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PubMed1981

[Molecular mechanism of action of benzodiazepines].

Recently, binding sites with high affinity and high specificity for the benzodiazepines have been discovered in mammalian brain. The affinity of the various benzodiazepines for these sites correlates well with the pharmacological potencies of these drugs. It is mainly for this reason that these binding sites are believed to represent the pharmacologically relevant "benzodiazepine receptors". Investigation of the binding of prazepam and metabolites to benzodiazepine receptors in rat brain homogenates reveals that prazepam has only a weak affinity to the receptor(s) with a KD of 1 microM. Its metabolite, descyclopropylmethyl-prazepam (= norprazepam) binds about 100 times more strongly (KD congruent to 15 nM). This shows that norprazepam which is the main pharmacokinetic metabolite (greater than 80% of all metabolites in plasma after oral administration of prazepam) is at the same time the biochemically active substance. Hydroxylation of the 7-membered ring of prazepam or norprazepam in position 3 does not lead to a marked increase in affinity. There is strong electrophysiological and biochemical evidence that the benzodiazepines potentiate GABAergic mechanisms in the CNS (GABA is the major inhibitory transmitter in brain). The molecular events by which the benzodiazepines modulate the GABA system are, however, completely unknown. Also, we do not know whether all pharmacological actions of the benzodiazepines (e.g. anxiolytic action, sedation, muscle relaxation) may be explained by the GABA-hypothesis. The existence of an endogenous substance--which binds to the benzodiazepine receptors--is still open to debate.

Animals↗

PubMed2005

Naltrexone plus benzodiazepine aids abstinence in opioid-dependent patients.

Naltrexone (NTX) is widely used to prevent relapse of opioid-dependent patients but its association with insomnia and "hyperexcitability" can result in treatment withdrawal. We evaluated whether NTX combined with the benzodiazepine prazepam was more effective than NTX in keeping patients opioid-free. We determined the relapse rate over 6 months in 56 opioid-dependent subjects, divided into 4 equal groups. All groups received psychological support and underwent urine tests for drug metabolites twice weekly. Group 1 did not receive pharmacological treatment (controls). Group 2 received NTX alone (one 50-mg tablet daily); group 3 received NTX (one 50-mg tablet daily) plus placebo (one tablet twice daily); and group 4 received NTX (one 50-mg tablet daily) plus prazepam (one 10-mg tablet twice daily). Ten patients of group 1 relapsed within 3 months, one after 6 months and three remained opioid-free. Six patients of group 2 relapsed within three months, two after 6 months, and six remained opioid-free. Seven patients of group 3 relapsed three months, one after 6 months and six patients remained opioid-free. In group 4, one patient relapsed within 3 months and one patient after 6 months; 12 patients of this group remained opioid-free. At urine tests, a significantly higher percent patients of group 4 remained free of Delta(9)-tetrahydrocannabinol versus patients of groups 2 and 3. In conclusion, many patients remained opioid-free on NTX alone or combined with prazepam, with a significant advantage for the NTX plus prazepam group.

Adult↗

PubMed2000

Anti-spasticity agents for multiple sclerosis.

BACKGROUND: Spasticity is a common problem in MS patients causing pain, spasms, loss of function and difficulties in nursing care. A variety of oral and parenteral medications are available. OBJECTIVES: To assess the absolute and comparative efficacy and tolerability of anti-spasticity agents in multiple sclerosis (MS) patients. SEARCH STRATEGY: Randomised controlled trials (RCTs) of anti-spasticity agents were identified using MEDLINE, EMBASE, bibliographies of relevant articles, personal communication, manual searches of relevant journals and information from drug companies. SELECTION CRITERIA: Double-blind, randomised controlled trials (either placebo-controlled or comparative studies) of at least seven days duration. DATA COLLECTION AND ANALYSIS: Two independent reviewers extracted data and the findings of the trials were summarised. Missing data were collected by correspondence with principal investigators. A meta-analysis was not performed due to the inadequacy of outcome measures and methodological problems with the studies reviewed. MAIN RESULTS: Twenty-three placebo-controlled studies (using baclofen, dantrolene, tizanidine, botulinum toxin, vigabatrin, prazepam and threonine) and thirteen comparative studies met the selection criteria. Only thirteen of these studies used the Ashworth scale, of which only three of the six placebo-controlled trials and none of the seven comparative studies showed a statistically significant difference between test drugs. Spasms, other symptoms and overall impressions were only assessed using unvalidated scores and results of functional assessments were inconclusive. REVIEWER'S CONCLUSIONS: The absolute and comparative efficacy and tolerability of anti-spasticity agents in multiple sclerosis is poorly documented and no recommendations can be made to guide prescribing. The rationale for treating features of the upper motor neurone syndrome must be better understood and sensitive, validated spasticity measures need to be developed.

