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This article is about the sleeping disorder. For other uses, see Insomnia (disambiguation).
Insomnia
SpecialtyNeurology, psychiatry Edit this on Wikidata

Insomnia is most often defined by an individual's report of sleeping difficulties.[1] While the term is sometimes used in sleep literature to describe a disorder demonstrated by polysomnographic evidence of disturbed sleep, insomnia is often defined as a positive response to either of two questions: "Do you experience difficulty sleeping?" or "Do you have difficulty falling or staying asleep?"[1]

Thus, insomnia is most often thought of as both a sign and a symptom[1][2] that can accompany several sleep, medical, and psychiatric disorders, characterized by persistent difficulty falling asleep and/or staying asleep or sleep of poor quality. Insomnia is typically followed by functional impairment while awake. One definition of insomnia is "difficulties initiating and/or maintaining sleep, or nonrestorative sleep, associated with impairments of daytime functioning or marked distress for more than 1 month."[3]

Insomnia can be grouped into primary and secondary, or comorbid, insomnia.[4][5][6] Primary insomnia is a sleep disorder not attributable to a medical, psychiatric, or environmental cause.[7] A diagnosis will usually differentiate between:

  • insomnia as secondary to another condition,
  • primary insomnia co-morbid with one or more conditions, or
  • free-standing primary insomnia.[citation needed]

Classification

Types of insomnia

Insomnia can be classified as transient, acute, or chronic.

  1. Transient insomnia lasts for less than a week. It can be caused by another disorder, by changes in the sleep environment, by the timing of sleep, severe depression, or by stress. Its consequences - sleepiness and impaired psychomotor performance - are similar to those of sleep deprivation.[8]
  2. Acute insomnia is the inability to consistently sleep well for a period of less than a month.[9]
  3. Chronic insomnia lasts for longer than a month. It can be caused by another disorder, or it can be a primary disorder. Its effects can vary according to its causes. They might include muscular fatigue, hallucinations, and/or mental fatigue; but people with chronic insomnia often show increased alertness.[citation needed] Some people that live with this disorder see things as if they are happening in slow motion, wherein moving objects seem to blend together. Can cause double vision.[8]

Patterns of insomnia

Sleep-onset insomnia is difficulty falling asleep at the beginning of the night, often a symptom of anxiety disorders or the delayed sleep phase disorder.

Nocturnal awakenings are characterized by difficulty returning to sleep after awakening in the middle of the night or waking too early in the morning: middle-of-the-night insomnia and terminal insomnia. The former may be a symptom of pain disorders or medical illness; the latter is often a characteristic of clinical depression.

Poor sleep quality

Poor sleep quality can occur as a result of, for example, restless legs, sleep apnea or major depression. Poor sleep quality is caused by the individual not reaching stage 3 or delta sleep which has restorative properties. There are, however, people who are unable to achieve stage 3 sleep due to brain damage who lead perfectly normal lives.[citation needed]

Major depression leads to alterations in the function of the hypothalamic-pituitary-adrenal axis, causing excessive release of cortisol which can lead to poor sleep quality.

Nocturnal polyuria, excessive nighttime urination, can be very disturbing to sleep.[10]

Subjective insomnia

Main article: Sleep state misperception

Some cases of insomnia are not really insomnia in the traditional sense. People experiencing sleep state misperception often sleep for normal durations, yet severely overestimate the time taken to fall asleep. They may believe they slept for only 4 hours while they, in fact, slept a full 8 hours.

Causes and co-morbidities

Symptoms of insomnia can be caused by or can be co-morbid with:

Sleep studies using polysomnography have suggested that people who have sleep disruption have elevated nighttime levels of circulating cortisol and adrenocorticotropic hormone They also have an elevated metabolic rate, which does not occur in people who do not have insomnia but whose sleep is intentionally disrupted during a sleep study. Studies of brain metabolism using positron emission tomography (PET) scans indicate that people with insomnia have higher metabolic rates by night and by day. The question remains whether these changes are the causes or consequences of long-term insomnia.[14]

A common misperception is that the amount of sleep required decreases as a person ages. The ability to sleep for long periods, rather than the need for sleep, appears to be lost as people get older. Some elderly insomniacs toss and turn in bed and occasionally fall off the bed at night, diminishing the amount of sleep they receive.[17]

Potential complications of insomnia.[18]

Diagnosis

Specialists in sleep medicine are qualified to diagnose the many different sleep disorders. Patients with various disorders including delayed sleep phase syndrome are often mis-diagnosed with primary insomnia. When a person has trouble getting to sleep, but has a normal sleep pattern once asleep, a circadian rhythm disorder is a likely cause.

