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At least 19 recordsLinked to original sources
PubMed1979

Concentrations of phenobarbital, flurazepam, and flurazepam metabolites in autopsy cases.

In five cases of death resulting from acute intoxication with phenobarbital and flurazepam, the blood, urine, brain, lung, liver, and kidney levels of these drugs as well as the levels of N-1 hydroxyethyl, N-1 desalkyl, and N-1 desalkyl-3-hydroxy flurazepam metabolites were determined. Concentration of flurazepam and its metabolites was determined by using new gas chromatographic conditions employing a selective detector for nitrogen-containing substances and a column of 1% SP-1000. In addition, the EMIT technique was also employed on blood and urine samples and the results compared with GLC data.

Adult↗
PubMed1977

[Electroencephalographic effects of flurazepam in rabbits (author's transl)].

Electroencephalographic (EEG) effects of flurazepam were investigated in unanesthetized, unrestrained rabbits with chronic electrode implants and compared with those of diazepam. Flurazepam, at doses of 0.5 approximately 5 mg/kg i.v., induced a drowsy EEG pattern, i.e. high voltage slow waves in the cortex and amygdaloid complex and desynchronization of the hippocampal theta waves. In addition, low voltage fast waves were superimposed, especially on the cortical EEG. Flurazepam suppressed the EEG arousal responses induced not only by auditory stimulation but also by electrical stimulation of the mesencephalic reticular formation, posterior hypothalamus and centromedian thalamus. The EEG arousal response induced by i.v. injection of physostigmine was suppressed by flurazepam. Flurazepam depressed the photic driving response and the augmenting response. The recruiting response was slightly enhanced by flurazepam. The limbic afterdischarges elicited by either hippocampal or amygdaloid stimulation were suppressed by flurazepam. Flurazepam caused reductions of pressor responses to stimulation of the posterior hypothalamus and the mesencephalic reticular formation in anaesthetized rabbits. There was little or no effect on pressor responses to the injection of noradrenaline, carotid artery occulusion and asphyxia with flurazepam. In general, these effects of flurazepam were similar to those of diazepam, but the drug induced actions which differed from those of diazepam.

Animals↗
PubMed1978

Comparative efficacy of triazolam, flurazepam and placebo in out-patients insomniacs.

The short-term hypnotic efficacy of triazolam was compared to that of flurazepam and placebo in 120 out-patient insomniacs. Each patient was studied with a two-night, double-blind crossover trial. Triazolam (0.5 mg) was compared to placebo and flurazepam (30 mg). Triazolam (0.25 mg) was compared to flurazepam (15 mg and 30 mg). Triazolam (0.5 mg) was preferred to both placebo and flurazepam (30 mg). Triazolam (0.5 mg) was superior to placebo in improving quality of sleep, shortening sleep onset, increasing sleep duration, and reducing the number of night-time awakenings. Triazolam (0.5 mg) was superior to flurazepam (30 mg) in speeding sleep onset and increasing the quality of sleep. Triazolam (0.25 mg) was preferred to flurazepam (15 mg) and was significantly better than flurazepam on all sleep questions. Triazolam (0.25 mg) was preferred by more patients than flurazepam (30 mg) and was judged equally efficacious on individual sleep questions. Reports of side-effects were minimal for both drugs.

Adult↗
PubMed1977

The gas chromatography mass spectrometry of the major metabolites of flurazepam.

Mass spectra and gas chromatographic data are presented for flurazepam and its metabolites; monodesethylflurazepam, didesethylflurazepam, hydroxyethylflurazepam, N1-desalkylflurazepam, N1-desalkyl-3-hydroxy-flurazepam, and flurazepam-N1-acetic acid. The on-column thermal degradation of didesethylflurazepam, N1-desalkyl-3-hydroxyflurazepam and flurazepam-N1-acetic acid is reported and discussed. Mass spectrometric and gas chromatographic data are also presented for the benzophenones obtained by acid hydrolysis of flurazepam and its metabolites. The occurrence of flurazepam metabolites in urine from five forensic cases after various treatments has been investigated. A possible new 'metabolite' of flurazepam was detected in two of these cases.

