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)

Focal injection of 2-amino-7-phosphonoheptanoic acid in the substantia nigra, pars reticulata or pars compacta, in rats produces a dose-dependent suppression of the tonic extensor seizure component in the electroshock test. Haloperidol pretreatment prevents stereotyped behaviour induced by 2-amino-7-phosphonoheptanoic acid, but does not change the effect on the electroshock test. This anticonvulsant effect of 2-amino-7-phosphonoheptanoic acid probably results from an antagonist action at a receptor site sensitive to N-methyl-D-aspartate leading to a decrease in activity in nigral efferent systems.
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PMID:Anticonvulsant action of 2-amino-7-phosphonoheptanoic acid in the substantia nigra. 652 64

The effects of trifluoperazine and haloperidol on protective activity of phenazepam were studied during seizures in mice treated with pentylenetetrazole (an index used for the appraisal of tranquilizing activity) as was their action on the phenazepam-induced depression of the test potential in the recovery cycles of somatosensory primary response. Trifluoperazine administered in doses of 0.1-0.5 mg/kg potentiated anticonvulsant action of phenazepam but did not change its effects on the recovery cycles of primary response. Haloperidol also potentiated anticonvulsant action of phenazepam. However, the doses administered were 4-5-fold lower than the tranquilizing doses of haloperidol. The drug also increased the depression of the test potential in the somatosensory recovery cycle, caused by phenazepam. This suggests an increment of GABA-positive effect of the tranquilizer. It appears that higher activity of haloperidol in elevating anticonvulsant and, probably, anxiolytic effects of phenazepam is determined by interaction of these drugs on the level of cortical GABA-ergic receptors.
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PMID:[Effect of triftazin and haloperidol on the activity of phenazepam]. 688 8

Before treatment 80 unselected patients suffering from delirium tremens were examined with regard to 13 psychopathological criteria. For the data a matrix of correlation was computed and it was factor analyzed according to the principal-component method. In consideration of the course of the value-curve two factors were interpreted. The result, however, is an undetailed classification. In addition to that, the data were cluster-analyzed according Ward. The results of the multivariate statistical analysis admit the assumption of two great, though heterogenous groups of symptoms (hallucination/vigilance). Factor I comprises the symptoms, disorder of orientation and consciousness, sweating, agitation and tremor on its positive pole, the duration of the delirant state on its negative pole. Factor II combines paranoid-hallucinatory symptoms, fearful affects and suggestibility on its positive pole, while on its negative, there are happy affect and grand-mal seizures. The bipolarity of this factor and additional diagnoses show that paranoid-hallucinatory symptoms without disorder of consciousness and grand-mal seizures mutually exclude each other. From this a differential therapy treating patients suffering from paranoid-hallucinatory symptoms with neuroleptics (e.g. Haloperidol) can be deduced, while the danger of grand-mal seizures has to be considered when disorders of consciousness appear.
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PMID:[Principle factors and symptom complexes in delirium tremens, factor and a group analytic study]. 717 1

1. The effects of some GABAergic and dopaminergic agents on pyrimethamine-induced tonic seizures were investigated in mice. 2. Pyrimethamine dose dependently induced seizures in mice. 3. Muscimol, AOAA and DABA significantly protected mice against pyrimethamine-induced seizures. 4. Bicuculline and picrotoxin effectively potentiated seizures elicited by pyrimethamine and significantly antagonized the protective effect of muscimol against the seizures. 5. Diazepam and phenobarbitone effectively protected mice against seizures elicited by pyrimethamine. 6. L-Dopa significantly potentiated pyrimethamine-induced seizures. 7. Apomorphine and pargyline significantly reduced the latency of seizures induced by pyrimethamine. 8. Haloperidol and pimozide effectively protected mice against pyrimethamine-elicited seizures and also significantly antagonized the potentiating effects of apomorphine and L-dopa on the seizures. 9. Disulfiram significantly potentiated seizures induced by pyrimethamine and also significantly enhanced the seizure-potentiating effect of L-dopa. 10. alpha-Methyl-p-tyrosine effectively protected against seizures induced by pyrimethamine. However, L-dopa significantly potentiated the seizures in alpha-methyl-p-tyrosine-pretreated animals. 11. Muscimol significantly attenuated the potentiating effect of L-dopa on pyrimethamine-induced seizures while bicuculline significantly enhanced the effect of L-dopa. Furthermore, haloperidol significantly potentiated the protective effect of muscimol against pyrimethamine-induced seizures. 12. These results suggest that both GABA and dopamine might be involved in the mechanism(s) of pyrimethamine seizures in mice.
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PMID:GABAergic and dopaminergic systems may be involved in seizures induced by pyrimethamine in mice. 787 56