Anti-Dyskinesia Agents↗

PubMed2006

Benzodiazepines prescription in Dakar: a study about prescribing habits and knowledge in general practitioners, neurologists and psychiatrists.

Benzodiazepines are relatively well-tolerated medicines but can induce serious problems of addiction and that is why their use is regulated. However, in developing countries like Senegal, these products are used without clear indications on their prescription, their dispensation or their use. This work focuses on the prescription of these medicines with a view to make recommendations for their rational use. Benzodiazepine prescription was studied with psychiatrists or neurologists and generalists in 2003. Specialist doctors work in two Dakar university hospitals and generalists in the 11 health centres in Dakar. We did a survey by direct interview with 29 of 35 specialists and 23 of 25 generalists. All doctors were interviewed in their office. The questionnaire focused on benzodiazepine indications, their pharmacological properties, benzodiazepines prescribed in first intention against a given disease and the level of training in benzodiazepines by doctors. Comparisons between specialists and generalists were made by chi-square test. Benzodiazepines were essentially used for anxiety, insomnia and epilepsy. With these diseases, the most benzodiazepines prescribed are prazepam against anxiety and insomnia and diazepam against epilepsy. About 10% of doctors do not know that there is a limitation for the period of benzodiazepine use. The principal reasons of drugs choice are knowledge of the drugs, habit and low side effects of drugs. All generalists (100%) said that their training on benzodiazepines is poor vs. 62.1% of specialists, and doctors suggest seminars, journals adhesions and conferences to complete their training in this field. There are not many differences between specialists and generalists except the fact that specialists prefer prazepam in first intention in the insomnia treatment where generalists choose bromazepam. In addition, our survey showed that specialists' training in benzodiazepines is better than that of generalists. Overall, benzodiazepine prescription poses problems particularly in training, and national authorities must take urgent measures for rational use of these drugs.

Anxiety↗

PubMed1980

Classification and assessment of cerebral bioavailability of lopirazepam (D-12524) by quantitative EEG and psychometric analysis.

In this double-blind, placebo-controlled study the CNS efficacy and pharmacodynamic properties of 3-hydroxy-5-(o-chlorophenyl)-7-chloro-1,2-dihydro-3H-pyrido[3,2-e]-1,4-diazepin-2-one (lopirazepam, D-12524) was investigated in a group of 10 normal volunteers. Quantitative EEG and psychometric analyses and clinical evaluations were done before as well as 2, 4, 6 and 8 h after oral administration of single doses of placebo, 3 mg, 5 mg and 10 mg lopirazepam and 10 mg prazepam. EEG digital computer period analysis demonstrated dose-dependent changes which are typical of the class of anxiolytics and which started in the 2nd hour, peaked in the 4th hour and lasted after 3 mg, 5 mg and 10 mg up to the 4th, 6th and 8th hour, respectively, 10 mg D-12524 produced an additional augmentation of slow waves indicating sleep-inducing qualities in this dosage. The equipotent dosage to 10 mg prazepam seems to be 5 mg. Psychometric analyses demonstrated an improvement in attention, psychomotor performance, mood and affectivity after 3 mg, opposite changes after 10 mg D-12524. Flickerlight fusion, reaction time, after-image and EAS score were determined as well. Data concerning side effects, pulse rate and blood pressure suggested a good tolerance of the drug.

Adult↗

PubMed1997

Anticonvulsant activity of azirino[1,2-d][1,4]benzodiazepines and related 1,4-benzodiazepines in mice.

