Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In electroshock test apomorphine appeared without effect, D, L-amphetamine and L-DOPA (in a high dose) elevated the convulsive threshold, while amantadine decreased it. Among investigated dopamine (DA) receptor blockers spiperone, pimozide and fluphenazine lowered the threshold, haloperidol being without effect. The convulsive threshold elevated by L-DOPA was not affected by neuroleptics and phentolamine but on the other hand DA receptor blockers and phentolamine anatagonized the effect of D, L-amphetamine. The effect of amantadine was not influenced by neuroleptics. In pentylenetetrazol (PTZ) test only amantadine and L-DOPA (in high doses) affected the threshold, increasing seizure susceptibility; the above effect was not abolished by pimozide. Our results seem to indicate that the activity of brain DA system seems not to be involved directly in the susceptibility to electrogenic or PTZ-induced seizures in mice.
Pol J Pharmacol Pharm
PMID:Brain dopamine and seizure susceptibility in mice. 74 May 53

By the condensation of 2-phenyl-3-acylchloride quinazolin (3H)-4-one with N-phenyl- and N-methyl piperazines or piperidine, 15 new 2-phenyl-3-piperidino/substituted piperazino acyl-quinazolin (3H)-4-ones 1--3 have been prepared. All the compounds barring one exhibited at the 100 mg/kg dose level significant activity against pentylenetetrazol induced seizures but these compounds did not afford any protection against electroshock induced seizures.
Pol J Pharmacol Pharm
PMID:Synthesis of some 2,3-disubstituted quinazolones as possible anticonvulsants. 74 May 59

Bilateral lesions involving the nucleus locus coeruleus produced a substantial decrease in the forebrain noradrenaline concentrations. Lesioned animals showed an increased susceptibility to audiogenic seizures. It is supposed that noradrenergic neurons, belonging to the locus coeruleus, play an inhibitory role in the seizure mechanism.
Acta Physiol Pol
PMID:Audiogenic seizures in rats: relation to noradrenergic neurons of the locus coeruleus. 74 2

The analysis was carried out in a group of 32 children with coexistent chronic urinary tract or respiratory infections. In 20 children an unfavourable effect of infection on the course of epilepsy was observed. Worsening of epilepsy during infection was observed mainly in children without evidence of nervous system damage with primarily generalized seizures, and in cases when the first attacks developed after protective vaccinations. The effect of urinary tract infections was particularly unfavourable. The authors put forward the hypothesis of immunological basis of exacerbation of epileptic seizures during chronic infections.
Neurol Neurochir Pol
PMID:[Effect of infections on the course and effectiveness of epilepsy treatment in children]. 80 69

The importance of various morphotic elements of EEG tracings in the diagnosis of seizures in children is discussed with particular reference to seizures connected with fever. The common neurophysiological mechanism of epileptic discharges in various epileptic seizures in children and adults is stressed calling attention to the fact that EEG investigation in only one of the elements on which the diagnostic process should be based. Attention is called also to the prognostic significance of duration of post-seizure slowing down of the background activity and occurrence of focal spike discharges at the site of greatest slowing of the activity - the greater is this slowing (above one week) the worse is the prognosis. In view of a considerable range of the concept of electroencephalographic normality in children it is stressed that EEG investigations should be repeated after the seizure to study the dynamics of bioelectric changes: the duration and type of EEG abnormalities.
Neurol Neurochir Pol
PMID:[Value of EEG studies in the differential diagnosis of seizures in children]. 80 65

