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

The appropriate use of hypnotics requires an understanding of the nature of the patient's insomnia and lifestyle. In the context of occupational medicine, the potential effects of these drugs on job skills and the persistence of such effects are also important considerations. This report reviews the factors that must be considered in the investigation of impaired performance due to hypnotics and the pharmacokinetic properties that determine the persistence of action of these drugs. Sleep disturbance associated with transmeridian flights (jet lag) is used to illustrate the place of hypnotics in the management of a transient form of insomnia.
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PMID:Hypnotics and occupational medicine. 218 65

Trazodone (150 mg to 400 mg) was administered to six depressed patients with significant sleep disturbances in an 8-week single-blind study design. Patients were evaluated psychologically by means of the Hamilton Rating Scales for Anxiety and Depression. Polysomnographic monitoring in the sleep laboratory was conducted at each of the time points corresponding to the psychiatric evaluations. Five of the six subjects completed treatment. Patients showed a significant improvement in symptoms of depression and in their polysomnographic-determined sleep architecture. There was a 44% improvement in persistent sleep latency, decreasing from a mean +/- SD of 51.0 +/- 59.3 minutes at baseline to 28.5 +/- 24.2 minutes after 5 weeks of active treatment. Total sleep time improved 14% from 387.1 +/- 59.2 minutes at baseline to 441.3 +/- 23.7 minutes after 5 weeks. Stage IV sleep more than doubled with an increase of 153% from 1.9 +/- 3.0% at baseline to a more normal 4.8 +/- 5.5%. There was no change in percentage of rapid eye movement (REM); however, REM latency increased 28% from a mean of 74.6 +/- 35.9 minutes at baseline to a mean of 95.6 +/- 28.8 minutes. Sleep efficiency improved from 80.6 +/- 12.3%, considered clinically significant insomnia, to 91.9 +/- 4.9%, which is well within normal sleep patterns.
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PMID:Sleep laboratory evaluation of the effects and efficacy of trazodone in depressed insomniac patients. 221 59

The clinical efficacy of a behavioral management program for treating insomnia secondary to chronic pain was evaluated within a multiple-baseline design across subjects. Treatment consisted of a combination of stimulus control and sleep restriction procedures. Daily sleep diaries and all-night polysomnographic (PSG) measures were used to document changes in sleep/wake patterns. The results showed that treatment was effective in improving sleep patterns in all three patients. A substantial decrease of time awake at night was obtained and this was reflected by reductions of sleep onset latency, wake time after sleep onset, and early morning awakenings. Sleep improvements were well maintained at follow-ups and were also paralleled by improved mood states. The findings indicate that behavioral procedures are effective for treating sleep disturbances associated with chronic pain conditions.
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PMID:Behavioral management of sleep disturbances secondary to chronic pain. 253 97

Rebound insomnia, a worsening of sleep compared with pretreatment levels, has been reported upon discontinuation of short half-life benzodiazepine hypnotics. This paper reviews the existing sleep laboratory studies for the presence or absence of rebound insomnia following treatment with triazolam, temazepam, and flurazepam in insomniac patients or poor sleepers and, when possible, in normals. The results indicate that rebound insomnia is a distinct possibility after discontinuation of triazolam in both insomniacs and normal controls. Compared with baseline, disturbed sleep was reported in insomniacs or poor sleepers for the first 1 or 2 nights of withdrawal in seven of nine polygraphically recorded sleep studies following triazolam 0.5 mg and in one of two studies following triazolam 0.25 mg. In one study conducted in normal volunteers, rebound insomnia was observed following triazolam 0.5 mg but not triazolam 0.25 mg. In another study, which used subjective reports of sleep rather than polygraphic recordings, rebound insomnia was significantly attenuated after triazolam 0.5 mg by tapering the dose over 4 nights. The risk of rebound insomnia after temazepam 15 or 30 mg was low. In keeping with its long elimination half-life, flurazepam (30 mg) continued to exert beneficial effects for the first 2-3 withdrawal nights, but the possibility of a mild rebound insomnia cannot be dismissed during the intermediate withdrawal period (nights 4-10) following prolonged, consecutive, nightly administration (more than 30 nights). The benzodiazepine hypnotics are generally preferred over other types (barbiturates or nonbenzodiazepine, nonbarbiturate), but there are advantages and disadvantages related to half-life of the benzodiazepines. The risk of rebound insomnia is greater with the short half-life as compared with the long half-life benzodiazepines.
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PMID:Rebound insomnia: a critical review. 256 41

The case of a patient with sleep-related painful erections is described. Insomnia and a slight depressive syndrome occurred along with a long history of this disorder. No physical abnormality was found. At a baseline recording of sleep electroencephalography (EEG) and nocturnal penile tumescence (NPT), a disturbed sleep pattern and impaired NPT were recorded. Attempts to treat the disorder with diazepam, amitriptyline, trimipramine, and biperidene did not prompt a stable improvement of the disorder, but a dosage of 25 mg clozapine was sufficient to achieve normalized sleep architecture, remission of the depressive symptomatology, and normalization of NPT. It is likely that marked sedation is the mode of action of clozapine.
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PMID:Examination and treatment of sleep-related painful erections--a case report. 275 20

