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At least 433 records · Page 24Linked to original sources
PubMed1985

SCH 23390 dissociated from conventional neuroleptics in apomorphine climbing and primate acute dyskinesia models.

SCH 23390 induced only a negligible incidence of the acute dyskinetic syndrome, a predictor of neuroleptic-induced extrapyramidal liability, in squirrel monkeys. However, haloperidol-induced dyskinesias were potentiated by SCH 23390 and were blocked by the D-1 agonist, SKF 38393. When administered orally or intraperitoneally to mice, SCH 23390 showed a considerably wider dose separation than did conventional neuroleptics between antagonism of apomorphine climbing and antagonism of stereotyped sniffing. Clinically relevant distinctions may exist between D-1 and D-2 antagonists, with D-1 antagonists (exemplified by SCH 23390) showing lower, although possibly not negligible, potential to cause extrapyramidal side effects.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1987

Carbamazepine as an adjunct of antipsychotic therapy.

The effect of low-dose haloperidol combined with the anticonvulsant carbamazepine was investigated in a 5-week placebo-controlled, double-blind study in acute schizophrenic patients. Weekly ratings showed a clinically pronounced and statistically significant improvement in both the carbamazepine and placebo groups. However, the patients on carbamazepine needed less neuroleptic and anticholinergic medication and experienced fewer side effects compared to the patients on placebo. Moreover, patients in the carbamazepine group showed a clear deterioration after discontinuation of carbamazepine (but maintenance of neuroleptic medication), while the placebo group did not change after discontinuation of placebo. Concomitant treatment with carbamazepine in psychotic patients may help to reduce neuroleptic dosages and unwanted side effects.

Adjuvants, Pharmaceutic↗
PubMed1967

Drug therapy.

Explore the source record for details and available documents.

Amphetamine↗
PubMed1977

Central nervous system activity of a novel class of annelated 1,4-benzodiazepines, aminomethylene-2,4-dihydro-1H-imidazo[1,2-a][1,4]benzodiazepin-1-ones.

The synthesis and CNS activity of a noval class of annelated 1,4-benzodiazepines, the aminomethylene-2,4-dihydro-1H-imidazo[1,2-a][1,4]benzodiazepines, are described. An investigation of the structure--activity relationships in the series derived from 8-chloro-2,4-dihydro-2-dimethylaminomethylene-6-phenyl-1H-imidazo[1,2-a][1,4]-benzodiazepin-1-one (10) led to the synthesis of a group of compounds with potent minor tranquillizer activity.

Aggression↗
PubMed1982

Amino acid amide derivatives of 2-[3-(aminomethyl)-4H-1,2,4-triazol-4-yl]benzophenones, a novel class of annelated peptidoaminobenzophenones.

A series of the title compounds was prepared via condensation of the 3-(aminomethyl)triazolylbenzophenone (5) with N-protected amino acids, followed by deprotection, amination of the 3-[(chloroacetamido)methyl]triazolylbenzophenone (6a,b), or reduction of the relevant azide derivative (6c). Some of the title compounds were also derived directly from the quinazolines 3 or 4 by acid-induced rearrangement, followed by deprotection. These new amino acid amide derivatives of the triazolylbenzophenones (2) were evaluated for central nervous system (CNS) activity. Members of this class of compounds exhibited a high level of CNS activities. For example, 2',5-dichloro-2-[3-[(glycylamino)methyl]-5-methyl-4H-1,2,4-triazol-4-yl] benzophenone (2c) was as active as triazolam, with an ED50 of 0.58 mg/kg (mice, po), against antifighting activity in the foot shock-induced fighting test. Other triazolylbenzophenone derivatives (2a-f) showed similar pharmacological activities.

Anesthesia↗
PubMed2000

Sensitivity of empirical metrics of rate of absorption in bioequivalence studies.

