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PubMed1991

A comparative study of diazepam and acupuncture in patients with osteoarthritis pain: a placebo controlled study.

Forty-four patients with chronic cervical osteoarthritis took part in this study. Patients were treated with acupuncture, sham-acupuncture, diazepam or placebo-diazepam in randomized order. Pain was rated on visual analogue scales before, during, and after treatment. Two scales were separately used to rate the intensity (sensory component) and the unpleasantness (affective component) of pain. The results analyzed from these trials show that diazepam, placebo-diazepam, acupuncture and sham-acupuncture have a more pronounced effect on the affective than on the sensory component of pain. Acupuncture was significantly more effective than placebo-diazepam (p less than 0.05), but not significantly more effective than diazepam or sham-acupuncture.

Acupuncture Analgesia↗

PubMed1986

Diazepam-induced changes in signal detection performance. A comparison with the effects on the Critical Flicker-Fusion Frequency and the Digit Symbol Substitution Test.

The effects of 10 mg diazepam on signal detection theory measures (stimulus sensitivity, response bias) and reaction times were studied in a 1-hour visual signal detection task with high and low signal probability, and on performance in two short-duration tasks: Critical Flicker-Fusion Frequency (CFF) and the Digit Symbol Substitution Test (DSST). 12 healthy volunteers participated in this placebo-controlled, double-blind cross-over study. Diazepam affected the stimulus sensitivity and the reaction times of hits in the signal detection task. DSST performance was also impaired while CFF did not change after diazepam treatment. No relationship between serum diazepam concentration and change in task performance was found. It is concluded that diazepam affects signal detection performance, independent of signal probability. A short-duration task like the DSST is as sensitive to the effects of diazepam as the (long-duration) signal detection task.

Adolescent↗

PubMed1997

Effects of the tranquillizer diazepam and the stimulant methylphenidate on alertness and memory.

Effects of alertness and memory of a single dose of diazepam (10 mg) and the central stimulant methylphenidate (20 mg) were studied in healthy volunteers. It was questioned whether opposite effects of diazepam and methylphenidate are not only observed with respect to alertness but also with respect to memory. It was also questioned whether the two drugs equally affect the first (primacy) and last (recency) items in both the immediate and delayed recall of newly learned words. The experiment was performed in a double-blind, placebo-controlled way. 12 subjects were exposed to a subjective alertness scale and a verbal memory test: a 15-word test. Subjective alertness was found to be decreased after diazepam and increased after methylphenidate. Anterograde amnesia was found after diazepam in the memory test. More specifically, the primacy but not the recency effect was reduced during the immediate recall and both were reduced in the delayed recall. methylphenidate had no effect on memory, however a ceiling effect might have obscured a putative drug effect. The results of a second experiment excluded this possibility. In all, the data demonstrate opposite effects of the two drugs on subjective alertness, suggesting opposite effects on vigilance. Opposite effects on memory were not established. This demonstrates that changes in alertness do not run in parallel with changes in memory. A scatter diagram, however, suggests a small effect of alertness on immediate recall. The effects of diazepam were also discussed in terms of the Atkinson and Shiffrin memory theory and it seems that diminished rehearsal processes are one of the key factors in explaining diazepam-induced amnesia.

Adult↗

PubMed1982

Body temperature response to cocaine and diazepam in morphine-treated rats.

Since cocaine or diazepam are used clinically and/or abused concomitantly with narcotics, this study was designed to determine if morphine-dependent, morphine-withdrawn, or acute morphine rats exhibit an altered core body temperature at 24 or 4 degrees C to either cocaine (10, 20, or 30 mg/kg i.p.) or diazepam (2 or 4 mg/kg i.p.). At 24 degrees C, each dose of cocaine manifested hyperthermia in all groups of rats except morphine-dependent whereas at 4 degrees C cocaine produced hypothermia in all groups except morphine-dependent. At both 24 and 4 degrees C, diazepam, 2 or 4 mg/kg, caused a hypothermic response in control, dependent, and withdrawn animals. At 24 degrees C, administration of acute morphine alone induced a hyperthermia which was antagonized by both doses of diazepam. At 4 degrees C, acute morphine alone induced an initial hypothermia followed by a hyperthermia; both doses of diazepam potentiated the hypothermic response to acute morphine. Thus, significant alterations in core body temperature may be induced following the administration of cocaine or diazepam to morphine-treated rats.