The anticonvulsant properties of several 1,4-benzodiazepine and azirino[1,2-d][1,4]benzodiazepine (ABDZ) derivatives were studied after intraperitoneal (IP) administration in DBA/2 mice (a strain genetically susceptible to sound-induced seizures) and in Swiss mice. The anticonvulsant effects were evaluated on seizures evoked by means of auditory stimulation (109 dB, 12-16 kHz) in animals placed singly under a hemispheric Perspex dome or on seizures induced by administration of pentylenetetrazole. The 1,4-benzodiazepines were generally more potent than the related ABDZ derivatives. The rank order of potency for anticonvulsant activity was flunitrazepam > diazepam > pinazepam > ABDZ5 > ABDZ4 > prazepam > halazepam > ABDZ1 > ABDZ3 > camazepam > ABDZ6 > ABDZ2. The impairment of locomotor performance following IP administration of these derivatives was also evaluated by means of the rotarod test. The rank order of potency for impairment of coordinated motor movements was pinazepam > flunitrazepam > diazepam > ABDZ5 > prazepam > halazepam > ABDZ4 > ABDZ3 > ABDZ1 > camazepam > ABDZ2 = ABDZ6. The potency of various 1,4-benzodiazepines and ABDZs as inhibitors of specific [3H]flumazenil binding to membranes from cerebellum or cortex was evaluated. In general, ABDZs were active as anticonvulsants and inhibited [3H]flumazenil binding in the micromolar range. Radioligand binding studies carried out in stable cell lines demonstrated that none of the ABDZs tested showed a particular subtype specificity. The pharmacological actions of ABDZ4 and ABDZ5, which appeared to be the most potent ABDZs as anticonvulsants, were significantly reduced by treatment with flumazenil (8.24 mumol/kg IP), suggesting a clear involvement of benzodiazepine mechanisms in the anticonvulsant activity of these compounds or their metabolites. The anticonvulsant activity of ABDZ4 and ABDZ5 was also evaluated against seizures induced in DBA/2 mice by two beta-carbolines: methyl-beta-carboline-3-carboxylate (beta-CCM) and methyl-6,6-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM). Both ABDZ4 and ABDZ5 give better protection against seizures induced by beta-CCM than DMCM, suggesting a preferential action on the benzodiazepine receptor subtype BDZ1.

Animals↗

PubMed1996

Azirino[1, 2-d][1, 4]benzodiazepine derivatives and related 1,4-benzodiazepines as anticonvulsant agents in DBA/2 mice.

1. The behavioral and anticonvulsant effects of several 1, 4-benzodiazepine (BDZ) and azirino[1,2-d] [1, 4]benzodiazepine (ABDZ) derivatives were studied after intraperitoneal administration in DBA/2 mice, a strain genetically susceptible to sound-induced seizures. 2. The anticonvulsant effects were evaluated on seizures evoked by means of auditory stimulation (109 dB, 12-16 kHz) in animals placed singly under a Perspex dome. 3. The 1,4-benzodiazepines were generally more potent than the related azirino[1,2-d] [1,4]benzodiazepine derivatives which, however, showed a remarkable anticonvulsant activity. The rank order of potency for anticonvulsant activity was flunitrazepam > diazepam > pinazepam > ABDZ5 > ABDZ4 > prazepam > halazepam > ABDZ1 > ABDZ3 > camazepam > ABDZ6 > ABDZ2. 4. The impairment of locomotor performance following intraperitoneal (IP) administration of the aforementioned derivatives was also evaluated by means of rotarod test. The rank order of potency for impairment of coordinated motor movements was pinazepam > flunitrazepam > diazepam > ABDZ5 > prazepam > halazepam > ABDZ4 > ABDZ3 > ABDZ1 > camazepam > ABDZ2 = ABDZ6. 5. A hypothermic activity was observed after the highest doses of the benzodiazepines studied. 6. The potency of various 1,4-benzodiazepines and azirino[1, 2-d][1,4]benzodiazepines as inhibitors of specific [3H]flumazenil binding to membranes from cerebellum or cortex was evaluated. In general, they inhibited [3H]flumazenil binding at the micromolar range. However, some ABDZ derivatives, although active as anticonvulsants, failed to displace [3H]flumazenil. 7. The azirino[1,2-d] [1,4]benzodiazepine derivatives are more lipophilic than the related benzodiazepines, but the different degree of anticonvulsant activity and impairment of coordinated motor movements cannot be directly related to the lipophilicity of the compounds studied. 8. The pharmacologic actions of ABDZ4 and ABDZ5, which appeared as the most potent anticonvulsants of the azirino[1,2-d] [1,4]benzodiazepine derivatives, were significantly reduced by treatment with flumazenil (8.24 mumol/kg IP) suggesting a clear involvement of benzodiazepine mechanisms in the anticonvulsant activity of these compounds or their metabolites. 9. The anticonvulsant activity of ABDZ4 and ABDZ5 was also evaluated against seizures induced by the two beta-carbolines, methyl beta-carboline-3-carboxylate (beta-CCM) and methyl6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), in DBA/2 mice. Both ABDZ4 and ABDZ5 gave better protection against the seizures induced by beta-CCM than DMCM, suggesting a preferential action on BDZ1 receptors.

