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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the most common of health problems, allergies afflict more than one of every six Americans. In the allergic reaction, mast cells degranulate, releasing inflammatory mediators such as histamine. These mediators in turn cause smooth muscle contraction, itch, mucus secretion, and vascular leakage. A number of pharmacologic agents, including the H1 receptor antihistamines and the sympathomimetic decongestants, have been developed in an attempt to minimize such effects. Antihistamines were first used clinically 50 years ago. Currently taken by approximately 30 million Americans each year, they are grouped by structure into six classes. Until recently, all of the classes, or first-generation antihistamines, were thought to be relatively equal in efficacy and, because of their ability to cross the blood-brain barrier, they all caused varying degrees of sedation. The effects of antihistamines on psychomotor reflexes and driving skills, antihistamine-induced drowsiness, and the interaction of antihistamines with alcohol and tranquilizers are reviewed. The centrally acting first-generation agents, and the performance decrements these agents commonly induce, are compared with the newer, nonsedating, second-generation antihistamines (eg, terfenadine, astemizole, cetirizine, and loratadine). Although decongestants do not appear to cause impaired performance, this needs to be evaluated further, particularly with regard to decongestant-induced insomnia.
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PMID:Antihistamine- and decongestant-induced performance decrements. 197 Aug 34

A multicenter, double-blind placebo-controlled clinical trial was designed to compare the safety and efficacy of estazolam compared with flurazepam as hypnotics. Outpatients complaining of insomnia were randomized to receive either estazolam 2 mg, flurazepam 30 mg or placebo for 7 consecutive nights. The analysis of efficacy was based on the patients' daily assessments of sleep and the investigators' global evaluations. Adverse events which were considered by the investigator to be attributable to, or of unknown relationship to the test medication were analyzed. The patient subjective questionnaire indicated that estazolam and flurazepam significantly improved all parameters (P less than .05) as compared to placebo. A marked or moderate improvement in sleep was reported by 81% (58/72), 78% (63/81) and 36% (27/76) of estazolam, flurazepam, and placebo recipients, respectively. There were no significant differences in hypnotic effect between estazolam and flurazepam. All efficacy parameters of the investigators' global evaluation improved significantly more (P less than .05) for patients receiving estazolam or flurazepam (except quality of sleep) than for those receiving placebo. The percentage of patients reporting any adverse experience was greatest for flurazepam (72%), followed by estazolam (59%), and placebo (43%). Somnolence and hypokinesia were the most commonly reported adverse events. An analysis of the global evaluation of side effects showed that flurazepam had a significantly worse side effect profile than estazolam (P less than .05) or placebo (P = .001). Estazolam and flurazepam effectively, and comparably, relieved insomnia when administered for 7 nights in adult patients complaining of insomnia. Estazolam demonstrated a more favorable side effect profile than flurazepam.
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PMID:Estazolam and flurazepam: a multicenter, placebo-controlled comparative study in outpatients with insomnia. 197 31

We carried out a four-week double-blind placebo-controlled study comparing remoxipride (n = 20) to chlorpromazine (n = 21) and placebo (n = 21) in the treatment of newly admitted schizophrenic patients with acute exacerbation. Chlorpromazine was found to be significantly better than remoxipride on the dropout rate due to inefficacy, Clinical Global Impression (CGI) of severity of illness and Brief Psychiatric Rating Scale (BPRS). Chlorpromazine tended to be better than placebo on the dropout rate related to inefficacy, Nurse's Global Impression (NGI) of severity and on the BPRS measures of positive symptoms (hallucinatory behaviour and thinking disturbance factor). We were unable to detect a difference between remoxipride and placebo except that remoxipride was better in patients who had previously responded well to neuroleptics. Both drugs induced significantly more parkinsonism than placebo, but differently so: chlorpromazine induced both types of parkinsonism hypo- and hyper-kinetic symptoms, whereas remoxipride induced hyperkinetic symptoms. Chlorpromazine caused more tachycardia, drowsiness, orthostatic dizziness, and dry mouth than the other two treatments, while patients on remoxipride suffered more from insomnia than those on the other two treatments.
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PMID:A placebo-controlled clinical trial of remoxipride and chlorpromazine in newly admitted schizophrenic patients with acute exacerbation. 197 69

