Insomnia Treatment & Management

  • Author: Ron A Shatzmiller, MD, MSc; Chief Editor: Selim R Benbadis, MD   more...
 
Updated: Jan 17, 2012
 

Approach Considerations

The 2008 AASM guideline states that the 2 primary goals of treatment are to improve sleep quality and to improve related daytime impairments.[3] The management of insomnia varies depending on the underlying etiology. If the patient has a medical, neurologic, or sleep disorder, direct treatment at the disorder. In particular, adequate pain control can greatly relieve the insomnia associated with pain syndromes.

If the patient has a psychiatric disorder, direct treatment at the disorder. Management may involve medications, psychotherapy, and possible referral to a psychiatrist, psychologist, or therapist. If the insomnia is related to medication or drug abuse, the offending medication or drug must be slowly tapered and withdrawn.

Even when comorbid causes of insomnia (ie, medical, psychiatric) are treated, however, variable degrees of insomnia persist that require additional interventions. These patients can benefit from cognitive behavioral therapy (CBT)[8] and a short course of a sedative-hypnotic or melatonin receptor agonist. In the case of a psychiatric disorder (eg, depression[52] or anxiety), CBT and a short-term sedative-hypnotic in conjunction with an antidepressant can be beneficial

The treatment of primary (psychophysiologic) insomnia begins with education about the sleep problem and appropriate sleep hygiene measures (elements of good sleep hygiene are described in Patient Education).

Before therapy is instituted, most patients are asked to maintain a sleep diary for 2-4 weeks (see Sleep Diary). This gives the physician a clearer picture of the degree of sleep disturbance and allows development of a tailored treatment.

CBT is now considered the most appropriate treatment for patients with primary insomnia.[9, 10, 11] Use of this therapy is based on the fact that primary insomnia is associated with physiologic, emotional, and cognitive arousal and conditioning to arousal in bed.

Strong evidence supports the use of nonpharmacologic interventions (eg, CBT) for insomnia. Head-to-head comparison has shown that the benefits of nonpharmacologic interventions are superior to those of medication.[53, 54, 55]

The 2008 AASM guideline recommends psychological and behavioral interventions (including, but not limited to, CBT) as effective in the treatment of chronic comorbid insomnia as well as primary insomnia. The guideline also encourages these interventions as initial therapy when appropriate.[3]

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Cognitive-Behavioral Therapy

Cognitive-behavioral therapy (CBT) is a group of techniques used to ameliorate factors that perpetuate or exacerbate chronic insomnia, such as poor sleep habits, hyperarousal, irregular sleep schedules, inadequate sleep hygiene, and misconceptions about sleep, and the consequences of insomnia. While CBT is most effective for primary insomnia, it is alos effective for comorbid insomnia as adjunctive therapy.[3]

Multiple randomized, controlled trials have demonstrated the efficacy of CBT. Sleep latency, total sleep time, duration of wakefulness, and sleep quality improve compared with placebo treatment. From 50-75% of patients attain clinically significant improvement. CBT also improves the absolute amount of slow-wave sleep by 30%. Six-month follow-up has shown sustained efficacy for this treatment modality.

The American Academy of Sleep Medicine (AASM) evidence-based practice parameter found that CBT (all components), as well as individual components of stimulus-control, paradoxical intention, relaxation training, and biofeedback were effective.[10] CBT has also been shown to be better in weaning patients from hypnotics compared with tapering medications alone.

Limitations of CBT are that providers must be trained in its use, and the technique is time consuming. Most studies of CBT used trained psychologists to work with patients over an average of 5.7 sessions over 6.5 weeks, with each session lasting at least 20-40 minutes. A study by Edinger et al showed that a total of 4 biweekly individual treatments represents the optimal dosing of CBT.[56]

Obviously, this would not be practical for most primary care providers or neurologists. In addition, it is currently not known how effective CBT can be when administered by a nonpsychologist.

