As humans live longer, a renewed focus on quality of life has made the prompt diagnosis and treatment of sleep-related disorders in older adults increasingly necessary.1 Normative aging results in multiple changes in sleep architecture, including decreased total sleep time, decreased sleep efficiency, decreased slow-wave sleep (SWS), and increased awakenings after sleep onset.2 Sleep disturbances in older adults are increasingly recognized as multifactorial health conditions requiring comprehensive modification of risk factors, diagnosis, and treatment.3
In this article, we discuss the effects of aging on sleep architecture and provide an overview of primary sleep disorders in older adults. We also summarize strategies for diagnosing and treating sleep disorders in these patients.
Elements of the sleep cycle
The human sleep cycle begins with light sleep (sleep stages 1 and 2), progresses into SWS (sleep stage 3), and culminates in rapid eye movement (REM) sleep. The first 3 stages are referred to as non-rapid eye movement sleep (NREM). Throughout the night, this coupling of NREM and REM cycles occurs 4 to 6 times, with each successive cycle decreasing in length until awakening.4
Two complex neurologic pathways intersect to regulate the timing of sleep and wakefulness on arousal. The first pathway, the circadian system, is located within the suprachiasmatic nucleus of the hypothalamus and is highly dependent on external stimuli (light, food, etc.) to synchronize sleep/wake cycles. The suprachiasmatic nucleus regulates melatonin secretion by the pineal gland, which signals day-night transitions. The other pathway, the homeostatic system, modifies the amount of sleep needed daily. When multiple days of poor sleep occur, homeostatic sleep pressure (colloquially described as sleep debt) compensates by increasing the amount of sleep required in the following days. Together, the circadian and homeostatic systems work in conjunction to regulate sleep quantity to approximately one-third of the total sleep-wake cycle.2,5
Age-related dysfunction of the regulatory sleep pathways leads to blunting of the ability to initiate and sustain high-quality sleep.6 Dysregulation of homeostatic sleep pressure decreases time spent in SWS, and failure of the circadian signaling apparatus results in delays in sleep/wake timing.2 While research into the underlying neurobiology of sleep reveals that some of these changes are inherent to aging (Box7-14), significant underdiagnosed pathologies may adversely affect sleep architecture, including polypharmacy, comorbid neuropathology (eg, synucleinopathies, tauopathies, etc.), and primary sleep disorders (insomnias, hypersomnias, and parasomnias).15
Box
The effects of aging on sleep architecture
It has long been known that sleep architecture changes significantly with age. One of the largest meta-analyses of sleep changes in healthy individuals throughout childhood into old age found that total sleep time, sleep efficiency, percentage of slow-wave sleep, percentage of rapid eye movement sleep (REM), and REM latency all decreased with normative aging.7 Other studies have also found a decreased ability to maintain sleep (increased frequency of awakenings and prolonged nocturnal awakenings).8
Based on several meta-analyses, the average total sleep time at night in the adult population decreases by approximately 10 minutes per decade in both men and women.7,9-11 However, this pattern is not observed after age 60, when the total sleep time plateaus.7 Similarly, the duration of wake after sleep onset increases by approximately 10 minutes every decade for adults age 30 to 60, and plateaus after that.7,8
Epidemiologic studies have suggested that the prevalence of daytime napping increases with age.8 This trend continues into older age without a noticeable plateau.
A study of a nationally representative sample of >7,000 Japanese participants found that a significantly higher proportion of older adults take daytime naps (27.4%) compared with middle-age adults (14.4%).12 Older adults nap more frequently because of both lifestyle and biologic changes that accompany normative aging. Polls in the United States have shown a correlation between frequent napping and an increase in excessive daytime sleepiness, depression, pain, and nocturia.13
While sleep latency steadily increases after age 50, recent studies have shown that in healthy individuals, these changes are modest at best,7,9,14 which suggests that other pathologic factors may be contributing to this problem. Although healthy older people were found to have more frequent arousals throughout the night, they retained the ability to reinitiate sleep as rapidly as younger adults.7,9
Primary sleep disorders
Obstructive sleep apnea (OSA) is one of the most common, yet frequently underdiagnosed reversible causes of sleep disturbances. It is characterized by partial or complete airway obstruction culminating in periods of involuntary cessation of respirations during sleep. The resultant fragmentation in sleep leads to significant downstream effects over time, including excessive daytime sleepiness and fatigue, poor occupational and social performance, and substantial cognitive impairment.3 While it is well known that OSA increases in prevalence throughout middle age, this relationship plateaus after age 60.16 An estimated 40% to 60% of Americans age >60 are affected by OSA.17 The hypoxemia and fragmented sleep caused by unrecognized OSA are associated with a significant decline in activities of daily living (ADL).18 Untreated OSA is strongly linked to the development and progression of several major health conditions, including cardiovascular disease, diabetes mellitus, hypertension, stroke, and depression.19 In studies of long-term care facility residents—many of whom may have comorbid cognitive decline—researchers found that unrecognized OSA often mimics the progressive cognitive decline seen in major neurocognitive disorders.20 However, classic symptoms of OSA may not always be present in these patients, and their daytime sleepiness is often attributed to old age rather than to a pathological etiology.16 Screening for OSA and prompt initiation of the appropriate treatment may reverse OSA-induced cognitive changes in these patients.21
The primary presenting symptom of OSA is snoring, which is correlated with pauses in breathing. Risk factors include increased body mass index (BMI), thick neck circumference, male sex, and advanced age. In older adults, BMI has a lower impact on the Apnea-Hypopnea Index, an indicator of the number of pauses in breathing per hour, when compared with young and middle-age adults.16 Validated screening questionnaires for OSA include the STOP-Bang Questionnaire (Table 122), OSA50, Berlin Questionnaire, and Epworth Sleepiness Scale, each of which is used in different subpopulations. The current diagnostic standard for OSA is nocturnal polysomnography in a sleep laboratory, but recent advances in home sleep apnea testing have made it a viable, low-cost alternative for patients who do not have significant medical comorbidities.23 Standard utilized cutoffs for diagnosis are ≥5 events/hour (hypopneas associated with at least 4% oxygen desaturations) in conjunction with clinical symptoms of OSA.24
Continue to: Treatment