Animals↗

PubMed1984

Failure to confirm consistent stimulation of growth hormone by diazepam.

Diazepam has been reported to influence pituitary hormone secretion, with several studies claiming that diazepam provokes growth hormone release. Normal volunteers were therefore examined for anterior pituitary responsiveness to 10 mg diazepam i.v. and p.o. The drug had no significant effect on the secretion of prolactin or thyrotropin when compared to control saline injections in all subjects. Growth hormone response was variable; serum growth hormone increased significantly in only 4 of 10 patients after i.v. diazepam and in only 1 of 7 subjects tested with oral diazepam. Serum cortisol rose in only 1 subject, precluding a stress-related explanation for the increase in growth hormone. We conclude that diazepam inconsistently stimulates growth hormone secretion and should not be relied upon as a test of growth hormone reserve.

Administration, Oral↗

PubMed1978

Diazepam and halazepam in anxiety: some prognostic indicators.

A multiple step-search regression procedure was applied to data obtained with 37 diazepam and 42 halazepam treated anxious outpatients. Good treatment outcome was predicted for those patients who reported a more adequate family adjustment, the presence of precipitating stress, and who either had no prior psychotropic drug treatment, or if they had received such treatment, had experienced a good response. Probably of greatest interest to the practicing clinician was the observation that patients high in initial anxiety but low in initial interpersonal problems improved the most with both medications. Differential drug effects indicated halazepam to do particularly poorly in less anxious patients and in those patients given a good prognosis by the doctor. Diazepam response was much less affected by these variables. It is speculated that the excessive sedating effect of the daily halazepam dosage (160 mg/d) used in this study may explain these differential drug effects. In the dosages employed, namely, diazepam 20 mg/d and halazepam 160 mg/d, diazepam produced the more consistent anti-anxiety effects. The indication that halazepam 160 mg/d was more effective than diazepam 20 mg/d in the initially sicker patients, while of interest, is probably simply a dose-related phenomenon, indicating that diazepam 20 mg/d was too low a daily dosage for severely anxious patients, a fact well known by most clinicians.

Adult↗

PubMed1998

Diazepam suppresses sleep apneas in rats.

To test the respiratory effects of benzodiazepines in an established animal model of central apnea, we administered nonhypnotic and hypnotic doses of diazepam to nine adult male Sprague-Dawley rats chronically instrumented for sleep staging. In random order on separate days, rats were recorded following intraperitoneal injection of: (1) saline; (2) 0.05 mg/kg diazepam; or (3) 5 mg/kg diazepam. Normalized inspiratory minute ventilation increased significantly during wakefulness and non-rapid eye movement (non-REM) sleep following each dose of diazepam (p < 0.003 in each case) and following the highest dose during rapid eye movement (REM) sleep (p = 0.01). In accord with this respiratory stimulation, non-REM-related spontaneous and post-sigh apnea expression decreased following each dose of diazepam (p = 0.006 to 0.04), but REM-related apnea expression was unaffected despite significant respiratory stimulation. The durations of non-REM and REM sleep were unaffected by the low dose, but following 5 mg/kg of diazepam non-REM sleep was increased (p = 0.03) and REM sleep was decreased (p = 0.009). We conclude that both hypnotic and non-hypnotic doses of benzodiazepines may be associated with suppression of sleep-related central apnea. We further conclude that non-REM and REM-related apneas arise from at least partially distinct mechanisms.

Analysis of Variance↗

PubMed1985

The effect of diazepam on genioglossal muscle activity in normal human subjects.

