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

Recent years have seen significant advances in sleep disorders medicine, including effective treatments for chronic psychophysiological insomnia and obstructive sleep apnea syndrome; greater understanding of biological rhythms and of the nature of sleep in depression, including seasonal affective disorder; and the discovery of REM behavior disorder. The author reviews selected developments in the sleep disorders field over the last three years. Developments are presented in the framework of the diagnostic classification of the American Sleep Disorders Association, with emphasis on areas relevant to the practice of psychiatry.
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PMID:Sleep disorders: a selective update. 264 52

The effect of zolpidem 10 mg p.o. on sleep in patients with persistent psychophysiological insomnia was assessed by polysomnographic recordings. An improvement in sleep with no rebound insomnia was observed during treatment for two weeks. Time awake after the onset of sleep was reduced after one week and increased after two weeks, whereas sleep latency remained reduced. Zolpidem markedly increased the duration of Stage 2 sleep without affecting either slow wave sleep or REM sleep. Subjective evaluation of improvement in sleep was well correlated with sleep laboratory findings. Zolpidem did not impair the immediate memory or psychomotor performance of patients on the morning after its administration. Side-effects during the period of drug administration included drowsiness, fatigue, headache, anxiety and irritability. They were mild or moderate and wore off soon after awakening.
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PMID:Effect of zolpidem on sleep in insomniac patients. 266 41

During depression, chronobiological disorders occur, such as disturbances in body temperature and early urinary excretion of a noradrenaline metabolite. Sleep patterns are disturbed in 90% of depressed patients; early REM sleep and shortened slow-wave sleep (stages 3 and 4), resulting in an increase in REM sleep, have been observed. Thus, an increase in REM sleep may be an indication of depression. Chronic insomnia is characterised by irregular sleep behaviour, an anxious attitude to sleep and increased cognition before sleep onset. Patients with this disorder can be divided into those with a disturbed ultradian rhythm (less than 2 REM-NREM cycles) and those with regular sleep structure (greater than 2 REM-NREM cycles). Most antidepressants reduce REM sleep, an effect evident from day 1 of administration. Trimipramine is an exception in that it has antidepressant and sedative effects without modifying REM sleep, and it possesses a different pharmacodynamic profile. Trimipramine is effective in depressed patients with chronobiological disorders such as chronic insomnia, although its mechanism of action is not fully understood.
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PMID:Depression, circadian rhythms and trimipramine. 269 50

Sleep-wakefulness and EEG responses to a chronic morphine treatment (2 mg/kg/day, IP, during 15 days) were studied in 8 cats provided with electrodes for EEG, EMG and EOG records. Results indicated that, in contrast to a resistance of the cats to exhibit overt signs of tolerance in the immediate behavioral and EEG responses to morphine, tolerance developed in sleep since: 1) there was a reduction in its onset latency after the initial insomnia period; 2) despite that the initial insomnia period was present throughout the treatment, compared to the effects of the first MS day, the total amount of both NREM sleep and REM sleep significantly increased in subsequent drug days, the total amount of REM sleep reached similar placebo values from day 5; 3) the restoration in the total amount of both sleep states was due to significant increases that occurred from day 5 after the first 6 hours of the MS injection. During the 19-24 hours after MS injections, increases of NREM and REM also resulted statistically significant compared to placebo values. A biphasic depressed and aroused response occurred during early withdrawal. REM sleep rebound was present after MS discontinuation and in the following week. Similarities with effects of opiate chronic administration in other species are discussed. These results support the potential use of the cat for the study of neural mechanisms involved in sleep chronic effects of opiates.
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PMID:Chronic morphine administration in cats: effects on sleep and EEG. 272 14

Benzodiazepines currently represent the most widely prescribed family of hypnotic drugs. They possess obvious advantages: actual hypnotic efficacy, at least with short-term use, low toxicity, and excellent tolerance. However, several side effects need to be mentioned: besides morning drowsiness (which represents the untoward continuation of their sedative properties), anterograde amnesia, increase of daytime anxiety, and rebound insomnia. Moreover, benzodiazepines significantly modify several sleep parameters: they decrease slow wave sleep and delay the first period of REM sleep. Any hypnotic benzodiazepine should only be prescribed in case of actual need and after exclusion of non-pharmacologic means. The "softest" agent, at the lowest dose, and during the shortest period should always be preferred.
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PMID:[Benzodiazepines and sleep]. 286 71

Psychobiological aspects of low-dose benzodiazepine dependence (LBD) and drug withdrawal were investigated in 76 middle-aged and elderly chronic insomniacs in a sleep laboratory. Comparison with drug-free insomniacs showed that LBD leads to a complete loss of hypnotic activity and substantial suppression of delta and REM sleep. Only small differences were found between benzodiazepines with different half-life time. Upon withdrawal, recovery from this suppression, especially in REM sleep, occurred, while insomnia did not increase. The patients, however, reported sleeping longer while taking the drug compared with withdrawal. This misperception seems to be a specific effect of benzodiazepines, and contrasts with the full awareness of insomnia upon withdrawal. It is concluded that these effects play a leading role in the patients' inability to escape their sleeping pills. The response of REM sleep to withdrawal should make this a useful measure to objectively confirm low-dose benzodiazepine dependence.
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PMID:Why low-dose benzodiazepine-dependent insomniacs can't escape their sleeping pills. 257 35

