Factors that Promote and Impair Sleep

It is well known that satisfying basic bodily needs, from hunger to sexual urgency, promote sleepiness. Conversely, all kinds of emotional distress tend to reduce sleep onset and quality. This effect is very prominent in the difficulty that depressed individuals commonly experience in falling asleep and sustaining sleep, and also in the disrupted sleep patterns found in various anxiety disorders, mania, and schizophrenia (Kryger et al., 2000). It is well known that physical exertion during the day tends to increase SWS, while mental and emotional exertions, as long as they are not too extreme, tend to increase REM (Panksepp, 1998).

Clearly there are several SWS generators in the brain, but one of the more prominent, highly localized, ones is in the lateral anterior lateral hypothalamus, which contains gamma-aminobutyric acid (GABA) as the main transmitter, which explains the utility of GABA facilitators (Table 4.1) to facilitate sleep (Kryger et al., 2000). The location of this generator helps explain one of the first findings in the neuroscience of sleep: von Economo's classic description of chronic insomnia in patients who had suffered damage to the anterior hypothalamus. On the other hand, the widely distributed waking generators, which are well represented by the acetylcholine and bio-genic amine systems (including dopamine, norepinephrine, and histamine), are more concentrated in the posterior hypothalamus, where damage has long been known to produce somnolence (Panksepp, 1998).

The REM generator in the lower brain stem appears to be a remnant of an ancient waking/arousal system that may, at some point in premammalian evolution, have been one of the major regulators of waking activities, perhaps of the emotional subroutines of the limbic system (Panksepp, 1998). It has recently been effectively argued that dreaming mechanisms can be dissociated from REM mechanisms (Solms, 2000). Even though they are typically coordinated, it seems that while REM sleep is critically dependent on the pontine generators, dreaming is much more dependent on arousal of various

TABLE 4.1. Sleep Medications Currently in Usea

Traditional Benzodiazepine (BZ) Hypnotics

Triazolam: Common initial dose: 0.25 mg; FDA AMDD: 0.5 mg Temazepam: Common initial dose: 15 mg; FDA AMDD: 30 mg Flurazepam: Common initial dose: 15-30 mg; FDA AMDD: 30 mg

Nonbenzodiazepine, Selective BZ Receptor Agonist Hypnotics

Zaleplon: Common initial dose: 10 mg; FDA AMDD: 20 mg Zolpidem: Common initial dose: 10 mg; FDA AMDD: 10 mg

Anxiolytic Benzodiazepines Used as Hypnotics (off-label)

Clonazepam: CID: 0.5 mg; FDA AMDD: 4 mg divided (for anxiety conditions) Lorazepam: CID: 1 mg; FDA AMDD: 6 mg divided (for anxiety conditions) Alprazolam: CID: 0.25 mg; FDA AMDD: 4 mg divided (for anxiety conditions)

Sedating Antidepressants Sometimes Used as Hypnotics (off-label)

Trazodone: CID: 50 mg; AMDD: FDA 400 mg divided (for depression) Amitriptyline: CID: 50 mg; FDA AMDD: 300 mg divided (for depression) Doxepin: CID: 50 mg; FDA AMDD: 300 mg divided (for depression) Fluvoxamine: CID: 50 mg; FDA AMDD: 300 mg divided (for OCD) Mirtazapine: CID: 15 mg; FDA AMDD: 45 mg (for depressions) Nefazodone: CID: 100 mg; FDA AMDD: 600 mg divided (for depressions)

aRecommended CID—adult common initial doses; half-dose is generally recommended in elderly; FDA AMDD—Food and Drug Administration Approved Maximum Daily Dose. For nonhypnotic use, doses for FDA approved indications, such as obsessive-compulsive behaviors (OCD) are listed.

limbic emotional circuits, with perhaps especially strong influences through ascending dopamine-based appetitive-motivation SEEKING systems (Gottesmann, 2002; Solms, 2000). Thus, it would seem likely that REM sleep is especially important in regulating emotional/affective homeostasis.

The main evidence for this is as follows: REM-deprived animals are generally hyperactive and hyperemotional, suggesting that the neuropsychological activities promoted by REM (i.e., dreams) are able to dissipate excessive emotional "energies"—to keep the emotional and cognitive aspects of key mental urges and processes balanced in favor of the cognitive side. In other words, during dreaming, organisms may reprocess emotionally salient information in such a way as to reduce its affective impact during waking. Perhaps this is achieved, in part, by the ability of the brain, during REM, to extract useful cognitive relationships from waking activities (Domhoff, 2002). This may allow organisms to more effectively pursue long-term as opposed to short-term plans, especially those related to emotional stressors (Panksepp, 1998), which may partially explain why people are typically less emotionally stressed after waking from a good nights sleep.

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