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)

1. Neither cannabichromene (CBC) nor delta 9-tetrahydrocannabinol (THC) protected mice from electroshock-induced seizures, although THC inhibited postictal mortality. Minor effects were produced on seizure latency and duration. 2. CBC had a weak analgetic action in mice; THC had a moderate and lengthy effect, which was potentiated at 2 hr by concurrent CBC. 3. Both CBC (10-75 mg/kg, i.p.) and THC (20 mg/kg) reduced motility of mice, the THC equalling the highest dose of CBC. 4. Performance of a conditioned avoidance response was strongly impaired by THC, but not by CBC, nor did CBC combined with THC have influence on the effects of THC.
Gen Pharmacol 1983
PMID:Neurobehavioral actions of cannabichromene and interactions with delta 9-tetrahydrocannabinol. 630 31

The effects of levodopa, apomorphine and 3,4-dihydroxyphenylserine (DOPS) on tonic seizures elicited by strychnine were investigated in mice. Levodopa (6.25-100 mg/kg), apomorphine (0.2-0.8 mg/kg) and FLA-63 (12.5 mg/kg) profoundly delayed the onset and reduced the incidence of strychnine seizures. In addition, these drugs decreased strychnine-induced mortality. DOPS (1-16 mg/kg) apparently shortened the onset of strychnine seizures and altered strychnine-induced mortality in a dose-dependent manner; low doses (1-2 mg/kg) enhanced while moderate doses (4-8 mg/kg) reduced the mortality rate. FLA-63 (12.5 mg/kg) potentiated the anticonvulsant effect of low doses of levodopa (6.25-12.5 mg/kg) while it had no significant influence on the anticonvulsant effect of higher doses (25-100 mg/kg) of levodopa. In addition, the onset of strychnine seizure was further delayed by FLA-63. Haloperidol (0.5 mg/kg) potentiated the convulsant effect of strychnine (1 mg/kg) as well as strychnine-induced mortality. It also antagonised the protective effect of levodopa (12.5 and 100 mg/kg) against strychnine (1 mg/kg). Phentolamine (5 mg/kg) and +/- propranolol (1 mg/kg) antagonised strychnine seizures. Strychnine-induced mortality was also reduced by these drugs. In addition, the effects of DOPS (2 mg/kg) on strychnine seizures were antagonised by phentolamine and propranolol. These results indicate that enhancement of dopaminergic and noradrenergic neurotransmission respectively attenuate and potentiate strychnine seizures in mice.
Gen Pharmacol 1984
PMID:Influence of levodopa, apomorphine and 3,4-dihydroxyphenylserine (DOPS) on strychnine-induced seizures in mice. 642 68

Administration of muscimol to mice in subcutaneous doses between 0.34 and 1.25 mg/kg produced partial protection against 3-mercaptopropionic acid (MPA)-induced seizures. Glycine at a dose of 750 mg/kg (10 mmol/kg) protected 20% of the animals 45 min after its administration. Combined treatment with the two compounds gave a near to complete protection against MPA-induced seizures. These observations suggest that the concomitant enhancement of glycinergic and GABAergic activities amplify the anticonvulsant effect of these neuronal systems against seizures induced by impairment of GABA-mediated transmission.
Gen Pharmacol 1984
PMID:Synergistic anticonvulsant effects of a GABA agonist and glycine. 648 32

The role of hypnosis as a tool in the treatment of problems commonly encountered among medical and surgical patients is examined. Hypnosis is defined as a change in state of mind far more akin to intense concentration than sleep. Diagnostic implications of differences in hypnotic responsivity are explored, and scales suitable for use in the clinic are examined. Uses of hypnosis in treating anxiety, pain, childbirth, psychosomatic symptoms, seizure disorders, neuromuscular dysfunction, and habits are described and evaluated. The phenomenon of hypnosis is presented as a means of exploring the mind-body relationship in a controlled fashion, providing information of diagnostic importance while at the same time allowing hypnotizable patients to intensify their concentration and interpersonal receptivity in the service of a therapeutic goal.
Gen Hosp Psychiatry 1983 Dec
PMID:Hypnosis with medical/surgical patients. 666 57

We have set up guidelines for the practice of electroconvulsive therapy, based on Scandinavian clinical experience and research. Because the therapeutic effect is a result of the cerebral seizure, and the organic side effects partly consequences of the electrical stimulation, the aim should be to induce maximal seizure activity using minimal electrical energy. Essential features of optimal therapy are (1) absence of therapy with benzodiazepines and other anticonvulsant drugs, (2) superficial narcosis, (3) abundant oxygen supply, (4) threshold stimulation with brief-pulse stimuli, and (5) unilateral, parietotemporal, nondominant application of the electrodes. Seizure duration should always be measured to make sure that maximum seizure activity has taken place.
Arch Gen Psychiatry 1983 May
PMID:Present practice of electroconvulsive therapy in Scandinavia. 683 35

