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

1. The clinical efficacy of mianserin, a tetracyclic compound, was compared with imipramine and placebo in 47 hospitalized depressed patients. 2. The clinical ratings showed that the three treatment groups improved equivalently during hospitalization. 3. Plasma levels of mianserin correlated with changes in the Hamilton Rating Scale for depression, total score and two of its factors (anxiety/somatization, and retardation) and the item 'late insomnia'. 4. Drowsiness was a more frequent side-effect among mianserin patients on day 4; no other side-effect distinguished the treatments. 5. No relationship between MHPG levels and treatment or treatment outcome were observed.
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PMID:Clinical study of mianserin, imipramine and placebo in depression: blood level and MHPG correlations. 34 42

Among the newer antihypertensive agents are the beta-blocking drugs, such as propranolol. These agents are useful as second-step drugs to be used if diuretic therapy alone is not effective. In mild to moderately severe hypertension, propranolol, in does of up to 480 mg/day in combination with a thiazide diuretic, has been found to be effective in over 80% of patients on long-term therapy. This degree of response is essentially similar to that noted with a combination of reserpine and a diuretic agent. Although some observers believe that propranolol produces many fewer side effects than the other step 2 drugs (reserpine and alpha-methyldopa), there are some patients who do experience restlessness, insomnia, and depression. Clonidine may be substituted for another step 2 drug, is of moderate potency, but may not be tolerated by a large number of patients because of the severe dry mouth and drowsiness that it produces. Prazosin appears to be a suitable substitute for hydralazine as an effective vasodialator if thiazides plus propranolol or thiazides plus reserpine or alpha-methyldopa are not effective. In some instances, it many be an acceptable second-step drug because of its alpha-adrenoreceptor-blocking properties. The angiotensin II competitive inhibitors or converting enzyme inhibitors may in the future have some place in the management of hypertension.
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PMID:Propranolol and newer antihypertensive drugs in the management of hypertension. 42 60

1 To assess the potential hazards of nitrazepam therapy of insomnia in the elderly, adverse reactions to nitrazepam were studied in 2111 hospitalized medical patients who received the drug. 2 Manifestations of unwanted central nervous system (CNS) depression (such as drowsiness or 'hangover') were reported in 49 nitrazepam recipients (2.3%), and signs of unwanted CNS stimulation (such as nightmares, insomnia, agitation, etc.) in 15 (0.7%). None of the adverse reactions were considered serious. 3 Physician-rated clinical efficacy of nitrazepam was not related to dose, but the frequency of both types of adverse reactions increased significantly at higher daily doses. CNS depression also was significantly more frequent in the elderly, being reported in 11% of those aged 80 years or older, whereas the frequency of CNS stimulation was not correlated with age. 4 The effect of age on the reported rate of unwanted CNS depression was most striking at high doses. Among patients aged 80 years or over whose daily dose averaged 10 mg or more, 55% experienced unwanted CNS depression attributed to nitrazepam. 5 Low doses of nitrazepam are safe for elderly individuals, but the elderly are readily susceptible to excessive CNS depression at high doses. The findings suggest that there is little reason to exceed 5mg doses of nitrazepam for most patients, particularly those who are elderly.
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PMID:Toxicity of nitrazepam in the elderly: a report from the Boston Collaborative Drug Surveillance Program. 65 80