Acoustic Stimulation↗

PubMed1995

Immunoassay detection of benzodiazepines and benzodiazepine metabolites in blood.

We evaluated the capability of commercially available benzodiazepine immunoassays from four vendors (Abuscreen radioimmunoassay [RIA-a] from Roche Diagnostic Systems and serum RIA-d from Diagnostic Products Corporation; X-systems serum and urine fluorescence polarization immunoassays [FPIA] from Abbott Laboratories; and EMIT TOX serum and EMIT urine enzyme immunoassays [EIA] from Syva) to detect 22 benzodiazepines and 16 benzodiazepine metabolites in blood samples. Drug-free bovine blood was fortified with the different compounds at concentrations relevant to blood analysis: 7, 30, and 70 ng/mL. One-milliliter samples were extracted with n-butyl chloride, dried, and reconstituted with 0.3 ml. of buffer. Results from the two urine-specific kits (EIA-u and FPIA-u) produced either equivalent or reduced cross-reactivity compared with their serum kit counterparts; these results are presented but not discussed further. Among the 38 compounds, the following were detected by all four assays at concentrations of 70 ng/mL or less: alprazolam, alpha-hydroxy-alprazolam, norclobazam, diazepam, estazolam, flunitrazepam, norflunitrazepam, miclazolam, 4-hydroxy-midazolam, nitrazepam, noradinazolam, oxazepam, prazepam, 3-hydroxy-prazepam, temazepam, and triazolam. 7-Amino-clonazepam, 7-acetamido-clonazepam, 3-hydroxy-7-acetamidoclonazepam, haloxazepam, loprazolam, 7-amino-nitrazepam, 7-acetamido-nitrazepam, and oxazolam were not detected by any of the assays at concentrations up to 70 ng/mL. A number of benzodiazepines or their metabolites were detectable by some but not all of the six assays: bromazepam, chlordiazepoxide, demoxepam, and 4-hydroxy-alprazolam (both RIAs and EIA); adinazolam (RIA-a, EIA, and FPIA); norchlordiazepoxide (both RIAs); clonazepam (RIA-a and EIA); bentazepam, clotiaze-pam, and mexazolam (EIA and FPIA); 7-amino-flunitrazepam and quazepam (EIA); and alpha-hydroxy-triazolam and medazepam (RIA-a).

Animals↗

PubMed1997

Analysis of the antiepileptic phenyltriazine compound lamotrigine using gas chromatography with nitrogen phosphorus detection.

A method is described for the determination of lamotrigine in serum or plasma, based on gas chromatography with nitrogen-phosphorus detection. The method requires minimal sample preparation. The drug is extracted from 1.0 ml of serum at pH 11 into butylacetate containing prazepam as internal standard. An aliquot of the organic phase is then injected onto an HP-5 fused silica capillary column and analyzed with temperature programming from 90 degrees to 250 degrees C. Lamotrigine is characterized by a relative retention time of 0.832 (+/-0.03) compared with prazepam. The method is competitive with the reported high-performance liquid chromatography procedures in terms of precision and sensitivity. Coefficients of variation, calculated from the results of between-run reproducibility tests, were 6.7%, 4.6%, 4.8%, and 6.2% for samples spiked with 0.20, 1.21, 2.42 and 10.84 micrograms/ml lamotrigine, respectively. The lower limit of quantitation of the method is 0.15 microgram/ml. The proposed procedure can be integrated easily in a comprehensive toxicology screening.

Anticonvulsants↗

PubMed1976

Benzodiazepines and reproduction of swiss-webster mice.

Chronic dietary administration of 6 different benzodiazepine tranquilizers (chlordiazepoxide, diazepam, oxazepam, prazepam, flurazepam, and nitrazepam) to breeding pairs of Swiss-Webster mice resulted in alterations of the normal patterns of reproductive behavior and fetal growth. Significant decreases in mating performance were seen among mice given diets containing 0.15% chlordiazepoxide, 0.05% diazepam, 0.05 and 0.15% oxazepam, 0.02 and 0.10% prazepam, 0.10% flurazepam, and 0.025% nitrazepam. Offspring in all drug treatments showed significantly depressed body weights at birth.