In many cases, insomnia is co-morbid with another disease, side-effects from medications, or a psychological problem. Approximately half of all diagnosed insomnia is related to psychiatric disorders.[19] In depression in many cases "insomnia should be regarded as a co-morbid condition, rather than as a secondary one;" insomnia typically predates psychiatric symptoms.[19] "In fact, it is possible that insomnia represents a significant risk for the development of a subsequent psychiatric disorder."[1]

Knowledge of causation is not necessary for a diagnosis.[19]

Treatment

It is important to identify or rule out medical and psychological causes before deciding on the treatment for insomnia.[20] Attention to sleep hygiene is an important first line treatment strategy and should be tried before any pharmacological approach is considered.[21] Pharmacological treatments have been used mainly to reduce symptoms in acute insomnia; their role in the management of chronic insomnia remains unclear.[4]

Non-pharmacological

Non-pharmacological strategies are superior to hypnotic medication for insomnia because tolerance develops to the hypnotic effects. In addition, dependence can develop with rebound withdrawal effects developing upon discontinuation. Hypnotic medication is therefore only recommended for short-term use, especially in acute or chronic insomnia.[22] Non pharmacological strategies however, have long lasting improvements to insomnia and are recommended as a first line and long term strategy of managing insomnia. The strategies include attention to sleep hygiene, stimulus control, behavioral interventions, sleep-restriction therapy, paradoxical intention, patient education and relaxation therapy.[23]

EEG biofeedback has demonstrated effectiveness in the treatment of insomnia with improvements in duration as well as quality of sleep.[24]

Stimulus control therapy is a treatment for patients who have conditioned themselves to associate the bed, or sleep in general, with a negative response. As stimulus control therapy involves taking steps to control the sleep environment, it is sometimes referred interchangeably with the concept of sleep hygiene. Examples of such environmental modifications include using the bed for sleep or sex only, not for activities such as reading or watching television; waking up at the same time every morning, including on weekends; going to bed only when sleepy and when there is a high likelihood that sleep will occur; leaving the bed and beginning an activity in another location if sleep does not result in a reasonably brief period of time after getting into bed (commonly ~20 min); reducing the subjective effort and energy expended trying to fall asleep; avoiding exposure to bright light during nighttime hours, and eliminating daytime naps.[citation needed]

A component of stimulus control therapy is sleep restriction, a technique that aims to match the time spent in bed with actual time spent asleep. This technique involves maintaining a strict sleep-wake schedule, sleeping only at certain times of the day and for specific amounts of time to induce mild sleep deprivation. Complete treatment usually lasts up to 3 weeks and involves making oneself sleep for only a minimum amount of time that they are actually capable of on average, and then, if capable (i.e. when sleep efficiency improves), slowly increasing this amount (~15 min) by going to bed earlier as the body attempts to reset its internal sleep clock. Bright light therapy, which is often used to help early morning wakers reset their natural sleep cycle, can also be used with sleep restriction therapy to reinforce a new wake schedule. Although applying this technique with consistency is difficult, it can have a positive effect on insomnia in motivated patients.

Paradoxical intention is a cognitive reframing technique where the insomniac, instead of attempting to fall asleep at night, makes every effort to stay awake (i.e. essentially stops trying to fall asleep). One theory that may explain the effectiveness of this method is that by not voluntarily making oneself go to sleep, it relieves the performance anxiety that arises from the need or requirement to fall asleep, which is meant to be a passive act. This technique has been shown to reduce sleep effort and performance anxiety and also lower subjective assessment of sleep-onset latency and overestimation of the sleep deficit (a quality found in many insomniacs).[25]

Cognitive Behavioral Therapy for Insomnia

A recent study found that Cognitive Behavioral Therapy for Insomnia (CBT-I) is more effective than hypnotic medications in controlling insomnia.[26] In this therapy, patients are taught improved sleep habits and relieved of counter-productive assumptions about sleep. Common misconceptions and expectations that can be modified include: (1) unrealistic sleep expectations (e.g., I need to have 8 hours of sleep each night), (2) misconceptions about insomnia causes (e.g., I have a chemical imbalance causing my insomnia), (3) amplifying the consequences of insomnia (e.g., I cannot do anything after a bad night's sleep), and (4) performance anxiety after trying for so long to have a good night's sleep by controlling the sleep process. Numerous studies have reported positive outcomes of combining cognitive behavioral therapy for insomnia treatment with treatments such as stimulus control and the relaxation therapies. Hypnotic medications are equally effective in the short-term treatment of insomnia but their effects wear off over time due to tolerance. The effects of CBT-I have sustained and lasting effects on treating insomnia long after therapy has been discontinued.[27][28] The addition of hypnotic medications with CBT-I adds no benefit in insomnia. The long lasting benefits of a course of CBT-I shows superiority over pharmacological hypnotic drugs. Even in the short term when compared to short-term hypnotic medication such as zolpidem (Ambien), CBT-I still shows significant superiority. Thus CBT-I is recommended as a first line treatment for insomnia.[29]