Benzonal was given to 52 epileptics. In 50 cases the duration of treatment ranged from 3 months to 7 years (mean 18 months) in doses of 100-500 mg daily, in 2 cases it had to be withdrawn after a short-term treatment because of intolerance. In all cases the drug was given together with other anticonvulsants: hydantoin, derivatives, mysodin, Tegretol, pheneturid or Ospolot in place of previously administered phenobarbital. It was found that benzonal reduced significantly the frequency of partial simple seizures (in 6 out of 20 cases) and grand mal seizures (in 24 out of 34 cases), while its action on the partial complex seizures was much weaker (improvement in only 7 out of 20 cases). The drug was usually well tolerated, side effects of greater intensity developed in 2 cases only, transient somnolence was observed in another 6 cases. In EEG records a slight favourable effect was exerted on pathological background activity with absent effect in focal changes and increase of seizure activity. The authors believe that in view of its favourable clinical action and good tolerance the drug may be widely used in properly selected cases of epilepsy.
Neurol Neurochir Pol
PMID:[Clinico-electroencephalographic observations in epileptic patients during long-term treatment with benzonal]. 81 1

The period of the so-called "maturation" of the epileptogenic focus creates a potential field for pharmacological prevention of further development of the disease. The author analysed the experimental investigations carried our by himself on the effects of epileptogenic foci and/or diphenylhydantoin on the process of learning, EEG tracings, and histological findings in the brain and internal organs, and believes that prophylactic administration of diphenylhydantoin in moderate therapeutic doses (20 mg daily) and for a relatively short time period (1 year) is associated with a much lower possibility of side effects than the risk of development of post-traumatic epilepsy. A condition of successful prophylaxis is the administration of the drug immediately after trauma since the experimental investigations of the author indicate that starting treatment at the time of epileptogenic focus development in the EEG, even before the appearance of clinical seizures is too late for complete prophylactic or even therapeutic success.
Neurol Neurochir Pol
PMID:[Pharmacological possibilities of preventing post-traumatic epilepsy]. 81 14

In the analysed material of 248 children with past craniocerebral trauma epilepsy developed in 25 cases (10%). In the group of post-traumatic epilepsy seizures developed twice as frequently after severe trauma than after light trauma. In EEG investigations in the group with light trauma the observed changes included slowing down of background activity, focal changes or lateralization as the only finding. In the group of severe trauma the EEG changes included slowing down of background activity with associated lateralization or focal changes. In the group of children with epilepsy following severe trauma the same changes were found in EEG curves prior to development of seizures. The authors believe that changes of this type may predict manifestation of epilepsy and may be regarded as sufficient for prophylactic treatment with anticonvulsants.
Neurol Neurochir Pol
PMID:[Problem of epilepsy prevention in children with abnormal EEG tracings following cranial trauma]. 81 15

The author demonstrated that a strong pressure exerted on the site of intraorbital branches of the trigeminal nerve can interrupt grand mal attack if exerted at the beginning of the seizure. In a group of 50 observed epileptics with frequent attacks it was possible in 29 cases to perform this procedure before the onset of convulsions and in all these cases the attack was prevented. On the other hand, the same procedure performed at the time of convulsions was without effect on the attack. The author discusses the neurophysiological bases of this observation.
Neurol Neurochir Pol
PMID:[Interruption of grand mal epileptic seizures by the trigeminal nerve stimulation]. 81 17

Pharmacological prevention of epilepsy, especially in cases of past cranial trauma, arose as one of the problems connected with this disease. Attention has been called, however, ever more frequently to the neurotoxic effects of antiepileptic drugs symptoms and signs of with brain damage. Drug-induced encephalopathy or neuropathy occur particularly in patients with disorders of anticonvulsant drug metabolism in liver diseases or due to inborn enzymatic defects. Teratogenic and even epileptogenic side effects has been described in cases treated with therapeutic doses of anticonvulsants. The author discusses in this aspect the indications to pharmacological prevention of epilepsy quoting cases observed by her in which cranial trauma was followed by one or several seizures in early post-traumatic period and presence of seizure potentials was found in EEG. During follow-up observations of severel years duration the seizures were not repeated and EEG has returned to normal.
Neurol Neurochir Pol
PMID:[Negative aspects of pharmacological prevention of epilepsy]. 81 16


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