The effects of bromocriptine and haloperidol, either alone or in combination, on ethanol withdrawal syndrome (EWS) have been investigated in rats. Bromocriptine (5 mg/kg 1P) inhibited wet dog shakes behavior and catatonia but potentiated the intensity of abnormal gait. The latency of the audiogenic seizures was prolonged by bromocriptine treatment. Haloperidol (0.5 mg/kg SC) decreased the intensity of stereotyped behavior but potentiated catatonia and agitation. It did not antagonize the behaviors induced by bromocriptine when injected in combination except the increased latency of the audiogenic seizures. The total intensity score of the EWS was not significantly different from that in untreated control. The results suggest that brain dopaminergic system may be involved to a limited extent in mediating the EWS in rats.
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PMID:Effects of bromocriptine and haloperidol on ethanol withdrawal syndrome in rats. 788 15

The effects of some beta-endorphin fragments with neuroleptic-like properties, i.e., tau-endorphin, des-tyr1-tau-endorphin (DT tau E), desenkephalin-tau-endorphin (DE tau E), in comparison with the dopaminergic antagonist haloperidol,- were studied on the EEG and behavioral alterations induced by beta-endorphin in the rabbit. beta-Endorphin administered i.c.v. (5-30 nmol) induced EEG nonconvulsive limbic seizures as well as EEG background and behavioral alterations which were antagonized by naloxone administered i.v. (1-2 mg/kg). Haloperidol, tau-endorphin, DT tau E and DE tau E were unable to prevent beta-endorphin-induced alterations when injected in a single dose i.v. (25-50 micrograms/kg), 15 min before beta-endorphin. Subchronic i.v. administration of DT tau E or DE tau E (25 micrograms/kg/day) for 4 consecutive days prevented completely EEG limbic seizures as well as EEG background and behavioral alterations induced by i.c.v. beta-endorphin injected 15 min after the fourth dose; however, haloperidol (30 micrograms/kg/day) administered with the same schedule as DT tau E or DE tau E was able to prevent only EEG epileptiform and EEG background alterations induced by beta-endorphin. tau-Endorphin administered i.v. for 4 consecutive days (25 micrograms/kg/day) did not consistently influence any of the beta-endorphin effects. Our results show that DT tau E and DE tau E, which are devoid of opioid activity, exert a strong antagonism on ictal seizures as well as on other EEG alterations and behavioral alterations induced by beta-endorphin, and suggest that the antagonism shown by these drugs and by haloperidol on the EEG effects induced by beta-endorphin are exerted at least in part through an indirect action, i.e., an interaction with the dopaminergic system.
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PMID:Subchronic treatment with fragments of beta-endorphin prevents electroencephalographic seizures and behavioral alterations induced by centrally administered beta-endorphin in the rabbit. 811 60

It has been shown that neuroleptics which interact selectively with either D-1 or D-2 dopamine receptors possess a marked difference in their propensity on seizures. The aim of this work was to investigate whether the D-1 antagonist SCH 23390 differs from haloperidol (D-2 antagonist) in models of experimental epilepsy induced by electrical stimulation of selected brain regions (hippocampus and amygdala), in rabbits. Haloperidol increased and SCH 23390 significantly decreased the susceptibility to seizures in both models investigated. The data suggest that the D-1 and D-2 receptor subtypes have different roles in the mechanisms underlying seizures.
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PMID:[Role of the dopaminergic system in experimental models of epilepsy]. 814 16