Medications

Many insomniacs rely on sleeping tablets and other sedatives to get rest, with research showing that medications are prescribed to over 95% of insomniac cases.[30] Certain classes of sedatives such as benzodiazepines and newer nonbenzodiazepine drugs can also cause physical dependence, which manifests in withdrawal symptoms if the drug is not carefully tapered down. The benzodiazepine and nonbenzodiazepine hypnotic medications also have a number of side-effects such as day time fatigue, motor vehicle crashes, cognitive impairments and falls and fractures. Elderly people are more sensitive to these side-effects.[31] The non-benzodiazepines zolpidem and zaleplon have not adequately demonstrated effectiveness in sleep maintenance. Some benzodiazepines have demonstrated effectiveness in sleep maintenance in the short term but in the longer term are associated with tolerance and dependence. Drugs that may prove more effective and safer than existing drugs for insomnia are in development.[32]

In comparing the options, a systematic review found that benzodiazepines and nonbenzodiazepines have similar efficacy that is not significantly more than for antidepressants.[33] Benzodiazepines did not have a significant tendency for more adverse drug reactions.[33] Chronic users of hypnotic medications for insomnia do not have better sleep than chronic insomniacs not taking medications. In fact, chronic users of hypnotic medications have more regular nighttime awakenings than insomniacs not taking hypnotic medications.[34] A further review of the literature regarding benzodiazepine hypnotic as well as the nonbenzodiazepines concluded that these drugs cause an unjustifiable risk to the individual and to public health and lack evidence of long-term effectiveness. The risks include dependence, accidents, and other adverse effects. Gradual discontinuation of hypnotics in long-term users leads to improved health without worsening of sleep. It is preferred that hypnotics be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible in the elderly.[35]

Benzodiazepines

General Prescribing Guideline
Insomnia Level Benzodiazepine Utilization
Mild to moderate Alprazolam†, Diazepam†, Flurazepam, Lorazepam†, Oxazepam† Quazepam
Moderate to severe Estazolam, Loprazolam, Lormetazepam, Midazolam§, Nitrazepam
Severe Brotizolam, Flunitrazepam, Nimetazepam, Temazepam, Triazolam
§Via the oral route (PO).
†Anxiolytic and/or anti-convulsive agent; off-label usage.

The most commonly used class of hypnotics prescribed for insomnia are the benzodiazepines. Benzodiazepines all bind unselectively to the GABAA receptor.[33] But certain benzodiazepines (hypnotic benzodiazepines) have significantly higher activity at the α1 subunit of the GABAA receptor compared to other benzodiazepines (for example, triazolam and temazepam have significantly higher activity at the α1 subunit compared to alprazolam and diazepam, making them superior sedative-hypnotics - alprazolam and diazepam in turn have higher activity at the α2 subunit compared to triazolam and temazepam, making them superior anxiolytic agents). Modulation of the α1 subunit is associated with sedation, motor-impairment, respiratory depression, amnesia, ataxia, and reinforcing behavior (drug-seeking behavior). Modulation of the α2 subunit is associated with anxiolytic activity and disinhibition. For this reason, certain benzodiazepines are better suited to treat insomnia than others. Hypnotic benzodiazepines include drugs such as temazepam, flunitrazepam, triazolam, flurazepam, midazolam, nitrazepam, and quazepam. These drugs can lead to tolerance, physical dependence, and the benzodiazepine withdrawal syndrome upon discontinuation, especially after consistent usage over long periods of time. Benzodiazepines, while inducing unconsciousness, actually worsen sleep as they promote light sleep while decreasing time spent in deep sleep.[36] A further problem is, with regular use of short-acting sleep aids for insomnia, daytime rebound anxiety can emerge.[37] Benzodiazepines can help to initiate sleep and increase sleep time, but they also decrease deep sleep and increase light sleep. Although there is little evidence for benefit of benzodiazepines in insomnia and evidence of major harm, prescriptions have continued to increase.[38] There is a general awareness that long-term use of benzodiazepines for insomnia in most people is inappropriate and that a gradual withdrawal is usually beneficial due to the adverse effects associated with the long-term use of benzodiazepines and is recommended whenever possible.[39][40]

Non-benzodiazepines

Nonbenzodiazepine sedative-hypnotic drugs, such as zolpidem, zaleplon, zopiclone, and eszopiclone, are a newer classification of hypnotic medications. They work on the benzodiazepine site on the GABAA receptor complex similarly to the benzodiazepine class of drugs. Some but not all of the nonbenzodiazepines are selective for the α1 subunit on GABAA receptors, which is responsible for inducing sleep and may therefore have a cleaner side-effect profile than the older benzodiazepines. Zopiclone and eszopiclone like benzodiazepine drugs bind unselectively to α1, α2, α3 and α5 GABAA benzodiazepine receptors. [41] Zolpidem is more selective and zaleplon is highly selective for the α1 subunit, thus giving them an advantage over benzodiazepines in terms of sleep architecture and a reduction in side-effects. Their activity at the α1 subunit on GABAA receptors is milder compared to most benzodiazepines, rendering them ineffective for moderately severe to severe insomnia.[42][43] However, there are controversies over whether these non-benzodiazepine drugs are superior to benzodiazepines. These drugs appear to cause both psychological dependence and physical dependence, though less than traditional benzodiazepines and can also cause the same memory and cognitive disturbances along with morning sedation.

