Primary Insomnia 

Primary Insomnia 

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Primary insomnia is sleeplessness that is not attributable to a medical, psychiatric, or environmental cause. Below are the diagnostic criteria for primary insomnia as set forth by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).

The predominant symptom according to the DSM-IV-TR is difficulty initiating or maintaining sleep, or suffering from nonrestorative sleep, for at least 1 month.

The second criterion is that the sleep disturbance (or associated daytime fatigue) causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

The third criterion is that the sleep disturbance not occur exclusively during the course of narcolepsy, breathing-related sleep disorder, circadian rhythm sleep disorder, or a parasomnia.

The fourth criterion is that the disturbance not occur exclusively during the course of another mental disorder (eg, major depressive disorder, generalized anxiety disorder, a delirium).

Finally, the fifth criterion is that the disturbance not be due to the direct physiological effects of a substance (eg, drug abuse, medication) or a general medical condition. [1]

The International Classification of Sleep Disorders (ICSD-2) diagnostic and coding manual consists of 3 primary insomnia categories:

Psychophysiological insomnia

Idiopathic insomnia

Paradoxical insomnia [2, 3]

The pathophysiology of primary insomnia is not well understood, and essential features assist in diagnosis. The focus of management is on symptoms. [4]

However, findings have strengthened the evidence that primary insomnia may be linked with mood disorders and is associated with hypothalamic-pituitary-adrenal (HPA) axis overactivity and excess secretion of corticotropin-releasing factor (CRF), adrenocorticotropin-releasing hormone, and cortisol.

The goal of insomnia management is to improve sleep quality and maintenance and limit daytime impairments. [5, 6, 7]

Inpatient care is not usually required for primary insomnia unless significant medical or psychiatric comorbidity exists.

Sleep disturbance is a reliable indicator of psychological and/or physical ill health. A report of disturbed sleep from the patient signals the need for further evaluation and close monitoring.

Go to Insomnia for more complete information on this topic.

The essential features of psychophysiologic insomnia include learned or behavioral insomnia and heightened arousal.

The primary components involved are intermittent periods of stress that result in poor sleep and maladaptive behaviors. These include (1) a vicious cycle of trying harder to sleep and becoming more tense (ie, patients “trying too hard to sleep”) and (2) bedroom habits and routines (eg, brushing teeth) that actually condition the patient to become frustrated and aroused. Patients often report “racing thoughts” and sensitivity to their environment.

Bad sleep habits, such as those naturally acquired during periods of stress, are occasionally reinforced. These are therefore not resolved and become persistent. Insomnia continues for years after the stress has abated, and is labeled persistent psychophysiologic insomnia.

The essential feature of idiopathic insomnia is lifelong sleeplessness, with onset in infancy or childhood. Idiopathic insomnia can be aggravated by stress or tension.

Lifelong sleeplessness is attributed to an abnormality in the neurologic control of the sleep-wake cycle for many areas of the reticular activating system (which promotes wakefulness), as well as in areas such as supra nuclei, raphe nuclei, and medial forebrain areas (which promote sleep).

Possibly, a so-called neuroanatomic, neurophysiologic, or neurochemical lesion exists in the sleep state, with patients tending to be on the extreme end of the spectrum toward arousal.

Paradoxical insomnia is also called sleep state misperception. [8] The essential feature is reports of severe insomnia without supporting objective evidence, such as daytime sleepiness.

Primary insomnia is diagnosed in approximately 15-25% of patients with insomnia who are referred to sleep disorder centers following exclusion of other predisposing conditions. However, the true incidence is not known. Primary insomnia is estimated to occur in 25% of all patients with chronic insomnia.

Whether the consequences associated with chronic insomnia outweigh the costs of treatment remains debatable. Despite that, various health-related associations with chronic insomnia have been noted.

Poor health and decreased activity occur in persons with chronic insomnia. Moreover, insomnia is the best predictor of the future development of depression.

An increased risk of mortality is associated with short sleep lengths. (Eg, the onset of insomnia in older patients is related to decreased survival.)

Catastrophic worry about the consequences of not sleeping is common among patients with chronic insomnia and serves to maintain the sleep disturbance.