A study by Buysse et al determined that brief behavioral treatment for insomnia (BBTI), which consisted of behavioral instructions delivered in 2 intervention sessions and 2 telephone calls, was a simple, efficacious, and durable intervention for chronic insomnia in older adults.[57]

Some sleep centers have behavioral medicine specialists who can administer CBT. Preliminary evidence by Morin indicated that providing written information about CBT can be helpful.[58] An internet-based CBT learning program for patients is also available for a nominal cost (see CBTforINSOMNIA.com).

The components of CBT include the following:

  • Sleep hygiene education
  • Cognitive therapy
  • Relaxation therapy
  • Stimulus-control therapy
  • Sleep-restriction therapy

Cognitive behavioral therapy for insomnia (CBT-I) is a term for the combination of cognitive therapy with behavioral therapy such as stimulus-control therapy or sleep-restriction therapy (with or without relaxation therapy).[3]

The 2008 AASM guideline recommends including at least one behavioral intervention in initial treatment. Multicomponent therapy that includes behavioral therapy without cognitive therapy is also recommended as effective in the treatment of chronic insomnia.[3]

Sleep hygiene education

Sleep hygiene education addresses behaviors that are incompatible with sleep. These include caffeine or alcohol use, environmental noise, inappropriate room temperature, and watching TV in bed. The 2008 AASM guideline recommends adherence to sleep hygiene rules for all patients with chronic insomnia but finds insufficient evidence of effectiveness when following these sleep hygiene rules as monotherapy and, thus, advises its use as adjunctive therapy.[3]

Cognitive therapy

In cognitive therapy, the patient is educated to correct inaccurate beliefs about sleep and to reduce catastrophic thinking and excessive worrying about the consequences of failing to obtain adequate sleep.

Relaxation therapy

Relaxation therapy comprises several techniques. In progressive relaxation, the patient is taught to recognize and control tension through a series of exercises that consist of first tensing and then relaxing each muscle group in a systematic way. Guided imagery and meditation teach the patient how to focus on neutral or pleasant targets in place of racing thoughts. Biofeedback techniques can also be used. These techniques have the advantages of providing the patient with immediate feedback regarding his or her level of tension and rapidly teaching the patient how to relax.

Stimulus-control therapy

Stimulus-control therapy works to reassociate the bed with sleepiness instead of arousal. Rules for its use include the following:

  • Use the bed only for sleeping and sexual activity (no reading, TV, eating, or working in bed)
  • Go to bed only when sleepy
  • If unable to fall asleep in 15-20 minutes, get out of bed to do something relaxing until sleepy; this can be repeated as often as needed
  • Do not spend more time in bed than is needed by establishing a standard wake-up time
  • Refrain from daytime napping

Sleep-restriction therapy

Sleep-restriction therapy is based upon the fact that excessive time in bed often perpetuates the insomnia. Limiting the time spent in bed leads to more efficient sleep that is both consolidated and more regular and predictable. Time in bed is allowed to increase as the patient demonstrates a continuing ability to sleep in an efficient and consolidated manner.

This treatment plan consists of limiting time in bed to the patient's estimated total sleep time (not less than 5 h) and increasing it by 20 minutes for a given week when the patient estimates that his or her sleep efficiency (SE; ratio of time asleep to time in bed) has reached greater than 85%. The amount of time in bed remains the same when the SE falls between 80 and 85%, and is decreased by 20 minutes for a given week when the SE is less than 85%. Periodic (weekly) adjustments are made until the optimal sleep duration is achieved.

Use sleep-restriction therapy with caution in commercial truck drivers, operators of heavy machinery, pilots, and patients in other occupations where sleep deprivation can have devastating consequences.