Urinary cyclic adenosine monophosphate (AMP-c) was measured morning and evening in 35 patients with alcohol withdrawal syndrome (AWS). 65% of the patients revealed a higher night time than day time concentration of AMP-c in the urine, reflecting increased sympathetic adrenergic activity. The circadian rhythm was lost in 88.55% of the 35 patients. The pathogenic factors and mechanisms involved in AWS are discussed and the contribution of sympathetic adrenergic hyperactivity to the onset of the withdrawal syndrome with its concomitant depression of the cholinergic and GABAergic systems is emphasised. Finally it is suggested that insomnia and the loss of REM sleep may also contribute to the onset of the condition.
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PMID:[Changes in the circadian rhythm of urinary cyclic adenosine monophosphate during the alcoholic withdrawal syndrome and related neurobiological correlations]. 299 62

The effects of 400-600 mg trazodone on the sleep patterns of ten depressed in-patients treated for 5 weeks were studied during the initial (days 1-3) and terminal (days 26-28) treatment periods. The sleep parameters were compared to those obtained from three sleep recordings performed just prior to the initiation of the treatment and after 2 adaptation nights at the end of a 2-week drug-free period. At the same time, the clinical evolution of patients was evaluated weekly using MADRS and Hamilton-Anxiety scales for anxiety-depression symptomatology and Spiegel and Norris sleep scales. Weekly blood samples were collected to measure plasma levels of trazodone and, at the end of the study, the elimination half-life at steady state was calculated by repeated measurements of plasma levels. Clinical improvement, as assessed by a reduction of more than 60% in MADRS scale scores, was accompanied by evidence of the definitely beneficial effects of trazodone on the disturbed sleep of these depressed patients. From the beginning of treatment, there was a hypnotic-like effect (increase in total duration of sleep and stage II, decrease in sleep latency and intrasleep awakenings). In addition, records at the end of the study showed an increase in delta sleep and an increase in REM latency, an effect classically associated with an antidepressant action. These particularly valuable effects of trazodone on sleep would suggest that this drug should especially be given in cases of depression with major insomnia.
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PMID:Effects of trazodone on the sleep of depressed subjects--a polygraphic study. 313 13

Hypnotic efficacy and safety of 3 weeks of daily doses of 2 mg lorazepam or 30 mg flurazepam were compared in a double-blind cross-over study in eight chronic insomniacs between the ages of 29 and 60 years. Subjects were monitored in the sleep laboratory twice weekly for a total of 25 nights. Also, subjective estimates of sleep, vigilance tests, and adverse effects were recorded throughout the study. Findings indicated lorazepam performed better than flurazepam in most sleep parameters. With lorazepam there was improvement from baseline in percentage of sleep time (P less than .05); in total wake time after sleep onset (P less than .01) and in last third of night (P less than .05); in percentage of stage 2 (P less than .05) (weeks 1, 2, 3) and in percentage of night in stage 4 (weeks 2 and 3). Only total wake time from baseline improved (P less than .05) with flurazepam (week 2). Objective and subjective sleep parameters did not correlate well for either drug. Neither drug impaired REM sleep or vigilance test performance. Side effects (grogginess, lethargy; flurazepam only) were few and none was unexpected; neither rebound insomnia nor early morning insomnia occurred with either drug. In summary, both lorazepam 2 mg at bedtime and flurazepam 30 mg at bedtime were found to be effective and safe for treating chronic insomnia, as measured by parameters of sleep and daytime functioning. Lorazepam had more favorable effects on sleep than did flurazepam.
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PMID:Comparison of lorazepam and flurazepam as hypnotic agents in chronic insomniacs. 328 Jun 15

Within the context of the comprehensive treatment of sleep disorders, which includes medical, neurologic, psychiatric, and social interventions, use of medication is often indicated. Among the three benzodiazepine hypnotics that are available in the United States for the treatment of insomnia, flurazepam is effective for both sleep induction and maintenance, and it retains most of its efficacy over a 4-week period of nightly administration; temazepam is effective only for sleep maintenance, and triazolam improves both sleep induction and maintenance with initial but not with continued administration. Rebound phenomena are more frequent and intense with the more rapidly eliminated drug, triazolam, and to a lesser degree with temazepam. Also, with triazolam, certain behavioral side effects, such as amnesia and psychotic-like symptoms, have been reported. With flurazepam, which is a slowly eliminated benzodiazepine, daytime sedation is more frequent than with the other two drugs. When insomnia is secondary to major depression, antidepressant medication should be administered. Methylphenidate, amphetamines, or other stimulant medications are used for the symptomatic treatment of the sleepiness and sleep attacks of narcolepsy and hypersomnia. For cataplexy and the other two auxiliary symptoms of narcolepsy, imipramine or other tricyclics are the drugs of choice. Protriptyline and medroxyprogesterone have been used in treating mild cases of obstructive sleep apnea, but their efficacy is limited. Similarly, for the treatment of central sleep apnea, medroxyprogesterone and acetazolamide have shown only limited effects. Medication for patients with sleepwalking, night terrors, or nightmares should be prescribed judiciously, and primarily when treatment of an underlying psychiatric condition is desired. The neuropharmacology of sleep should also consider drugs that may cause sleep disorders. Medications with sleep disturbing effects include various antihypertensives, bronchodilators, and the energizing antidepressants. Withdrawal of REM-suppressant drugs, such as the barbiturates, may cause nightmares in association with a REM rebound. Occasionally, a drug or a combination of drugs may produce somnambulistic-like activity in some patients.
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PMID:Clinical neuropharmacology of sleep disorders. 333 64


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