Animals↗

PubMed1984

In vitro and ex vivo inhibition by flutoprazepam of [3H]flunitrazepam binding to mouse brain receptors.

The ability of flutoprazepam, a new antianxiety drug of the benzodiazepine class, to inhibit [3H]flunitrazepam binding to mouse brain receptors was investigated in vitro and ex vivo (measurement of [3H]flunitrazepam binding in vitro after in vivo treatment of animals with unlabelled drugs). The Ki values for [3H]flunitrazepam binding in vitro were as follows: flutoprazepam (13.0 nM), diazepam (2.7 nM), nitrazepam (5.3 nM), prazepam (68.5 nM) and chlordiazepoxide (234 nM). Two metabolites of flutoprazepam, N-desalkyl-flutoprazepam (Ki = 3.1 nM) also inhibited [3H]flunitrazepam binding in vitro with higher potencies than that of flutoprazepam. Flutoprazepam was found to be more active in inhibiting [3H]flunitrazepam binding ex vivo and in preventing pentetrazol convulsions than predicted from Ki values. The ID50 values for inhibiting [3H]flunitrazepam binding ex vivo were 0.32 mg/kg, p.o. (flutoprazepam), 0.89 mg/kg, p.o. (diazepam), 0.94 mg/kg, p.o. (nitrazepam), 1.98 mg/kg, p.o. (prazepam) and 23.3 mg/kg, p.o. (chlordiazepoxide), respectively. The correlation between ID50 values ex vivo and ED50 values for preventing pentetrazol convulsions was highly significant (r = 0.929). These results suggest that flutoprazepam can exert its pharmacological activities by itself and that two metabolites also play an important role in the effects of flutoprazepam in vivo.

Animals↗

PubMed1982

The potentiation of cardiac responses to adenosine by benzodiazepines.

The concentration-related sensitization of guinea-pig left atria to adenosine produced by six benzodiazepines and dipyridamole was analyzed with a quantitative procedure which theoretically yields the pKI (-log equilibrium dissociation constant) of an uptake inhibitor for the site of uptake. Four benzodiazepines produced sensitization of atria to adenosine and no alteration of responses to 2-chloroadenosine (a purine agonist which is not a substrate for adenosine uptake or degradation), the rank order of potency being diazepam (pKI = 5.6) much greater than oxazepam (pKI = 4.6) greater than clonazepam (pKI = 4.3) = lorazepam (pKI = 4.2). Chlordiazepoxide and prazepam produced little sensitization to adenosine, but a concentration-related antagonism of responses to 2-chloroadenosine. Prior inhibition of adenosine uptake with dipyridamole unmasked antagonism of responses to adenosine by these two benzodiazepines as well, indicating a dual self-cancelling effect (for inhibition of adenosine uptake; chlordiazepoxide, pKI = 5.0; prazepam, pKI = 4.8). Although benzodiazepines have been shown to inhibit uptake of adenosine in the central nervous system, the potency of these drugs and dipyridamole is more in accord with inhibition of a myocardial uptake process distinct from the synaptosomal transport of adenosine.

2-Chloroadenosine↗

PubMed1976

The effect of minor tranquilizers on psychomotor performance.

The effect of a standard daily regimen of chlordiazepoxide, prazepam (a new benzodiazepine tranquilizer), and placebo were examined in a three way double-blind comparison for a sample of normal volunteers. The criteria include a limited spectrum of psychomotor functions. A learning effect was conspicuous for all drugs on all criteria during the day-long sequence of ten trials. For the most part the differences between the drug groups were insignificant, but there were distinctive modifications in the performance of the chlordiazepoxide group. The clearest effect of the tranquilizer medications was found in the time estimation tests. Paradoxically, the drugs correct a naturally occurring perceptual error.

Adult↗

PubMed1992

Comparative metabolism of clinically important precursors of N-desmethyldiazepam using phenobarbitone-pretreated rat liver microsomes.

