Підхід до пацієнта з розладом сну або неспання

History of present illness should include duration and age at onset of symptoms and any events (eg, a life or work change, new drug, new medical disorder) that coincided with onset. Symptoms during sleeping and waking hours should be noted.

The quality and quantity of sleep are identified by determining

• Bedtime

• Latency of sleep (time from bedtime to falling asleep)

• Number and time of awakenings

• Final morning awakening and arising times

• Frequency and duration of naps

• Quality of sleep (whether it is refreshing)

Having patients keep a sleep log for several weeks is more accurate than questioning them. Bedtime events (eg, food or alcohol consumption, physical or mental activity) should be evaluated. Intake of and withdrawal from medications, alcohol, caffeine, marijuana, and nicotine as well as level and timing of physical activity should also be included.

If excessive daytime sleepiness is the problem, severity should be quantified based on the propensity for falling asleep in different situations (eg, resting comfortably versus when driving a car). The Epworth Sleepiness Scale may be used; a cumulative score ≥ 10 represents excessive daytime sleepiness.

Review of systems should check for symptoms of specific sleep disorders, including

• Snoring, interrupted breathing patterns, witnessed apneic events, nocturnal gasping and choking, and nocturia (sleep apnea syndromes)

• Depression, anxiety, mania, and hypomania (psychiatric sleep disorders)

• Restlessness in the legs, an irresistible desire to move them, and jerking leg or arm movements (restless legs syndrome, periodic limb movement disorder)

• Cataplexy, sleep paralysis, and hypnagogic hallucinations (narcolepsy)

Bed partners or other family members can best identify some of these symptoms.

Past medical history should check for known disorders that can interfere with sleep, including chronic obstructive pulmonary disease (COPD), asthma, heart failure, hyperthyroidism, gastroesophageal reflux, neurologic disorders (particularly movement and degenerative disorders), urinary incontinence, other urinary disorders, and painful disorders (eg, rheumatoid arthritis). Risk factors, symptoms, and diseases associated with obstructive sleep apnea include obesity, heart disorders, hypertension, stroke, smoking, snoring, retrognathia, tonsillar hypertrophy, and nasal trauma. Drug history should include questions about use of any medications or substances associated with sleep disturbance.

Клінічний калькулятор

Шкала сонливості Епворта (ESS)

The physical examination is useful mainly for identifying signs associated with obstructive sleep apnea:

• Obesity with fat distributed around the neck or midriff

• Large neck circumference (≥ 43.2 cm [17 in] in males, ≥ 40.6 cm [16 in] in females)

• Mandibular hypoplasia and retrognathia

• Nasal obstruction

• Enlarged tonsils (palatine or lingual), adenoid, tongue, uvula, lateral walls of the pharynx or soft palate (modified Mallampati score 3 or 4—see figure Modified Mallampati Scoring)

• Decreased pharyngeal patency

• Redundant lateral pharyngeal mucosa

Модифікована шкала оцінки Малампаті

Modified Mallampati scoring is as follows: Class 1: Tonsils, uvula, and soft palate are fully visible. Class 2: Hard and soft palate, upper portion of tonsils, and uvula are visible. Class 3: Soft and hard palate and base of the uvula are visible. Class 4: Only the hard palate is visible.

The chest should be examined for expiratory wheezes and kyphoscoliosis. Signs of right ventricular failure, including lower-extremity edema, should be noted. A thorough neurologic examination should be performed.

The following findings are of particular concern:

• Falling asleep while driving or other potentially dangerous situations

• Repeated sleep attacks (falling asleep without warning)

• Breathing interruptions or awakening with gasping reported by bed partner

• Unstable cardiac or pulmonary status

• Recent stroke

• Status cataplecticus (continuous cataplexy attacks)

• History of violent behaviors or injury to self or others during asleep

• Frequent sleepwalking or other out-of-bed behavior

Inadequate sleep hygiene and situational stressors are usually apparent in the history. EDS that disappears when sleep time is increased (eg, on weekends or vacations) suggests inadequate sleep syndrome. EDS that is accompanied by cataplexy, hypnagogic/hypnopompic hallucinations, or sleep paralysis suggests narcolepsy.

