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

In the article, the author develops an analysis of external and intrapsychic factors related to adults' insomnia. First she undertakes a literature review to describe semiological, evolutive and etiological levels of insomnia. From a semiological point of view, it is usual to differenciate initial insomnia (associated to the first phase of sleeping), intermittent insomnia (related to frequent awakenings) and final insomnia (related to early morning awakenings). From an evolutive point of view, we can identify transitory insomnia (characterized by frequent awakenings) and chronic insomnia. On the other hand, we are allowed to distinguish organic insomnia (disorder where an organic cerebral injury is demonstrated or suspected) from insomnias related to psychiatric or somatic disease or idiopathic one. Then, the author makes a literary review to identify various insomnia causes and points out. Social factors: insomnia rates are higher by divorced, separated or widowed people. Percentages are higher when scholastic level is weak, domestic income is less then 915 O a month, or by unemployed people. Besides, sleep quality is deteriorated by ageing. Sleeping and waking rhythm is able to loose its synchronization. Complaints about insomnia occur far frequently from women than men. Environmental factors: working constraints increase sleep disorders. It is possible to make the same conclusion when we have to face overcharge of external events, deep intrapsychic conflicts (related to grief, unemployment, damage or hospitalization) or interpersonal conflicts' situations where we are confronted to stress related to socio-affective environment, lack of social support or conjugal difficulties. Medical and physiologic causes: legs impatience syndrome, recurrent limbs shakings syndrome, breathe stop during sleep, narcolepsy, excessive medicine or hypnotic drugs use, some central nervous system injuries, every nocturnal awakening (related to aches.), surgical operation. Chronobiological factors: night working or day-night shift produce insomnia by desynchronization. It is the same for time lag related to jet-lag flights. Significant gaps between the internal biological clock and environmental synchronizators, such as phase delay sleep, phase advance sleep, sleep-waking cycle longer than 24 (25) hours, or variations in sleep-awakening cycle, are of less importance. Toxic factors are numerous: amphetamines, antidepressors, medication against anorexia and tubercular disease, caffeine and alcohol excessive use, chronic alcoholism. Behavioral factors: enduring insomnias are related to poor nightroutines (to go to sleep too early, to read or to look at T.V. when going to bed). The same effect is produced by regular intellectual activities close to bedtime or by a late meal in the evening, by an noisy or unhealthy environment, by physical hyperactivity or sleeping after each lunch. Psychiatric factors: insomnia often appears with psychiatric disorders such as a major depressive episode, an anxiety disorder or schizophrenia. Insomnia also is able to open a delirious disorganization or a manic access. Psychological factors: overstimulation of waking system (related to stress overdose or intellectual hyperactivity), conditioning phenomena, fear of not falling asleep, intrapsychic and interpersonal conflicts. Third, the author put hypothesis about psychodynamic etiology of chronic insomnia. Following a first assumption, insomnia should be a result of anguish excess related to intrapsychic (and not interpersonal) conflicts which can't lead to a mental elaboration. These conflicts run over dream protective function, generating a breakdown of dream symbolization function. At a clinical level, we are in some cases in front of people enduring sleeping insomnia but more often, we are confronted with an intermittent or early waking insomnia sometimes associated with nightmares. Following a second assumption, insomnia should be a result of psychic functioning invalidation. Here, failure of dream protective and symbolization function is related to anguish excess associated with an amount of external conflicts. Overwhelmed by concretude, insomniac patients present an alexythimic intrapsychic functioning forbiding dream realization. These persons have no possibility to elaborate conflicts especially external overcharge, using dreams or imagination to escape from an intrusive reality and regress to sleeping. Here we are in front of initial sleep insomnia. Following a third hypothesis, some insomnias are related to wakings associated with repetitive nightmares. This type of insomnia should be related to a past traumatic event or activated by actual existential context and produces a too important anguish charge to follow a mental elaboration process and lead to mental symbolic representation. Following a fourth hypothesis, some insomnias are in relation with an impossibility to accept passive position. The last one will expose to a danger consisting either of castration or loneliness and death. To conclude, the author suggests some preventive perspective to face insomnia. Especially, she points out limits of pharmalogical treatments. She underlines the necessity to promote no medical methods to facilitate sleep induction and maintenance, including sleep hygiene measures, relaxation, psychotherapic approach and behavioral methods. She emphasizes the danger of a reductive approach of insomnia which would be focused on a single medical, psychological or environmental dimension. Last but not least, she makes methodological propositions to test from a clinical point of view the four psychodynamic exposed hypotheses.
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PMID:[Etiology of adult insomnia]. 1250 61