In persons with chronic insomnia, there is an increased risk for the development of anxiety, alcohol and drug use disorders, and nicotine dependence.

Primary insomnia is more common in women than in men.

Persons of any age may be affected, although primary insomnia is more common in the older population. [9, 10, 11, 12, 13]

A thorough clinical interview with the patient and his or her sleep partner is critical in making the correct diagnosis of primary insomnia.

Sleep disturbance in these patients ranges from mild to severe. Insomnia may manifest as difficulty falling asleep or as frequent nocturnal awakenings.

Patients often find that they can sleep well anywhere else but in their own bedroom.

Patients with this type of insomnia tend to be more tense and dissatisfied compared to people who sleep well. Emotionally, they typically are repressors, denying problems.

In patients with this condition, the insomnia is long-standing, typically beginning in early childhood.

Patients often present with other hard-to-localize neurologic signs and symptoms, such as difficulty with attention or concentration, hyperactivity, and mild, nonfocal electroencephalographic abnormalities.

Emotionally, persons with childhood-onset insomnia are often repressors, denying and minimizing emotional problems. These individuals often show atypical reactions, such as hypersensitivity or insensitivity, to medications.

Patients report insomnia subjectively, while sleep duration and quality are completely normal.

Physical characteristics that indicate sleep deprivation and fatigue can include features such as eye redness. Depending on the origin of the sleep dysfunction, other physical findings would be included to rule out secondary causes (ie, weight, neck circumference, thyroid).

A complete neurologic examination is included in the evaluation of insomnia, to assess for comorbid conditions. Recognition of mental disorders that may be contributing to insomnia is key to effectively managing symptoms. [14]

When performing a complete Mental Status Examination, drowsiness and mood changes, such as irritability, anxiety, and sad feelings from underlying depression, may be noted. The clinician should also note the patient’s orientation, memory, judgment, insight, and the presence of any hallucinations or delusions. [15]

As with any mental status (but especially with the concern about depression), assess the patient’s suicide potential. For completeness, assess the patient’s homicidal potential as well.

The exclusion of common causes of insomnia is required to make the diagnosis of primary insomnia.

Medical causes of insomnia include the following:

Chronic pain, especially neuropathic pain

Primary sleep disorders (eg, sleep apnea, periodic limb movements, restless legs syndrome)

Dyspnea from any cause

Pregnancy

Drug use or withdrawal (eg, selective serotonin reuptake inhibitors, stimulants, antihistamines, caffeine, diet pills, herbal preparations containing ma huang, anticonvulsants, steroids)

Psychiatric and/or psychological causes of insomnia include the following:

Anxiety disorders (eg, generalized anxiety, panic attacks, obsessive-compulsive disorder)

Substance abuse (eg, alcohol or sedative/hypnotic withdrawal)

Major life stressors and/or events

Mood disorders (eg, depression, mania)

Environmental causes of insomnia include the following:

Noise

Jet lag or shift work

Bedroom too hot or cold

Symptoms of the following conditions can mimic those of primary insomnia:

Adjustment Disorders

Alcohol-Related Psychosis

Amphetamine Abuse

Anxiety Disorders

Apnea, Sleep

Bipolar Affective Disorder

Caffeine-Related Psychiatric Disorders

Circadian rhythm sleep disorder

Cocaine-Related Psychiatric Disorders

Depression

Hyperthyroidism

Obstructive Sleep Apnea-Hypopnea Syndrome

Parasomnias

Postpartum Depression

Posttraumatic Stress Disorder

Schizophrenia

Substance abuse can cause insomnia during the intoxication phase, during the sustained use phase, and during withdrawal.

Laboratory studies essentially are not required for the diagnosis of primary insomnia. However, tests are required to exclude other causes of insomnia, including the following:

Thyroid function tests (hyperthyroidism)

Blood alcohol levels (alcohol-related psychosis)

Neuroimaging studies may be helpful if a structural lesion is suspected to cause insomnia.

This is a questionnaire (shown below) completed by the patient each morning to describe the previous night’s sleep.

Data from the sleep diary may help to minimize distortions in sleep information recalled in the physician’s office.