We examined the effect of diazepam on the respiratory electromyographic (EMG) activity of the genioglossal muscle using a double-blind, placebo-controlled, randomized protocol. Control measurements of minute ventilation, tidal volume, frequency, end-tidal CO2, and peak integrated inspiratory genioglossal EMG activity were made in 10 normal awake male subjects during quiet breathing and CO2 rebreathing. Subjects then received either 10 mg of diazepam orally or a placebo, and all respiratory measurements were repeated after 45 min. Each subject was studied on 2 separate days, receiving each treatment on a different day. The placebo had no effect on any of the measured variables. After diazepam, we observed an increase in end-tidal CO2 rebreathing, diazepam was associated with a reduction in minute ventilation, tidal volume, and frequency. When compared at equal end-tidal CO2 levels, genioglossal EMG activity and tidal volume were significantly reduced after diazepam. However, only older subjects demonstrated a reduction in EMG activity when compared at equal tidal volumes during CO2 rebreathing. We conclude that diazepam selectively decreases genioglossal EMG activity during CO2 rebreathing only in older subjects.

Adult↗

PubMed1997

Alterations in pharmacodynamics of anxiolytics in abstinent alcoholic men: subjective responses, abuse liability, and electroencephalographic effects of alprazolam, diazepam, and buspirone.

Subjective responses, including those associated with abuse liability and changes in frontal electroencephalographic activity, were assessed in abstinent alcoholic men and control subjects after administration of alprazolam, diazepam, buspirone, and placebo. Plasma concentrations of alprazolam, diazepam, and desmethyldiazepam also were determined. Abuse liability scales were elevated for alcoholic participants above control levels after alprazolam and diazepam. Areas under the concentration-time curve differed only for desmethyldiazepam, which was lower for the alcoholic participants. Compared with control subjects, alcoholic participants had greater declines in the absolute power of the alpha band after diazepam challenge. Alcoholic participants, unlike control subjects, had areas under the effect-time curve for alpha and theta bands that were lower after administration of alprazolam or diazepam than they were after receiving placebo. These results suggest that alprazolam and diazepam are more likely to be abused by alcoholic men than by nonalcoholic men and that alcoholic men have enhanced sensitivity to the effects of benzodiazepines on alpha and theta activity.

Adult↗

PubMed2001

Effects of clonidine and diazepam on prepulse inhibition of the acoustic startle response and the N1/P2 auditory evoked potential in man.

Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (prepulse inhibition). We examined the effects of two sedative/anxiolytic drugs, diazepam and clonidine, on prepulse inhibition of these two responses in healthy volunteers. Fifteen males (aged 18-35 years) participated in three sessions in which they received oral doses of placebo, diazepam 10 mg and clonidine 0.2 mg according to a balanced double-blind protocol. Thirty-minute simultaneous recordings of the electromyographic (EMG) responses of the orbicularis oculi muscle of the right eye and the vertex auditory evoked potentials took place 120 min after ingestion of clonidine and 60 min after ingestion of diazepam. Sound stimuli (1 kHz) were presented in 60 trials separated by variable intervals (mean 25 s): (i) 40-ms 115-dB ('pulse alone', 20 trials); (ii) 40-ms 85-dB (20 trials); (iii) 40-ms 85-dB, followed after 120 ms by 40-ms 115-dB ('prepulse/pulse', 20 trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. The amplitude of the EMG response was significantly reduced both by diazepam and by clonidine; neither drug significantly altered prepulse inhibition of the EMG response. Diazepam, but not clonidine, significantly reduced the amplitude of the N1/P2 potential; neither drug significantly affected prepulse inhibition of the N1/P2 potential. Both drugs reduced self-rated alertness and anxiety, and systolic blood pressure; clonidine, but not diazepam reduced diastolic blood pressure and salivation. The results confirm previous findings that sedative drugs can suppress the startle response without affecting prepulse inhibition of this response, and provide new information on the effects of these drugs on the N1/P2 potential and its inhibition by prepulses.

Acoustic Stimulation↗

PubMed2005

Diazepam suppresses the acquisition but not the expression of 'fear-potentiation' of the acoustic startle response in man.