Anti-Anxiety Agents↗
PubMed1977

Metabolism of flurazepam by the small intestine.

The metabolism of flurazepam-5-14C has been studied in man following catheterization of the portal and hepatic veins. Flurazepam was administered through a tube into the stomach in one patient and into the duodenum in two patients. Thin-layer chromatographs of portal vein blood showed that there was a rapid and early appearance of metabolites of flurazepam consistent with the metabolism of the flurazepam by the intestinal mucosa and at times when the concentrations in the hepatic vein and peripheral blood were very much lower than those in the portal vein. The major metabolites identified in portal vein blood were the mono- and didesetyl metabolies of flurazepam. Considerable hepatic uptake of flurazepam and its metabolites occurred, as evidenced by the lower concentrations of the parent compound and metabolites in the hepatic vein. Thus, "first-pass" metabolism of flurazepam following oral administration occurs in the small bowel mucosa of man as well as in the liver.

Adult↗
PubMed1979

[A fatal monointoxication by flurazepam (Dalmadorm). Problems of the toxicological interpretation (author's transl)].

A death case following a suicidal overdose of flurazepam (Dalmadorm) is reported. The body was found after 3 month near a highway. The course of the intoxication is in question as benzodiazepines are believed to be relatively save drugs. The death might have occured rapidly because of the acute toxic actions of the drug overdose as well as after a protracted course involving additional complications like inflammatory alteration of the myocard or hypothermia during a coma. Flurazepam and its major metabolites were analysed in blood and urine. The toxic levels of flurazepam (0.51 mg/l), N1-desalkylflurazepam (0.14 mg/1) and N1-hydroxyethylflurazepam (9.0 mg/1) in the blood amounted to 20--50 times higher than therapeutic levels, with flurazepam and metabolites being in only slight altered relation to each other. The overdose is considered to have been above 2.4 g (80 tablets). The resorption of the drug was complete. The analytical findings in blood and urine as well as in the GI-tract are in satisfactory agreement. The analytical data of flurazepam and its metabolites are discussed in detail, taking metabolic and pharmacokinetic parameters, autopsy findings and case circumstances into consideration. A final decision about the course of the intoxication is not possible. This case shows however the fatal consequences of a flurazepam overdose although alcohol or other drugs were not involved.

Autopsy↗
PubMed1975

Flurazepam hydrochloride, a benzodiazepine hypnotic.

Flurazepam hydrochloride is a benzodiazepine derivative marketed for use as a hypnotic agent. Flurazepam is more effective than placebo and is as effective as other hypnotic drugs in most short-term controlled studies. In long-term dosage studies, flurazepam's efficacy persists while other hypnotics become ineffective. Flurazepam has relatively minor effects upon rapid eye movement (REM) sleep and does not lead to REM rebound; this may reduce the likelihood of drug dependence. Flurazepam does not cause enzyme induction and probably presents little hazard of abuse or overdosage. The rational use of hypnotic agents depends as much upon the underlying cause of the sleep disorder as upon the choice of a particular drug. When hypnotic therapy is indicated, flurazepam appears to have advantages over other drugs currently available in the United States.

Animals↗
PubMed1975

Comparison of the hypnotic activity of triazolam, flurazepam hydrochloride, and placebo.