This technique makes use of an activity monitor to record activities during sleep and waking. It is useful in the diagnosis of circadian rhythm sleep disorders, sleep state misperception, and other types of primary insomnia. In older adults treated for chronic primary insomnia, the clinical use of actigraphy is still suboptimal in detecting wakefulness. [16]

Full-night polysomnography (PSG) is indicated when suspicion of sleep apnea or movement disorders arises, when initial diagnosis is uncertain, when treatment fails, or when precipitous arousal occurs with violent or injurious behavior. [17, 18, 19, 16, 20]

Psychophysiologic insomnia and idiopathic insomnia manifest as increased sleep latency, reduced sleep efficiency, and an increase in the number and duration of awakenings.

Sleep state misperception manifests as normal sleep latency (15-20 min), normal number of arousals and awakenings, and normal sleep duration (6.5 h). The multiple sleep latency test shows normal daytime vigilance. Sleep state misperception can be diagnosed only in the laboratory because of the need to document that sleep duration and quality are normal when a person claims to have poor sleep.

The active agent in many over-the-counter medications is one of the sedating antihistamines. These medications are generally safe but have anticholinergic adverse effects, such as dry mouth, blurred vision, urinary retention, and confusion in older patients, that can be potentially more serious in patients with dental caries, glaucoma, prostatic enlargement, and dementia (or delirium), respectively.

These medications are minimally effective in inducing sleep and may reduce sleep quality. Discourage patients from using them on a routine basis.

The use of various herbal preparations (eg, herbal tea) and nutritional substances are reported to be beneficial by users, but no supporting trials have been performed.

Studies have shown that melatonin may be useful for short-term adaptation to jet lag or other circadian rhythm sleep disorders. [21]

One study showed that ramelteon, a highly selective agonist for melatonin subtypes 1 and 2 receptors, is a good option for the treatment of insomnia characterized by difficulty falling asleep. In patients with insomnia, treatment with ramelteon was generally well tolerated and resulted in modest, but statistically significant, decreases in the latent period for sleep. [22] Ramelteon was the first melatonin receptor agonist drug to have been approved by the US Food and Drug Administration (FDA). [23]

Patients need to be observed closely and have regular follow-up visits to review their response to and any adverse effects from drugs used to treat insomnia.

The American Academy of Sleep Medicine guidelines include the following recommendations for the pharmacologic management of primary insomnia, listed in the following preferred medication sequence: [17]

Short- or intermediate-acting benzodiazepine receptor agonists (BzRAs), whether a benzodiazepine such as temazepam or a newer BzRA, such as zolpidem, eszopiclone, or zaleplon

Other short- or intermediate-acting BzRAs or ramelteon if the initial agent was unsuccessful

Sedating low-dose antidepressant, such as trazodone, nefazodone, amitriptyline, doxepin, and mirtazapine, [24] especially in patients with depression or anxiety

Combination BzRA or ramelteon and sedating antidepressant

Amitriptyline should not be used in older patients because of a high anticholinergic side-effect profile.

According to evidence-based recommendations on sleep disorders in older persons published in the Journal of American Geriatrics Society in 2009, clinically significant adverse effects can be associated with all FDA-approved medications for the treatment of insomnia (evidence level A), and the safest and most effective medications currently available are nonbenzodiazepines and melatonin receptor agonists (evidence level B or moderate). [25, 23] Prescriptions not recommended include the following: [17]

Chloral hydrate, barbiturates, and nonbarbiturate nonbenzodiazepine drugs (ie, meprobamate), due to significant adverse effects and tolerance

Off-label use of antiepileptic (gabapentin, tiagabine) and atypical antipsychotics (quetiapine, olanzapine)

Regarding the above recommendation against the off-label use of antiepileptic and atypical antipsychotic drugs, there is Insufficient evidence of efficacy when these agents are used alone, and adverse effects can occur. They may be considered for patients with comorbid conditions and insomnia.