Sudden auditory stimuli elicit a short-latency muscular response (acoustic startle response) which is enhanced during presentation of a Pavlovian conditioned stimulus (CS) that has previously been paired with an aversive unconditioned stimulus (US) ('fear-potentiation'). In rodents, acute treatment with benzodiazepines blocks both the acquisition of fear-potentiation and the expression of fear-potentiation induced by prior exposure to CS/US pairing. We examined the effect of diazepam on the acquisition and expression of fear-potentiation of the acoustic startle response in man. Forty-six male volunteers (18-30 years) participated in two sessions separated by 7 days. In session 1, they were exposed to 20 2-s presentations of a light (CS), 50% of which terminated with an electric shock to the wrist (1.8 mA, 50 ms: US). Somatosensory potentials evoked by the US were recorded from the scalp at Cz, and skin conductance responses from electrodes taped to the second and fourth fingers. In session 2, the CS was presented 20 times without the US; a random 50% of CS presentations terminated with a sound pulse (40-ms 115-dB 1-kHz); an equal number of sound pulses was presented without the CS. Electromyographic responses of the orbicularis oculi muscle to the acoustic stimuli were recorded from electrodes placed on the lower eyelid, late-latency auditory evoked potentials were recorded at Cz, and skin conductance responses from electrodes taped to the second and fourth fingers. In each session, alertness was measured using visual analogue self-rating scales and critical flicker fusion frequency. Subjects received placebo or diazepam 10mg in the two sessions in a double-blind protocol: group 1 (n 12) placebo/placebo; group 2 (n 11) placebo/diazepam; group 3 (n 12) diazepam/placebo; group 4 (n 11) diazepam/diazepam. Diazepam reduced alertness as measured by visual-analogue self-rating scales and critical flicker fusion frequency. In session 1, diazepam reduced the amplitude of the somatosensory potentials and skin conductance responses evoked by the CS. In session 2, the acoustic startle response, the N1/P2 auditory evoked response and the skin conductance response evoked by the sound stimuli were enhanced in the presence of the CS. This fear-potentiation was attenuated in subjects who received diazepam in session 1, but was not affected by the treatment given in session 2. The results indicate that diazepam blocks the acquisition of fear-potentiation of startle responses in man, as in animals, but does not prevent the expression of a previously learned response.

Acoustic Stimulation↗

PubMed1999

Comparison of the effects of diazepam on the fear-potentiated startle reflex and the fear-inhibited light reflex in man.

It has been shown previously that the amplitude of the acoustic startle reflex is enhanced, and the amplitude of the light reflex reduced, when subjects anticipate an aversive event, compared to periods when subjects are resting ('fear-potentiated startle reflex' and 'fear-inhibited light reflex'). We examined whether the anxiolytic diazepam would reverse the effects of threat on the startle and pupillary reflexes. Twelve male volunteers participated in three weekly sessions in which they received oral treatment with placebo, diazepam 5 mg and diazepam 10 mg, according to a balanced crossover double-blind design. One hour after ingestion of the treatments, miotic responses to light pulses and electromyographic responses of the orbicularis oculi muscle to sound pulses were elicited during alternating periods in which the threat of an electric shock (electrodes attached to the subject's wrist) was present (THREAT) and absent (SAFE). The THREAT condition was associated with a significant increase in the amplitude of the electromyographic (EMG) response, a significant reduction of the miotic response amplitude, and an increase in self-rated anxiety. Diazepam attenuated all these effects of THREAT. Diazepam did not affect the amplitude of the miotic response under the SAFE condition, but did suppress the EMG response under this condition. These results confirm the validity of the fear-potentiated startle reflex and fear-inhibited light reflex as laboratory models of human anxiety, and reveal some differences between the effects of diazepam on the two reflexes.

Acoustic Stimulation↗

PubMed1979

A double-blind comparison of prazepam with diazepam, chlorazepate dipotassium and placebo in anxious out-patients.

