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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insomnia is defined as difficulty with the initiation, maintenance, duration, or quality of sleep that results in the impairment of daytime functioning, despite adequate opportunity and circumstances for sleep. In most countries approximately every third inhabitant has insomnia. Insomnia can be classified as primary and secondary. The pathogenesis of primary insomnia is unknown, but available evidence suggests a state of hyperarousal. Insomnia secondary to other causes is more common than primary insomnia. Cerebral hypoperfusion can be the cause of insomnia in some cases. In such patients the cerebral blood flow should be improved using parenteral vascular therapy. If insomnia persists despite treatment, then therapy for primary insomnia should be instituted using benzodiazepine-receptor agonists such as Zolpidem, Zopiclone, or Zaleplon. In those cases Midazolam cannot be used for the treatment of insomnia due to its marked negative effect on cerebral blood flow. In Hungary there is a need to organize multidisciplinary Insomnia Clinics because insomnia is more than a disease, it is a public health problem in this century.
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PMID:[Insomnia and cerebral hypoperfusion]. 1798 72

According to the National Institutes of Health, approximately 30 percent of all Americans complain of sleep disruption, while 10 percent display symptoms congruent with chronic insomnia. One of the most common treatments for insomnia is prescription sleep medications that help people fall asleep and remain asleep. Historically barbiturates were initially popular for treating insomnia, but their long "hangover" effect made them easily replaced with the introduction of the benzodiazepines. Triazolam (Halcion), diazepam (Valium), and oxazepam (Serax) rapidly became the treatment of choice for insomnia. Recently a new class of nonbenzodiazepines---the "z-sedatives"--has overtaken the older benzodiazepines as the most commonly prescribed sleep medications. The three most popular z-drugs are zolpidem (Ambien), zaleplon (Sonata), and eszopiclone (Lunesta). The Food and Drug Administration (FDA) also recently approved the production of zolpidem tartrate, a generic form of Ambien. Many dentists prescribe these medications for patients who have difficulty sleeping the night prior to an appointment or as a procedural sedative. With 43 million prescriptions for sleep medications filled in 2005, generating $2.7 billion for pharmaceutical companies, it is important that dentists be aware of these drugs' mechanism of action and potential drug interactions.
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PMID:What every dentist should know about the "z-sedatives". 1806 95

Zolpidem is a unique nonbenzodiazepine sedative hypnotic drug that selectively binds to omega-1 gamma-aminobutyric acid receptors in the brain. Although used for years in Israel and abroad for insomnia, there have been periodic reports of unusual or remarkable neurologic effects in patients with various brain pathologies. Here, we report on a 50-year-old woman 18 months after severe anoxic brain injury in a minimally conscious state. Residual deficits included mutism, athetoid movements of the extremities, and complete dependence for all personal care. After the administration of 5 to 10mg of zolpidem, within 45 minutes, the patient's condition improved markedly, including the cessation of athetoid movements, regained speaking ability, and ability to perform various tasks including self-feeding. These effects lasted 3 to 4 hours, after which the patient returned to her former state. This effect was repeatable on a daily basis. Existing evidence and possible mechanisms to explain zolpidem's effects in brain injury are described.
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PMID:Transient reversal of anoxic brain injury-related minimally conscious state after zolpidem administration: a case report. 1822 67

Zolpidem is among the most frequently prescribed hypnotic drugs for those who suffer from insomnia. Recent media reports drew attention to driving impairment after zolpidem misuse. This review summarizes the available data on the effects of recommended use and misuse of zolpidem on driving ability and traffic safety. Both experimental studies and roadside evidence were taken into account. From these studies it must be concluded that patients should fully comply with the prescription instructions of zolpidem, i.e. to take the medication just prior to a full 8 hours of uninterrupted sleep. If this strategy is adopted, zolpidem is a safe alternative to benzodiazpine hypnotics and zopiclone who do show significant driving impairment the morning following bedtime administration. However, to ensure traffic safety higher dosages than recommended (10 mg) or allowing less than 8 hours between zolpidem intake and actual operation of a motor vehicle should be avoided.
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PMID:Zolpidem and traffic safety - the importance of treatment compliance. 1869 Sep 71