Alcohol

Alcohol is often used as a form of self-treatment of insomnia to induce sleep. However, alcohol use to induce sleep can be a cause of insomnia. Long-term use of alcohol is associated with a decrease in NREM stage 3 and 4 sleep as well as suppression of REM sleep and REM sleep fragmentation. Frequent moving between sleep stages occurs, with awakenings due to headaches, polyuria, dehydration, and diaphoresis. Glutamine rebound also plays a role as when someone is drinking; alcohol inhibits glutamine, one of the body's natural stimulants. When the person stops drinking, the body tries to make up for lost time by producing more glutamine than it needs. The increase in glutamine levels stimulates the brain while the drinker is trying to sleep, keeping him/her from reaching the deepest levels of sleep.[44] Stopping chronic alcohol use can also lead to severe insomnia with vivid dreams. During withdrawal REM sleep is typically exaggerated as part of a rebound effect.[45]

Opioids

Opioid medications such as hydrocodone, oxycodone, and morphine are used for insomnia that is associated with pain due to their analgesic properties and hypnotic effects. Opioids can fragment sleep and decrease REM and stage 2 sleep. By producing analgesia and sedation, opioids may be appropriate in carefully selected patients with pain-associated insomnia.[12]

Antidepressants

Some antidepressants such as amitriptyline, doxepin, mirtazapine, and trazodone can often have a very strong sedative effect, and are prescribed off label to treat insomnia.[46] The major drawback of these drugs is that they have properties that can lead to many side-effects; for example, amitriptyline and doxepin both have antihistaminergic, anticholinergic, and antiadrenergic properties, which contribute to their side-effect profile, while mirtazapines side-effects are primarily antihistaminergic, and trazadones side-effects are primarily antiadrenergic. Some also alter sleep architecture. As with benzodiazepines, the use of antidepressants in the treatment of insomnia can lead to withdrawal effects; withdrawal may induce rebound insomnia.

Mirtazapine is known to decrease sleep latency, promoting sleep efficiency and increasing the total amount of sleeping time in patients suffering from both depression and insomnia.[47][48]

Melatonin and melatonin agonists

The hormone melatonin, sold as a "dietary supplement" in some countries, is effective in several types of insomnia. Melatonin has demonstrated effectiveness equivalent to the prescription sleeping tablet zopiclone in inducing sleep and regulating the sleep/waking cycle.[49] One particular benefit of melatonin is that it can treat insomnia without altering the sleep pattern, which is altered by many prescription sleeping tablets. Another benefit is it does not impair performance related skills.[50][51]

Melatonin agonists, including ramelteon (Rozerem) and tasimelteon, seem to lack the potential for misuse and dependence. This class of drugs has a relatively mild side-effect profile and low likelihood of causing morning sedation. While these drugs show good effect for the treatment of insomnia due to jet lag[52] and the chronic circadian rhythm disorders, the results for other forms of insomnia are less promising.[53]

Natural substances such as 5-HTP and L-Tryptophan have been said to fortify the serotonin-melatonin pathway.[54]

Antihistamines

The antihistamine diphenhydramine is widely used in nonprescription sleep aids such as Benadryl. The antihistamine doxylamine is used in nonprescription sleep aids such as Unisom (USA) and Unisom 2 (Canada). In some countries, including Australia, it is marketed under the names Restavit and Dozile. It is the most effective over-the-counter sedative currently available in the United States, and is more sedating than some prescription hypnotics.[55]

While the two drugs mentioned above are available over the counter in most countries, the effectiveness of these agents may decrease over time, and the incidence of next-day sedation is higher than for most of the newer prescription drugs. Anticholinergic side-effects may also be a draw back of these particular drugs. Dependence does not seem to be an issue with this class of drugs.

Cyproheptadine is a useful alternative to benzodiazepine hypnotics in the treatment of insomnia. Cyproheptadine may be superior to benzodiazepines in the treatment of insomnia because cyproheptadine enhances sleep quality and quantity, whereas benzodiazepines tend to decrease sleep quality.[56]

Atypical antipsychotics

Low doses of certain atypical antipsychotics such as quetiapine, olanzapine, and risperidone are also prescribed for their sedative effect, but the danger of neurological, metabolic, and cognitive side-effects makes these drugs a poor choice to treat insomnia. Over time, quetiapine may lose its effectiveness as a sedative. The ability of quetiapine to produce sedation is determined by the dosage. Higher doses (300 mg - 900 mg) are usually taken for its use as an antipsychotic, while lower doses (25 mg - 200 mg) have a marked sedative effect; e.g., if a patient takes 300 mg, he/she will more likely benefit from the drug's antipsychotic effects, but ,if the dose is brought down to 100 mg, it will leave the patient feeling more sedated than at 300 mg, because it works primarily as a sedative at lower doses.

Eplivanserin is an investigational drug with a mechanism similar to those of these antipsychotics, but probably with fewer side-effects.

