Evidence-Based Reviews

Treatment-resistant insomnia? Ask yourself 8 questions

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References

Order sleep laboratory testing for patients at risk for sleep apnea, based on their history, physical exam—including obesity, upper airway anatomy, and neck circumference (collar size ≥17 inches)—and informant reports of snoring and breathing patterns.

3 Is the patient taking medications with stimulating effects?

Because insomnia is highly comorbid with mood and anxiety disorders, patients with insomnia often are prescribed antidepressants. Although some are sedating, antidepressants such as selective serotonin reuptake inhibitors are likely to be stimulating.

Recommendation. When insomnia persists, assess the potential effects of prescribed and over-the-counter (OTC) medications. Consider possible pharmacologic effects of aging that can make patients more sensitive to medications.

Also educate patients about the long-acting effects of caffeine and its varied sources, such as energy drinks and OTC products. Some patients will benefit from completely avoiding caffeine, whereas others may do fine restricting coffee to 1 or 2 cups in the morning. A good general practice is to avoid all caffeine after lunchtime.

Box 2

‘3 Ps’: Framework for evaluating treatment-resistant insomnia

Predisposing factors. Some personalities may be predisposed to insomnia. Persons who tend to be anxious, depressive, or emotionally reactive may be at increased risk for developing insomnia.

Precipitating factors may include situational crises, schedule changes, substance or medication use, and psychiatric, medical, and sleep disorders. A careful history allows you to consider precipitating events.

Perpetuating factors that may reinforce and maintain chronic insomnia include:

  • maladaptive behaviors, such as napping or using alcohol as a sleep aid
  • conditioned hyperarousal, whereby insomnia sufferers experience anxiety and tension associated with preparing for and getting into bed. Sleepless time in bed may reinforce the conditioning, contribute to anxiety and tension, and undermine sleep on future nights.

Source: Reference 2

4 Does the patient’s insomnia have a homeostatic component?

Circadian rhythms and a homeostatic sleep drive are temporally linked in regulating the normal routine of nighttime sleep alternating with day and evening wakefulness.5,6 The sleep drive promotes a sleep-to-waking ratio of approximately 1:2 (an average of 8 hours sleep per 24 hours). Adequate sleep, from the homeostatic perspective, could be achieved during any hours of the day or night.

Acute sleep deprivation may result from extended wakefulness—such as staying up all night to study for an exam. Chronic sleep deprivation may occur during successive 24-hour periods with insufficient sleep. Both patterns are associated with increasing subjective sleepiness and ultimately with cognitive impairment.

The circadian process optimizes sleep to occur at night through entrainment with the photoperiod (daylight exposure). The master CNS timekeeper is coordinated by the tiny paired suprachiasmatic nuclei (SCN) in the anterior hypothalamus, where neurons maintain approximate 24-hour periodicity through complex transcription-translation feedback loops involving several genes. Circadian rhythm is reinforced by SCN control of pineal gland production and secretion of melatonin, which normally:
  • is low throughout the daytime
  • rises during the evening as bedtime approaches
  • plateaus during nighttime sleep hours
  • decreases as the normal morning wake time approaches.
The homeostatic sleep drive accumulates from awakening until sleep occurs again. In the late afternoon and evening, however, homeostatic sleep pressure is opposed by an arousal signal from the circadian system.

Typically, people are more alert in the evening than at any other time in the 24-hour cycle. As bedtime approaches, rising melatonin interacts with SCN melatonin receptors and decreases circadian arousal. Normal sleep onset then can occur rapidly at bedtime, when the homeostatic sleep drive is unopposed.

Nighttime sleep initially is promoted by the homeostatic sleep drive. However, the homeostatic sleep pressure is reversed by sleep and thus decreases as sleep continues during the night. The circadian system promotes minimum stimulation during the latter sleep hours, sustaining total sleep for approximately 8 hours.

Consequences. Individual circadian timing tendencies may affect when people experience alertness and sleepiness and may be associated with persistent complaints of sleep onset difficulty or early morning awakening.7 Napping may reduce the homeostatic sleepiness available to aid bedtime sleep onset. Mismatched homeostatic and circadian processes often prevent shift workers from achieving satisfactory sleep.

Recommendation. Have the patient keep a sleep log to identify the time and duration of sleep episodes throughout the 24-hour cycle. Actigraphy may provide useful information about sleep-wake patterns.

5 Are circadian rhythm patterns contributing to insomnia?

Overlooking circadian rhythms’ effects on insomnia can lead to apparent treatment failure.8 Although the circadian system typically promotes sleep from about 10 pm to midnight until about 6 to 8 am, some individuals have long-standing predispositions for earlier or later sleep episodes.

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