Zolpidem, a non-benzodiazepine hypnotic of the imidazopyridine class, is very effective in treating insomnia with previous claims of little adverse effects. However, zolpidem-induced somnambulism and amnesic sleep-related behavioral problems were begun to be reported in literature but no systemic investigation has been undertaken in non-Western cultures. In our current retrospective survey, 5.1% (13 out of 255) of Taiwanese patients reported change in sleep-related behavior as adverse effects. This serves as a reminder for clinicians to inquire regarding any unusual behavior of parasomniac activities when prescribing zolpidem.
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PMID:Zolpidem-induced amnesia and somnambulism: rare occurrences? 1881 79

In 1993, Zolpidem (Ambien), a non-benzodiazepine hypnotic agent, was approved for use in the United States for the short-term treatment of insomnia. Zolpidem has a rapid onset of action and short elimination half-life, rendering it ideal as a sleep aid. The objective of this study was to evaluate, and retrospectively compare, the use of the Immunalysis ELISA kit and gas chromatograpy-mass spectrometry (GC-MS) to screen blood/urine specimens for zolpidem. In addition, results for the incidence of zolpidem in suspected DUI drivers in 2007 are compared to previous years' data. The ELISA kit was evaluated for cross-reactivity with zaleplon and zopiclone and zolpidem metabolite I. Urine samples (n = 100) and blood samples (n = 100) were selected from specimens received into the DUI laboratory in 2007 and were screened via the Immunalysis Zolpidem ELISA kit and on GC-MS in full EI scan mode following an alkaline liquid-liquid extraction. Results show 5% of the urine and blood samples screened positive for zolpidem using the ELISA kits, and all 5% confirmed positive for zolpidem using GC-MS. The ELISA kit demonstrated no cross-reactivity to zaleplon or zopiclone at a spiked urine concentration of 1000 ng/mL. Ten cases of suspected DUI drivers in 2007 confirmed positive for zolpidem by ELISA and GC-MS in blood/urine, a higher incidence rate than in the previous years. Because of the low percentage elimination of the parent compound in urine, a screening method for the detection of the main metabolite of zolpidem may be needed for better detection of drug impairment driving due to zolpidem.
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PMID:The incidence of Zolpidem use in suspected DUI drivers in Miami-Dade Florida: a comparative study using immunalysis Zolpidem ELISA KIT and gas chromatography-mass spectrometry screening. 1900 22

Caffeine is the world's most popular stimulant and is known to disrupt sleep. Administration of caffeine can therefore be used in healthy volunteers to mimic the effects of insomnia and thus to test the hypnotic effects of medication. This study assessed the effects of caffeine on sleep architecture and electroencephalography (EEG) spectrum alone and in combination with two different sleep-promoting medications. Home polysomnography was performed in 12 healthy male volunteers in a double-blind study whereby subjects received placebo, caffeine (150 mg), caffeine plus zolpidem (10 mg) and caffeine plus trazodone (100 mg) at bedtime in a randomised crossover design. In addition to delaying sleep onset, caffeine decreased total sleep time (TST), sleep efficiency (SE) and stage 2 sleep without significantly altering wake after sleep onset or the number of awakenings. Zolpidem attenuated the caffeine-induced decrease in SE and increased spindle density in the caffeine plus zolpidem combination compared with placebo. Trazodone attenuated the decrease in SE and TST, and it also increased stage 3 sleep, decreased the number of awakenings and decreased the spindle density. No significant changes in rapid eye movement (REM) sleep were observed, neither was any significant alteration in slow wave activity nor other EEG spectral measures, although the direction of change was similar to that previously reported for caffeine and appeared to 'normalise' after trazodone. These data suggest that caffeine mimics some, but not all of the sleep disruption seen in insomnia and that its disruptive effects are differentially attenuated by the actions of sleep-promoting compounds with distinct mechanisms of action.
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PMID:Effects on sleep stages and microarchitecture of caffeine and its combination with zolpidem or trazodone in healthy volunteers. 1935 1