The effects of high-dose fluoxetine (median 80 mg/day), standard-dose imipramine (median 200 mg/day), and placebo were studied in 706 outpatients meeting DSM-III criteria for major depressive disorder. Baseline psychomotor activity of each patient was prospectively categorized as agitated, retarded, or neither. Rates of occurrence of total and significant (leading to discontinuation) activating adverse events (insomnia, agitation, anxiety, nervousness) and sedating events (somnolence, asthenia) were compared between treatments on an overall basis and within categories of baseline psychomotor activity. Additionally, these rates were compared across baseline psychomotor activity for each treatment. Efficacy was evaluated on an overall basis and with respect to baseline psychomotor activity. There was more total activation with fluoxetine than placebo (p = 0.008), but total activation with fluoxetine (28%) showed only a trend (p = 0.092) for being greater than with imipramine (21%). Discontinuations for activation with fluoxetine (5%) did not differ from imipramine (5%). Sedation and discontinuations for sedation with both fluoxetine and imipramine significantly exceeded placebo. The only drug-drug difference in discontinuations was for sedation where imipramine (11%) exceeded fluoxetine (5%; p = 0.008). Only for the occurrence of sedation with imipramine (47% among patients retarded at baseline) was there a significant association with baseline psychomotor activity (p = 0.021). Both fluoxetine and imipramine were superior to placebo and equal in efficacy in decreasing total Hamilton Rating Scale for Depression (HAM-D), the sleep disturbance HAM-D factor, and the anxiety/somatization HAM-D factor scores. These improvements were independent of baseline psychomotor activity.
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PMID:High-dose fluoxetine: efficacy and activating-sedating effects in agitated and retarded depression. 162 94

Two hundred forty-one elderly depressed patients entered the 8-week, double-blind phase of this parallel-group, multicenter study; 161 patients were randomized to receive sertraline (50-200 mg/day) and 80 were randomized to receive amitriptyline (50-150 mg/day). Among evaluable patients, there were no statistically significant differences between treatments in any of the primary efficacy variables: change in total Hamilton Rating Scale for Depression (HAM-D) score (17 items), percentage change in HAM-D score, change in HAM-D Item 1, change in Clinical Global Impressions (CGI) Severity score, change in the Depression Factor of the 56-item Hopkins Symptom Checklist, and the CGI Improvement score at the last visit. Similar results were obtained using data from all patients (intention-to-treat analysis), except that amitriptyline was superior in HAM-D Total score (p = .044). The two drugs produced a similar degree of response: on the basis of the HAM-D criterion, 69.4% of sertraline patients and 62.5% of amitriptyline patients responded, and, on the basis of CGI criterion, 79.5% of sertraline and 73.4% of amitriptyline patients responded. Twenty-eight percent of the sertraline patients withdrew from the study because of a treatment-related side effect and 2.5% (4) because of a laboratory abnormality. In comparison, 35% of the amitriptyline patients withdrew because of treatment-related side effects. Sertraline was associated with a statistically lower frequency of somnolence, dry mouth, constipation, ataxia, and pain and a higher frequency of nausea, anorexia, diarrhea/loose stools, and insomnia; thus, anticholinergic effects were less common and gastrointestinal effects were more common with sertraline than with amitriptyline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Double-blind, multicenter comparison of sertraline and amitriptyline in elderly depressed patients. 225 79

A therapeutic committee was established in Toulouse Regional University Hospital in order to prescribe zidovudine in patients suffering from AIDS. Using an informatic card, the side effects were evaluated in the 125 patients treated by Zidovudine since the creation of the Committee (from July 1987 to January 1989). Zidovudine was prescribed from May 1987 to June 1988 at the total dose of 1,200 mg daily from June 1988 at 900 mg daily. The most frequent side effects were hematologic: zidovudine used alone (or associated with non hematotoxic drugs) elicited in 21.2% of patients a neutropenia (defined as a number of neutrophils less than 1,000/mm3), in 2.4% anaemia (haemoglobin less than or equal to 9 g/100 ml) and in 4.8% neutropenia associated with anaemia. When zidovudine was administered with hematotoxic drugs, neutropenia, anaemia or the association of both were observed in 12.0%, 3.2% and 2.4% of patients respectively. These hematologic side effects were always regressive after drug cessation. However, it is important to underline the low incidence of hematological side effects on red cells of zidovudine in the present study. This result is unexpected. The other side effects of Zidovudine (used alone) did not led to modification in drug treatment: gastrointestinal disturbances (30.4%), headaches (16.8%), insomnia (13.6%), somnolence (6.4%).... These side effects appeared during the four first months and decreased with the continuation of drug treatment. Their imputation was difficult to define and differentiate to evolution of the disease.
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PMID:[Evaluation of the pharmacovigilance follow-up of zidovudine]. 226 33