Triazolam, 0.4 and 0.8 mg, flurazepam, 15 and 30 mg, and placebo were compared in a double-blind, randomized 5-night crossover study in 25 inpatient insomniacs. These patients all complained difficulty falling asleep; all said they usually slept less than 5 hr a nigh and woke up too early in the morning. Results of the patients' global evaluation of the medications shows that all of the treatments were rated significantly higher than placebo, with the exception of triazolam, 0.4 mg, which was not significantly different from flurazepam, 15 or 30 mg, or from placebo. In subjective evaluation of sleep onset, only triazolam, 0.4 and 0.8 mg, was rated faster than placebo. All 4 active medications increased duration of sleep. Triazolam, 0.8 mg, and flurazepam, 30 mg, were rated as providing deeper sleep than placebo while all treatments except flurazepam, 15 mg, decreased the number of awakenings below that on placebo. A significant dose-response curve was obtained with triazolam and flurazepam for some of the parameters. Very few adverse effects were reported. One patient reported feeling groggy and drowsy on 0.4 mg triazolam while 2 reported nightmares on placebo.

Adult↗
PubMed1976

Sleep laboratory studies of flurazepam: a model for evaluating hypnotic drugs.

The results from six separate evaluations of flurazepam 30 mg in the sleep laboratory were combined to determine the effectiveness of the drug in inducing and maintaining sleep and its effects on sleep stages in a large sample of insomniac subjects. The combined studies provide a model from which a detailed profile of the effects of a hypnotic drug over short-, intermediate-, and long-term conditions can be thoroughly evaluated. Although sleep was significantly improved on the first night of flurazepam administration, peak effectiveness of the drug did not result until the second and third consecutive drug nights. Flurazepam continued to be effective in inducing and maintaining sleep with intermediate-and long-term drug use with only a slight loss of effectiveness with long-term use. Sleep was also significantly improved on the first and second nights of drug withdrawal. Carryover effectiveness of active metabolites of flurazepam from one drug night to the next drug night and to withdrawl nights is discussed. The clinical implications are discussed with regard to the time of peak effectiveness of the drug, dosage recommendations and schedule, minimizing possible effects of the drug on daytime performance, and the rationale and method for using drug holidays in the treatment regimen. With this comprehensive profile of the drug's actions, the physician is able to more rationally and effectively utilize the drug in treating the insomniac patient. With short-term administration, flurazepam produced a slight decrease in rapid eye movement (REM) sleep and an increase in REM latency. These effects were much more pronounced with intermediate-term drug administration, again possibly due to the accumulation of active metabolites. After withdrawal there was no rebound in REM sleep. Stages 3 and 4 sleep decreased progressively through short and intermediate drug administration. With initial withdrawal, there was a slight recovery in both sleep stages.

Anti-Anxiety Agents↗
PubMed1977

Toxicity of high-dose flurazepam in the elderly.

To assess the potential hazards of flurazepam (Dalmane) therapy of insomnia in the elderly, the relation of dosage and patient age to the frequency of flurazepam-attributed adverse reactions was studied in 2,542 hospitalized medical patients. Adverse reactions, predominantly unwanted residual drowsiness, were reported in 78 flurazepam recipients (3.1%). None of the adverse reactions were serious. The frequency of reported toxicity increased with average daily dose, ranging from 1.3% among those receiving less than 15 mg/day to 12.3% at doses of 30 mg/day or more (p less than 0.001). Toxicity increased with age, progressively from 1.9% among those under 60 to 7.1% among those 80 or over (p less than 0.001). Unwanted effects of high-dose flurazepam were observed much more commonly in the elderly. Only 2.0% of those 70 years of age or older experienced adverse reactions at doses under 15 mg/day, as opposed to 39.0% at 30 mg or more per day. Low doses of flurazepam appear to be safe for elderly individuals, but they are susceptible to unwanted central nervous system depression at high doses.

Adult↗
PubMed1977

Multiclinic double-blind comparison of triazolam and flurazepam for seven nights in outpatients with insomnia.