Lower zolpidem doses were recommended by the FDA in January 2013, owing to the risk of next-morning mental impairment. Data show that zolpidem blood levels may remain high enough the morning after nighttime usage to impair activities that require alertness, including driving. This next-morning impairment is highest for the controlled-release dosage form and is more prevalent in women because of their slower elimination compared with men. The revised labeling recommends a 5-mg dose for women for immediate-release products (Ambien, Edluar, and ZolpiMist) and 6.25 mg for extended-release products (Ambien CR). The recommendations also urge prescribers to consider lower doses in men. [26]

In May 2014, the recommended dose for eszopiclone (Lunesta) was lowered to 1 mg at bedtime for nonelderly and elderly adults because of next day drowsiness. [27]

Basic principles for the rational treatment of insomnia are to use the lowest effective dose, use intermittent dosing (2-3 nights/wk), use short term (2-3 wk at a time), discontinue after slow taper if the patient has been taking it regularly, and use agents with short and/or intermediate half-life to minimize daytime sedation. (See the table below.)

Pharmacokinetic properties and risk-benefit ratio are the key factors in selecting the most appropriate medication. [28]

Table 1. FDA-Approved Hypnotics for Insomnia (Open Table in a new window)

Duration

Agent

Trade Name

Dose

Half-life

Comments

Benzodiazepine

Long acting

Flurazepam

Dalmane

15-30 mg

48-120 h

Do not use in older adults due to long half-life

Quazepam

Doral

7.5-15 mg

41 h

Do not use in older adults due to long half-life

Intermediate acting

Estazolam

ProSom

1-2 mg

10-24 h

Sleep maintenance

Temazepam

Restoril

7.5-30 mg

3.5-18 h

Sleep maintenance

Lorazepam*

Ativan

0.5-4 mg; 1 mg in elderly

12-20 h

May be used if duration of action meets patients needs

Short acting

Triazolam

Halcion

0.125-0.5 mg

1.5-5.5 h

Caution, rebound anxiety; not first-line agent

Nonbenzodiazepine

Intermediate acting

Eszopiclone

Lunesta

1 mg starting dose; may increase to 2-3 mg in nonelderly adults or 2 mg or elderly/debilitated patients

6 h

Sleep onset and maintenance

Short-to-intermediate

Zolpidem

Ambien

Women: 5 mg

Men: 10 mg; consider lower dose

5 mg in elderly or hepatic impairment

2.5 h

Primary use, sleep onset

Zolpidem ER

Ambien CR

Women: 6.25 mg

Men: 12.5 mg; consider lower dose

6.25 mg in elderly or hepatic impairment

2.8 h

Primary use, sleep onset and maintenance

Zolpidem

Intermezzo

Women: 1.75 mg SL prn

Men: 3.5 mg SL prn

1.75 mg with hepatic impairment

2.5 h

Middle of night awakening

Short acting

Zaleplon

Sonata

10 mg, 5 mg in elderly or hepatic impairment or use with cimetidine

0.9-1 h

Primary use, sleep onset; maintenance up to 4 h

Orexin Receptor Antagonist

Intermediate acting

Suvorexant

Belsomra

10 mg; if tolerated but not effective, may increase not to exceed 20 mg

12 h

Sleep onset and maintenance

Melatonin Receptor Agonist

Short acting

Ramelteon

Rozerem

8 mg

1-2.6 h

Primary use, sleep onset

* Not FDA approved for sleep

Anterograde amnesia and withdrawal effects may occur, especially with short-acting BZD (not with zolpidem and zaleplon).

Residual daytime sedation with intermediate-acting and long-acting drugs may occur, depending on dosage and half-life.

Rebound insomnia may occur with short-acting and intermediate-acting BZD after discontinuation.

A small study conducted in The Netherlands to evaluate the next-morning residual effects of ramelteon (8 mg) and zopiclone (7.5 mg) found that driving, cognitive, memory, and psychomotor performance were significantly impaired the morning following bedtime administration in healthy volunteers. However, when compared with zoplicone, ramelteon produced no balance impairments. Further research is required to replicate this finding, especially in subjects suffering from insomnia. [29]

Dosage, pharmacokinetic properties, and risk-benefit ratio are the key factors in selecting the most appropriate medication.

Short-acting agents are recommended for patients with difficulty falling asleep, while intermediate-acting drugs are indicated for problems with sleep maintenance.

Avoid long-acting agents, especially in older people, because they cause daytime sedation and impair cognition, thereby increasing the risk of falls.

