Psychiatric Annals

CME Article 

Insomnia in Older Adults

Chandra M. Cherukuri, MD, MS; Neeraj Kaplish, MD; Deepthi C. Malepati, MD; Imran S. Khawaja, MBBS, FAASM; Shashi K. Bhatia, MD, FACPsych; Subhash C. Bhatia, MD, FACPsych

Abstract

Insomnia disorder in older adults is associated with dissatisfaction with quality or quantity of sleep and is also associated with difficulty falling asleep, maintaining sleep, or early morning awakening. It is frequently associated with an age-related decrease in restorative stage 3 of nonrapid eye movement sleep as well as advance phase shift leading to early morning awakening. Sleep disturbances in older adults, as in younger patients, have a bidirectional relationship with many medical and psychiatric disorders as well as polypharmacy. The health consequences of insomnia in the elderly may also include manifestation or magnification of cognitive deficits. Diagnosis of insomnia is based on history from the patient, the bed partner, self-administered questionnaire or sleep diary, comprehensive evaluation for comorbid medical/psychiatric disorders, and comprehensive medication history. Both nonpharmacological and pharmacological strategies are effective in the management of insomnia. Cognitive-behavioral therapy for insomnia (CBT-I) should be considered as an initial intervention for chronic insomnia. Pharmacological treatment with short-acting hypnotics is a valuable adjunct to CBT-I for acute insomnia for a brief period followed by a slow taper. Any treatment intervention should be in collaboration with the patient and/or family and include a discussion of the risks, benefits, and costs. [Psychiatr Ann. 2018;48(6):279–286.]

Abstract

Insomnia disorder in older adults is associated with dissatisfaction with quality or quantity of sleep and is also associated with difficulty falling asleep, maintaining sleep, or early morning awakening. It is frequently associated with an age-related decrease in restorative stage 3 of nonrapid eye movement sleep as well as advance phase shift leading to early morning awakening. Sleep disturbances in older adults, as in younger patients, have a bidirectional relationship with many medical and psychiatric disorders as well as polypharmacy. The health consequences of insomnia in the elderly may also include manifestation or magnification of cognitive deficits. Diagnosis of insomnia is based on history from the patient, the bed partner, self-administered questionnaire or sleep diary, comprehensive evaluation for comorbid medical/psychiatric disorders, and comprehensive medication history. Both nonpharmacological and pharmacological strategies are effective in the management of insomnia. Cognitive-behavioral therapy for insomnia (CBT-I) should be considered as an initial intervention for chronic insomnia. Pharmacological treatment with short-acting hypnotics is a valuable adjunct to CBT-I for acute insomnia for a brief period followed by a slow taper. Any treatment intervention should be in collaboration with the patient and/or family and include a discussion of the risks, benefits, and costs. [Psychiatr Ann. 2018;48(6):279–286.]

Humans spend as much as one-third of their lifespan sleeping. With an increasing knowledge of sleep as an essential component of physical and mental well-being, the National Sleep Foundation recommends approximately 7 to 8 hours of sleep per night in older adults.1 In the United States, the population of older adults (age ≥65 years) has been steadily growing and is expected to double in the next 25 years to about 72 million; by the year 2030, approximately 1 in 5 Americans will be age 65 years or older.2 With the increase in the size of the aging population and the high prevalence of sleep disturbances in elderly people and their impact on health, it will be even more important for health care professionals to be aware of sleep disorders in the elderly.

Over the past decade, there has been a significant rise in clinic visits and prescription medications for insomnia, accounting for more than 5.5 million clinic visits annually.3 It is estimated that the prevalence of insomnia symptoms in older adults is as high as 65%.4 Despite the high prevalence of insomnia, it is often missed, treated ineffectively, or treatment is deferred. This could be related to the popular belief that less sleep at night and sleepiness during the day is a normal part of the aging process.