Schedule-dependent sleep problems tend to increase as the youngster moves from middle childhood through preadolescence and into adolescence. This is partly because the youngster becomes more independent and parental control over both the selection of particular sleep schedules and the consistent maintenance of these schedules across weekends diminishes. Even accurate descriptions of the existing problem may become difficult to obtain. Nevertheless, specific syndromes are common and may be identified and treated. There may be increased demands at both ends of the sleep period leading to later bedtimes, earlier wakings, insufficient sleep, and daytime sleepiness. Periods of wakefulness confined to one portion of the night (beginning, middle, or end) may occur if sleep requirements are overestimated. Insomnia coupled with trouble waking may imply a circadian phase shift abnormality or a 'school-refusal' variant. And, variable sleep difficulties may be seen in a youngster with irregular schedules and poor sleep hygiene. Guidelines to the understanding, evaluation, and treatment of these syndromes are presented.
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PMID:Sleep schedule-dependent causes of insomnia and sleepiness in middle childhood and adolescence. 231 36

This study was undertaken to determine whether a single night's use of triazolam by normal healthy sleepers leads to withdrawal insomnia on the subsequent night, and whether there is a dose response relationship to this phenomenon. Thirty normal sleepers of both sexes were randomly assigned to three parallel treatment groups. All subjects were studied for five consecutive nights by means of pre- and post-sleep questionnaires and all night polysomnography. Multiple sleep latency tests were conducted on the days following the second, third, and fourth nights in the laboratory. All subjects received placebo capsules on the first, second, fourth, and fifth nights in the laboratory and either placebo, 0.25 mg triazolam or 0.5 mg triazolam according to their assigned group on the third night. Both doses of the drug increased subjective estimates of sleep duration, but no objective increase was found. Neither dose altered daytime measures of sleepiness. No changes were found in any of the sleep parameters on withdrawal of the 0.25 mg dose of triazolam. However, discontinuation of the 0.5 mg dose did lead to significant objective and subjective withdrawal effects. It was concluded that higher doses of triazolam could lead to withdrawal effects in normal sleepers even when this drug was used for only a single night.
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PMID:The effects of a single night's dosing with triazolam on sleep the following night. 235 5

We report 38 consecutive patients referred to a sleep disorder clinic who on diagnostic polysomnography showed excessive amounts of brief fragmentary myoclonus throughout all stages of NREM sleep. Almost all patients were male despite a reasonably equal sex distribution of referral. The phenomenon was found associated with sleep-related respiratory problems, periodic movements in sleep (PMS), narcolepsy, intermittent hypersomnia and (rarely) insomnia. It also occurred associated with excessive daytime sleepiness (EDS) as an isolated polysomnographic finding apart from some degree of sleep fragmentation.
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PMID:Excessive fragmentary myoclonus in NREM sleep: a report of 38 cases. 241 Feb 21

Aminoglutethimide (AG) was administered as palliative therapy in 112 patients with metastatic breast cancer. In 36 patients, the dose level was 1000 mg/day; 76 patients received a dose level of 500 mg/day. Patients with brain or liver metastasis were excluded, as were patients with tumors determined to be negative for estrogen receptors. Objective regression was observed in 35 (31%) patients, with the duration of response ranging from 4 to 36 + months (mean, 12 months; median, 10 months). Response was observed in 11 of 31 (35%) patients with soft tissue metastasis; 16/59 (27%) patients with osseous metastasis; and 8 of 22 (36%) having visceral metastasis. In 93 patients with positive estrogen receptor (ER), 33 responded (35%), whereas in 19 patients with unknown ER status, two responded (11%). Response to previous treatment with tamoxifen (TAM) had occurred in 31 patients; of these, response to AG was noted in 11 (35%). Of 24 patients failing to respond to prior treatment with tamoxifen, four (17%) responded to subsequent therapy with AG. Thirteen patients had previously received combination chemotherapy, and response to AG was noted in two (15%). The side effects observed in this study included skin rash in ten patients, fever in eight, somnolence in three, weakness and dizziness in one, headache in one, insomnia in one, dyspnea in one, and ataxia in one. Treatment had to be discontinued in eight patients, due to the severity of the side effects. As expected, patients receiving AG at the lower dose level of 500 mg/day experienced fewer and less severe side effects than those treated with the higher dose. The response rate in the 1000 mg/day group was 10/36 (28%) and in the 500 mg/day group, it was 25/76 (33%). The lower dosage was better tolerated without apparent compromise in therapeutic efficacy.
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PMID:Aminoglutethimide in patients with metastatic breast cancer. 246 35


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