Caution and close monitoring is needed in the administration of hypnotics to older people and to patients with hepatic, renal, or pulmonary disease.

Contraindications of these agents are as follows:

Pregnancy

Untreated obstructive sleep apnea

History of substance abuse

New experimental drugs have been under investigation as possible insomnia treatments. [30, 31]

For example, initial studies of indiplon showed significant improvement in subjective measures of sleep induction and maintenance in elderly women with chronic insomnia, at a dose of 5-10 mg. Indiplon is a unique nonbenzodiazepine experimental drug that acts on a specific site of the gamma-aminobutyric acid (GABA)-A receptor. [32, 33]

A randomized, double-blind, placebo-controlled trial using low-dose doxepin for elderly patients with primary insomnia revealed improved sleep maintenance and some effect on sleep onset, at doses of 1 mg, 3 mg and 6 mg, with no anticholinergic side effects. Doxepin is a histamine-H(1) antagonist. [34]

Psychological treatment for insomnia consists primarily of patient education and short-term cognitive-behavioral therapies. The focus is primarily on sleep hygiene or factors presumed to perpetuate insomnia. These therapies seek to modify maladaptive sleep habits and to educate patients about healthier sleep practices. [35]

The purpose of this treatment is to reestablish the connection between the bed and sleep by prohibiting the patient from engaging in nonsleep activities while in bed. The instructions given to the patient are (1) to go to bed only when sleepy, (2) to use the bed and bedroom only for sleep and intimacy, (3) to avoid trying to force sleep (go into another room whenever unable to fall asleep within 20-30 min and return to bed only when sleepy again), (4) to get up at the same time each morning regardless of how much the patient slept the previous night, and (5) to avoid daytime napping.

This involves limiting the amount of time the patient spends in bed to the actual amount of time the patient usually spends sleeping. This results in sleep deprivation, which accumulates and causes more rapid sleep onset on subsequent nights. As sleep improves, the patient is allowed to gradually increase time in bed by 15-30 minutes.

Relaxation-based interventions are indicated based on the observation that patients with insomnia often display high levels of arousal (physiologic and cognitive) at night and during the daytime. The various techniques available to deactivate the arousal system are (1) progressive muscle relaxation, (2) biofeedback, and (3) imagery training and thought stopping.

Cognitive behavior therapy (CBT) consists of identifying patient-specific dysfunctional sleep cognitions, challenging their validity, and replacing them with more adaptive substitutes, such as reattribution training, reappraisal, and attention shifting.

A randomized clinical trial determined that 4 individual, biweekly sessions represent the optimal dosing for cognitive behavioral intervention. [36]

This method consists of persuading a patient to engage in his or her most feared behavior (ie, staying awake). This serves to eliminate performance anxiety so that sleep may come more easily.

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% [43/74 and 32/59] vs 43% [34/75 and 28/68]). The long-term outcome was optimized when medication was discontinued during maintenance CBT. [37]

Consultation with a sleep disorders specialist may be necessary if the standard pharmacologic and behavioral treatments are not effective.

The following sleep hygiene recommendations, which include environmental and lifestyle modifications, should be used as an adjunct to other forms of therapy:

Elimination of the use of caffeine, especially after noon

No tobacco or alcohol use near bedtime

Avoidance of heavy meals close to bedtime (may eat a light snack at bedtime)

Engagement in exercise early in the day before dinner to alleviate stress, but not before bedtime

Avoidance of daytime naps and establishment of a regular schedule for going to bed and getting up

Maintenance of the bedroom at a comfortable temperature, and minimization of light and noise

Family education and patient self-help information are also important. Resources on sleep disorders can be found at the National Sleep Foundation Web site.

For patient education information, see eMedicineHealth’s Mental Health Center and Sleep Disorders Center.

Also, see eMedicineHealth’s patient education articles Primary Insomnia, Insomnia, Disorders That Disrupt Sleep (Parasomnias), Insomnia Medications, Sleep Disorders in Women, Sleep Disorders and Aging, and Sleeplessness and Circadian Rhythm Disorder.