Phenobarbitone-pretreated male Sprague-Dawley rat liver microsomes were used to examine C3-hydroxylation and N-dealkylation of four clinically important benzodiazepines: diazepam (DZP), prazepam (PZP), pinazepam (PIN) and halazepam (HZP). These substrates differ only in the nature of the N-substituent of the B ring and N-desmethyldiazepam (DMD) is the N-dealkylation product in each case. C3-Hydroxylation was accordingly also studied with DMD as substrate. All monooxygenations were studied with substrates at a concentration of 10 microM, in the absence of solubilizing agents, and under conditions where the production of secondary metabolites was minimized. A 20-fold variation in the rate of C3-hydroxylation was recorded across the five substrates with HZP showing the highest rate and DMD showing the lowest rate. An almost equally large range of variation was shown for the N-dealkylation reaction, with PZP undergoing this biotransformation more than 17 times faster than DZP. Log P values (a measure of lipophilicity) for the five substrates were determined using an HPLC method and a remarkable lack of correspondence between this substrate parameter and either of the monooxygenations was noted. This suggests that multiple substrate determinants govern the relative rates of these monooxygenations. It was, however, notable that the additive rate of metabolism of these substrates by both monooxygenase routes did show an excellent correlation with substrate lipophilicity.

Animals↗

PubMed1993

A salt-free isocratic high-pressure liquid chromatographic method for the quantitation of benzodiazepines in serum.

A simple, rapid high-pressure liquid chromatography (HPLC) method was developed for detecting and quantifying benzodiazepines in serum. Seven major benzodiazepines were extracted from spiked serum samples using solid-phase extraction with prazepam as the internal standard. The eluted drugs were then resolved isocratically by HPLC within 11 min using a reversed-phase C8 column with a mobile phase consisting of acetonitrile, methanol, water, and perchloric acid. All drugs gave responses that varied linearly with concentration over the ranges studied. Within-day imprecision (CV) varied from 3.9 to 14.9%, day-to-day CV from 4.8 to 17.0%, absolute recoveries from 67% to 114%, and detection limits from 10 to 110 ng/mL. Tricyclic antidepressants did not interfere, and clinical results were in good agreement with those obtained by a gas chromatographic method. The advantage of this method is that it uses a salt-free isocratic mobile phase that can be easily manipulated to effect difficult benzodiazepine separations.

Anti-Anxiety Agents↗

PubMed1996

Simultaneous high-performance liquid chromatographic analysis of flunitrazepam and four metabolites in serum.

A high-performance liquid chromatographic method for the simultaneous determination of flunitrazepam and four metabolites, desmethylflunitrazepam (DMF), 7-aminodesmethylflunitrazepam (7-NH2DMF), 7-aminoflunitrazepam (7-NH2F) and 3-hydroxyflunitrazepam (3-OHF), in serum is described. The method involves a simple extraction from alkalinized plasma (pH 9.5) into diethyl ether-chloroform (80:20, v/v). Prazepam was used as an internal standard for the quantification of the five compounds. Separation was achieved with a 10 microns RSil CN column (300 x 3.9 mn I.D.). The detection wavelength was set at 242 nm. The limits of detection ranged from 2.5 to 5 micrograms/l with a limit of quantification of 10 micrograms/l for all analytes.

Anti-Anxiety Agents↗

PubMedDate not supplied

Development of a supercritical fluid extraction method for the determination of temazepam in whole blood.

A supercritical fluid extraction (SFE) procedure for the analysis of temazepam from whole blood was developed. Quantitative recoveries were obtained by high-performance liquid chromatography using prazepam as an internal standard and carefully monitoring the extraction temperature and pressure. The results were found to compare well with those obtained by solid-phase extraction techniques, but they also had the advantages of reduced solvent consumption and minimal sample handling. The application of this method to authentic forensic blood specimens showed the SFE method to be useful as an alternative procedure for the extraction of temazepam in the toxicology laboratory.

Chromatography, High Pressure Liquid↗

PubMed1982

Tranquillizer effects in an experimental analog of group psychotherapy.

In an experimental analog of group psychotherapy situations, the effects of two dosages of a tranquillizing agent (prazepam) are compared with those of placebo treatment. Pulse frequency and psychic strain on 24 healthy young volunteers was measured in different social interactions. Variations of social situations induced great changes both in physiological and in psychological measures. The drug acted differentially as to sex and dosage, but showed no situation-specific action. These and further results indicated that group dynamics are an efficient tool in proving drug effects.

Adult↗