4,7 Secondary insomnia can result from medical,

neurologi

4,7 Secondary insomnia can result from medical,

neurological, environmental, drugs, or psychiatric causes. Medical causes include pain, thyroid disease, acid reflux, coronary artery disease, pulmonary disease (chronic obstructive pulmonary disease, asthma, sleep apnea, central alveolar hypoventilation syndrome), chronic renal insufficiency, eating disorders, thyroid dysfunction, fibromyalgia, menstrual-associated sleep disorder, and pregnancy.34-36 Neurological causes of insomnia Inhibitors,research,lifescience,medical include headaches, Parkinson’s disease, and sleep-related movement disorders (nocturnal myoclonus, RLS). Environmental sleep disorders can be triggered by excessive noise, noxious odors, bright light, or extremes of ambient temperature. Alcohol-, hypnotic-, and stimulant-dependent sleep disorders also contribute to chronic insomnia. Psychiatric disorders are characterized by sleep-onset difficulties, frequent arousals, sleep fragmentation, shortened total sleep

time, and Inhibitors,research,lifescience,medical decreased sleep efficiency. These disorders include alcoholism, anxiety disorders, mood disorders, panic disorders, and psychoses. Preliminary data indicate that chronic insomnia may precede depressive episodes by several years, and the question of systematic treatment of chronic insomnia as a means of avoiding depression is being studied. Stressful life events can precipitate chronic insomnia in predisposed Inhibitors,research,lifescience,medical individuals with neurotic depression, rumination, chronic anxiety, inhibition of emotions, and inability to express anger.36 PSG in anxiety disorders Inhibitors,research,lifescience,medical shows increased sleep www.selleckchem.com/products/crenolanib-cp-868596.html latency, decreased rapid eye movement (REM) sleep, and reduced sleep efficiency, while PSG in mood disorders demonstrates frequent arousals and awakenings, decreased slow-wave sleep (SWS), decreased REM latency, increased first REM period duration, and increased REM density.34 Insomnia assessment tools can utilize self-reporting methods (sleep diary and Pittsburgh Sleep Quality Index) and objective methods include Inhibitors,research,lifescience,medical actigraphy and PSG.26,37 Treatment for insomnia can

be categorized into pharmacological and nonpharmacological treatments. Pharmacological strategies must achieve a balance between hypnotic and adverse effects. Hypnotics are indicated in psychophysiological insomnia for Cilengitide occasional intermittent use or short-term (2 weeks) administration. Benzodiazepine usage can result in impaired sleep quality, residual sedation, memory or functional impairment the day following drug administration, or rebound insomnia. Other they problems may include increased rates of falls, drowsiness, dizziness, cognitive impairment, and automobile accidents.35,38-40 Nonbenzodiazepine hypnotics, type I selective γ-aminobutyric acid (GABA) receptor agents, such as Zolpidem (ti/2=2.4 h), zopiclone (tia=5 h), and zaleplon (ti/2=l h), have hypnoscdative action similar to the benzodiazepines and interact preferentially with δ1 receptors.

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