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

Case histories are presented for four psychotic patients who ingested large quantities of water and subsequently developed grand mal seizures and serum sodium levels of less than 121 meq/liter. The physiology of psychogenic polydipsia and related disorders is reviewed. The relation of this disorder to temporal lobe seizures and to the use of phenothiazines is considered.
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PMID:Polydipsia, hyponatremia, and seizures in psychotic patients. 0 49

Significant correlation in 11 different 1,4-benzodiazepinones has been established between log k2 (the second order rate constant for the reduction of the "azepinones" by sodium borohydride) and their ED50 against leptazol-induced seizures in mice. The results suggest a possible involvement of the carobnyl group at the receptor site.
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PMID:Structure activity relation for some 1,4-benzodiazepinones: correlation between rate constants for reduction by sodium borohydride and antileptazol ED50. 2 91

The antagonism of various seizure and time-related components of the convulsions resulting after IV injection of D,L-allylglycine into male Wistar rats were assessed in a standard test procedure. Trimethadione and ethosuximide did not antagonize the seizure components, whereas clonazepam, phenobarbital, diphenylhydantoin, primidone, valproate sodium, aminoxyacetic acid, etomidate, acetazolamide, flunarizine, pipamperone and baclofen did. The allylglycine test may thus represent a relatively specific method of differentiating between drugs effective against partial or generalized convulsive seizures from those effective against absence seizures. The neuroleptics haloperidol and pimozide were completely inactive in contrast to their reported antagonism of bicuculine seizures. The spectra of the active substances are discussed with respect to Principal Component and Cluster Analysis. Noteworthy are the similarities between baclofen and etomidate; between aminoxyacetic acid, phenobarbital and valproate sodium; and between diphenylhydantoin and flunarizine.
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PMID:Effects of some anti-epileptic, neuroleptic and gabaminergic drugs on convulsions induced by D,L-allylglycine. 4 Dec 64

Of thirty-five patients with various types of epilepsy treated with sodium valproate, 15 achieved complete seizure control on that drug alone, 12 other patients benefited and eight failed to improve on the drug. Excellent results were more likely in those with petit mal epilepsy and in those whose epilepsy was controlled with other drugs at the expense of side effects. Three patients were unable to tolerate valproate, but in general few patients experienced side effects and several patients felt much better on valproate than on their previous drugs. A twice daily dosage regime was satisfactory. Plasma valproate levels at the final dose covered a wide range, 0.21 - 1.2mmol/l (34 to 190 microgram/ml) and did not correlate with response, lack of response or side effects.
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PMID:Sodium valproate (Epilim) in epilepsy: a trial. 10 32

A child with pattern sensitive epilepsy is reported. She had both absences and generalised seizures. The latter occurred spontaneously but the former followed concentration on patterned materials. These self-induced seizures appeared to have an affective component. The EEG showed generalised atypical spike and wave discharges both in the resting state and during intermittent photic and pattern stimulation. The patient responded to sodium valproate.
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PMID:Pattern sensitive epilepsy: a case report. 11 7

Two epileptic patients developed an acute toxic encephalopathy consisting of altered behavior, deteriorating seizure control, and confusion while taking sodium valproate alone. Serum valproate levels were greater than 100 microgram/ml in both. Toxic symptoms resolved when the dose of valproate was reduced, with a consequent fall in serum concentration of the drug.
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PMID:Acute intoxication with sodium valproate. 11 82

Sodium valproate and clonazepam were given in combination to 17 refractory epileptic patients and their progress was reviewed clinically and by EEG's. Even though plasma concentrations of sodium valproate and conventional anticonvulsants were monitored and adjusted according to individual requirements, combination therapy consisting of valproate and clonazepam was ineffective in controlling seizures in the majority of patients. A further 40 patients receiving clonazepam were reviewed in relation to adverse reactions. 22 patients in this group suffered from undesirable effects attributable to clonazepam. These effects were managed by cessation of the drug or a reduction in the dose. The commonest side effects were drowsiness, loss of concentration, irritability and aggression.
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PMID:Some aspects of the clinical use of clonazepam in refractory epilepsy. 12 7

The (Na+ 4 K+)- and Mg2+-dependent ATPase distribution in several brain areas has been investigated in Quaking mutant mice characterized by myelin deficiency. A marked decrease of (Na+ + K+)-ATPase activity has been found in limbic structures, hypothalamus and cerebellum. The Mg2+-dependent activity did not change. A possible involvement of the impairment of the (Na+ + K+)-ATPase activity in the seizure susceptibility of this mice is discussed.
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PMID:The (Na+ + K+)-ATPase activity in brain of Quaking mice. 12 35

Drug treatment of status epilepticus is reviewed. Tonic-clonic, focal motor, complex partial and absence status epilepticus are discussed. In managing tonic-clonic status epilepticus one should: (1) maintain vital functions at all times, (2) identify and treat precipitating factors and (3) administer an intravenous loading dose of phenytoin sodium or phenobarbital sodium. Careful use of i.v. diazepam sometimes helps to achieve these objectives. Intravenous phenytoin sodium and phenobarbital sodium provide definitive, long-term control of tonic-clonic seizures but must be administered slowly and require time to reach peak brain concentrations. Intravenous diazepam appears to enter and exit from the brain rapidly and may control seizures while therapeutic brain concentrations of long-acting drugs are being achieved. Phenytoin, phenobarbital and diazepam should not be administered intramuscularly in treating status epilepticus. Treatment of focal motor and complex partial status epilepticus is similar to that of tonic-clonic status epilepticus, but i.v. diazepam is required less frequently and loading doses of phenytoin and phenobarbital sometimes can be given more slowly. Status epilepticus of the absence type is managed with i.v. acetazolamide sodium or diazepam. Paraldehyde, muscle relaxants, general anesthesia and lidocaine may be tried when conventional therapies fail.
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PMID:Drug therapy reviews: drug therapy of status epilepticus. 15 Feb 28

Post-tetanic potentiation (PTP) of monosynaptic reflex was estimated in spinal cords in the drug-free state after the administration of a convulsant dose of penicillin and after the administration of phenytoin. There was no apparent correlation between the degree of depression of PTP and the efficacy of controlling seizure activity by phenytoin. Extracellular potassium levels were measured with ion-selective microelectrodes. The post-stimulation clearing of [K+]0 was not accelerated by phenytoin, and frequently it was slowed. Post-stimulus undershooting of [K+]0 was diminished. Oxidation of NADH in cortex and of cytochrome a, a3 in spinal cord were measured by optical methods. Stimulus-evoked transient oxidation responses evoked by electrical stimulation were depressed by phenytoin. It is concluded that systemic administration of phenytoin in therapeutic doses does not stimulate Na+-K+-activated membrane ATPase in cortex and spinal cord. Unlike other depressants, phenytoin did not cause a reduction of "resting" redox levels of respiratory enzymes. The local regulation of blood flow remained unaltered after phenytoin administration. Phenytoin caused a moderate but consistent depression of the stimulus-evoked responses of potassium activity, electric potential, and oxidative enzymes, consistent with diminished outflow of potassium from cells, owing either to lesser activation of cells or to a lesser exchange of ions.
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PMID:Phenytoin, electric, ionic, and metabolic responses in cortex and spinal cord. 19 41


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