The treatment of obesity is one of the major measures available today in the field of preventive medicine. In particular, the coronary epidemic of Western civilisation would be halted, and most cases of maturity-onset diabetes prevented, if obesity were to be treated effectively. Anorectic drugs act mainly on the satiety centre in the hypothalamus to produce anorexia. They also have various metabolic effects involving fat and carbohydrate metabolism, but many of these may be secondary to loss of weight. Most of the drugs are related directly or indirectly to amphetamine and in addition act by increasing general physical activity. Anorectic drugs tend to lose their effect after some months, and part of this reduction in effect may be due to chemical alterations produced by the drugs in the brain. All the drugs, with the exception of fenfluramine, have a stimulant effect on the central nervous system in some individuals, resulting in restlessness and nervousness, irritability and insomnia. Fenfluramine commonly produces drowsiness in normal doses, but has stimulant effects with overdosage. Dexamphetamine, phenmetrazine and benzphetamine all tend to cause euphoria and the risk of addiction is therefore considerable. Euphoria occasionally occurs with diethylpropion, phentermine and chlorphentermine, but to a much lesser extent. Side-effects also occur due to sympathetic stimulation and gastro-intestinal irritation. These side-effects may cause some individuals to stop taking the drug, but are never serious or dangerous. Drug interactions may occur with monoamine oxidase inhibitors and to a clinically unimportant extent, with antihypertensive drugs. The anorectic drugs have a very definite part to play in the treatment of obesity, mainly for those individuals who have altered their eating habits but have come to a plateau of weight which they find difficult to get below. The drugs are best given in a long-acting form and can safely be continued as long as weight loss persists, provided that the clinician exercises careful supervision. Dexamphetamine, phenmetrazine and benzphetamine should rarely be used because of the danger of addiction, and chlorphentermine is potentially hazardous for long-term use. Diethylpropion emerges as the drug of first choice, as fenfluramine has a tendency to cause depression and has a higher incidence of side-effects. Fenfluramine is mainly useful for people who are especially tense and for obese maturity-onset diabetics who have been unable to lose weight with the biguanides. Mazindol and phentermine appear to be useful as alternative drugs.
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PMID:Anorectic drugs: use in general practice. 78 35

Mianserin in a dosage of 20 mg 3 times daily, was given to 13 patients with bipolar affective illness, who were previously maintained on lithium. 3 patients left the trial at their own request within a few days due to drowsiness in 2 cases and insomnia in the third. Of the remaining 10 patients, 6 became manic within the 3-month trial period. This result indicates that mianserin may be capable of precipitating mania in susceptible subjects with bipolar affective illness. This may be a general property of antidepressants, since it has been previously described with other groups of antidepressants.
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PMID:Mianserin in the prophylactic treatment of bipolar affective illness. 89 30

An obese patient with a ten year history of respiratory failure presented with insomnia and marked daytime somnolence. Respriatory failure had been attributed to obesity, respiratory centre insensitivity to carbon dioxide, and to diffuse airways obstruction. To investigate the possible role of episodic apnoea with frequent nocturnal arousals, continous recordings were obtained during sleep of arterial oxygen saturation, oesophageal pressure and the motions of the rib-cage and abdomen/diaphragm. Repeated episodes of hypoventilation and profound hypoxaemia were found which were due to intermittent obstruction of the upper airway rather than to cessation of breathing efforts. During the episodes of hypoxaemia, values of arterial O2 tension fell to as low as 24 mmHg. Episodic hypoxaemia was relieved but not abolished, by the use of a collar, designed to hold the mandible forward. Previous reports indicated that recognition of intermittent obstruction of the upper airway during sleep and treatment by a permanent tracheostomy, resulted in a significant long-term imporvement of pulmonary and cardiac function and relief of insomnia and day-time somnolence. When tracheostomy is inadvisable, as in the present patient, it is hoped that similar long-term benefits will result from a supportive collar.
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PMID:Intemittent obstruction of the upper airway during sleep causing profound hypoxaemia. A neglected mechanism exacerbating chronic respiratory failure. 107 82

Very few epidemiological surveys have specifically studied relationships between sleep disturbances and psychiatric diseases. In this review, we preferred to use the classification proposed in 1979 by the Association of Sleep Disorders Centers. It includes four main categories: insomnias, excessive sleepiness, troubles of the wake/sleep schedule and parasomnias. Evaluating psychiatric disorders among general populations is easier owing to DSM III and DSM III-R criteria, but there are not equivalent criteria in evaluating sleep disorders. It is almost impossible to realize polysomnographic recordings in large samples, therefore sleep disorders are to be detected by questionnaires. It has been shown that there is a good correlation between self-reports and polysomnographic recordings among clinical and general samples. The prevalence of insomnia, defined as difficulties of initiating and maintaining sleep, is estimated between 9 and 31%. It is higher among women, elderly people, separated and divorced subjects, and low educational levels' groups. It has to be noticed that polysomnographic records of some subjective insomniacs are not different from those of good sleepers, sleep latency excepted. These subjective (and not objective) insomniacs have high scores in anxiety scale, depression scale, or psychologic distress. Insomnia is more frequently noted amongst subjects with psychiatric diagnoses, especially major depressive disorders and anxiety disorders. Depressive disorders are present in 21-40% of insomniacs versus 0-1% of non-insomniacs, and anxiety disorders in 13-24% of insomniacs versus 3-10% of non-insomniacs. In depressive disorders, sleep alterations are frequently noted: they are difficulties of initiating and maintaining sleep, decreasing proportion of slow-wave sleep, decreasing time of REM (rapid eye movement) sleep and REM sleep latency, and increasing density of REM sleep. Of these modifications, the last two ones seem to be specific for depression. The relationships between sleep, aging and depression are more complex than previously noted. For example, differences between depressed and non-depressed subjects depend on the age of the population. The prevalence of hypersomnia is lower than the insomnia's. It varies between 2 and 4%. It is more frequently noted among young people, and never married subjects. Two specific aetiologies must be looked for: sleep apnea syndrome and narcolepsy. These diagnoses are respectively found in 45% and 24% of hypersomniacs examined in American Sleep Centers. Hypersomnias are objectived by the Multiple Sleep Latency Test, which measures the physiologic sleep tendency.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Sleep disorders in psychiatric diseases. Epidemiological aspects]. 129 83