In this two-clinic seven-day double-blind study, 0.5 mg triazolam (Halcion) was compared to flurazepam (Dalmane) in the treatment of insomnia. Two clinical investigators completed 118 outpatients, 61 on triazolam and 57 on flurazepam. Five patients, four on triazolam and one on flurazepam, discontinued because of side effects; and three patients, one on triazolam and two on flurazepam, discontinued because of ineffectiveness of the medication. Analysis of pooled data for the 110 evaluable patients showed that 0.5 mg triazolam was significantly better than 30 mg flurazepam on the following parameters: (1) how much the medication helped the patients sleep, (2) onset of sleep, (3) duration of sleep, (4) evaluation of duration of sleep, and (5) feeling of restfulness in the morning. The trend for all other parameters favored triazolam treatment, but the values did not reach statistical significance. Side effects were similar in both groups, with drowsiness being reported most frequently. No change in efficacy indicating tolerance development during the seven days of drug administration was observed in either group.

Adolescent↗
PubMedDate not supplied

Long-term hypnotic efficacy and safety of triazolam and flurazepam.

Both triazolam and flurazepam are effective hypnotics when administered nightly for 12 consecutive weeks. However, at the dosages tested, 0.6 mg triazolam had a significantly faster onset of activity than 30 mg flurazepam. Long-term administration of either treatment did not influence the patient's capability to recognize the difference between active drug and placebo. This supports the conclusion that there was no tolerance development on either treatment. There were no deleterious effects attributable to either treatment as measured by the 35-Item Hopkins Symptom Checklist or by physical examinations, laboratory tests, ECGs, and ophthalmologic examinations. Side effects occurred more often on flurazepam than on triazolam, and the number of patients experiencing side effects was significantly higher in the flurazepam group. Drowsiness and grogginess were reported most frequently on both treatments, and the number of patients reporting drowsiness or grogginess was also significantly higher in the flurazepam group.

Adult↗
PubMed1979

The effects of flurazepam hydrochloride on brain electrical activity during sleep.

To further evaluate the effects of flurazepam on EEG during sleep, following 7 nights of placebo baseline, flurazepam (30 mg) was administered to 6 young adult poor sleepers for 10 additional nights while 6 other young adult poor sleepers continued to receive placebo capsules in a double-blind paradigm. Three placebo follow-up nights were recorded 2--3 weeks post-treatment. Twelve good sleepers received only placebo capsules for the first 7 nights. Delta waves, 0.5--2 c/sec, and sleep spindles were counted on-line by a phasic detector. Delta activity was also analyzed off-line by PDP-12 computer for only the first 4 h of sleep and involved a comparison over stages of sleep. Click-evoked K-complexes during NREM sleep were analyzed for 6 good sleepers and 11 poor sleepers. Repeated use of flurazepam caused a gradual decrease in delta amplitude and count, and a gradual increase in sleep spindle rate. The decrease in delta amplitude was seen in all sleep stages, but the decrease was significant only during SWS and stage 2. The decrease in delta amplitude was significant by the 3rd drug night, but the rate of amplitude decrease tended to slow with continued treatment. The decrease in delta count was less pronounced and more gradual over drug nights than the rate of decrease in amplitude. Flurazepam also significantly reduced evoked K-complex amplitude but did not affect latency. Sleep spindle rate was significantly increased by drug night 5. Results of this study indicate that the reduction of SWS with flurazepam during the initial drug nights is due primarily to the decrease in delta amplitude, but, with continued use, the decrease in delta count also contributes to the decrease in stage 4 sleep.

Adult↗
PubMed1975

A clinical and psychometric evaluation of flurazepam.

1 The efficacy of flurazepam (15 mg or 30 mg) as a hypnotic, and the residual effects of each dose were compared with placebo in a double-blind cross-over trial involving thirty patients in a general practice setting. Patients received each medication for one week. Daily self-ratings of onset, duration and quality of sleep, together with reports of any untoward effects were made. At the end of each period of medication psychomotor tests (reaction time, pursuit rotor, tapping speed) were administered at 09.00 hours. 2 Both doses of flurazepam were significantly more effective than placebo in inducing sleep, improving the quality of sleep and extending its duration. 3 'Hangover' effects were marked following 30 mg, but not after flurazepam (15 mg). Flurazepam (30 mg, but not 15 mg) significantly impaired performance on the pursuit rotor test and tapping speed. Flurazepam thus appears to be an effective hypnotic drug with the optimum dose for use in general practice being 15 mg at night.