Other substances

Some insomniacs use herbs such as valerian, chamomile, lavender, hops, and passion-flower. Valerian has undergone multiple studies and appears to be modestly effective.[57][58][59]

Insomnia may be a symptom of magnesium deficiency, or low magnesium levels, but this has not yet been proven. A healthy diet containing magnesium can help to improve sleep in individuals without an adequate intake of magnesium.[60]

L-Arginine L-aspartate, S-adenosyl-L-homocysteine, and Delta sleep-inducing peptide (DSIP) may be also helpful in alleviating insomnia.[61] There is some evidence showing that 3 grams of L-Glycine before bedtime improves sleep quality.[62]

Disability-adjusted life year for insomnia per 100,000 inhabitants in 2002.
  no data
  less than 25
  25-30.25
  30.25-36
  36-41.5
  41.5-47
  47-52.5
  52.5-58
  58-63.5
  63.5-69
  69-74.5
  74.5-80
  more than 80

Epidemiology

A survey of 1.1 million residents in the United States conducted by the American Cancer Society found that those that reported sleeping about 7 hours per night had the lowest rates of mortality, whereas those that slept for fewer than 6 hours or more than 8 hours had higher mortality rates. Getting 8.5 or more hours of sleep per night increased the mortality rate by 15%. Severe insomnia - sleeping less than 3.5 hours in women and 4.5 hours in men - also led to a 15% increase in mortality. However, most of the increase in mortality from severe insomnia was discounted after controlling for co-morbid disorders. After controlling for sleep duration and insomnia, use of sleeping pills was also found to be associated with an increased mortality rate.[63]

The lowest mortality was seen in individuals who slept between six and a half and seven and a half hours per night. Even sleeping only 4.5 hours per night is associated with very little increase in mortality. Thus, mild to moderate insomnia for most people is associated with increased longevity and severe insomnia is associated only with a very small effect on mortality.[63]

As long as a patient refrains from using sleeping pills, there is little to no increase in mortality associated with insomnia, but there does appear to be an increase in longevity. This is reassuring for patients with insomnia in that, despite the sometimes-unpleasantness of insomnia, insomnia itself appears to be associated with increased longevity.[63] It is unclear why sleeping longer than 7.5 hours is associated with excess mortality.[63]

Insomnia is 40% more common in women than in men.[64]

Prevalence

The National Sleep Foundation's 2002 Sleep in America poll showed that 58% of adults in the U.S. experienced symptoms of insomnia a few nights a week or more.[65] Although insomnia was the most common sleep problem among about one half of older adults (48%), they were less likely to experience frequent symptoms of insomnia than their younger counterparts (45% vs. 62%), and their symptoms were more likely to be associated with medical conditions, according to the poll of adults between the ages of 55 and 84.[65]

As explained by Thomas Roth,[1] estimates of the prevalence of insomnia depend on the criteria used as well as the population studied. About 30% of adults report at least one of the symptoms of insomnia. When daytime impairment is added as a criterium, the prevalence is about 10%. Primary insomnia persisting for at least one month yields estimates of 6%.

