Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method has been developed for the quantitative determination of heptabarbital [5-(1-cyclohepten-1-yl)-5-ethylbarbituric acid] in human plasma after administration of single therapeutic doses of the drug. It involves a single extraction step followed by gas chromatography with alkali flame ionization detection, and the results were linear in the concentration range 0.125 - 5.0 mug/ml plasma. The pharmacokinetics and relative bioavailability of heptabarbital and heptabarbital sodium were studied in a crossover design in 7 healthy volunteers after oral administration of 20 tablets containing 200 mg heptabarbital and hard gelatine capsules containing an equivalent amount of its sodium salt. Heptabarbital concentrations in plasma were determined at regular intervals. The absorption of heptabarbital from the tablets absorbed more rapidly and peak concentrations occurred between 1/3 and 2 h. In all cases the elimination of heptabarbital could be described by a single first-order process with an average half-life of 7.6 h (range 6.1 - 11.2 h). The half-life of the drug in each individual was about the same in the two trials. The relative bioavailability in each volunteer was estimated by comparing the areas under the plasma concentration curves. The sodium salt had an average bioavailability of 83% relative to the free acid. In some volunteers urinary excretion of unchanged heptabarbital was measured; cumulative excretion amounted to 0.16 - 0.30% of the administered dose. Four volunteers received one tablet each night for eight or ten days, but no accumulation was found. In three volunteers the half-life of the drug prior to and after these experiments did not change, whereas in the other volunteer the half-life decreased from 7.1 to 4.6 h. The possibility of enzyme induction should be considered when heptabarbital is taken regularly. It was concluded that heptabarbital was a suitable drug for the treatment of insomnia, since its half-life was rather short. Heptabarbital sodium may be used for induction of sleep, whereas Medomin tablets, i.e. heptabarbital free acid, may be prescribed when the maintenance of sleep is the primary reason for treatment with a hypnotic drug.
Eur J Clin Pharmacol 1975 Dec 19
PMID:Pharmacokinetics and relative bioavailability of heptabarbital and heptabarbital sodium after oral administration to man. 0 99

Of 23 hospitalized chronic schizophrenic patients, all under neuroleptic medication, hypnotics taken previously for a long time could be totally withdrawn in 16 cases, and in 7 cases, the dosage was diminished by 30%, without any sleep impairment. The gradual reduction of hypnotics was accompanied by a shift of neuroleptic dosage to the evening and bedtime, with reduction of the morning and midday dose, without change of the total daily dose. A significant improvement in the psychic state was observed in 16 patients after withdrawal of the hypnotic; 7 patients showed a slight improvement after reduction of the hypnotic. Monthly or bimonthly reassessment of insomnia in the hospitalized population of chronic schizophrenics is indispensable to avoid the deleterious effects and abuse of hypnotic drugs.
Biol Psychiatry 1979 Dec
PMID:The utilization of hypnotics in chronic schizophrenics: some critical remarks. 4 5

The relation between reduced nutritional intake, with consequent weight loss, and sleep disturbance was studied by comparing certain sleep encephalogram patterns in a group of inpatients with anorexia nervosa before, during, and after a regimen of refeeding with a normal diet to a matched population mean weight. At low body weights patients had less sleep and more restlessness, especially in the last four hours of the night. During refeeding and weight gain slow-wave sleep initially increased and then tended to decrease during the final stage of restoration of weight back to matched population mean levels. With the overall weight gain, however, there was a significant increase in length of sleep and rapid eye movement sleep, the latter increasing especially during the later stages of weight gain. These results reaffirm that insomnia, and especially early morning waking, is associated with low body weight in anorexia nervosa, and their implications are discussed with particular reference to a hypothetical association between various anabolic profiles and the need for differing components of sleep.
Br Med J 1975 Dec 06
PMID:Weight gain and the sleeping electroencephalogram: study of 10 patients with anorexia nervosa. 17 48