Seizure durations in electroconvulsive therapy (ECT) were determined by both EEG and BP cuff methods in 20 patients receiving 225 seizures. The estimates were highly correlated, with cuff estimates 10% shorter than those by EEG. Routine monitoring of seizure duration by the BP cuff method is recommended, particularly in unilateral ECT. Monitoring seizure time should resolve controversies over the efficacy of different forms of ECT, as well as improve clinical practice where disturbing reports of missed seizures are now documented.
Arch Gen Psychiatry 1982 Oct
PMID:Monitoring the duration of electroconvulsive therapy seizures: 'cuff' and EEG methods compared. 712 48

The characteristics of 9,365 patients admitted to public hospitals in a one-year period were analyzed in relation to the presence of assaultive or suicidal problems prior to admission. There were definite differences in the occurrence of assaultive or suicidal problems in relation to sex, age, primary diagnosis, education, race, marital status, prior private care, and source of referral to the hospital. There were no significant differences in regard to the history of previous psychiatric admissions, veteran status, or history of seizures. These findings demonstrate the usefulness of a large, routinely collected data base in the study of specific psychiatric problems and offer directions for intervention and future research in the field of life-threatening behavior.
Arch Gen Psychiatry 1980 Feb
PMID:Assault, suicide, and mental illness. 735 48

In the long QT syndrome (LQT), individuals suffer from syncope, seizures and sudden death due to cardiac arrhythmias, specifically torsade de pointes and ventricular fibrillation. Many of these individuals also have prolongation of the QT interval on electrocardiograms, suggesting abnormal cardiac repolarization. To improve our understanding of the mechanisms underlying LQT and to facilitate presymptomatic diagnosis, we have begun to study families with autosomal dominant LQT. In 1991, we reported tight linkage between the LQT phenotype and the Harvey ras-1 gene (HRAS) in several families of Northern European descent. This discovery localized an LQT gene to chromosome 11p15.5 and made presymptomatic diagnosis in some families possible. In initial experiments, no recombination between HRAS and LQT was observed, making this protoncogene a candidate for LQT. This hypothesis was supported by physiologic data; other investigators had shown that ras proteins modulate cardiac potassium channels and an abnormality of potassium homeostasis could explain LQT. We eliminated HRAS as a candidate, however, by sequencing the coding region in 10 unrelated patients and finding no mutations. This indicated that the LQT locus was nearby, but not HRAS. Autosomal dominant LQT was previously thought to be genetically homogeneous and the first seven LQT families we studied were linked to 11p15.5. In 1992, however, several groups, including my laboratory, identified locus heterogeneity for LQT. Recently we identified a second LQT locus, LQT2, on chromosome 7q35-36. Because several families were unlinked, at least one more LQT locus exists. This degree of heterogeneity presents opportunities. It seems likely, for example, that proteins encoded by distinct LQT genes interact to modulate cardiac repolarization.(ABSTRACT TRUNCATED AT 250 WORDS)
Soc Gen Physiol Ser 1995
PMID:Molecular genetics of long QT syndrome. 767 24

1. The premorbid behaviors produced by the administration of cocaine, ethanol, their combination, as well as a metabolite produced by their co-administration, viz. cocaethylene, were defined, determined and quantified in the HS strain of mice. 2. The LD50 for ethanol was 9.71 g/kg in males and 9.45 g/kg in females, whereas the LD50 values in male and female mice for cocaine were 101.55 and 90.00 mg/kg, respectively. 3. The data indicate that clonic-tonic seizures continued into status epilepticus after cocaine administration and prior to cocaine-induced lethality. In contrast, administration of the cocaine-ethanol metabolite cocaethylene produced status epilepticus without producing clonic-tonic seizures yet still resulted in lethality. 4. Thus, both cocaine and cocaethylene may produce their lethal effects in mice through neuro-regulatory mechanisms mediating protracted seizure induction.
Gen Pharmacol 1995 Jan
PMID:Premorbid behaviors produced by cocaine, ethanol and cocaethylene in the mouse. 771 72

1. The behaviour and EEG effects of the dopamine and sigma (sigma) ligands (+) 3-(3-hydroxyphenyl)-N-(1-propyl)piperidine ((+)3-PPP) were studied in mice. 2. (+) 3-PPP dose-dependently (60-100 mg/kg i.p.) produced behavioural and electrical tonic-clonic seizures. 3. The incidence of the tonic seizures elicited by 100 mg/kg of the drug was significantly (P < 0.05) prevented by spiperone (0.5 mg/kg i.p.) and haloperidol (0.5 mg/kg i.p.). 4. The results show an influence on the behavioural and electrical threshold of convulsions by (+) 3-PPP depending on a prevalent interference on dopamine receptors.
Gen Pharmacol 1995 May
PMID:3-(3-Hydroxyphenyl)-N-(1-propyl)piperidine elicits convulsant effects in mice. 778 37


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