Studies have shown occasional evidence of increased physiological activity in patients with primary insomnia. We hypothesized that metabolic rate, as measured by overall oxygen use (VO2), might be a more general index of increased physiological activity. An initial experiment found elevated VO2 both at night and during the day in patients with primary insomnia as compared with matched normal sleepers. A second experiment found significant but more modest increases in VO2 in patients with Sleep State Misperception Insomnia [who complain of poor sleep but who had normal sleep by electroencephalographic (EEG) criteria]. In a third experiment, normal young adults were given caffeine 400 mg three times per day (TID) for 1 week as a means of increasing VO2 and possibly producing other symptoms of insomnia. Participants developed many symptoms consistent with those seen in patients with primary insomnia (poor sleep, increased latency on the Multiple Sleep Latency Test, increasing fatigue despite physiological activation, and increased anxiety on the Minnesota Multiphasic Personality Inventory (MMPI)). In a final experiment, physiological arousal was again produced by caffeine to determine if sleep with elevated arousal would be less restorative. All subjects (Ss) slept for 3.5 h after being given 400 mg of caffeine. During 41 h of sleep deprivation that followed, there was no significant condition difference for the Multiple Sleep Latency Test or mood measures. The results provided only weak support for the idea that sleep is less restorative after physiological arousal.
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PMID:Insomnia, metabolic rate and sleep restoration. 1282 40

Sleep hygiene (SH) refers to a list of behaviors, environmental conditions, and other sleep-related factors that can be adjusted as a stand-alone treatment or component of multimodal treatment for patients with insomnia. This paper presents a review of SH, how this concept has been applied and often modified over the past 24 years, and how it relates to the modern sleep disorder nosology, particularly Inadequate Sleep Hygiene. Although a recognized and commonly utilized treatment option, there is no absolute consensus about which steps must be included to constitute SH treatment, and there is much overlap between SH and other cognitive-behavioral treatments for insomnia such as Stimulus Control Procedures and Sleep Restriction Therapy. The literature on the effects of manipulations of individual components of SH under experimental conditions (e.g. effects of presleep alcohol or caffeine intake) in normal sleepers show mixed results. Empirical data demonstrating the role of poor SH as a contributor to insomnia, or showing that good SH improves sleep in patients with insomnia, is not available. Instead of evaluating the impact of a comprehensive list of SH recommendations, a focus on guidelines for use of individual rules is needed.
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PMID:Use of sleep hygiene in the treatment of insomnia. 1292 19

Relationships between common lifestyle practices important to sleep hygiene (e.g., smoking cigarettes, drinking alcohol, ingesting caffeine, exercising, bed times, getting-up times) and nocturnal sleep have not been documented for women with insomnia in their home environments. This community-based sample of 121 women, ages 40 to 55 years, included 92 women who had experienced insomnia for at least 3 months and 29 women with good-quality sleep. Women recorded lifestyle practices and sleep perceptions (time to fall asleep, awakenings during sleep, feeling rested after sleeping, and overall sleep quality) in diaries while undergoing 6 nights of somnographic sleep monitoring at home. Compared to women with good-quality sleep, women with insomnia reported greater night-to-night variation in perceived sleep variables, poorer overall sleep quality (M = 2.8, SD = 0.7 vs. M = 1.9, SD = 0.5, P < 0.05), and longer times to fall asleep (M = 25 min, SD = 14.2 vs. M= 12.9 min, SD = 5.8, P < 0.05). Correlations between mean individual lifestyle practice scores and mean perceived or somnographic sleep variables were low, ranging from 0 to 0.20. An aggregated sleep hygiene practice score was not associated with either perceived or somnographic sleep variables. Regression analysis using dummy variables showed that combinations of alcohol, caffeine, exercise, smoking, and history of physical disease explained 9% to 19% of variance in perceived or somnographic sleep variables. Lifestyle practices, and combinations thereof, do warrant consideration when assessing or treating insomnia, but these data fail to support a dominant relationship between lifestyle practices and either perceived or somnographic sleep variables.
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PMID:Lifestyle practices and nocturnal sleep in midlife women with and without insomnia. 1518 7