Anti-Anxiety Agents↗
PubMed1978

Comparison of oxazepam, flurazepam and chloral hydrate as hypnotic sedatives in geriatric patients.

In a four-week study, a comparison was made of oxazepam, flurazepam and chloral hydrate as hypnotic sedatives in 17 geriatric patients. Each drug was given alone for six nights, with a two-night placebo interval following each phase. Each patient completed an additional placebo phase (up to six nights) before each drug phase. The number of awakenings per night and the sleep latency (time required to fall asleep) were determined from the patients' reports and from the reports of a nurse-observer. Only for oxazepam was the number of patient-reported awakenings per night significantly less than for placebo, although with both oxazepam and flurazepam the awakenings were fewer than with chloral hydrate. According to the patient-reports, sleep latency was significantly lower with flurazepam than with placebo; for oxazepam and chloral hydrate the latencies were not significantly different from those for flurazepam or placebo. Only for oxazepam were the patients' ratings of sleep quality significantly greater than for placebo. The objective assessment of sleep by the nurse-observer usually confirmed the patients' assessments. Morning drowsiness was the most common side effect, reported equally for placebo and for the active drugs. Drowsiness during the day was reported less frequently for oxazepam than for flurazepam, chloral hydrate or placebo. It is concluded that oxazepam is safe and efficacious for the short-term management of insomnia in the elderly.

Aged↗
PubMed1979

Effects of microiontophoretically applied flurazepam on responses of cerebral cortical neurones to putative neurotransmitters.

Utilizing standard microiontophoretic techniques and recording extracellularly in cats, we studied the effects of flurazepam, a water-soluble benzodiazepine, on the spike activity of single cerebral neurones and its interactions with several excitatory and inhibitory putative neurotransmitters. Large iontophoretic doses (5--30 nA, 0.1 M solution) of flurazepam induced a depression of spike amplitude. Smaller doses (less than 5 nA, 0.1 M solution or 20--50 nA, 20 mM in 0.16 M NaCl) reduced the excitation produced by glutamate, aspartate, and homocysteate, but antagonism of acetylcholine-evoked excitations required large flurazepam doses (up to 30 nA, 0.1 M solution). Even lower doses of flurazepam (less than 10 nA, 20 mM in 0.16 M NaCl) enhanced the inhibitory effect of gamma-aminobutyric acid (GABA) but antagonized that of 5-hydroxytryptamine, and had no effect on dopamine-induced inhibition of firing. Hence, only GABA-evoked inhibitions were significantly potentiated by flurazepam. These results demonstrate the multiple possible interactions between a benzodiazepine and different putative neurotransmitters in the mammalian cerebral cortex.

Acetylcholine↗
PubMed1976

The use of flurazepam (dalmane) as a substitute for barbiturates and methaqualone/diphenhydramine (mandrax) in general practice.

A twelve-week study involving fifty-three patients is described as taking place in a practice with a higher than average geriatric population. The purpose of the study was to substitute flurazepam for habitually used barbiturates or methaqualone/diphenhydramine. Of the original fifty-three patients admitted to the study, fifty-one completed; the two drop-outs resulting from concomitant physical illness. Eighty-four per cent of patients were successfully changed to flurazepam. Of those who did not accept flurazepam, eight per cent accepted nitrazepam, while six per cent of patients were motivated to stop all hypnotics. During the three month period of the study none of the well-known disadvantages of the barbiturates and methaqualone/diphenhydramine were seen with flurazepam. The author found flurazepam to be a very efficient hypnotic of relatively low toxicity which could be easily substituted fro barbiturates and methaqualone/diphenhydramine in the treatment of long-term insomnia.

Adult↗