Efficacy of CBT versus sedative-hypnotics for primary insomnia

Several randomized trials comparing CBT against hypnotics for primary insomnia have been published. Morin and colleagues compared temazepam with CBT in older patients and found similar short-term effects, but continued efficacy after discontinuation of therapy in the CBT group only. A study by Jacobs et al comparing zolpidem with CBT showed continued efficacy for the patients treated with CBT.[54]

A European study by Sivertsen and colleagues showed that CBT was superior to zopiclone. In fact, zopiclone was no different than placebo on 3 of 4 outcome measures.[59] CBT, on the other hand, reduced total awake time by 52%, improved sleep efficiency, and increased slow-wave sleep. At 6 months, sleep efficiency was still improved with CBT.

The limitation of this last study was that it consisted of 44 older subjects using zopiclone (not available in the United States). Zopiclone is a racemic mixture of an inactive and an active isomer with the active isomer equivalent to eszopiclone. Furthermore, the dose used was slightly higher than the maximal recommended dose of eszopiclone.

Efficacy of combined CBT and sedative-hypnotics

Several studies have demonstrated that after 10-24 months follow-up, the CBT group demonstrated sustained benefit that was not seen in the combined CBT-hypnotic group. This could be due to patients being less willing to practice CBT techniques during the initial phase if they have obtained rapid, short-term improvement of sleep with a sedative-hypnotic. In this regard, many sleep experts feel that CBT should be considered as initial therapy for primary insomnia and adjunctive therapy for secondary insomnia.

CBT and hypnotic medications are efficacious for short-term treatment of insomnia, but few patients achieve complete remission with any single treatment. Morin et al studied 160 adults with persistent insomnia and demonstrated that CBT used singly or in combination with zolpidem produced significant improvements in sleep latency, time awake after sleep onset, and sleep efficiency during initial therapy. Combined therapy produced a higher remission rate compared with CBT alone during the 6-month extended therapy phase and the 6-month follow-up period (56% vs 43%). Long-term outcome was optimized when medication was discontinued during maintenance CBT.[60]

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Pharmacologic Treatment of Insomnia

The pharmacologic treatment of insomnia has made great advances in the last 2 decades. In the early 19th century, alcohol and opioids were used as sleeping medications. In the late 19th century, chloral hydrate was used (and misused, in combination with alcohol, as “knockout drops” or a “Mickey Finn”). Barbiturates were used from the early 20th century until the early 1960s, when benzodiazepine receptor agonists (BZRAs) were first FDA-approved for the treatment of insomnia (ie, flurazepam and quazepam).

BZRAs include long-acting (flurazepam, quazepam), intermediate-acting (temazepam, estazolam), and short-acting forms (triazolam). The long-acting agents are rarely used today for insomnia because of daytime sedation, cognitive impairment, and increased risk for falls in elderly patients.

BZRAs were commonly used until the 1980s, when concerns about tolerance, dependence, and daytime side effects were recognized as major limitations of these agents, particularly those with long elimination half-lives. Temazepam is still used for a short-term course (ie, days to 1-2 w).

In the 1990s, antidepressants were widely used for primary insomnia, and they continue to be widely used, despite the fact that no randomized controlled trials have demonstrated their efficacy in treating primary insomnia.

At present, sedative-hypnotics remain the most commonly prescribed sleep medications.

Sedative-hypnotic drugs

Sedative-hypnotic medications do not cure insomnia, but they can provide symptomatic relief as sole therapy or as an adjunct with CBT. Furthermore, some patients cannot adhere or do not respond to CBT and are candidates for these agents, particularly benzodiazepine receptor agonist (BzRAs).

The most appropriate use of BzRA drugs is for transient and short-term insomnia in combination with nonpharmacologic treatment. Most authorities now agree that they should infrequently be the only therapy for chronic insomnia.

In the past, most studies of the efficacy of sedative-hypnotics had been short-term trials, generally less than 4 weeks. Use for longer than 4 weeks was thought to result in tolerance and decreased efficacy, although supportive findings are scarce, and epidemiologic literature suggests that patients report continued efficacy with continued use. Nevertheless, because of the addictive nature of benzodiazepines, most authorities believe that the duration of use of these drugs should be limited.