Sleep hygiene education is a basic component of behavioral treatment for chronic insomnia, yet the actual sleep hygiene practices of people with insomnia have not been well documented. In this descriptive secondary analysis, midlife women ages 41-55 years with either chronic insomnia (n = 92) or good sleep (n = 29) kept diaries of sleep perceptions and sleep hygiene practices during 6 nights of somnographic monitoring at home. In both groups few reported smoking cigarettes (<10%), most drank caffeine (>80%), and many averaged 30 min of exercise per day ( approximately 50%). Very few in either group (<10%) had regular (<30 min variation) bedtimes or getting-up times. Compared to women with good sleep, those with insomnia reported drinking less caffeine per day, being more abstinent from alcohol, and having smaller variations in day-to-day alcohol intake and bedtimes. Although some women with insomnia limit or refrain from caffeine and alcohol intake, many have not optimized behaviors believed to help prevent or modulate insomnia.
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PMID:Variations in sleep hygiene practices of women with and without insomnia. 1526 62

The concomitant use of benzodiazepines and caffeine was studied to learn if caffeine consumption varied as a function of benzodiazepine use. Caffeine may antagonize the effects of benzodiazepine and even relatively small amounts can aggravate symptoms associated with anxiety disorders. In addition, caffeine can cause or aggravate insomnia, one of the main reasons cited for use by the subjects in this analysis. Given this, there would seem to be sufficient reason for at least some users of benzodiazepines to consider, with their physicians, avoiding or limiting caffeine consumption. Data from the Third National Health and Nutrition Examination Survey were analyzed to obtain a nationally representative sample of benzodiazepine users. Subjects included 253 individuals (64% women) whose median age was 54 yr. Approximately 88% of benzodiazepine users reported caffeine consumption in the 24-hr. Dietary Recall. 26% of benzodiazepine users and 23% of nonusers reported consuming greater than 250 mg of caffeine during the 24-hr. reference period. In regression analyses, no significant relationships were found between reported caffeine consumption and benzodiazepine use. This study suggests that users and nonusers of benzodiazepines ingest similar amounts of caffeine even though some users should probably avoid or limit caffeine use.
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PMID:Caffeine consumption among adults on benzodiazepine therapy: United States 1988-1994. 1546 Mar 74

The relation between smoking and sleep was examined in a randomly selected sample of 769 individuals (379 men and 390 women, ages 20 to 98). Participants completed 2 weeks of sleep diaries, provided a global report on their sleep, indicated the number of cigarettes smoked per day, and supplied information on health, depressive symptoms, anxiety, and caffeine and alcohol use. After controlling for demographic, health, psychological, and behavioral variables, light smoking (< 15 cigarettes per day), but not heavier smoking, was associated with self-reported chronic insomnia and reduced sleep diary total sleep time and time in bed. Smokers did not differ significantly from nonsmokers on diary measures of sleep-onset latency, number of awakenings during the night, wake time after sleep onset, or sleep efficiency.
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PMID:The relation between smoking and sleep: the influence of smoking level, health, and psychological variables. 1560 Feb 25