Hypnotic drugs designed to treat insomnia in adults are now increasingly used in children, but the effects of these compounds on neonatal sleep are poorly understood. We investigated the hypnotic effects of the commonly prescribed non-benzodiazepine sleep agent Zolpidem (Ambien) on sleep architecture and electroencephalographic (EEG) activity in the neonatal ferret. Six ferret kits were surgically prepared for EEG/electromyographic (EMG) recordings using techniques adopted for use in neonatal animals. They were then administered in a counter-balanced design vehicle, or Zolpidem (2 mg/kg or 20 mg/kg) via intraperitoneal injection (1x/day over three days at 1 p.m.). Zolpidem did not increase non-rapid-eye-movement (NREM) or total sleep time. Instead Zolpidem reduced REM sleep and total sleep amounts and increased NREM sleep bout duration. Zolpidem also increased higher-frequency EEG energies during REM and NREM sleep and transiently produced a behavioral state that appeared intermediate between wake and sleep. Our findings demonstrate that hypnotics that improve sleep quality in adults may produce profoundly different behavioral changes in neonates.
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PMID:Paradoxical effects of the hypnotic Zolpidem in the neonatal ferret. 1942 39

Gaboxadol is a selective extrasynaptic GABA(A) receptor agonist previously in development for the treatment of insomnia. Due to its short half-life (1.5-2 h) it is expected to be free from residual effects the next morning. The present study assessed the residual effects of evening and middle-of-the-night administration of 15 mg of gaboxadol on cognitive, psychomotor and driving performance. Twenty-eight healthy volunteers entered the study with 25 (12 women; mean age 31.4 years) completing a double-blind, placebo-controlled, active-referenced five-way cross-over study. Each treatment night subjects ingested one capsule at 23:00 hours and one at 04:00 hours. Treatments were placebo at both times, 15 mg gaboxadol or 7.5 mg zopiclone followed by placebo, and placebo followed by 15 mg gaboxadol or 10 mg zolpidem. Effects on cognition and psychomotor performance were assessed between 07:30 and 08:30 hours and on driving between 09:00 and 10:00 hours. Driving, as measured by standard deviation of lateral position in an on-the-road driving test, was almost significantly (P < 0.07) impaired after evening administration of gaboxadol for the all-subjects-completed set (n = 25) but significantly (P < 0.05) in the full analysis set (n = 28). Effects of all other active treatments on driving were significant. Evening administration of gaboxadol had minor effects on divided attention only, whereas middle-of-the-night administration impaired performance significantly in all tests except memory. Zolpidem and zopiclone impaired performance significantly in every test except tracking after zopiclone; 15 mg of gaboxadol can produce minor residual effects on driving after evening administration. Administration later at night is associated with moderately impairing residual effects on driving and psychomotor performance but not on memory.
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PMID:Highway driving performance and cognitive functioning the morning after bedtime and middle-of-the-night use of gaboxadol, zopiclone and zolpidem. 1955 33

Drugs that act as allosteric activators at the benzodiazepine site of the gamma-aminobutyric acid (GABA(A)) receptor complex are used commonly to treat insomnia but relatively little is known of how such use affects learning and memory. Although anterograde effects on memory acquisition have been shown, possible retrograde effects on consolidation are more relevant when such agents are administered at bedtime. We tested the effects of two GABA(A) allosteric activators on sleep-dependent motor skill memory consolidation in 12 healthy male subjects. Subjects slept in a sleep laboratory for four consecutive nights (one accommodation night followed by three experimental nights). Placebo, triazolam 0.375 mg, and zolpidem 10 mg were given to each subject in counterbalanced order on the experimental nights. Polysomnographic (PSG) sleep measurement and sleep-dependent motor learning were assessed at each condition. Triazolam was associated with longer total sleep time and increased Stage 2 sleep. Both zolpidem and triazolam were associated with increased latency to rapid eye movement (REM) sleep. Overnight motor learning correlated with total sleep time in the placebo condition but not in the triazolam or zolpidem conditions. A statistically significant impairment in motor performance occurred overnight in the triazolam condition only. Triazolam, given in sufficient doses to prolong sleep in healthy people, affected overnight motor learning adversely. Zolpidem, in a dose sufficient to prolong REM onset latency but without other effects on PSG-measured sleep, degraded the relationship between total sleep time and overnight motor learning. These data indicate that non-selective or alpha1-preferring benzodiazepine site allosteric activators can interfere with sleep-dependent memory consolidation.
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PMID:Retrograde effects of triazolam and zolpidem on sleep-dependent motor learning in humans. 1968 31


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