The authors compared the sleep laboratory recordings of 122 drug-free subjects who complained of chronic insomnia with the subjects' estimates of their habitual sleep characteristics and their estimated sleep time on the morning after sleeping in the laboratory. Most subjects consistently underestimated the amount of time they slept and overestimated the amount of time it took them to get to sleep in comparison with laboratory data. All subjects consistently underestimated the number of arousals they experienced. The authors discuss the implications of these findings for the treatment and definition of insomnia and for further research.
Am J Psychiatry 1976 Dec
PMID:Self-reports versus sleep laboratory findings in 122 drug-free subjects with complaints of chronic insomnia. 18 19

In a 13-night sleep laboratory study, each of 18 normal young adult males twice received 1 cup of warm water, 1-, 2-, and 4-cup equivalents of regular coffee, a 4-cup equivalent of decaffeinated coffee, and a 4-cup equivalent of caffeine. All beverages were administered 30 min before bedtime according to a balanced Latin-square design. Regular coffee produced dose-related changes in most standard electroencephalogram-electrooculogram (EEG-EOG) sleep parameters, and the 4-cup equivalents of regular coffee and caffeine produced equivalent effects. Decaffeinated coffee had no effect. Regular coffee and caffeine caused rapid eye movement (REM) sleep to shift to the early part of the night and stages 3 and 4 sleep to shift to the later part. Coffee also produced dose-related changes in several subjects estimates of sleep characteristics. These results suggest that coffee and caffeine may be used in normal subjects to induce symptoms mimicking those of insomnia. Such a tool should promote further understanding of insomnia.
Clin Pharmacol Ther 1976 Dec
PMID:Dose-related sleep disturbances induced by coffee and caffeine. 18 23

Under sleep-laboratory control, the efficacy of flurazepam hydrochloride (15 mg) was evaluated in 6 women (age range, 67-82 years) with objectively verified insomnia. A 15-night, single-blind, crossover procedure was followed. Sleep records obtained during 3 placebo-baseline nights, 7 consecutive flurazepam nights, and 3 placebo-withdrawal nights were evaluated by means of electroencephalographic, electro-oculographic, and electromyographic criteria. A statistically significant reduction in sleep latency and total awake time and a corresponding increase in total sleep time (P less than 0.05) were demonstrated during the active drug period. No evidence of diminishing effectiveness was observed during the 7 days of drug administration. For the rapid-eye-movement (REM) stage, a significant decrease (P less than 0.05) in mean REM percent was noted during the drug period despite an increase in mean absolute REM time. No REM rebound occurred upon drug withdrawal. There were no significant changes in mean percentages for stages 3 and 4 during the drug period and the withdrawal period. Adverse reactions were rare (chiefly some daytime drowsiness in 2 subjects).
J Am Geriatr Soc 1979 Dec
PMID:Insomnia in the elderly: treatment with flurazepam hydrochloride. 22 46

Enhanced voluntary motor inhibition regularly accompanies conditioned increases in the sensorimotor rhythm (SMR), a 12--14-Hz Rolandic EEG rhythm in cats.A similar rhythm, presumably SMR, has also been identified in the human EEG. The clinical effectiveness of SMR operant conditioning has been claimed for epilepsy, insomnia, and hyperkinesis concurrent with seizure disorders. The present report attempts to follow up and replicate preliminary findings that suggested the technique's successful application to hyperkinesis uncomplicated by a history of epilepsy. SMR was defined as 12--14-Hz EEG activity in the absence of high-voltage slow-wave activity between 4 and 7 Hz. Anticipated treatment effects were indexed by systematic behavioral assessments of undirected motor activity and short attention span in the classroom. EEG and behavioral indices were monitored in four hyperkinetic children under the following six conditions: (1) No Drug, (2) Drug Only, (3) Drug and SMR Training I, (4) Drug and SMR Reversal Training, (5) Drug and SMR Training II, (6) No Drug and SMR Training. All hyperkinetic subjects were maintained on a constant drug regimen throughout the phases employing chemotherapy. Contingent increases and decreases in SMR occurred in three of four training subjects and were associated with similar changes in classroom assessments of motor inactivity. Combining medication and SMR training resulted in substantial improvements that exceeded the effects of drugs alone and were sustained with SMR training after medication was withdrawn. In contrast, these physiological and behavioral changes were absent in one highly distractible subject who failed to acquire the SMR task. Finally, pretraining levels of SMR accurately reflected both the seve-ity of original motor deficits and the susceptibility of hyperkinetic subjects to both treatments. Although the procedure clearly reduced hyperkinetic behavior, a salient, specific therapeutic factor could not be identified due to the dual EEG contingency imposed combined with associated changes in EMG. Despite these and other qualifying factors, the findings suggested the prognostic and diagnostic value of the SMR in the disorder when overactivity rather than distractibility is the predominant behavioral deficit.
Biofeedback Self Regul 1979 Dec
PMID:Operant conditioning of EEG rhythms and ritalin in the treatment of hyperkinesis. 52 75

