Sleep induction

Abstract: OBJECTIVE Because of the role of psychological factors in insomnia, the shortcomings of hypnotic medications, and patients' greater acceptance of nonpharmacological treatments for insomnia, the authors conducted a meta-analysis to examine the efficacy and durability of psychological treatments for the clinical management of chronic insomnia. METHOD A total of 59 treatment outcome studies, involving 2,102 patients, were selected for review on the basis of the following criteria: 1) the primary target problem was sleep-onset, maintenance, or mixed insomnia, 2) the treatment was nonpharmacological, 3) the study used a group design, and 4) the outcome measures included sleep-onset latency, time awake after sleep onset, number of nighttime awakenings, or total sleep time. RESULTS Psychological interventions, averaging 5.0 hours of therapy time, produced reliable changes in two of the four sleep measures examined. The average effect sizes (i.e., z scores) were 0.88 for sleep latency and 0.65 for time awake after sleep onset. These results indicate that patients with insomnia were better off after treatment than 81% and 74% of untreated control subjects in terms of sleep induction and sleep maintenance, respectively. Stimulus control and sleep restriction were the most effective single therapy procedures, whereas sleep hygiene education was not effective when used alone. Clinical improvements seen at treatment completion were well maintained at follow-ups averaging 6 months in duration. CONCLUSIONS The findings indicate that nonpharmacological interventions produce reliable and durable changes in the sleep patterns of patients with chronic insomnia.

Abstract: Sleep is believed to play an important role in memory consolidation. We induced sleep on demand by expressing the temperature-gated nonspecific cation channel Transient receptor potential cation channel (UAS-TrpA1) in neurons, including those with projections to the dorsal fan-shaped body (FB). When the temperature was raised to 31°C, flies entered a quiescent state that meets the criteria for identifying sleep. When sleep was induced for 4 hours after a massed-training protocol for courtship conditioning that is not capable of inducing long-term memory (LTM) by itself, flies develop an LTM. Activating the dorsal FB in the absence of sleep did not result in the formation of LTM after massed training.

Abstract: Most antidepressants change sleep; in particular, they alter the physiological patterns of sleep stages recorded overnight with EEG and other physiological measures. These effects are greatest and most consistent on rapid eye movement (REM) sleep, and tend to be in the opposite direction to the sleep abnormalities found in major depression, but are usually of greater degree. Reductions in the amount of REM sleep and increases in REM sleep onset latency are seen after taking antidepressants, both in healthy volunteers and in depressed patients. Antidepressants that increase serotonin function by blocking reuptake or by inhibiting metabolism have the greatest effect on REM sleep. The decrease in amount of REM sleep appears to be greatest early in treatment, and gradually diminishes during long-term treatment, except after monoamine oxidase inhibitors when REM sleep is often absent for many months. Sleep initiation and maintenance are also affected by antidepressants, but the effects are much less consistent between drugs. Some antidepressants such as clomipramine and the selective serotonin receptor inhibitors (SSRIs), particularly fluoxetine, are sleep-disturbing early in treatment and some others such as amitriptyline and the newer serotonin 5-HT2-receptor antagonists are sleep promoting. However, these effects are fairly short-lived and there are very few significant differences between drugs after a few weeks of treatment. In general, the objectively measured sleep of depressed patients improves during 3-4 weeks of effective antidepressant treatment with most agents, as does their subjective impression of their sleep. Sleep improvement earlier in treatment may be an important clinical goal in some patients, perhaps when insomnia is particularly distressing, or to ensure compliance. In these patients, the choice of a safely used and effective antidepressant which improves sleep in short term is indicated. Patients with other sleep disorders such as restless legs syndrome and REM sleep behaviour disorder should be identified before choosing a treatment, as some antidepressants worsen these conditions. Conversely, there is evidence that some antidepressants may be useful in the treatment of sleep disorders such as night terrors.