As part of the National Institute of Mental Health Epidemiologic Catchment Area study, 7954 respondents were questioned at baseline and 1 year later about sleep complaints and psychiatric symptoms using the Diagnostic Interview Schedule. Of this community sample, 10.2% and 3.2% noted insomnia and hypersomnia, respectively, at the first interview. Forty percent of those with insomnia and 46.5% of those with hypersomnia had a psychiatric disorder compared with 16.4% of those with no sleep complaints. The risk of developing new major depression was much higher in those who had insomnia at both interviews compared with those without insomnia (odds ratio, 39.8; 95% confidence interval, 19.8 to 80.0). The risk of developing new major depression was much less for those who had insomnia that had resolved by the second visit (odds ratio, 1.6; 95% confidence interval, 0.5 to 5.3). Further research is needed to determine if early recognition and treatment of sleep disturbances can prevent future psychiatric disorders.
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PMID:Epidemiologic study of sleep disturbances and psychiatric disorders. An opportunity for prevention? 276 6

Sleep disturbance has become a subject of serious study only over the past few years, but even so there is already an increasing awareness of the nature of insomnia and a greater understanding of the role which hypnotics should play in clinical medicine. An hypnotic may be used to shorten sleep onset when there is difficulty in falling asleep, to reduce nocturnal wakefulness, or to provide an anxiolytic effect during the next day when insomnia is accompanied by a marked element of anxiety. The purpose of an hypnotic is to meet one or more of these clinical problems; to ensure that the patient is given the most useful medication, consideration must be given to duration of activity. This depends on the absorption, distribution and elimination characteristics of the drug. It is now appreciated that the most appropriate use of hypnotics is in the individual with insomnia of recent origin. An hypnotic with the most relevant pharmacokinetic profile should be used for the shortest period of time and then only as required, while low doses will ensure freedom from adverse effects. The place of hypnotics in chronic insomnia remains less certain. Their careful use may well be of benefit, though it must be part of a well defined clinical strategy. Assessment of the patient is essential to identify any specific conditions which would impair sleep.
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PMID:Hypnotics. Their place in therapeutics. 286 77

Many centrally acting drugs which are prescribed for hypertension, depression, epilepsy, insomnia and asthma may also affect fetal brain neurotransmission and behavioral states. Nearly all these drugs enter the fetal circulation following maternal administration. The immaturity of the blood-brain barrier and greater accumulation in the developing brain make the fetal brain a major target of its mother's medication. Adverse effects that are seen in the fetus are not necessarily evident in its mother. We have shown that drugs like clonidine (an antihypertensive) and clomipramine (an antidepressant), which act on noradrenaline and serotonin neurotransmission in the brain, suppress rapid eye movement sleep in the developing rat. In adulthood, the neonatally treated rats showed hyperactivity, hyperanxiety, reduced sexual behavior, disturbed sleep patterns and reduced cerebral cortical size. Furthermore, such treatment induced an increase in voluntary alcohol consumption and a decreased adaptability of responses to changes in water deprivation in a Y-maze. Little is known about long-lasting consequences of centrally acting drugs used during late gestation in humans. Minor neurological disturbances, such as delayed visual motor performance, smaller head circumference, increased anxiety and disturbed sleep-wake patterns, have been reported in children born to hypertensive mothers treated with clonidine or alpha-methyl-dopa.
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PMID:Neurochemical and electrophysiological disturbances mediate developmental behavioral alterations produced by medicines. 287 4

The dose effects of temazepam tablets (15 and 30 mg) were studied at two sleep centres in 48 volunteers who had objective polysomnographic evidence of sleep onset insomnia. Volunteers slept in the laboratory, retiring at their usual bedtime after taking placebo or temazepam 30 min earlier, and were monitored for 8 h using standard polysomnographic techniques. Acute (nights 5-7) and short term (nights 11-13) temazepam, both 15 and 30 mg, improved the sleep of these volunteers by reducing sleep latency and increasing sleep time compared to the placebo baseline (nights 2-4). Dose differences were found primarily on the measurement of sleep staging, with 30 mg having a greater or more consistent effect than 15 mg. No residual effects were observed on the basis of questionnaires and objective tests of performance and no consistent evidence of disturbed sleep after discontinuing treatment was seen.
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PMID:Dose effects of temazepam tablets on sleep. 287 58

Clonazepam (1 mg h.s.) and temazepam (30 mg h.s.) were studied in 10 patients diagnosed as having insomnia with nocturnal myoclonus. Each subject underwent two nocturnal polysomnographic recordings while drug-free, two during treatment with clonazepam, and two during treatment with temazepam. Treatment sessions were 7 days long, and recordings were done on nights 6 and 7 of the treatment sessions. A 14-day washout period separated the treatment sessions. The order of drugs used in the first and second treatment sessions was randomized. Objective and subjective sleep laboratory data showed that both drugs improved the sleep of patients with insomnia in association with nocturnal myoclonus. Neither drug significantly reduced the number of nocturnal myoclonic events. Sleep changes were consistent with those produced by sedative benzodiazepines in general. Thus, the data support clinical reports that clonazepam, a benzodiazepine marketed for the indication of seizure, is useful in improving sleep disturbances associated with nocturnal myoclonus. Temazepam, a benzodiazepine marketed for the indication of insomnia, was found to be a suitable alternative to clonazepam in the treatment of insomnia associated with nocturnal myoclonus. The present data and other studies suggest the need for a model that explains why leg movements and sleep disturbances may wax and wane independently.
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PMID:Nocturnal myoclonus: treatment efficacy of clonazepam and temazepam. 287 85


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