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The Psychiatric Dimensions of Sleep Medicine by Karl Doghramji MD

By Karl Doghramji MD

This factor is the definitive instruction manual at the most crucial psychiatric features of sleep drugs. issues contain a historic viewpoint of sleep and psychiatry; the psychology of sleep and dreaming; the superiority, effect, pathogenesis, differential prognosis, and assessment of insomnia; pharmacological administration of, in addition to nonpharmacological techniques for, insomnia; over the top daylight hours somnolence and fatigue within the psychiatric sufferer; parasomnias; sleep in temper problems, schizophrenia, and anixiety problems; behavioral sleep issues in kids and kids; sleep problems particularly in seniors and in girls; and seasonal affective disease and phototherapy.

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For example, in the previously cited study of trimipramine in primary insomniacs, dizziness, dry mouth, headache, and nausea were more frequent than with the comparator drug, lormetazepam [67]. With trazodone, orthostatic hypotension, weakness, and lightheadedness are common; cardiac conduction abnormalities have been reported in patients who have pre-existing heart disease; and, although rare, priapism is a potentially serious side effect [71–74]. Antipsychotics The antipsychotics quetiapine and olanzapine also are used frequently as hypnotics in people who have primary insomnia.

The transmitter systems altered by the three leading sedating antidepressants differ. Trazodone antagonizes serotonin 2a (5HT2a), 5HT2c, and alpha1-adrenergic receptors and also inhibits 5HT reuptake [58,59]. Amitriptyline blocks acetylcholine and histamine binding and inhibits reuptake of norepinephrine and 5HT [60–62]. Mirtazepine antagonizes alpha1-adrenergic, 5HT2a, 5HT2c, and 5HT3 receptors, and is a strong histamine receptor type 1 (H1) antagonist [63,64]. Amitriptyline and mirtazepine share antihistaminergic activity, which may produce hypnotic effects.

Despite speculations in the medical literature, tolerance to the hypnotic effects of BzRAs did not develop in most studies, at least at the therapeutic doses for the periods of time that have been studied. Investigations that often are cited as evidence for the development of tolerance (eg, the study by Mitler and colleagues [55]) show gradual improvement over time in the placebo group versus a constant effect in the drug group, resulting in loss of statistical significance. The sleep in the active drug groups does not worsen with time with a stable dose of drug, as the definition of tolerance requires.

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