See also

References

  1. ^ a b c d e Roth, Thomas (15 August 2007). "Insomnia: Definition, Prevalence, Etilogy, and Consequences" (Full text). J Clin Sleep Med. 3(5 Suppl). American Academy of Sleep Medicine: S7–S10. Retrieved 21 September 2010. {{cite journal}}: Cite has empty unknown parameters: |laydate=, |laysource=, |laysummary=, and |month= (help)
  2. ^ Hirshkowitz, Max (2004). "Chapter 10, Neuropsychiatric Aspects of Sleep and Sleep Disorders (pp 315-340)". In Stuart C. Yudofsky and Robert E. Hales, editors (ed.). Essentials of neuropsychiatry and clinical neurosciences (4 ed.). Arlington, Virginia, USA: American Psychiatric Publishing. ISBN 9781585620050. ...insomnia is a symptom. It is neither a disease nor a specific condition. (from p. 322) {{cite book}}: |access-date= requires |url= (help); |editor= has generic name (help); |format= requires |url= (help); Cite has empty unknown parameters: |origmonth=, |month=, |origdate=, and |coauthors= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
  3. ^ Morin, Charles M. (2000). "The Nature of Insomnia and the Need to Refine Our Diagnostic Criteria" (Editorial). Psychosomatic Medicine. 62 (4): 62:483–485. PMID 10949092. Retrieved 2010-01-07.
  4. ^ a b "Dyssomnias" (pdf). WHO. pp. 7–11. Retrieved 2009-01-25.
  5. ^ Buysse, Daniel J. (2008). "Chronic Insomnia" (Full text). Am J Psychiatry 165:678-686, June 2008. 165 (6). American Psychiatric Association: 678–86. doi:10.1176/appi.ajp.2008.08010129. PMC 2859710. PMID 18519533. Retrieved 2010-09-22. For this reason, the NIH conference [of 2005] commended the term "comorbid insomnia" as a preferable alternative to the term "secondary insomnia." {{cite journal}}: Unknown parameter |month= ignored (help)
  6. ^ Erman, Milton K. (2007). "Insomnia: Comorbidities and Consequences". Primary Psychiatry. 14 (6): 31–35. Retrieved 2010-09-22. Two general categories of insomnia exist, primary insomnia and comorbid insomnia. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
  7. ^ World Health Organization (2007). "Quantifying burden of disease from environmental noise" (PDF). p. 20. Retrieved 2010-09-22. "In his e-mail dated 10.8.2005, Colin Mathers gives the following statement referring to this question: 'Primary insomnia is sleeplessness that is not attributable to a medical, psychiatric or environmental cause. …' {{cite web}}: Cite has empty unknown parameters: |month= and |coauthors= (help)
  8. ^ a b Roth, Thomas (2004-02-25). "Insomnia: Epidemiology, characteristics, and consequences". Clinical Cornerstone. 5 (3): 5–15. doi:10.1016/S1098-3597(03)90031-7. PMID 14626537. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  9. ^ "Insomnia - sleeplessness, chronic insomnia, acute insomnia, mental ..." driectoryM articles. Archived from the original on March 29, 2008. Retrieved 2008-04-29.
  10. ^ Sleep issues in Parkinson’s disease. Neurology. 2005. pp. 64, S12–20. Retrieved June 2007. {{cite book}}: Check date values in: |accessdate= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  11. ^ Lawrence KR, Adra M, Keir C (2006). "Hypoglycemia-induced anoxic brain injury possibly associated with levofloxacin". J. Infect. 52 (6): e177–80. doi:10.1016/j.jinf.2005.08.024. PMID 16269178. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  12. ^ a b Ramakrishnan, K.; Scheid, DC. (2007). "Treatment options for insomnia". Am Fam Physician. 76 (4): 517–26. PMID 17853625. {{cite journal}}: Unknown parameter |month= ignored (help)
  13. ^ Gelder, M., Mayou, R. and Geddes, J. 2005. Psychiatry. 3rd ed. New York: Oxford. pp167.
  14. ^ a b Mendelson WB (2008). "New Research on Insomnia: Sleep Disorders May Precede or Exacerbate Psychiatric Conditions". Psychiatric Times. 25 (7).
  15. ^ Schenkein J, Montagna P (2006). "Self management of fatal familial insomnia. Part 1: what is FFI?". MedGenMed : Medscape general medicine. 8 (3): 65. PMC 1781306. PMID 17406188.
  16. ^ The epidemiological survey of exercise-induced insomnia in chinese athletes Youqi Shi, Zhihong Zhou, Ke Ning, Jianhong LIU. Athens 2004: Pre-olympic Congress.
  17. ^ American Family Physician: Chronic Insomnia: A Practical Review
  18. ^ Mayo Clinic > Insomnia > Complications By Mayo Clinic staff. Retrieved on May 5, 2009
  19. ^ a b c Wilson, S. J. (2 September 2010). "British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders". J Psychopharm. 0 (0). Sage: 2, 4. doi:10.1177/0269881110379307. PMID 20813762. {{cite journal}}: |access-date= requires |url= (help); Cite has empty unknown parameters: |laydate=, |laysummary=, |laysource=, and |month= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  20. ^ Wortelboer U, Cohrs S, Rodenbeck A, Rüther E (2002). "Tolerability of hypnosedatives in older patients". Drugs Aging. 19 (7): 529–39. doi:10.2165/00002512-200219070-00006. PMID 12182689.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ Flamer HE (1995). "Sleep problems". Med. J. Aust. 162 (11): 603–7. PMID 7791648. {{cite journal}}: Unknown parameter |month= ignored (help)