The influence of some dopaminergic and noradrenergic agents on seizures induced by chloroquine (45-100 mg/kg, i.p.) was investigated in mice. Apomorphine (0.2-0.8 mg/kg, s.c.). L-dopa (25-50 mg/kg, s.c.) benserazide (5 mg/kg, i.p.) plus L-dopa (50 mg/kg, s.c.), pargyline (100 mg/kg, i.p.), FLA-63 (10-20 mg/kg, s.c.) and FLA-63 (10 mg/kg, s.c.) plus L-dopa (50 mg/kg, s.c.) profoundly shortened the latency of seizures induced by chloroquine (65 mg/kg, i.p.). L-Dopa (50 mg/kg, s.c.) weakly reduced the latency and weakly increased the incidence of chloroquine (50 mg/kg, i.p.)-induced seizures. alpha-Methyl-p-tyrosine (25-100 mg/kg, i.p.) dose-dependently and significantly reduced the incidence and significantly prolonged the latency of chloroquine (65 mg/kg, i.p.)-induced seizures. However, L-dopa (50 mg/kg, s.c.) effectively increased the proportion of animals convulsing and effectively reduced the latency of seizures induced by chloroquine (65 mg/kg, i.p.) in alpha-methyl-p-tyrosine-pretreated mice. Haloperidol (0.25-1.0 mg/kg, i.p.) and pimozide (2-4 mg/kg, i.p.) markedly reduced the incidence and markedly prolonged the latency of seizures induced by chloroquine (65 mg/kg, i.p.) in a dose-related manner. However, apomorphine (0.4-0.8 mg/kg, s.c.) and L-dopa (25-50 mg/kg, s.c.) profoundly attenuated the protective effects of haloperidol (0.5 mg/kg, i.p.) and pimozide (4 mg/kg, i.p.) against chloroquine (65 mg/kg, i.p.)-induced seizures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chloroquine-induced seizures in mice: the role of monoaminergic mechanisms. 847 29

1. The differential role played by blockade of D-1 or D-2 dopamine receptors in mechanisms underlying seizures was studied in a model of EEG after-discharge induced by electrical stimulation of selective brain regions (dorsal hippocampus and amygdala) in the rabbit. 2. The D-2 antagonist haloperidol (1 mg/Kg) increased significantly after-discharge duration after stimulation of either hippocampus or amygdala and lowered after-discharge threshold in few animals. 3. The D-1 antagonist SCH 23390 (0.3 mg/Kg) caused no changes following stimulation of amygdala and reduced after-discharge duration when hippocampus was stimulated. 4. Haloperidol exerted a proconvulsant action in this experimental model, having a clearer influence on D-2 receptors. SCH 23390 had no effect on amygdala whereas it exerted protection on the hippocampus. 5. The present data suggest that D-1 and D-2 receptors have different roles in generating and spreading the epileptic activity.
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PMID:Role of dopamine D-1 and D-2 antagonists in a model of focal epilepsy induced by electrical stimulation of hippocampus and amygdala in the rabbit. 853 28

Haloperidol levels in blood were measured monthly in 43 refractory chronic schizophrenic patients referred to a locked skilled nursing facility for long-term treatment. Gross toxic side effects (seizures, catatonia, confusion) and Neuroleptic Induced Deficit Syndrome in conjunction with blood levels over 30 ng/ml were identified in 13 of our 43 patients. Blood level reductions contributed to a reduction of side effects and clinical improvement and led to the expedited discharge of 6 of these 13 patients of the toxic subgroup. Considerable blood level variation was evident in single samples, and four levels appeared necessary to develop confidence for accuracy. Significant dose to blood level interindividual variability was identified, thereby bringing into question fixed-dose approaches to patients. The results strongly suggest the utility of haloperidol blood levels in the clinical setting.
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PMID:Haloperidol dose and blood level variability: toxicity and interindividual and intraindividual variability in the nonresponder patient in the clinical practice setting. 883 64


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