Studies have indicated, however, that BzRAs have long-term efficacy for 6-12 months without the development of tolerance. Eszopiclone was the first sedative-hypnotic to be tested over a 6-month period.[61] This study showed continued efficacy over the 6-month period. A subsequent multicenter, randomized, placebo-controlled trial of long-term (6 mo) eszopiclone showed improved quality of life, reduced work limitations, and reduced global insomnia severity.[62] Another study demonstrated continued efficacy at 12 months.[63]

Eszopiclone and zolpidem are believed to be less habit-forming than benzodiazepines and, therefore, represent important advances in the long-term treatment of chronic insomnia.

Krystal et al showed long-term efficacy and safety of sustained-release zolpidem (Ambien-CR) for 6 months in a double-blind, placebo-controlled trial.[64]

Zolpidem can be dosed at 5 or 10 mg at bedtime for sleep-onset insomnia, and zolpidem-controlled release at doses of 6.25 mg or 12.5 mg can be used for patients with sleep maintenance insomnia or patients with both sleep onset and maintenance insomnia.

Eszopiclone has a half-life of 5-7 hours and can be used for sleep-maintenance insomnia. It can be used starting with either a 2 mg or 3 mg dose at bedtime or a 1 mg starting dose in elderly or debilitated patients.

Zaleplon has a very short half-life of 1 hour and is indicated for sleep-onset insomnia at doses ranging from 5-20 mg. It can also be used for sleep-maintenance insomnia if taken at the time of awakening during the night. However, the patient should allow at least 4 hours for remaining sleep to avoid possible daytime sedation.

Intermediate-acting benzodiazepines, such as temazepam, are still sometimes used in a short course at a dose of 15-30 mg at bedtime.

The following general precautions should be taken when using sedative-hypnotics:

  • Therapy should be instituted with a low dose and maintained at the lowest effective dose
  • Continued nightly use should be avoided; patients should be encouraged to use them only when truly necessary.
  • Use for more than 2-4 weeks should be avoided if possible.
  • Long-term hypnotic pharmacotherapy may be necessary in patients with severe or treatment-resistant insomnia or chronic comorbid disorders but must include regular assessment of necessity, efficacy, and adverse effects.[3]
  • Long-term administration of hypnotics may be intermittent, as needed, or nightly.[3]
  • If possible, during long-term therapy, patients should receive an adequate trial of CBT.[3]
  • Counsel patients to allow for at least 8 hours of sleep.
  • A hypnotic free of residual effects in the morning is preferable (eg, zolpidem, zaleplon).
  • Hypnotics with a rapid onset of action, such as zolpidem or zaleplon, are preferable when the problem is falling asleep.
  • If the problem is staying asleep, a hypnotic with a slower rate of elimination may be more appropriate (eg, temazepam, estazolam, flurazepam).
  • If the patient is depressed, an antidepressant with sedative properties, such as trazodone, mirtazapine, or amitriptyline, may be preferable to a hypnotic.
  • Hypnotics should never be used with alcohol.
  • In general, pregnancy is a contraindication.
  • Benzodiazepines should be avoided in patients with known or possible sleep apnea.
  • Lower doses should be used in elderly patients.

Use with caution in patients with a history of insufficient sleep syndrome, particularly in patients prone to alcohol use, since this group can be predisposed to the development of parasomnias (eg, sleep-walking or sleep-related eating disorder[65, 66] )

  • In most patients, the risk of dependency is low (most rarely escalate the dose or use more frequently than prescribed); however, sedative-hypnotics use should be avoided in patients with a history of substance abuse.

Rebound insomnia may develop when a sedative-hypnotic is abruptly withdrawn. This is more likely to occur with larger doses and with the short-acting agents. Using smaller doses and tapering the drug can avoid rebound insomnia. The 2008 AASM guideline states that these measures are aided by concurrent CBT-I.[3]

Ramelteon

Ramelteon (Rozerem), a melatonin receptor agonist, has been approved by the US Food and Drug Administration (FDA) for use in persons with insomnia. It has been shown to have no potential for abuse and, as such, is the first nonscheduled prescription drug available in the United States for the treatment of insomnia.