Insomnia negatively affects quality of life, increases the risk of psychiatric or medical morbidity as well as mortality,5 and also significantly increases risk for all-cause dementia.6 Moreover, independent of depressive symptoms, subjective experience of poor quality and quantity of sleep in older adults is associated with increased risk of death by suicide even 10 years later.7 Sleep problems (in particular sleep initiation) independently and in combination with sleep medication use among community-dwelling older adults and nursing home residents are associated with a higher risk of falls.8,9 Self-reported insomnia among elderly men was a significant predictor of shortened time to nursing home placement.10 In addition, community-dwelling older adults reporting more than one symptom of insomnia have greater odds of hospitalization and use of health care or home health services; those reporting more than two symptoms were associated with even greater odds of nursing home placement.11 Early recognition and intervention of insomnia may mitigate greater risk of hospitalization, reduce use of costly health services, and improve quality of life.

Age-Related Changes in Sleep in Older Adults

It has been described that as we age sleep becomes more fragmented, lighter, and is associated with changes in sleep architecture as well as other parameters including reduction in total sleep time and sleep efficiency.12 Wakefulness after sleep onset increases with advancing age. With normal aging, the total time spent in sleep stages N1 and N2 (ie, the lighter stages of sleep) increases, whereas stage N3 (deeper and restorative sleep) and rapid eye movement (REM; cognitive consolidative sleep) decrease. Most of these changes in sleep occur between adulthood and age 60 years except for sleep efficiency, which continues to decline.12

Neurobiology of Sleep

Sleep is initiated by inhibition of arousal systems (Table 1). Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter that plays an important role in promoting sleep by inhibiting neurons of the arousal system, so most commonly prescribed hypnotic drugs target the GABA receptors.

Wake and Sleep-Promoting Neurotransmitters

Table 1:

Wake and Sleep-Promoting Neurotransmitters

Insomnia Disorders

The International Classification of Sleep Disorders, third edition (ICSD-3)13 simplified the insomnia disorders to chronic insomnia, short-term insomnia, and other insomnia. Previous versions of ICSD required diagnostic classification and subtyping, which was onerous and susceptible to inter-clinician variability. Insomnia may be related to family history, aging, lower socioeconomic and status (predisposing factor); stressful life events like changing homes or loss of loved ones can disrupt sleep (precipitating factor). Even if the stress resolves, the patient may start to worry during the day about not being able to sleep or worry about lack of sleep causing ill effects on health or quality of life (perpetuating factor), which may result in insomnia as a learned behavior.13 Diagnostic criteria for insomnia are listed in Table 2. A polysomnogram (overnight sleep study) or home sleep apnea test is usually not recommended unless there is concern for another sleep-related disorder as a cause for sleep disturbance.

Criteria for Clinical Diagnosis of Insomnia Disorder

Table 2:

Criteria for Clinical Diagnosis of Insomnia Disorder

A diagnosis of “other insomnia disorder” is reserved for people who have difficulty initiating and maintaining sleep but do not meet the full criteria for either chronic or short-term insomnia disorder.13 Older adults are particularly susceptible to comorbid insomnia (ie, insomnia occurring in association with other clinical disorder). Comorbid insomnia can be related to other psychiatric or sleep-related disorders such as obstructive sleep apnea, restless leg syndrome, REM behavioral disorder, nightmares, and circadian rhythm sleep disorder (older adults tend to have an advanced sleep phase shift leading to earlier bedtime and early morning awakening). In addition, older adults may have chronic medical and psychiatric illnesses or polypharmacy that could contribute to comorbid insomnia. Some of the commonly observed clinical problems in the elderly that can disrupt sleep include menopausal vasomotor symptoms like hot flashes or nocturia due to enlarged prostrate or overactive bladder; diabetes or use of diuretics; chronic pain from osteoarthritis or medical problems; neurological deficits from stroke or dementia; breathing difficulties due to congestive heart failure or chronic obstructive lung diseases; and mood or anxiety or psychotic disorder. Medication side effects from polypharmacy (eg, antidepressants, stimulants, corticosteroids, thyroid hormone, analgesics with caffeine, beta blockers, opioids, anticholinergic medications, over-the-counter [OTC] hypnotics) can contribute to daytime and nighttime symptoms leading to insomnia.14

Treatment of Insomnia in Older Adults

Regardless of the therapeutic modality used for insomnia, the primary goal is to improve sleep quality and quantity along with insomnia-related daytime impairments. Before initiating therapy for insomnia, management of comorbid conditions mentioned above may improve insomnia symptoms. It is also important to review and eliminate both OTC and prescribed medications contributing to increased arousal, which worsens insomnia.14 If an alternative medication with less sleep disruption is available, a change to such medication should be considered.