Difficulty falling asleep (sleep-onset insomnia) should be distinguished from difficulty maintaining sleep and early awakening (sleep maintenance insomnia).

Sleep-onset insomnia suggests delayed sleep phase syndrome, chronic psychophysiologic insomnia, restless legs syndrome, or childhood phobias.

Sleep maintenance insomnia suggests major depression, central sleep apnea, obstructive sleep apnea, periodic limb movement disorder, or aging.

Falling asleep early and awakening early suggest advanced sleep phase syndrome.

Clinicians should suspect obstructive sleep apnea in patients with significant snoring, frequent awakenings, and other risk factors. The STOP-BANG score can help predict risk of obstructive sleep apnea (see table STOP-BANG Risk Score for Obstructive Sleep Apnea).

Sleep tests are usually performed when specific symptoms or signs suggest obstructive sleep apnea, nocturnal seizures, narcolepsy, periodic limb movement disorder, or other disorders whose diagnosis relies on identification of characteristic polysomnographic findings. Tests are also performed when the clinical diagnosis is in doubt or when response to initial presumptive treatment is inadequate. If symptoms or signs strongly suggest certain causes (eg, restless legs syndrome, poor sleep habits, transient stress, shift work disorder), testing is not required.

Polysomnography is particularly useful when obstructive sleep apnea, narcolepsy, nocturnal seizures, periodic limb movement disorder, or parasomnias are suspected. It also helps clinicians evaluate violent and potentially injurious sleep-related behaviors (REM behavioral disorder). It monitors brain activity (via EEG), eye movements, heart rate, respirations, oxygen saturation, and muscle tone and activity during sleep. Video recording may be used to identify abnormal movements during sleep (1). Polysomnography is typically performed in a sleep laboratory; home sleep studies are now commonly used to diagnose obstructive sleep apnea, but not other sleep disorders (2).

Multiple sleep latency testing assesses speed of sleep onset in 4 to 5 daytime nap opportunities 2 hours apart during the patient’s typical daytime. Patients lie in a darkened room and are asked to sleep. Onset and stage of sleep (including REM) are monitored by polysomnography to determine the degree of sleepiness. This test’s main use is in the diagnosis of narcolepsy.

For the maintenance of wakefulness test, patients are asked to stay awake in a quiet room during 4 wakefulness opportunities 2 hours apart while they sit in a bed or a recliner.

Patients with EDS may require laboratory tests of renal, liver, and thyroid function.

1. 1. Kushida CA, Littner MR, Morgenthaler T, et al: Practice parameters for polysomnography and procedures: An update for 2005. Sleep 28(4):499-519.

2. 2. Rosen IM, Kirsch DB, Chervin RD, et al: Clinical use of a home sleep apnea test: An American Academy of Sleep Medicine Position Statement. J Clin Sleep Med 13 (10):1205-1207, 2017. doi: 10.5664/jcsm.6774

Cognitive-behavioral therapy for insomnia focuses on managing the common thoughts, worries, and behaviors that interfere with sleep. It is typically performed in 4 to 8 individual or group sessions and can be performed face-to-face, via telehealth remotely, or digitally. Most studies show that telehealth is noninferior to in-person CBT-I (2, 3). However, evidence for the effectiveness of digital CBT-I is weaker (4), although more data are needed to substantiate this.

Cognitive-behavioral therapy for insomnia consists of the following:

• Helping patients improve sleep hygiene, particularly restricting time spent in bed, establishing a regular sleep schedule, and controlling stimuli

• Teaching patients about the effects of sleeplessness and helping them identify inappropriate expectations about how much sleep they should get

• Teaching patients relaxation techniques

• Using other cognitive therapy techniques as needed

Restricting the amount of time spent in bed aims to limit the time patients spend lying in bed trying unsuccessfully to sleep. Initially, time in bed is limited to the average nightly total sleep time, but not to < 5.5 hours. Patients are asked to get out of bed in the morning at a fixed time and then calculate a bed time based on total sleep time and remaining awake until that time (called sleep restriction therapy). After a week, this approach typically improves quality of sleep. Then, the time spent in bed can be increased by gradually making bed time earlier, as long as awakenings in the middle of the night remain minimal.