Ramelteon is a specific melatonin receptor agonist that binds to the melatonin MT1 and MT2 receptors. It has a half-life of 1-3 hours. The MT1 receptor attenuates the alerting signal of the suprachiasmatic nucleus (SCN) clock and the MT2 receptor phase shifts (advances) the SCN clock to promote sleep.

Controlled trials have shown a decrease in sleep latency, but no change in wake time after sleep onset and no next-morning residual effects.[67] Additionally, studies thus far on elderly patients have shown no impairment in night balance, mobility, or memory compared with placebo.[68]

This medication is suited for patients with sleep-onset insomnia, and particularly for elderly patients with gait disorders who have an increased fall risk and in patients with a history of substance abuse. The typical starting dose is 8 mg prior to bedtime. Ramelteon is not effective for sleep-maintenance insomnia.

Sedating antidepressants

Although there is a paucity of clinical data on the use of sedating antidepressants for the treatment of primary insomnia without mood disorders, these agents are still sometimes used. Many clinicians believe that sedating antidepressants have fewer adverse effects than NBZRAs; however, this is not the case.

Sedating tricyclic antidepressants, such as amitriptyline, nortriptyline, and doxepin and the tetracyclic drug mirtazapine have been used. Tricyclic drugs and mirtazapine can cause daytime sedation, weight gain, dry mouth, postural hypotension, and cardiac arrhythmias. Trazodone can cause priapism in men, daytime sedation, and hypotension.

Antihistamines

Antihistamines are the major ingredient of over-the-counter (OTC) sleep aids and are the ingredient in cold and sinus formulas sold as bedtime-use medications. Nevertheless, common antihistamines (ie, first-generation H1-receptor antagonists such as diphenhydramine, hydroxyzine, and doxylamine) are not indicated for the treatment of sleeplessness.

While H1 antihistamines have sedative effects in healthy individuals, no study has established an effective dose range for these agents’ hypnotic effect in patients with insomnia. These agents may have some subjective benefit, but long-term efficacy and safety have not been demonstrated. Thus, their regular use in individuals with insomnia is not advised.[3]

Melatonin

Melatonin has also become a popular OTC sleep aid. Melatonin is a naturally occurring hormone secreted by the pineal gland. The concentration of melatonin is highest in the blood during normal times of sleep and lowest during normal times of wakefulness. The general consensus is that melatonin given during normal waking hours has hypnotic properties.

However, the timing of evening administration is critical as to whether a hypnotic effect occurs. Melatonin given early in the evening appears to increase sleep time; however, administration 30 minutes before a normal bedtime has not resulted in a decreased sleep latency or an increase in sleep time.

Most studies of melatonin have been small and of limited duration, and the results have conflicted somewhat with several studies that have shown limited or no effect.[12] Most of the data, however, seem to suggest that melatonin taken before bedtime decreases sleep latency and may increase total sleep time[69, 70] and entrain irregular circadian rhythms.

Studies of melatonin in individuals with chronic insomnia have not demonstrated objective changes in patient sleep habits or changes in mood or alertness the day after treatment. In addition, a dose-response relationship has not been determined. OTC melatonin is also sold at doses much higher than those that naturally occur in the blood. The 2008 AASM guideline notes a relative lack of safety data as well as efficacy data and, therefore, states that melatonin is not recommended for the treatment of chronic insomnia.[3]

Alternative and herbal medications

Alternative and herbal medications have also been tried in the treatment of insomnia. Among the most widely used and studied of these is valerian root extract. A 2006 meta-analysis of 16 randomized controlled trials of valerian for the treatment of insomnia had conflicting results.[71] The pooled data did seem to show evidence of improved sleep; however, the authors noted a possible publication bias that may have contributed to this result.