After a single oral dose of aminopyrine (9 mg/kg), mean salivary aminopyrine half-lives (t 1/2s) and metabolic clearance rates in 12 normal male volunteers exhibited diurnal variations. Salivary aminopyrine t 1/2s were approximately 50% longer at 8 P.M. (2.1 +/- 0.7 hr) than at 8 A.M. (1.4 +/- 0.3 hr). Mean aminopyrine metabolic clearance rates decreased 20% from 8 A.M. (418.2 +/- 152.0 ml/min) to 8 P.M. (335.3 +/- 107.6 ml/min). There were large interindividual variations in the magnitude of these diurnal changes in aminopyrine t 1/2 and metabolic clearance rates. There were nonsignificant changes in mean aminopyrine apparent volumes of distribution (aVd) which increased only slightly from 53.1 +/- 20.6 L at 8 A.M. to 59.7 +/- 26.5 L at 8 P.M. There were diurnal variations in plasma 11-hydroxycorticosteroids (11-OHCS), mean values of which decreased 60% from 16.2 +/- 4.2 microgram/100 ml at 8 A.M. to 6.5 +/- 1.9 microgram/100 ml at 8 P.M. Sleeplessness for 24 or 48 hr under the conditions of this experiment failed to affect diurnal rhythms in aminopyrine metabolism or plasma 11-OHCS concentrations.
Clin Pharmacol Ther 1978 Dec
PMID:Diurnal rhythms of aminopyrine metabolism: failure to sleep deprivation to affect them. 56 34

A double-blind randomized multicenter parallel group comparison of prazepam in divided doses vs. placebo was conducted by 15 investigators among 847 patients presenting with anxiety alone or concurrent with other medical illnesses. Study groups were well matched for age, sex and level of pre-treatment symptomatology. Efficacy evaluation by a physician questionnaire included serial assessment of global improvement plus 10 target signs/symptoms during the 2 to 4 weeks of treatment. Prazepam was statistically significantly superior to placebo as shown on final on-treatment scores for global improvement ratio and for the target symptoms of anxiety, tension, irritability/hostility, depressive mood, insomnia and somatization.
J Clin Psychiatry 1978 Dec
PMID:Prazepam in the treatment of anxiety: a placebo-controlled multicenter evaluation. 72 88

This article reviews all the prospective, double-blind controlled studies that have evaluated the prediction of response to imipramine hydrochloride and amitriptyline hydrochloride in depressed patients. Despite widely divergent methodologies, an attempt is made to extract clinically useful conclusions from these data. Critiques of each study and the criteria used in their evaluation are presented, with suggestions for future research included. The predictors of positive response to imipramine and amitriptyline are as follows: upper socioeconomic class, insidious onset, anorexia, weight loss, middle and late insomnia, and psychomotor disturbance. The predictors of poor response are the following: neurotic, hypochondriacal, and hysterical traits, multiple prior episodes, and delusions. Pretreatment urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) levels may some day be useful in predicting to which of these two tricyclic antidepressants a patient will respond.
Arch Gen Psychiatry 1976 Dec
PMID:Prediction of tricyclic antidepressant response: a critical review. 79 64


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