Effective treatments for chronic insomnia in older adults includes behavioral therapy strategies like stimulus control, relaxation techniques, cognitive-behavioral therapy, cognitive-behavioral therapy for insomnia (CBT-I), or pharmacotherapy.15,16 It is the opinion of authors that pharmacotherapy in older adults should only be considered after a comprehensive assessment for burden of sleep dysfunction, comorbidities, risks, and after careful consideration for nonpharmacological options such as CBT-I.

Nonpharmacological Interventions

Behavioral and psychological therapy is a recommended treatment for chronic insomnia after optimizing treatment for underlying comorbid conditions and prior to pharmacotherapy.14,15 Numerous behavioral and psychological treatments including sleep education, sleep hygiene, stimulus control, sleep restriction, relaxation, cognitive therapy, biofeedback, and paradoxical intention individually or as a multicomponent treatment package (ie, CBT-I) have been shown to be effective in the treatment of chronic insomnia. Clinical trials have shown that CBT-I has outperformed medical management both in terms of long-term benefit and safety in older adults.14,15 CBT-I can be provided by a trained therapist or secured through self-guided online programs. Implementation of cognitive and behavioral strategies for insomnia in the elderly is not profoundly different from younger adults. Common techniques, principles, and goals of CBT-I are summarized in Table 3.17,18

Overview of Principles Used in Cognitive-Behavioral Therapy for Insomnia

Table 3:

Overview of Principles Used in Cognitive-Behavioral Therapy for Insomnia

Adherence and efficacy of a technique are increased when the justification and instructions are explained. The patient's progress and difficulties are carefully monitored in daily sleep logs and addressed in subsequent follow-up sessions.

Pharmacotherapy for Insomnia

Pharmacotherapy for chronic insomnia should be considered only if patients are unable to participate in CBT-I, or selectively as a temporary adjunct to CBT-I or for those who still have symptoms despite CBT-I.16 It is most appropriate for elderly patients with acute insomnia of 3 months or less.19 For optimal benefits, medication use should be adjunctive to CBT-I. The American Geriatric Society (AGS) has strongly recommended not to use benzodiazepines (BZDs) or other sedative hypnotics in older adults as a first choice for insomnia intervention due to limited effect on sleep and significantly increased risk of hospitalization and mortality after falls and hip fractures and motor vehicle accidents (MVA).20 Medications approved by the US Food and Drug Administration for insomnia and their recommended dosage in older adults are outlined in Table 4.16,21,22

US Food and Drug Administration-Approved Prescription Medications for Insomnia

Table 4:

US Food and Drug Administration-Approved Prescription Medications for Insomnia

Benzodiazepines. BZDs bind to the GABA-A receptor alpha-1, alpha-2, alpha-3, and alpha-5 subunits in the brain.21 Older adults are more susceptible to the potential adverse effects of BZDs because of increased sensitivity and altered pharmacokinetics and pharmacodynamics that come with aging.22 Short- and intermediate-acting BZDs in older adults are associated with increased risk of cognitive impairment, delirium, ataxia, falls, fractures, and MVAs.23 Additionally, long-acting agents are frequently associated with residual sedation and impaired motor coordination. All BZDs have the potential risk of dependence, tolerance, and abuse. Triazolam has a rapid onset of action with a short half-life, making it optimal for sleep onset insomnia; however, it has significant adverse effects of rebound insomnia and anterograde amnesia,24 so it should be used cautiously. As a whole, the benefits of benzodiazepines may not justify their use due to the increased risk of adverse events in older adults.