  22. ^ National Prescribing Service (2009). "Addresing hypnotic medicines use in primary care". NPS News, Vol 67. Available at http://www.nps.org.au/health_professionals/publications/nps_news/current/nps_news_67
  23. ^ Kirkwood CK (1999). "Management of insomnia". J Am Pharm Assoc. 39 (5): 688–96, quiz 713–4. PMID 10533351.
  24. ^ Lake, James A. (31 October 2006). Textbook of Integrative Mental Health Care. Thieme Medical Publishers. p. 313. ISBN 1-58890-299-4.
  25. ^ Kierlin L (2008). "Sleeping without a pill: nonpharmacologic treatments for insomnia". J Psychiatr Pract. 14 (6): 403–7. doi:10.1097/01.pra.0000341896.73926.6c. PMID 19057243.
  26. ^ Cognitive behavior therapy and pharmacotherapy for insomnia: a randomized controlled trial and direct comparison, http://www.ncbi.nlm.nih.gov/pubmed/15451764?dopt=Abstract
  27. ^ Jacobs, Gregg (September 27, 2004). "Cognitive Behavior Therapy and Pharmacotherapy for Insomnia: A Randomized Controlled Trial and Direct Comparison". Archives of Internal Medicine. 164 (17): 1888–1896. doi:10.1001/archinte.164.17.1888. PMID 15451764. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  28. ^ Morin, C. M.; Colecchi, C; Stone, J; Sood, R; Brink, D (1999). "Behavioral and Pharmacological Therapies for Late-Life Insomnia: A Randomized Controlled Trial". JAMA the Journal of the American Medical Association. 281 (11): 991–9. doi:10.1001/jama.281.11.991. PMID 10086433.
  29. ^ KARL E. MILLER, M.D. (2005). "Cognitive Behavior Therapy vs. Pharmacotherapy for Insomnia". American Family Physician. {{cite journal}}: Unknown parameter |month= ignored (help) [dead link]
  30. ^ Harrison C, Britt H (2009). "Insomnia". Australian Family Physician, 32:283. Available at http://www.racgp.org.au/afp/200905/200905beach.pdf and http://www.nps.org.au/news_and_media/media_releases/repository/New_clinical_program_addresses
  31. ^ Glass J, Lanctôt KL, Herrmann N, Sproule BA, Busto UE (2005). "Sedative hypnotics in older people with insomnia: meta-analysis of risks and benefits". BMJ. 331 (7526): 1169. doi:10.1136/bmj.38623.768588.47. PMC 1285093. PMID 16284208. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  32. ^ Rosenberg, RP. (2006). "Sleep maintenance insomnia: strengths and weaknesses of current pharmacologic therapies". Ann Clin Psychiatry. 18 (1): 49–56. doi:10.1080/10401230500464711. PMID 16517453. {{cite journal}}: Unknown parameter |month= ignored (help)
  33. ^ a b c Buscemi N, Vandermeer B, Friesen C, Bialy L, Tubman M, Ospina M, Klassen TP, Witmans M. (2007). "The efficacy and safety of drug treatments for chronic insomnia in adults: a meta-analysis of RCTs". J Gen Intern Med. 22 (9): 1335–1350. doi:10.1007/s11606-007-0251-z. PMC 2219774. PMID 17619935. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  34. ^ Ohayon MM, Caulet M (1995). "Insomnia and psychotropic drug consumption". Prog. Neuropsychopharmacol. Biol. Psychiatry. 19 (3): 421–31. doi:10.1016/0278-5846(94)00023-B. PMID 7624493. {{cite journal}}: Unknown parameter |month= ignored (help)
  35. ^ "What's wrong with prescribing hypnotics?". Drug Ther Bull. 42 (12): 89–93. 2004. doi:10.1136/dtb.2004.421289. PMID 15587763. {{cite journal}}: Unknown parameter |month= ignored (help)
  36. ^ Tsoi, Wf (1991). "Insomnia: drug treatment". Annals of the Academy of Medicine, Singapore. 20 (2): 269–72. ISSN 0304-4602. PMID 1679317. {{cite journal}}: Unknown parameter |month= ignored (help)
  37. ^ Montplaisir J (2000). "Treatment of primary insomnia" (PDF). CMAJ. 163 (4): 389–91. PMC 80369. PMID 10976252. {{cite journal}}: Unknown parameter |month= ignored (help)
  38. ^ D. Maiuro PhD, Roland (13 December 2009). Handbook of Integrative Clinical Psychology, Psychiatry, and Behavioral Medicine: Perspectives, Practices, and Research. Springer Publishing Company. pp. 128–130. ISBN 0-8261-1094-0.
  39. ^ Lader, Malcolm Harold; P. Cardinali, Daniel; R. Pandi-Perumal, S. (22 March 2006). Sleep and sleep disorders: a neuropsychopharmacological approach. Georgetown, Tex.: Landes Bioscience/Eurekah.com. p. 127. ISBN 0-387-27681-5.
  40. ^ Authier, N.; Boucher, A.; Lamaison, D.; Llorca, PM.; Descotes, J.; Eschalier, A. (2009). "Second Meeting of the French CEIP (Centres d'Evaluation et d'Information sur la Pharmacodépendance). Part II: Benzodiazepine Withdrawal". Therapie. 64 (6): 365–370. doi:10.2515/therapie/2009051. PMID 20025839.
  41. ^ WHO (2006). "World Health Organisation - Assessment of Zopiclone" (PDF). who.int.
  42. ^ Rowlett JK, Woolverton WL (1996). "Assessment of benzodiazepine receptor heterogeneity in vivo: apparent pA2 and pKB analyses from behavioral studies" (PDF). Psychopharmacology (Berl.). 128 (1): 1–16. doi:10.1007/s002130050103. PMID 8944400. {{cite journal}}: Unknown parameter |month= ignored (help)
  43. ^ Noguchi H (2004). "Electroencephalographic properties of zaleplon, a non-benzodiazepine sedative/hypnotic, in rats" (pdf). J Pharmacol Sci. 94 (3): 246–51. doi:10.1254/jphs.94.246. PMID 15037809. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  44. ^ http://health.howstuffworks.com/hangover5.htm