Other herbal remedies, such as chamomile and St. Johns Wort, have also not shown efficacy for insomnia. Furthermore, potential risks have been associated with the use of some OTC remedies such as dogwood, kava kava, alcohol, and l-tryptophan.[72] For these reasons, the 2008 AASM guideline states that valerian and other alternative or herbal medications are not recommended for treatment of chronic insomnia.[3]

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Acupressure for Insomnia

A longitudinal study by Sun et al found that acupressure treatment can improve insomnia, with effects lasting after the end of intervention. In a randomized controlled trial in 50 residents in long-term care facilities, 5 weeks of standard acupressure on the HT7 (Shenmen) points of both wrists significantly reduced insomnia, with the benefit persisting for up to 2 weeks afterward.[73]

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Dietary Modification to Manage Insomnia

Avoid caffeinated beverages in the late afternoon or evening, since the stimulant activity of adenosine antagonism can promote hyperarousal.

Avoid alcohol in the evening since this can worsen sleep-disordered breathing leading to frequent arousals. Furthermore, while alcohol promotes sleep early in the night, it leads to more sleep disruption later in the evening.

Avoid large meals near bedtime, particularly in patients with gastroesophageal reflux disease or delayed gastric emptying.

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Activity

Exercise in the late afternoon or early evening (at least 6 hours before bedtime) can promote sleep. However, vigorous physical activity in the late evening (< 6 hours before bedtime) can worsen insomnia.

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Treatment of Insomnia in Elderly Patients

The satisfaction of sleep declines with age. This probably is related to changes in sleep associated with age, such as a decrease in slow-wave sleep, increased time awake after sleep onset, and a tendency to go to bed early and rise early. Although napping is highly prevalent among elderly persons, it has not been consistently correlated with sleep disturbance.[74]

However, aging should not be assumed to be the explanation for insomnia.[75] Multiple factors affect sleep in the elderly, including nocturia, pain syndromes, and many medical disorders (eg, heart failure, COPD, Parkinson disease). Other factors include restless legs syndrome, periodic leg movement disorder, sleep apnea (all of which have increased frequency in the elderly), dementia, and, frequently, changing situational factors such as retirement, bereavement, or financial difficulties, which lead to anxiety and depression.[76]

As in younger patients, nonpharmacologic treatment should take precedence over pharmacologic treatment. Psychological and behavioral interventions are effective in older adults, according to the 2008 AASM guideline.[3]

Hypnotics should be prescribed cautiously and in lower doses than for younger patients. Drugs tend to have longer duration of effect due to changes in metabolism and elimination. This can lead to increased incidence of falls and resulting bone fractures at night (if the patient gets up to use the bathroom when not fully awake or ataxic) and decrements in daytime alertness and performance (including increased incidence of motor vehicle accidents).

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Consultations

Primary care physicians should be able to diagnose and treat transient or short-term insomnia. Chronic insomnia is often more difficult to treat and when primary or associated with a sleep or psychiatric disorder, referral to a specialist may be indicated. Patients with comorbid medical conditions may benefit from referral to the appropriate specialist.

Patients should be referred to a sleep specialist in the following cases:

  • If the history suggests obstructive sleep apnea or restless legs syndrome/periodic leg movement disorder
  • In cases of primary insomnia, particularly if it is psychophysiologic insomnia and of long duration
  • The patient requires daily or near-daily sedative-hypnotics for insomnia for 30 days or more

Many sleep centers have a staff psychologist who specializes in treating insomnia. The advantages include experience in cognitive-behavioral techniques and providing sleep education, greater available time for the often-frequent follow-up that is needed, and the ability to ascertain whether other psychological factors are present that may need further evaluation by a psychiatrist.

Patients with a history of depression should be treated with an antidepressant or referred to a psychiatrist, based on the physician's comfort level in treating depression, the severity of depression, and the response to therapy. In addition, patients with a history of substance abuse or another major psychiatric disorder should also be referred to a psychiatrist.