Nonbenzodiazepine benzodiazepine receptor agonists (“Z drugs”). “Z drugs” bind preferentially to the GABA-A alpha-1 subunit, which improves their side effect profile compared to BZDs.21 However, use of “Z drugs” in older adults is also associated with increased risk of delirium, falls, fractures, MVA, increased emergency department visits, and hospitalizations with minimal improvement in sleep and should be avoided in patients with dementia/cognitive impairment or a history of falls. The AGS has recommended that “Z drugs” should not be initiated without consideration of duration of use and to avoid using them for more than 90 days due to the risk of adverse effects.23 Data suggest the rebound insomnia is limited to the first night after discontinuation of zolpidem, but is not a significant concern with other “Z drugs.”16 “Z drugs” should be administered on an empty stomach, as taking them with or immediately after meals may delay absorption and onset of action. Zolpidem is a protein-bound agent and the dose should be reduced in patients with hepatic and renal failure. In patients with cirrhosis of the liver, the half-life of zolpidem is increased to about 10 hours.22 Anterograde amnesia, complex sleep-related behaviors such as sleep walking, sleep eating, and “sexsomnia” have been described with use of zolpidem, so it should be used with caution in patients with a history of parasomnias.25

Melatonin receptor agonists. Ramelteon has a strong affinity for the melatonin receptors, which control drowsiness by weakening wake-promoting signals from the suprachiasmatic nucleus. Ramelteon is associated with somnolence, dizziness, nausea, and fatigue, without effects on fertility.

Histamine antagonists (antihistamines). Doxepin, a tertiary tricyclic antidepressant (at higher doses), has more selective histamine (H1) antagonist action at doses of 3 to 6 mg. At doses of <6 mg, doxepin is without significant anticholinergic side effects (as it is highly selective to the histamine receptor with minimal to no effect on adrenergic or serotonergic receptors) and seems appropriate for use in the elderly. Minimal adverse effects of headache or somnolence are reported at lower doses. Higher doses of doxepin are associated with antiadrenergic actions, which have a potential for cardiovascular effects such as hypotension and abnormal cardiac conduction.16

Orexin antagonist. Suvorexant is a relatively new drug that acts by inhibiting the orexin receptors, which play a significant role in maintaining wakefulness. Although it has been shown to be effective in sleep maintenance,16 there are limited data on the efficacy and adverse effects of this drug in older adults. Some of the adverse effects related to this drug include sleep paralysis, daytime sleepiness, and falls.

In conclusion, in older adults the choice of hypnotic drugs should be individualized depending on type of symptom pattern of insomnia, therapeutic effects needed (Table 5),16 prior treatment responses, medication interactions and side effects, comorbid medical, psychological, and other sleep disorders, and side effect profile of the medication, with frequent reassessments. OTC herbal or nutritional products, antihistamines, and other agents labeled as “sleep aids” are not recommend in older adults due to lack of safety and efficacy data.16

Insomnia Medication Choices for Older Adults

Table 5:

Insomnia Medication Choices for Older Adults

Combined CBT-I and Pharmacotherapy

Available current literature in adults about combination therapy favors CBT-I treatment alone as more effective in improving insomnia symptoms after 2 years when compared to CBT-I plus temazepam for 8 weeks.26 Another trial comparing CBT-I alone with CBT-I plus zolpidem for 6 weeks versus CBT-I plus zolpidem on an as-needed basis for 6 weeks demonstrated CBT-I plus zolpidem had added benefit of improving insomnia symptoms during acute therapy, but long-term outcome was better when medication was discontinued during maintenance CBT-I.27,28 Based on these data, if a patient requires medication for insomnia it is advantageous to combine it with CBT-I rather than treat insomnia with medication alone.

Summary and Recommendations for Insomnia in Older Adults

Based on a review of the literature and available guidelines, the following are the summary and recommendations for management of insomnia in older adults.

  1. Treat all comorbid medical, neuropsychiatric, menopausal, and substance use disorder(s) as well as precipitating or perpetuating factors associated with the insomnia.

  2. Pharmacotherapy is most appropriate for acute insomnia and has greater effectiveness if combined with CBT-I.

  3. Long-term treatment with medication alone should be avoided.

  4. Review current medications the patient is taking. Most OTC sleeping pills have drugs with antihistaminic and anticholinergic effects (eg, diphenhydramine). These pills should be discontinued.

  5. Provide coping skills training for stressful life events related to loss of health, income, spouse, and friends.

  6. Many elderly patients resort to relatively heavy alcohol use as self-medication for insomnia that must be addressed.

  7. Provide general behavioral recommendations particularly advice regarding healthy sleep practices such as reduce time in bed, get up at the same time every morning irrespective of day of the week and amount of sleep, go to bed only when sleepy, don't stay in bed unless asleep, and to practice relaxation and mindfulness techniques.

