode record. Another abnormal pattern was a period of ECoG and neuronal inactivity subsequent to the negative transients. These series of sharp and slow waves and of inactivity were interrupted by tonic and clonic ECoG seizures characterized by regular surface positive spikes. Development of seizures, but not of interictal phenomena, could be prevented by intravenous application of Diazepam (1 mg), Nembutal (30 mg/kg) and--less effectively--by Phenhydane (20 mg/kg).
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PMID:The effects of a spirolactone derivative on EEG and cortical single unit activity in the cat. 5 40

The effects of cortically kindled seizure responses of procaine hydrochloride, diazepam and combinations of these two drugs were tested in this study. The cortex was stimulated until seizure responses developed past the focal stage (accompanied primarily by brief tonic convulsions) to the cortico-generalized stage (accompanied, typically, by an early brief tonus followed by a longer clonic seizure that is characteristic of subcortically triggered seizures). Diazepam was found to block the generalized component of the cortico-generalized electrographic and motor seizure leaving the tonus only slightly suppressed. Procaine blocked the tonus leaving the clonic seizure and discharge that is characteristic of the generalized response relatively intact. Combinations of half doses of the two drugs completely blocked all electrographic and motor seizure responses in about half the animals. The remaining animals had a very brief discharge with no convulsive responses.
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PMID:The effect of procaine hydrochloride and diazepam, separately or in combination, on cortico-generalized kindled seizures. 9 13

Intramuscular injection of diazepam to rats at doses of 0.01 and 2 mg/kg 25-30 min after penicillin application to the rat brain cortex leads to alteration of periodic appearance of epileptic seizures (ES), to changes in the seizure pattern, and to emergence of periodic acceleration of epileptiform discharges (ED). Injection of diazepam at a dose of 2 mg/kg 20 min before penicillin application results in the reduction of ED latency in the epileptogenic focus and in a decrease in their frequency before seizures as compared to the control animals without diazepam injection. ES appear irregularly, their quantity is markedly reduced while duration is increased. Diazepam injection leads to disappearance of the rat moving reaction during ER and ES. In vivo experiments diazepam (2 mg/kg) does not influence brain cortex Na, K-ATPase of crude synaptosomes. However, diazepam leads to an increase in Na, K-ATPase activity both in the primary and dependent secondary epileptogenic foci. It is suggested that the anticonvulsant action of diazepam may be underlain by its activating effect on Na, K-ATPase of neuronal membranes in the epileptogenic focus.
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PMID:[Effect of diazepam on the Na, K-ATPase state in a penicillin--induced hyperactivity focus in the cerebral cortex]. 22 25

The history, symptoms, diagnosis and treatment of phencyclidine hydrochloride (PCP) intoxication and the pharmacology of PCP are reviewed. Intoxication with low to moderate doses of PCP (5-20 mg) resembles an acute, confusional state generally lasting four to six hours. High doses (greater than 20 mg) may cause serious neurologic and cardiovascular complications and the patient is often comatose for several days. Treatment involves supportive psychological and medical measures. Evacuation of the stomach with activated charcoal and a saline cathartic may be indicated and succinylcholine chloride may ease intubation. Diazepam and chlorpromazine may be used to control the combative patient and the "PCP psychosis" patient, respectively. Antihypertensive agents are not usually needed, but diazoxide and hydralazine hydrochloride have been used to treat hypertensive crises. Diazepam and phenytoin have been used to treat seizures. Ion-trapping by continuous gastric suctioning and by urine acidification with ammonium chloride may increase clearance of PCP. Forced diuresis with furosemide in conjunction with acidification may further increase PCP clearance. Use of physostigmine is based on conjecture.
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PMID:Phencyclidine intoxication: a literature review. 36 Aug 32