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Duration

Agent

Trade Name

Dose

Half-life

Comments

Benzodiazepine

Long acting

Flurazepam

Dalmane

15-30 mg

48-120 h

Do not use in older adults due to long half-life

Quazepam

Doral

7.5-15 mg

41 h

Do not use in older adults due to long half-life

Intermediate acting

Estazolam

ProSom

1-2 mg

10-24 h

Sleep maintenance

Temazepam

Restoril

7.5-30 mg

3.5-18 h

Sleep maintenance

Lorazepam*

Ativan

0.5-4 mg; 1 mg in elderly

12-20 h

May be used if duration of action meets patients needs

Short acting

Triazolam

Halcion

0.125-0.5 mg

1.5-5.5 h

Caution, rebound anxiety; not first-line agent

Nonbenzodiazepine

Intermediate acting

Eszopiclone

Lunesta

1 mg starting dose; may increase to 2-3 mg in nonelderly adults or 2 mg or elderly/debilitated patients

6 h

Sleep onset and maintenance

Short-to-intermediate

Zolpidem

Ambien

Women: 5 mg

Men: 10 mg; consider lower dose

5 mg in elderly or hepatic impairment

2.5 h

Primary use, sleep onset

Zolpidem ER

Ambien CR

Women: 6.25 mg

Men: 12.5 mg; consider lower dose

6.25 mg in elderly or hepatic impairment

2.8 h

Primary use, sleep onset and maintenance

Zolpidem

Intermezzo

Women: 1.75 mg SL prn

Men: 3.5 mg SL prn

1.75 mg with hepatic impairment

2.5 h

Middle of night awakening

Short acting

Zaleplon

Sonata

10 mg, 5 mg in elderly or hepatic impairment or use with cimetidine

0.9-1 h

Primary use, sleep onset; maintenance up to 4 h

Orexin Receptor Antagonist

Intermediate acting

Suvorexant

Belsomra

10 mg; if tolerated but not effective, may increase not to exceed 20 mg

12 h

Sleep onset and maintenance

Melatonin Receptor Agonist

Short acting

Ramelteon

Rozerem

8 mg

1-2.6 h

Primary use, sleep onset

* Not FDA approved for sleep

Catherine McVearry Kelso, MD, MS Associate Professor of Internal Medicine, Virginia Commonwealth University School of Medicine; Medical Director, Hospice and Palliative Care, Site Director, Palliative Care Fellowship, Ethics Consultation Coordinator, Hunter Holmes McGuire Veterans Affairs Medical Center

Catherine McVearry Kelso, MD, MS is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Geriatrics Society, American Society for Bioethics and Humanities

Disclosure: Nothing to disclose.

Antony Fernandez, MD, FRCPsych(UK) Professor of Psychiatry, Virginia Commonwealth University School of Medicine; Attending Physician, Mental Health Service, McGuire Veterans Affairs Medical Center, Richmond

Antony Fernandez, MD, FRCPsych(UK) is a member of the following medical societies: American Society of Addiction Medicine

Disclosure: Nothing to disclose.

Angela Gentili, MD Director of Geriatric Medicine Fellowship Program, Professor of Internal Medicine, Division of Geriatric Medicine, Virginia Commonwealth University Health System and McGuire Veterans Affairs Medical Center, Richmond, VA

Angela Gentili, MD is a member of the following medical societies: Virginia Geriatrics Society, American Geriatrics Society

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: Received salary from Medscape for employment. for: Medscape.

Iqbal Ahmed, MBBS, FRCPsych(UK) Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Uniformed Services University of the Health Sciences; Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine

Iqbal Ahmed, MBBS, FRCPsych(UK) is a member of the following medical societies: Academy of Psychosomatic Medicine, American Neuropsychiatric Association, American Society of Clinical Psychopharmacology, Royal College of Psychiatrists, American Association for Geriatric Psychiatry, American Psychiatric Association

Disclosure: Nothing to disclose.

Jennifer S Morse, MD Associate Medical Director, Optum Health

Jennifer S Morse, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, Aerospace Medical Association, American Psychiatric Association

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Aparna Ranjan, MD, and Kirk L Nelson, MD, to the development and writing of the source article.

Primary Insomnia 

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