The study compared prazepam with diazepam, chlorazepate dipotassium, and placebo in the treatment of anxious out-patients. Patients were screened for participation in the study to be sure they met the criteria for inclusion. Patients were excluded if they had complicating physical or mental problems. All patients signed an informed consent. Seventy-three patients entered the study, thirteen did not complete at least two weeks of treatment and were not used in the data analysis. Of these thirteen, ten did not return and were lost to follow-up, tow entered the hospital for reasons unrelated to the drug study, and one patient on diazepam was terminated because of increased anxiety. Six patients were used in the data analysis, thirty-six males and twenty-four females with an age range of 21-61 years. Side-effects were minimal. Drowsiness was reported by two people in the placebo group, one taking chlorazepate dipotassium, three on prazepam and one on diazepam. One diazepam patient reported nausea and vomitting. Scores on the Zung Self-Rating Scale for Anxiety showed all three drug groups to be superior to placebo. The Hopkins Symptom Check-list found prazepam and diazepam to be superior to placebo and chlorazepate. No differences among the groups were found in the Hamilton Anxiety Scale. Prazepam may offer advantages over the other available benzodiazepines since it may be more readily absorbed than chlorazepate and has less side-effects than diazepam.

Adolescent↗

PubMed1998

Refractory status epilepticus in children: role of continuous diazepam infusion.

To determine efficacy of continuous diazepam infusion in the treatment of refractory status epilepticus in a retrospective study, we analyzed data of 62 children admitted consecutively to our Pediatric Intensive Care Unit with a diagnosis of refractory status epilepticus. The unit followed a standard treatment protocol for diazepam infusion; if it failed, thiopental infusion was used. The mean age of patients was 2.80 years (range, 1.5 to 11.5 yr). Thirty-six patients (60%) had acute infections of the central nervous system and 10 (16%) had idiopathic epilepsy. Diazepam infusion was used in 57 patients. This treatment controlled seizures in 86% of patients (49/57), on average within 40 minutes (median, 30 min; range, 10-120 min), at a mean infusion rate of 0.017 mg/kg/min (range, 0.01-0.03 mg/kg/min). The mean total duration of infusion was 68 hours (range, 12-220 hr). Diazepam infusion was associated with hypotension in one patient, respiratory depression requiring ventilatory support in 12% of patients (6/49), and death in 14% of patients (7/49). Thiopental infusion was used in nine patients, including eight in whom diazepam infusion had failed. Thiopental infusion controlled seizures in all nine patients, but all of them needed mechanical ventilation, and seven needed vasopressor support for hypotension; four patients (44%) died. We conclude that continuous diazepam infusion is a reasonably effective modality to control refractory status epilepticus in children and is associated with reduced need for ventilatory and vasopressor support.

Anticonvulsants↗

PubMed1986

Comparison of controlled-release diazepam capsules and placebo in patients in general practice.

A multi-centre, randomized double-blind parallel study was carried out to compare the efficacy and tolerance of a single daily dose of controlled-release (CR) capsules of diazepam (10 mg and 15 mg) with placebo under conditions close to those of general practice. All patients between 16 and 60 years of age, presenting an anxiety syndrome as a result of neurotic disturbance, for whom benzodiazepine treatment was indicated for at least 3 weeks, were accepted for the study. The results from 231 patients (119 on placebo, 55 on 10 mg and 57 on 15 mg diazepam) were analyzed after 1 and 3 weeks of treatment. Complaints were found to have improved after 1 week and 3 weeks in the controlled-release diazepam groups whereas the corresponding results with placebo were clearly less favourable. After 1 week, and even more strikingly after 3 weeks, evaluation of the general effects of treatment showed better results with diazepam than with placebo. The obviously higher rate of drop-outs on placebo confirmed its less reliable effect. The controlled-release capsules were well tolerated and notably better than placebo. The most frequent side-effect reported on diazepam was fatigue, and this was probably due to a relative overdosage from use of a standardized dose throughout treatment. Other reported side-effects could not definitely be ascribed to the drug. At the end of a week, successful results were achieved in 48.2% of the patients on controlled-release diazepam compared with only 14.3% of those on placebo. After 3 weeks, these figures were 73.2% and 30.3%, respectively.