General guidelines for use of hypnotics (see table Guidelines for the Use of Hypnotics) aim at minimizing abuse, misuse, and addiction.

For commonly used hypnotics, see table Oral Hypnotics in Common Use. All hypnotics (except ramelteon, low-dose doxepin, and orexin receptor antagonists) act at the benzodiazepine recognition site on the gamma-aminobutyric (GABA) receptor and augment the inhibitory effects of GABA.

Hypnotics differ primarily in elimination half-life and onset of action. Medications with a short half-life are used for sleep-onset insomnia. Medications with a longer half-life are useful for both sleep-onset and sleep maintenance insomnia, or, in the case of low-dose doxepin, primarily for sleep maintenance insomnia. Some hypnotics (eg, older benzodiazepines) have greater potential for daytime carryover effects, especially after prolonged use and/or in older adults. Newer medications with a very short duration of action (eg, low-dose sublingual zolpidem) can be taken in the middle of the night, during a nocturnal awakening, as long as patients stay in bed for at least 4 hours after use. Ambien can have serious side effects including fall risk, memory impairment, and complex sleep behaviors (sleep-walking, sleep-driving, and sleep-texting).

Patients who experience daytime sedation, incoordination, or other daytime effects should avoid activities requiring alertness (eg, driving), and the dose should be reduced, the medication stopped, or, if needed, another medication used. Other adverse effects include amnesia, hallucinations, incoordination, and falls. Falling is a significant risk with all hypnotics.

When benzodiazepines are to be stopped, they should be tapered and not stopped abruptly.

Three dual orexin receptor antagonists (daridorexant, lemborexant, suvorexant) can be used to treat sleep-onset and maintenance insomnia. They block orexin receptors in the brain, thereby blocking orexin-induced wakefulness signals and enabling sleep initiation. Dual orexin receptor antagonists block orexin receptors-1 and -2. The orexin receptor-1 is involved in suppressing the onset of rapid eye movement (REM) sleep; the orexin receptor-2 is involved in suppressing non-REM sleep onset and, to some extent, in controlling REM sleep. However, the mechanism of action for dual orexin receptor antagonists is not fully understood. They are used to treat sleep-onset and/or sleep-maintenance insomnia and may improve cognitive performance in patients with mild cognitive impairment or Alzheimer disease (5).

• Daridorexant is taken once a day within 30 minutes of going to bed (has the shortest half-life [8 hours] of the dual oxexin receptor antagonists)

• Lemborexant is taken once a day within 30 minutes of going to bed (can be increased based on patient response and tolerability)

• Suvorexant is taken no more than once a night and taken within 30 minutes of going to bed, with at least 7 hours before the planned time of awakening (somnolence is most common adverse effect)

Low-dose doxepin (3 mg, 6 mg), a tricyclic antidepressant with antihistaminic activity, is also indicated for sleep maintenance insomnia. Doxepin has not been directly compared with other hypnotics, but a risk-benefit analysis suggested it had the most favorable profile when making indirect comparisons with other hypnotics (6). Doxepin is potentially the best first-line therapy (6).

Hypnotics should be used cautiously in patients with pulmonary insufficiency. In older patients, any hypnotic, even in small doses, can cause restlessness, excitement, falls, or exacerbation of delirium and dementia. Rarely, hypnotics can cause complex sleep-related behaviors, such as sleepwalking and even sleep driving; use of higher-than-recommended doses and concurrent consumption of alcoholic beverages may increase risk of such behaviors. Rarely, severe allergic reactions occur.

Prolonged use of hypnotics is typically discouraged because tolerance can develop and because abrupt discontinuation can cause rebound insomnia or even anxiety, tremor, and seizures. These effects are more common with benzodiazepines (particularly triazolam) and less common with nonbenzodiazepines. Difficulties can be minimized by using the lowest effective dose for brief periods and by tapering the dose before stopping the medication (see also Withdrawal and detoxification).

Many medications and substances not specifically indicated for insomnia are used to induce and maintain sleep.