  45. ^ Lee-chiong, Teofilo (24 April 2008). Sleep Medicine: Essentials and Review. Oxford University Press, USA. p. 105. ISBN 0-19-530659-7.
  46. ^ Bertschy G, Ragama-Pardos E, Muscionico M; et al. (2005). "Trazodone addition for insomnia in venlafaxine-treated, depressed inpatients: a semi-naturalistic study". Pharmacol. Res. 51 (1): 79–84. doi:10.1016/j.phrs.2004.06.007. PMID 15519538. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  47. ^ Winokur A, DeMartinis NA 3rd, McNally DP, Gary EM, Cormier JL, Gary KA. ; et al. (2003). "Comparative effects of mirtazapine and fluoxetine on sleep physiology measures in patients with major depression and insomnia". J Clin Psychiatry. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: numeric names: authors list (link)
  48. ^ Schittecatte M, Dumont F, Machowski R, Cornil C, Lavergne F, Wilmotte J ; et al. (2002). "Effects of mirtazapine on sleep polygraphic variables in major depression". Neuropsychobiology year=2002. 46 (4): 197–201. doi:10.1159/000067812. PMID 12566938. {{cite journal}}: Explicit use of et al. in: |author= (help); Missing pipe in: |journal= (help)CS1 maint: multiple names: authors list (link)
  49. ^ Paul MA, Gray G, Sardana TM, Pigeau RA (2004). "Melatonin and zopiclone as facilitators of early circadian sleep in operational air transport crews". Aviat Space Environ Med. 75 (5): 439–43. PMID 15152897. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  50. ^ Paul MA, Gray G, Kenny G, Pigeau RA (2003). "Impact of melatonin, zaleplon, zopiclone, and temazepam on psychomotor performance". Aviat Space Environ Med. 74 (12): 1263–70. PMID 14692469. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  51. ^ Zhdanova IV, Tucci V (2003). "Melatonin, Circadian Rhythms, and Sleep". Curr Treat Options Neurol. 5 (3): 225–229. doi:10.1007/s11940-003-0013-0. PMID 12670411. {{cite journal}}: |format= requires |url= (help); External link in |format= (help); Unknown parameter |month= ignored (help)
  52. ^ Rajaratnam, SMW (2 December 2008). "Melatonin agonist tasimelteon (VEC-162) for transient insomnia after sleep-time shift: two randomised controlled multicentre trials". Lancet. 373 (9662): 482–91. doi:10.1016/S0140-6736(08)61812-7. PMID 19054552. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  53. ^ Zammit G, Erman M, Wang-Weigand S, Sainati S, Zhang J, Roth T (2007). "Evaluation of the efficacy and safety of ramelteon in subjects with chronic insomnia". J Clin Sleep Med. 3 (5): 495–504. PMC 1978328. PMID 17803013. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  54. ^ Morton Walker, DPM - The Restoration of L-Tryptophan with Its Numerous Physiological Benefits
  55. ^ DrugBank: DB00366 (Doxylamine)
  56. ^ Tokunaga S (2007). "Effects of some H1-antagonists on the sleep-wake cycle in sleep-disturbed rats" (pdf). J Pharmacol Sci. 103 (2): 201–6. doi:10.1254/jphs.FP0061173. PMID 17287588. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)
  57. ^ Donath F, Quispe S, Diefenbach K, Maurer A, Fietze I, Roots I (2000). "Critical evaluation of the effect of valerian extract on sleep structure and sleep quality". Pharmacopsychiatry. 33 (2): 47–53. doi:10.1055/s-2000-7972. PMID 10761819.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  58. ^ Morin CM, Koetter U, Bastien C, Ware JC, Wooten V (2005). "Valerian-hops combination and diphenhydramine for treating insomnia: a randomized placebo-controlled clinical trial". Sleep. 28 (11): 1465–71. PMID 16335333.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  59. ^ Meolie AL, Rosen C, Kristo D; et al. (2005). "Oral nonprescription treatment for insomnia: an evaluation of products with limited evidence". Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 1 (2): 173–87. PMID 17561634. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  60. ^ Hornyak M, Voderholzer U, Hohagen F, Berger M, Riemann D (1998). "Magnesium therapy for periodic leg movements-related insomnia and restless legs syndrome: an open pilot study". Sleep. 21 (5): 501–5. PMID 9703590.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  61. ^ Billiard, M, Kent, A (2003). Sleep: physiology, investigations, medicine. pp. 275–7. ISBN 9780306474064.{{cite book}}: CS1 maint: multiple names: authors list (link)
  62. ^ Yamadera W, Inagawa K, Chiba S, Bannai M, Takahashi M, Nakayama K (2007). "Glycine ingestion improves subjective sleep quality in human volunteers, correlating with polysomnographic changes". Sleep and Biological rhythms. 5 (2): 126–131. doi:10.1111/j.1479-8425.2007.00262.x.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  63. ^ a b c d Kripke DF, Garfinkel L, Wingard DL, Klauber MR, Marler MR (2002). "Mortality associated with sleep duration and insomnia". Arch. Gen. Psychiatry. 59 (2): 131–6. doi:10.1001/archpsyc.59.2.131. PMID 11825133. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  64. ^ "Several Sleep Disorders Reflect Gender Differences". Retrieved 2008-09-05.
  65. ^ a b "2002 Sleep in America Poll". National Sleep Foundation. Archived from the original on June 14, 2008. Retrieved 2008-08-13.
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