  8. For chronic insomnia consider CBT-I as an initial option rather than medication. If CBT-I option is not available then provide brief behavioral treatment education (as in #7 above).

  9. For patients who require medication for sleep maintenance, consider short or intermediate half-life medication. Avoid long half-life agents so as not to interfere with daytime cognitive function or operating machinery due to drowsiness. With any medication, a patient should be warned about daytime drowsiness, impaired ability to operate machinery, driving, dizziness, and lightheadedness.

  10. For patients who respond to combined behavioral and pharmacologic intervention, the medication may be tapered while continuing the behavioral intervention for few more sessions.

  11. Continue to evaluate response to recommended intervention(s).

  12. For treatment-resistant insomnia disorder, consult with a sleep disorder specialist for further evaluation for sleep-wake cycle disorder and sleep apnea.

References

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Wake and Sleep-Promoting Neurotransmitters

Wake-promoting/arousal neurotransmitters <list-item>

■ Acetylcholine

</list-item><list-item>

■ Dopamine

</list-item><list-item>

■ Histamine

</list-item><list-item>

■ Hypocretin/orexin peptides

</list-item><list-item>

■ Norepinephrine

</list-item><list-item>

■ Serotonin

</list-item>
Sleep-promoting neurotransmitters <list-item>

■ Adenosine

</list-item><list-item>

■ Galanin

</list-item><list-item>

■ Gamma-aminobutyric acid

</list-item><list-item>

■ Melatonin

</list-item>

Criteria for Clinical Diagnosis of Insomnia Disorder

Symptoms Duration
Dissatisfaction with quantity or quality of sleep
  Difficulty initiating/maintaining sleep or waking earlier than desired If >3 months: chronic insomnia
  Associated with impaired daytime function
  Occurs with adequate opportunity and optimal environment for sleep If <3 months: short-term insomnia
  Not adequately explained by medical or psychiatric disorders
  Occurs at least 3 times per week for 3 months

Overview of Principles Used in Cognitive-Behavioral Therapy for Insomnia

Technique Goal
Sleep hygiene Encourage consistent practices that promote sleep <list-item>

Regular sleep and wake times, including weekends

</list-item><list-item>

Avoid daytime naps, especially late evening

</list-item><list-item>

No clock watching in bed. If unable to sleep, get out of bed

</list-item><list-item>

Regular exercise 3–4 hours before bed time

</list-item><list-item>

Resolve concerns or worries before going to bed

</list-item><list-item>

Have encouraging sleep environment <list-item>

Cooler, darker, and quieter bed room with comfortable bed

</list-item>

</list-item><list-item>

Avoid stimulating behavior and stimulant or stimulating activity closer to bedtime or in bedroom <list-item>

Avoid caffeinated drinks, nicotine, heavy alcohol use, or arguing with significant other. Have an early light dinner; don't force self to go to sleep

</list-item><list-item>

Avoid bright light-emitting screens (television/computer/tablets/smart phones) as these can interfere with circadian clock

</list-item>

</list-item>
Stimulus control <list-item>

Strengthens conditioning reflex of the bed and bedroom as a cue for sleep; go to bed only when tired

</list-item><list-item>

Use bed only for sleep and sex

</list-item><list-item>

If unable to sleep after 15 to 30 minutes (based on own estimation without looking at clock): <list-item>

Leave the bedroom

</list-item><list-item>

Engage in quiet, relaxing activity, and

</list-item><list-item>

Return to bedroom when tired again

</list-item>

</list-item>
Sleep restriction therapy Restricting total time in bed to increase sleep drive and consolidation of sleep <list-item>

Based on sleep diary, prescribe a total time in bed based on average need for sleep including naps and sleep time outside bedroom. Enhance sleep efficiency, which is the ratio of duration of sleep divided by total time in bed

</list-item><list-item>

Once sleep efficiency improves to >85% for 1 week, then increase time in bed by 15–30 minutes at weekly intervals until optimal improvement in daytime functioning

</list-item><list-item>

If sleep efficiency <85%, then decrease total time in bed by 15–30 minutes until sleep efficiency is >85%

</list-item>
Relaxation training To reduce levels of arousal and anxiety before bedtime and at night <list-item>