Adolescent↗

PubMed1983

Effect of the benzodiazepine derivative, diazepam, on the clonidine-stimulated human growth hormone secretion.

gamma-Aminobutyric acid (GABA) has both stimulatory and inhibitory effect on human GH secretion. We previously reported that the benzodiazepine derivative diazepam, which exerts its main pharmacological effect by facilitating GABA-mediated transmission, is able to reduce the GH response to L-dopa and apomorphine. To establish whether diazepam affects the alpha-adrenergic regulation of GH secretion, the GH response to clonidine (an alpha-agonist) was investigated in seven volunteers after placebo and diazepam premedications. After placebo pretreatment, clonidine (0.15 mg iv infused over 20 min) significantly stimulated GH secretion: the mean serum GH level rose from a basal level of 4.7 +/- 1.1 (+/- SEM) ng/ml to a maximum of 10.8 +/- 1.6 ng/ml (P less than 0.025). After 3 days of diazepam treatment, a similar GH response to clonidine was observed; the mean serum GH level rose from a basal value of 2.3 +/- 0.3 ng/ml to a maximum of 9.4 +/- 1.3 ng/ml. It is concluded that the inhibitory effect of diazepam on human GH secretion is mediated via inhibition of dopaminergic transmission, whereas the alpha-adrenergic control of GH release is not affected. Since diazepam potentiates GABAergic transmission, its effect may reflect the role of endogenous GABA in human GH secretion.

Adult↗

PubMed1992

Sedation and recovery of psychomotor function after intravenous administration of various doses of midazolam and diazepam.

A placebo-controlled, double-blind, crossover trial in 11 healthy male volunteers compared clinical sedation and psychomotor function after intravenous injection of midazolam (0.05, 0.1, or 0.15 mg/kg), diazepam (0.15 or 0.3 mg/kg), or placebo (saline). The depth of sedation was estimated at 5-10-min intervals during the first hour after injection. A comprehensive battery of psychomotor tests was used to collect objective data of psychomotor performance before drug injection and 1, 3, 5, and 7 h after injection. Midazolam (0.15 mg/kg) produced the highest scores of sedation and most impairment of psychomotor performance. In most tests, the maximal psychomotor effects seen after 0.3 mg/kg of diazepam did not reach those of 0.1 mg/kg of midazolam. Although the strongest psychomotor effects were induced by midazolam, these effects disappeared sooner than those of diazepam. By 5 h after injection, 0.3 mg/kg of diazepam showed the highest scores of psychomotor impairment. The authors conclude that at least four times as much diazepam as midazolam is needed to produce equally severe psychomotor impairment. That the residual effects of midazolam terminate sooner than those of diazepam probably accounts for the occasional underestimation of the potency of midazolam in clinical practice.

Adult↗

PubMed2005

Remifentanil for fetal immobilization and maternal sedation during fetoscopic surgery: a randomized, double-blind comparison with diazepam.

Obstetric endoscopy procedures are routinely performed at our institution to treat selected complications of monochorionic twin gestation. We perform these procedures under combined spinal epidural anesthesia plus maternal sedation. In the absence of general anesthesia, fetal immobilization is not achieved. We hypothesized that remifentanil would induce adequate maternal sedation and provide fetal immobilization, which is equal or superior to that induced by diazepam. Fifty-four second trimester pregnant women were included in this randomized, double-blind trial. After combined spinal epidural anesthesia, maternal sedation was initiated using either incremental doses of diazepam or a continuous infusion of remifentanil. Maternal sedation, hemodynamics, side effects, and fetal hemodynamics and immobilization were evaluated before, during, and for 60 min after surgery. Remifentanil produced adequate maternal sedation with mild but clinically irrelevant respiratory depression (respiratory rate 13 +/- 4 breaths/min and Pco(2) 38.6 +/- 4 mm Hg at 40 min of surgery), whereas diazepam resulted in a more pronounced maternal sedation but no respiratory depression (respiratory rate 18 +/- 3 breaths/min and Pco(2) 32.7 +/- 3 mm Hg at 40 min of surgery). Compared with diazepam, fetal immobilization with remifentanil occurred faster and was more pronounced, resulting in improved surgical conditions; the number of gross body and limb movements was 12 +/- 4 (diazepam) versus 2 +/- 1 (remifentanil) at 40 min of surgery. Because of this, the mean (range) duration of surgery was significantly shorter in the remifentanil-treated patients, 60 (54-71) min versus 80 (60-90) min in the diazepam group. We conclude that remifentanil produces improved fetal immobilization with good maternal sedation and only minimal effects on maternal respiration.

Adult↗