Five newborn infants (birth weight 2900--3600 g) were given diazepam (Valium, LaRoche) for convulsive disorders in 4 equal doses intravenously, intramuscularly, rectally and orally with at least 24 hours intervals. Three infants were given doses of 1 mg diazepam/kg body weight, and 2 0.5 mg/kg. The parenteral solution of the drug was given intravenously, intramuscularly and rectally. Powder of tablets was given orally. After intravenous administration very high peak values of plasma-diazepam concentration were obtained (5775--10800 ng/ml after 1 mg/kg, 2750 and 6450 ng/ml after 0.5 mg/kg). Next to intravenous administration rectal administration caused the most rapid increase in plasma-diazepam concentration. Presumed anticonsulsive concentrations (150--300 ng/ml) were obtained within 5 min with 1 mg/kg as well as 0.5 mg/kg rectally. Rectal administration therefore could be a suitable treatment for seizures in the newborn infant. Accumulation of the main depressive metabolite N-desmethyldiazepam occurred in all infants. This phenomenon must be taken into account when repeated doses of diazepam are administered.
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PMID:Plasma concentrations of diazepam and N-desmethyldiazepam in newborn infants after intravenous, intramuscular, rectal and oral administration. 36 1

Interrupting petit-mal status in infantile myoclonic seizures (n = 11), Lennox syndrom (n = 32), and in myoclonicastatic petit mal (n = 13) diazepame (Valium) and clonazepame (Rivotril) have been injected intraveneously in 56 patients during continuous EEG monitoring (38 patients with diazepame, 18 patients with clonazepame) (Table 1). A judgement according to the EEG findings and the apparent vigilance was performed thirty minutes after the injection was completed (Fig. 1 und 2; Table 3). Following results are presented: 1) There are no significant differences between clonazepame and diazepame with respect to therapeutic success (Table 3). 2. There are almost no differences concerning therapeutic success in the three forms of petit-mal status listed above (Table 3). 3) The initial success was 57%: 46% in infantile myoclonic seizures, 56% in Lennox syndrome, 70% in myoclonic-astatic petit-mal. The number of relapses for all forms was high: On the day following the injection only 18% of all patients did not show continued petit-mal-status: 18% in infantile myoclonic seizures, 15% in Lennox syndrome, 23% in myoclonicastatic petit mal (Table 3). 4) 13 patients were no longer in a status on the following day. 3 children were out of status spontaneously, independent from the intravenous application, 4 patients, one with infantile myoclonic seizures and 3 with Lennox syndrome, showed a focal EEG, 6 patients, 2 with infantile myoclonic seizures, 3 with Lennox syndrome, 4 with myoclonic-astatic petit mal, were further demonstrating generalised paroxysms (Fig. 1 und 2). 5) In infantile myoclonic seizures and in the Lennox syndrome almost always a focal EEG could be seen that accompanied the decrease of generalised paroxysms (hypsarrhythmia or 2/sec slow wave and spike). This finding has not been seen in the myoclonic-astatic petit mal, another sign that the latter is of primary generalised, "centrencephal" origin in contrast to the first two forms of convulsive disorders (Fig. 1, 2).
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PMID:[Intraveneous therapy of petit mal status with diazepame and clonazepame (author's transl)]. 40 24

A 20-year-old mentally retarded woman, who had a history of intractable epileptic seizures since early childhood, had prolonged episodes of confusion, decreased responsiveness and automatic behavior lasting as long as 2 days. These are believed to represent epileptic status of the complex partial (psychomotor) type because the electroencephalogram (EEG) recorded during two such periods showed continuous high amplitude, semirhythmic, 4 to 6 cycles per second (cps), spike activity over both frontotemporal regions; several interictal tracings revealed a consistent spike focus in the right anterior temporal area. Diazepam given intravenously during one such episode terminated both the abnormal behavior and the ictal discharges in the EEG.
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PMID:Complex partial status epilepticus (psychomotor status). 56

Diazepam 0.05-0.25 mg/kg increased the dose of lignocaine required to cause seizures in Rhesus monkeys by 24-34%. Spontaneous ventilation was maintained adequately during lignocaine administration following diazepam treatment and no adverse cardiovascular effects occurred. Before the onset of lignocaine-induced seizures in non-treated animals, the animals appeared to be drowsy. However, prior to administration of diazepam masked this effect. Convulsions were controlled by smaller doses of diazepam in non-treated animals than in diazepam-treated animals. Also, the animals that were pretreated with diazepam had a greater duration of depression after seizure.
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PMID:Diazepam in the prophylaxis of lignocaine seizures. 81 22


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