The "revolution" in pharmacologic treatment of insomnia began in 1970 with the availability of flurazepam, the first of the benzodiazepine hypnotics. Flurazepam largely replaced all other hypnotics during the decade of the 1970s. The second revolution began in the early 1980s as shorter half-life hypnotics, triazolam and temazepam, became available and began to replace flurazepam. The decade of the 1990s will probably see a more balanced pattern of benzodiazepine hypnotic use, as well as use of newer nonbenzodiazepine hypnotics. Among available benzodiazepines, all have the capacity to produce dose- and concentration-dependent sedation, drowsiness, performance impairment, and amnesia. Benzodiazepine-induced amnestic effects are characterized by either impairment of information acquisition, impairment of consolidation and storage, or both. In general, apparent clinical differences among benzodiazepine hypnotics are explained by differences in pharmacokinetic properties of absorption, distribution, elimination, and clearance.
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PMID:Pharmacology of benzodiazepine hypnotics. 131 29

An electro-behaviour dissociation was described, at first by animals next about the man, in experiment testing and in the drug addictions. This non concordance appear as lesser if it is be considered not only the sleeping waves but also all the electrical signs of the vigil state: non-existent, fluctuating, limited in topography, behind the stimulation, incomplete or emphasized. In this view we study some pathological states: narcotic and alcoholic addictions, confusion and pre-senile illness. Sometimes it is the abnormal sleep (coma or amazement) which alter the vigil state: absent, decreased, etc. Sometimes the vigilance is "numbed", the behaviour and the recording are those of lethargy. Sometimes also, the drowsiness has insomnia characteristics, associating a deep sleep loss, a reactivity to stimulations at once emphasized and undiscriminated, and "strangeness" insurmontable for the consciousness (perplexity, delusions, nightmare and level anomalies).
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PMID:[Alterations of arousal in some psychopathologic states]. 134 49

Phenindamine, an H1-receptor antagonist that was developed almost 50 years ago, has been associated with both drowsiness and insomnia. Since its central nervous system profile has not been well characterized, we used a series of psychomotor tests to conduct two studies. In the first, 12 subjects received single oral doses of phenindamine (25 mg), diphenhydramine (50 mg), terfenadine (60 mg), or placebo in a four-way crossover study. Psychomotor tests included choice reaction time (CRT), tracking, and hand steadiness (HS). In the second trial, 15 subjects received single oral doses of phenindamine (25 mg), pseudoephedrine (60 mg), phenindamine and pseudoephedrine, diphenhydramine (50 mg), or placebo in a five-way crossover study. Psychomotor tests included CRT, HS, and a task that divided attention between tracking and reaction time. Introspective drowsiness was measured in both trials with use of a visual analog scale (VAS) and the Stanford Sleepiness Scale (SSS). All assessments were made before and 1, 3, and 5 hours after drug administration. In the first trial, diphenhydramine produced significant impairment relative to placebo (p < 0.05) in CRT, tracking, and HS tasks and higher SSS and VAS scores, with peak effect noted at 3 hours. Phenindamine did not significantly differ from placebo or terfenadine. In the second trial, diphenhydramine produced significant impairment relative to placebo (p < 0.05) in CRT, divided attention, HS, and VAS, and SSS, also peaking at 3 hours. Stanford Sleepiness Scale scores after phenindamine were greater than placebo at 3 hours (p < 0.05) but significantly less than diphenhydramine (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of phenindamine tartrate on sleepiness and psychomotor performance. 136 Sep 91


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