Progressive muscle relaxation <list-item>

Successive tensing and relaxing of muscles—start with face and move down

</list-item>

</list-item><list-item>

Relaxation response <list-item>

Slow breathing with thoughts focused on hand movement on abdomen or peaceful word or image

</list-item>

</list-item><list-item>

Mindfulness <list-item>

Being aware of mental and physical states by focusing attention on the present (eg, in and out of breath)

</list-item>

</list-item>
Cognitive therapy Restructuring sleep-related maladaptive thoughts/expectations/beliefs to reduce cognitive arousal <list-item>

Address and help deal with the patient's beliefs and attitudes related to: <list-item>

Unrealistic sleep expectation (“I must sleep 8 hours every night”)

</list-item><list-item>

Performance anxiety (“I must fall asleep tonight to perform well at work”)

</list-item><list-item>

Exaggerated attributions to sleep (“I feel fatigued, anxious, and irritable during the day because I did not sleep well”)

</list-item><list-item>

Hopelessness (“I won't fall asleep tonight again”)

</list-item>

</list-item>

US Food and Drug Administration-Approved Prescription Medications for Insomnia

Drug Starting Dose in Elderly Patients (mg) Onset of Action (minutes) Duration of Action Half-Life of Parent Drug or Metabolite in Elderly Patients (hours)
Benzodiazepine receptor agonists
Estazolam 0.5 15–60 Intermediate 10–24
Flurazepam 7.5 30–60 Long 1.5–5.5
Quazepam 7.5 20–45 Long 39–73
Temazepam 7.5 45–60 Intermediate 3.5–18.4
Triazolam 0.125 15–30 Short 1.5–5.5
Nonbenzodiazepine benzodiazepine receptor agonists (“Z drugs”)
Eszopiclone 1–2 15–30 Intermediate 9
Zaleplon 5 15–30 Very short 1
Zolpidem 5 <30 Short 2.9–3.7
Zolpidem CR 6.25 <30 Intermediate 1.9–7.3
Zolpidem SL 1.75 20 Very short 1.4–3.6
Melatonin receptor agonists
Ramelteon 8 15–30 Short 1–2.6
H1 antagonists (antihistamines)
Doxepin 3 30 Long 15.3–31
Orexin receptor antagonist
Suvorexant 10–20 30 Intermediate 12

Insomnia Medication Choices for Older Adults

Sleep onset insomnia <list-item>

■ Ramelteon

</list-item><list-item>

■ Zaleplon

</list-item><list-item>

■ Zolpidem

</list-item>
Sleep maintenance insomnia <list-item>

■ Doxepina

</list-item><list-item>

■ Zaleplonb

</list-item><list-item>

■ Zolpidem SLb

</list-item>
Sleep onset and maintenance insomnia <list-item>

■ Eszopiclone

</list-item><list-item>

■ Zolpidem CR

</list-item>
Authors

Chandra M. Cherukuri, MD, MS, is an Assistant Professor, Department of Family Medicine, University of Minnesota; and a Faculty Physician, Department of Family Medicine, and Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center. Neeraj Kaplish, MD, is the Medical Director, University of Michigan Health System Sleep Disorder Laboratories; and an Assistant Professor, Department of Neurology, University of Michigan. Deepthi C. Malepati, MD, is a Resident Physician, Department of Internal Medicine, Hennepin County Medical Center. Imran S. Khawaja, MBBS, FAASM, is the Medical Director, Center for Sleep Medicine, VA North Texas Health Care System; and an Associate Professor of Psychiatry and Neurology and Neurotherapeutics, UT Southwestern Medical Center. Shashi K. Bhatia, MD, FACPsych, is a Professor, Department of Psychiatry and Pediatrics, Creighton University School of Medicine. Subhash C. Bhatia, MD, FACPsych, is a Distinguished Professor and the Senior Associate Chair for Academic Affairs and Faculty Development, Department of Psychiatry, Creighton University School of Medicine.

Address correspondence to Chandra M. Cherukuri, MD, MS, Department of Family Medicine, University of Minnesota, 2810 Nicollet Avenue, Minneapolis, MN 55408; email: chandra.cherukuri@hcmed.org.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/00485713-20180514-01

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