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Sleep architecture

Erman MK (2001) Sleep architecture and its relationship to insomnia. J Clin Psychiatry 62 (Suppl. 10) 9—17... [Pg.1137]

Poor sleep architecture and fragmented sleep secondary to OSA can cause excessive daytime sleepiness (EDS) and neu-rocognitive deficits. These sequelae can affect quality of life and work performance and may be linked to occupational and motor vehicle accidents. OSA is also associated with systemic disease such as hypertension, heart failure, and stroke.21-23 OSA is likely an independent risk factor for the development of hypertension.24 Further, when hypertension is present, it is often resistant to antihypertensive therapy. Fatal and non-fatal cardiovascular events are two- to threefold higher in male patients with severe OSA.25 OSA is associated with or aggravates biomarkers for cardiovascular disease, including C-reactive protein and leptin.26,27 Patients with sleep apnea often are obese and maybe predisposed to weight gain. Hence, obesity may further contribute to cardiovascular disease in this patient population. [Pg.623]

Zolpidem (Ambien ) Zolpidem CR (AmbienCR ) 2-2.6 6-8 Perhaps longer 5-10 6.25-12.5 Oxidation Short-moderate duration, no effects on sleep architecture... [Pg.627]

Gervasoni, D., Panconi, E., Henninot, V. et al. (2002). Effect of chronic treatment with milnacipran on sleep architecture in rats compared with paroxetine and imipramine. Pharmacol. Biochem. Behav. 73, 557-63. [Pg.101]

Reymond Shaw, I., Lavigne, G., Mayer, P. Choiniere, M. (2005). Acute intravenous administration of morphine perturbs sleep architecture in healthy pain-free young adults a preliminary study. Sleep 28, 677-82. [Pg.141]

All antidepressant drugs have some effects on sleep architecture. Suppression of REM sleep associated with the treatment of depression was such a consistent finding in early studies that it was seen as essential for the antidepressant action. [Pg.437]

Polulin J., Daoust A M., Forest G., Stip E., Godbout R. (2003). Sleep architecture and its clinical correlates in first episode and neuroleptic-naive patients with schizophrenia. Schizophr. Res. 62, 147-53. [Pg.458]

Winokur A., Sateia M. J., Boyd Hayes J. el al. (2000). Acute effects of mirtazapine on sleep continuity and sleep architecture in depressed patients a pilot study. Biol. Psychiatry 48, 75-7. [Pg.461]

Barbiturates. The next advance in treatment was the introduction of the barbiturates in the early 1900s. These medications are not only effective sleep inducers, but they also treat epilepsy and alcohol withdrawal at higher doses they produce anesthesia. The barbiturates can help one to fall asleep and to sleep soundly through the night. However, they markedly alter sleep architecture, reducing REM sleep. [Pg.268]

Thalidomide. Thalidomide is a chemically unique sleep medication that was introduced in the 1950s. It is not clear how thalidomide works, but in contrast to most sleep agents, it has beneficial effects on sleep architecture. [Pg.268]

Sleep architecture in narcolepsy is distinctly abnormal. Recall that sleep normally begins in a NREM phase and that the first phase of REM does not occur until about 90 minutes after falling asleep. The patient with narcolepsy, in sharp contrast, experiences REM onset within 15 minutes of falling asleep. [Pg.275]

Increasing evidence indicates that patients with DLB experience changes in sleep behaviour and sleep architecture, both of which add to carer burden and may lead to prescription of additional medication. Sleep in DLB has not been as extensively investigated as in AD in which reductions in REM sleep (Ancoli-Israel et ah, 1994) nocturnal wandering and confusion (Ancoli-Israel et ah,... [Pg.274]

Sleep. All of the SSRIs can potentially alter sleep architecture and decrease sleep efficiency, which may manifest itself as daytime sedation or trouble concentrating. The SSRIs may have differing effects on sleep. Fluoxetine has been reported to increase rapid eye movement (REM) latency, increase the number of awakenings, decrease sleep efficiency, and suppress... [Pg.276]

Nefazodone is generally well tolerated. It has been shown to improve sleep architecture (Armitage et ah, 1994), and has minimal associated sexual dysfunction. The adverse effects associated with nefazodone, in descending order of frequency, are dry mouth, somnolence, dizziness, nausea, constipation, blurred vision, and postural hypotension (Preskorn, 1993). Nefazodone does not slow cardiac conduction therefore, it has been tolerated in intentional overdoses of up to 11,200 mg. [Pg.300]

In this chapter the basics of the available atypical antidepressants and those that may soon to come on the market have been reviewed. The atypical antidepressants are less readily used, and their benefits for treating depression and anxiety are not fully appreciated. The atypical antidepressants may provide benefit for conditions such as ADHD or offer an alternative to other antidepressants with problematic side effects (i.e., activation on SSRIs). They may also provide specific relief for troublesome symptoms (i.e., nefazodone s normalization of sleep architecture). [Pg.306]

Benzodiazepines (such as clonazepam) are used widely to induce sleep, but they disrupt the normal sleep architecture. Children also have a tendency to become more irritable and hyperactive with hypnotics. In severe cases, benzodiazepines could be given for 3-5 days to facilitate a behavioral treatment program. Trazodone, though not specifically studied in children, may be a safer alternative for more chronic sleep problems if over-the-counter (OTC) diphenhydramine does not work. [Pg.627]

Zopiclone. Zopiclone is a full agonist that has been shown to have sedative properties in experimental animals and to be a potent hypnotic in humans. It has a short duration of action and minimal effects on sleep architecture, which means that it has few residual effects on waking. It appears to cause less tolerance and problems on withdrawal than the classic benzodiazepines and is currently marketed as a hypnotic. [Pg.458]

Levine J, Barak Y, Gonsalves M, et al A double-blind controlled trial of inositol treatment of depression. Am J Psychiatry 152 792-794, 1995a Levine J, Pomerantz T, Stier S, et al Lack of effect of 6 g inositol treatment on post-ECT cognitive function in humans. J Psychiatr Res 29 487-489, 1995b Levy A, Zohar J, Belmaker RH The effect of chronic lithium pretreatment on rat brain muscarinic receptor regulation. Neuropharmacology 21 1199-1201, 1983 Levy AB, Dixon KN, Schmidt H Sleep architecture in anorexia nervosa and bulimia. Biol Psychiatry 23 99-101, 1988... [Pg.683]

Buspirone may be an effective anxiolytic in the elderly patient and less likely than BZDs to produce excessive sedation ( 352, 353, 354 and 355). Dizziness, however, may be a problem. Zolpidem or zaleplon, particularly in lower doses (i.e., 2.5 to 5.0 mg at bedtime) may be viable alternatives ( 356). The elimination half-life of these two agents is approximately 3 hours in the elderly. Although it has sleep-enhancing properties similar to BZD hypnotics, it is less likely to alter sleep architecture. Whereas antidepressants and b -blockers may be useful alternatives in younger patients, no data document their effectiveness for anxiety in elderly patients ( 307). Although antipsychotics may be helpful in reducing severe agitation, their side effect profile makes them unsuitable for use in subjective anxiety states ( 300, 307). [Pg.292]

Clinical studies in patients with sleep disorders have shown that oral melatonin supplementation may alter sleep architecture. Subjective improvements in sleep quality and improvements in sleep onset and sleep duration have been reported. However, the significance of these findings is impaired by many study limitations. [Pg.1365]


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