A number of medicinal plants are traditionally endowed with anxiolytic or sedative properties and, in the context of this revue, both indications are considered since the former may induce a mood conducive to the latter. For any sleep-inducing drug to be effective, a tranquil ambience needs to be established a priori. Thus, physical ailments (i.e. pain), factors interfering with sleep (i.e. noise), psychological conditions causing stress, psychiatric illnesses (i.e. depression) and other drugs that interfere with sleep (i.e. caffeine) need to be controlled, if possible. Kava-kava is a well-established hypnotic drug, with a rapid onset of effect, adequate duration of action and minimal morning after-effects. However, reports of serious hepatotoxicity with this preparation have led to it being banned in most countries worldwide. On the other hand, side-effects with valerian would appear to be bland indeed. However, it's slow onset of effect (2-3 weeks) renders it unsuitable for short-term use (i.e. 'jet-lag'), but it does have profound beneficial effects on sleep architecture (augments deep sleep) that may make it particularly suitable for long-term use and for the elderly. In a personal trial (not double-blind) in stress-induced insomnia, both kava and valerian improved sleep and the ill-effects of stress, and the combination of the two was even more effective for the control of insomnia. Aromatherapy (lavender, chamomile, Ylang-Ylang) would appear to improve sleep, but how practical a form of treatment this may be remains to be determined. The only other plant drug that may have some effect on sleep is melissa, but reports are too scanty to form any opinion about this. Based on animal experiments, passion flower (passiflora) may have a sedative action, but the sedative action of hops has not been investigated in any detail. In conclusion, there is a need for longer-term controlled studies with some of these compounds (particularly valerian). Aromatherapy constitutes a tantalising possibility. In the interpretation of this review, it should be borne in mind that the evidence on which it is based is often incomplete or missing, but that is all that is available. Consequently some conjecture on the part of the author is inevitable and should be appreciated as such.
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PMID:Medicinal plants for insomnia: a review of their pharmacology, efficacy and tolerability. 1598 98

Although a multitude of pharmaceutical agents are available for the treatment of mood disorders, anxiety and insomnia, many patients have difficulty tolerating the side effects, do not respond adequately, or eventually lose their response. Many therapeutic herbs and nutrients have far fewer side effects and may provide an alternative treatment or can be used to enhance the effect of prescription medications. In the article, the authors review the quality of the evidence supporting the clinical effects of a number of commonly used types of complementary/alternative medicine (CAM) for mood disorders, anxiety, and insomnia. They review data on the use of St. John's Wort, S-adenosyl-methionine (SAM-e), B vitamins, inositol, omega-3 fatty acids, and choline for mood disorders; data on the use of kava and other herbal agents and fish extract for anxiety and insomnia; and data on valerian and melatonin for insomnia. The authors also discuss the use of CAM to treat migraines, which may be comorbid with mood and anxiety disorders, and obesity, which can occur as a side effect of psychotropic medications. They consider the data on feverfew and butterbur for migraines and on chromium picolinate and the combination of ephedrine and caffeine for obesity. The authors also review issues related to comorbid medical illness, side effects, drug interactions, dosage, and brand selection.
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PMID:Herbs and nutrients in the treatment of depression, anxiety, insomnia, migraine, and obesity. 1599 May 9

The population suffering from insomnia in old age onset (LOI) is quite large. LOI might include a larger scale of syndromes ranging from typical psychophysiological insomnia to night delirium. The correlation between the biological, biochemical changes and the quantitative as well as the qualitative alterations of the sleep process through aging has not been fully explored. One can suppose that any cerebral lesion leading to a dysfunction in mental performance can also act on the sleep. The majority of LOI brain metabolic disturbances might therefore have some etiological role. The authors suggest the application of this concept in the clinical evaluation of LOI. The authors constructed a heuristic model for the pathophysiology and treatment of LOI. It is a bipolar axis containing the most typical symptoms of LOI. On the opposite margins psychophysiological insomnia and organic/metabolic insomnia (up to delirious states) are settled. The position on the axis (i.e., its distance from the "edge syndromes") gives information on the probability of its organic nature. Based on their clinical experiences and considering the data of the very few studies, they suppose that with the help of a detailed analysis of the symptoms of LOI and using some additional (electrophysiological and neuroimaging) laboratory methods most patients with LOI can get a strict diagnostic position on the LOI axis. Using the LOI axis not only a detailed evaluation of the symptomatology but also more sophisticated therapeutic interventions become possible. Symptoms on the "metabolic side" can be cured by a single evening application of any drugs improving the function of the brain (like nootropics, neuroprotective agents or even slight stimulants, e.g., caffeine) might show a "paradoxical hypnotic" effect, or in combination with sleeping pills they can cause an additive effect in LOI patients. The efficacy of this treatment can also have a diagnostic value: i.e., it helps to differentiate between the primary (organic) and psychophysiological (exogenous or emotional/psychic) forms of LOI.
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PMID:From psychophysiological insomnia to organic sleep disturbances: a continuum in late onset insomnia - with special concerns relating to its treatment. 1612 34


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