Some antidepressants (other than low-dose doxepin) taken in low doses at bedtime (eg, paroxetine 5 to 20 mg, trazodone 50 mg, trimipramine 75 to 200 mg) may improve sleep because of their sedating side effects. However, their use in these low doses should be limited to when standard hypnotics are not tolerated (rare) or in higher (antidepressant) doses when depression is present.

Melatonin is a hormone that is secreted by the pineal gland (and that occurs naturally in some foods). Darkness stimulates secretion, and light inhibits it. By binding with melatonin receptors in the suprachiasmatic nucleus, melatonin mediates circadian rhythms, especially during physiologic sleep onset.

Oral melatonin (typically 0.5 to 5 mg at bedtime) may be effective for sleep problems due to delayed sleep phase syndrome. When used to treat this disorder, it must be taken at the appropriate time (a few hours before the evening increase in endogenous melatonin secretion—in early evening for most people, typically 3 to 5 hours before the intended bedtime) and at a low dose of 0.5 to 1 mg; taken at the wrong time, it can aggravate sleep problems. There are delayed release preparations of melatonin but it is not clear if these preparations are more effective than the normal release versions.

For other forms of insomnia, melatonin's efficacy is largely unproved.

Melatonin can cause headache, dizziness, nausea, and drowsiness. However, after widespread use, no other worrisome adverse effects have been reported. Available preparations of melatonin are unregulated, so content and purity cannot be ensured, and the effects of long-term use are unknown.

Over-the-counter (OTC) antihistamines (eg, doxylamine, diphenhydramine) can induce sleep but should not be used to treat insomnia. Efficacy is unpredictable, and these agents have long a half-life and have adverse effects such as daytime sedation, confusion, urinary retention, and other systemic anticholinergic effects, which are particularly worrisome in older adults.

Alcohol should also not be used to help with sleep because it produces unrefreshing, disturbed sleep with frequent nocturnal awakenings, often increasing daytime sleepiness. Alcohol can further impair respiration during sleep in patients with obstructive sleep apnea and other pulmonary disorders such as chronic obstructive pulmonary disease (COPD).

Cannabinoids include the following:

• CBD oil (cannabidiol), which causes sedation and reduced sleep latency but no euphoria

• CBN (cannabinol), which causes sedation, reduces pain, and increases appetite

• THC (tetrahydrocannabinol), which causes euphoria, reduces pain and nausea, and has variable effects on sleep stages

• Dronabinol, which is a synthetic analog

Whether cannabis is effective for insomnia is unclear, but it is useful for chronic pain.

Tolerance can develop; stopping cannabis after long-term use results in insomnia.

1. 1. Qaseem A, Kansagara D, Forciea MA, C et al: Management of Chronic Insomnia Disorder in Adults: A Clinical Practice Guideline From the American College of Physicians. Ann Intern Med 165(2):125-133, 2016. doi: 10.7326/M15-2175

   2. Arnedt JT, Conroy DA, Mooney A, et al: Telemedicine versus face-to-face delivery of cognitive behavioral therapy for insomnia: a randomized controlled noninferiority trial. Sleep 44(1):zsaa136, 2021. doi: 10.1093/sleep/zsaa136

2. 3. Gehrman P, Gunter P, Findley J, et al: Randomized noninferiority trial of telehealth delivery of cognitive behavioral treatment of insomnia compared to in-person care. J Clin Psychiatry 82(5):20m13723, 2021. doi: 10.4088/JCP.20m13723

3. 4. Bullock G, Johnson GS, Pattridge SG, et al: A homozygous MAN2B1 missense mutation in a Doberman Pinscher dog with neurodegeneration, cytoplasmic vacuoles, autofluorescent storage granules, and an α-mannosidase deficiency. Genes (Basel)14(9):1746, 2023. doi: 10.3390/genes14091746

4. 5. Zhou M, Tang S: Effect of a dual orexin receptor antagonist on Alzheimer's disease: Sleep disorders and cognition. Front Med (Lausanne) 9:984227, 2023. doi: 10.3389/fmed.2022.984227

5. 6. Cheung JMY, Scott H, Muench A, et al: Comparative short-term safety and efficacy of hypnotics: A quantitative risk-benefit analysis. J Sleep Res e14088, 2023. doi: 10.1111/jsr.14088