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Contributor Information and Disclosures
Author

Ron A Shatzmiller, MD, MSc  Assistant Clinical Professor, Department of Neurology, Keck School of Medicine of the University of Southern California; Specialty Lead Physician, Healthcare Partners Medical Group, Arcadia, California

Ron A Shatzmiller, MD, MSc is a member of the following medical societies: American Academy of Neurology and American Academy of Sleep Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Erasmo A Passaro, MD, FAAN  Director, Comprehensive Epilepsy Program/Clinical Neurophysiology Lab, Bayfront Medical Center, Florida Center for Neurology

Erasmo A Passaro, MD, FAAN is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association, and American Society of Neuroimaging

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; UCB Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching; Forest Honoraria Speaking and teaching

Chief Editor

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Additional Contributors

Carmel Armon, MD, MSc, MHS Professor of Neurology, Tufts University School of Medicine; Chief, Division of Neurology, Baystate Medical Center

Carmel Armon, MD, MSc, MHS is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, American College of Physicians, American Epilepsy Society, American Medical Association, American Neurological Association, American Stroke Association, Massachusetts Medical Society, Movement Disorders Society, and Sigma Xi

Disclosure: Avanir Pharmaceuticals Consulting fee Consulting

Kendra Becker, MD, MPH Sleep Medicine Department, Kaiser Permanente Fontana Medical Center

Kendra Becker, MD, MPH is a member of the following medical societies: American Academy of Sleep Medicine, American College of Physicians, and American Medical Association

Disclosure: Nothing to disclose.

Jose E Cavazos, MD, PhD, FAAN Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director of the San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and American Neurological Association

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device. No conflict with any of the eMedicine articles that I wrote or edited.

Zab Mosenifar, MD Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Consulting Staff, Pulmonary Disease and Critical Care Medicine Service, Henry Ford Health System

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

James A Rowley, MD Professor, Fellowship Program Director, Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine

James A Rowley, MD is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Silverio M Santiago, MD Clinical Professor of Medicine, University of California at Los Angeles School of Medicine; Chief, Department of Pulmonary and Critical Care Medicine, Medical Director, Sleep Disorders Center, Veterans Affairs Medical Center of West Los Angeles

Silverio M Santiago, MD is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Peter Smethurst, MD Attending Physician, Pulmonary, Critical Care and Sleep Medicine, St Joseph's Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Gregory Tino, MD Director of Pulmonary Outpatient Practices, Associate Professor, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care, University of Pennsylvania Medical Center and Hospital

Gregory Tino, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

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Theoretical model of the factors causing chronic insomnia. Chronic insomnia is believed to primarily occur in patients with predisposing or constitutional factors. These factors may cause the occasional night of poor sleep but not chronic insomnia. A precipitating factor, such as a major life event, causes the patient to have acute insomnia. If poor sleep habits or other perpetuating factors occur in the following weeks to months, chronic insomnia develops despite the removal of the precipitating factor. Adapted from Spielman AJ, Caruso LS, Glovinsky PB: A behavioral perspective on insomnia treatment. Psychiatr Clin North Am. 1987 Dec;10(4):541-53.
Mallampati airway scoring.
Diagnostic algorithm for major depression.
Diagnostic criteria for generalized anxiety disorder.
Sleep diary.
GABAA receptor subunit function(s).
GABAA receptor complex subunits and schematic representation of agonist binding sites.
Sleep-wake cycle.
The ascending arousal system. Adapted from Saper et al. Hypothalamic Regulation of Sleep and Circadian Rhythms. Nature 2005;437:1257-1263.
Ventrolateral pre-optic nucleus inhibitory projections to main components of the arousal system to promote sleep.
Schematic flip-flop switch model. Adapted from Saper C et al. Hypothalamic regulation of sleep and circadian rhythms. Nature 2005;437:1257-1263.
Epworth Sleepiness Scale.
Frequency of insomnia causes.
 
 
 
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