PURPOSE: The sensitivity and effectiveness of indirect metrics proposed for the assessment of comparative absorption rates in bioequivalence studies [Cmax, Tmax, partial AUC (AUCp), feathered slope (SLf), intercept metric (I)] were originally tested by assuming first-order absorption. The present study re-evaluates their sensitivity performances using the more realistic inverse Gaussian (IG) model characterizing the input process for oral drug administration. METHODS: Simulations were performed for both the first-order or exponential model (EX) which is determined by only one parameter, the mean absorption time (MAT = 1/k(a)), and the IG model, which additionally contains a shape parameter, the relative dispersion of absorption time distribution (CV2A). Kinetic sensitivities (KS) of the indirect metrics were evaluated from bioequivalence trials (error free data) generated with various ratios of the true parameters (MAT and CV2A) of the two formulations. RESULTS: The behavior of the metrics was similar with respect to changes in MAT ratios with both models: KS was low with Cmax, moderate with SLf and AUCp, and high with I and Tmax following correction for apparent lag time (Tlag). Changes of the shape parameter CV2A, however, were not detectable by Cmax, Tmax, SLf, and AUCp. Changes in both MAT and CV2A were well reflected by I with CV2A - ratio > 1. I exhibited approximately full KS also with CV2A - ratio < 1 when a correction was first applied for the apparent lag time. CONCLUSIONS: The time profile of absorption rates is insufficiently characterized by only one parameter (MAT). Indirect metrics which are sensitive enough to detect changes in the scale and shape of the input profile could be useful for bioequivalence testing. Among the tested measures, I is particularly promising when a correction is applied for Tlag.

Antipsychotic Agents↗
PubMedDate not supplied

Gamma-hydroxybutyrate versus chlorprothixene/phenobarbital sedation in children undergoing MRI studies.

BACKGROUND: Few clinical studies have assessed gamma-hydroxybutyrate and chlorprothixene/phenobarbital sedation in children. This prospective trial compared the two regimes in children, in particular concerning differences in recovery time. METHODS: 28 pediatric oncology patients undergoing elective MRI studies at a university hospital were randomly assigned to either receive gamma-hydroxybutyrate or chlorprothixene/phenobarbital sedation. Time to induce deep sedation (Ramsay score of 5) and recovery time, the incidence of failure of sedation, the frequency of side effects, the need for therapeutic interventions, and the number of patients receiving additional midazolam were recorded. Analysis of hemodynamic parameters was performed at five defined time points. RESULTS: All 28 MRI studies were successfully completed. Recovery time was significantly shorter with gamma-hydroxybutyrate (p < 0.01). There were more side effects with chlorprothixene/phenobarbital, in particular tachycardia and hyperexcitation. Vomiting was the side effect most often seen in gamma-hydroxybutyrate sedation. Therapeutic interventions were not required in any patient. Additional midazolam was necessary to maintain satisfactory sedation in six children receiving gamma-hydroxybutyrate and four receiving chlorprothixene/phenobarbital. CONCLUSIONS: Due to its significantly shorter recovery time, gamma-hydroxybutyrate is a reasonable sedative drug for children undergoing non-invasive diagnostic procedures, and is superior to chlorprothixene/phenobarbital. In pediatric oncology patients gamma-hydroxybutyrate appears to be associated more often with vomiting. The long recovery time and its great variability make chlorprothixene/phenobarbital a less valuable alternative.

Adolescent↗
PubMed1987

Rebound insomnia in neuroleptic drug withdrawal neurophysiologic characteristics.

Rebound insomnia is one of the medical effects of reduction in dosage or discontinuation of neuroleptic drugs. The electrophysiologic features of sleep dysfunction are reported and discussed in 3 patients manifesting withdrawal-related DIMS. Electrographic anachronism and cyclic alternating pattern are signs of N-Rem sleep dysfunction. Clinical and neurophysiologic data suggest that rebound insomnia in neuroleptic withdrawal is due to an enhancement of physiologic mechanisms and rebound supersensitivity of cholinergic transmission in the ARAS.

Adult↗