There has been a documented change in the distribution of sleep stages with older adults spending more time in the lighter sleep stages (N1 and N2) and less time in deep sleep (N3; slow wave sleep) and dream sleep (REM or R sleep) compared to younger adults. This reduction in slow wave sleep is progressive with advancing age. However, as Ohayon et al. (2) have shown, slow wave sleep is already decreasing in middle-age and by age 60, stabilizes. However, there are more frequent shifts from one sleep stage to another and more transient arousals lasting for only a few seconds, which result in more fragmented sleep and more subjective complaints of poor sleep.

As many as 57% of older adults complain of significant sleep disruption and almost 20% complain of early morning awakening despite wanting to sleep later (3). This decreased sleep time results in insufficient sleep, which has been shown to be associated with negative consequences including impaired immune functioning, depression, hypertension, and increased mortality.

Homeostatic and circadian changes dramatically affect sleep and wake regulation, and these changes have been documented in the older adult (4). The homeostatic process involves the need or drive to sleep building up throughout the day and then dissipating during sleep. In insomnia, the drive to sleep is weaker than the drive to
stay awake. Sleep maintenance problems may be due to homeostatic mechanisms declining too quickly and the sleep drive only being sufficient in the first part of the night and losing momentum during the second part.

As mentioned, slow wave sleep declines with age and this decline may also be indicative of reduced sleep drive (5,6). Some studies show that after sleep deprivation and therefore after a buildup of sleep drive, older patients sleep much longer and show more deep sleep delta activity compared to their sleep before sleep deprivation. This is further evidence supporting the notion that older individuals may have a reduced homeostatic drive that interferes with their sleep.

Another fundamental change that occurs with age is a dampening in the amplitude of circadian rhythms. This disruption may produce changes in body temperature (where minimum temperature occurs much earlier in the nocturnal sleeping period), hormonal levels, urinary electrolytes, and rest/activity profiles.

Several studies have indicated that with age comes a desynchronization of the internal circadian rhythm. For instance, Wever reported that 70% of older subjects and only 20% of younger subjects became desynchronized during “free running” (e.g., not synchronized to environmental time cues and fluctuating on a cycle slightly longer than 24 hours) (7).

Circadian rhythms and oscillations in neurons and hormones throughout a 24-hour cycle are controlled by the suprachiasmatic nucleus (SCN), situated in the anterior part of the hypothalamus. In adults over the age of 80 years, the volume of the SCN decreases by 40% (8). Further evidence for age-related disruptions in circadian rhythmicity comes from animal studies showing that lesioned SCNs result in disrupted circadian rhythms with animals wakeful during the night, sleepy during the day, and napping more during the day (9). This sleep pattern is very similar to that of older patients, thus supporting one theory that age-related decay of the SCN may play a pivotal role in sleep disturbances.

Another hypothesis for major changes in circadian rhythms in older adults has to do with the environment. Deficient zeitgebers, or exogenous cues that synchronize endogenous time-keeping biological clocks, cause circadian rhythms to become disrupted with age (10). Exposure to bright light, the strongest zeitgeber, is reduced in older patients. One study reported that the median amount of time community-dwelling older adults spent in light over 1000 lux was only 4% (11). Older adults also have less exposure to other zeitgebers that entrain the SCN. For instance, it has been widely reported that physical activity helps normalize sleep/wake cycles; therefore, older adults who may be functionally impaired are more likely to have more disturbed sleep.

Sleep and circadian rhythms are also controlled by melatonin, a hormone secreted during darkness from the pineal gland. However, melatonin levels decrease with age in part due to less bright light exposure and a significant decline in the number of beta-adrenergic receptors in the pineal gland (12).

The most common sleep-related complaint in the elderly is insomnia. Insomnia is defined as both persistent difficulties falling and/or staying asleep despite the opportunity for rest, which result in the disruption in one’s ability to carry out daily affairs.

Since older adults have high rates of medical and psychiatric disorders they often take multiple prescription and over-the counter medications. These medications can alter and severely interfere with sleep.

Commonly used medications in older patients, such as beta-blockers, bronchodilators, corticosteroids, decongestants, and diuretics, as well as other cardiovascular, neurological, psychiatric, and gastrointestinal medications, can all adversely affect sleep. Antidepressants, such as selective serotonin reuptake inhibitors (SSRIs) and serotonergic and noradrenergic reuptake inhibitors, are known to have side effects that disrupt sleep and cause insomnia or produce daytime fatigue. Sedating antihistamines commonly taken to relieve colds or allergies, even if over-the-counter, often contain substances like pseudoephedrine or phenylpropanolamine that may induce drowsiness or cause sleeplessness, respectively.
Sometimes, individuals self-medicate and use alcohol to induce sleep. Th is has paradoxical effects because although alcohol may decrease the time required to fall asleep, the second half of the sleep period is often disrupted, leading the individual to wake up in the middle of the night. This sleep disruption can have a dangerous cumulative effect, leading to daytime sleepiness and fatigue.

Polypharmacy and prescriptions of sedative drugs is increasingly prevalent among older adults (32), often without consideration of its effect on the patient’s sleep. When possible, sedating medications should be administered prior to bedtime, while stimulating medications and diuretics should be taken during the day. In the elderly, the risk of falls, cognitive impairment, and respiratory depression are of particular concern, although recent data suggest that insomnia and disrupted sleep, and not hypnotics, increase the risk of falls (16,33, 34 and 35). Recent studies by Stone and colleagues further support this finding, by demonstrating an increase in risk of falls associated with sleep duration and fragmentation in subjective and objective measures of sleep in older women independent of benzodiazepine use and other risk factors for falls (36,37).

As with all sleep disorders, a thorough sleep history is required in order to evaluate and make the diagnosis of insomnia. To best identify precipitating and perpetuating factors related to insomnia, it is helpful to obtain a history about a typical 24-hour day. It is also helpful to have the patient keep a sleep diary to estimate the amount of time it takes to fall asleep, number of awakenings, sleep quality, duration, and timing. Other information about the sleep environment, medical and psychiatric history, and use of alcohol, medications, and caffeine should also be obtained.

In 2005, the NIH State of the Science conference on insomnia concluded that the most effective and safe treatment for insomnia is cognitive-behavioral therapy (CBT) (38). CBT includes both the cognitive component of challenging irrational or distorted beliefs about sleep, and the behavioral component, which includes education on proper sleep hygiene, relaxation techniques, sleep restriction, and stimulus control therapy. In older adults, CBT-I has been shown to be as effective as medications in the short-run and to have better long-term outcomes in the treatment of insomnia (39). Although pharmacological treatments may be of more immediate help, particularly in the acute treatment phase, in order to maintain long-term clinical gains, nonpharmacological or combined approaches may be more effective.

When prescription medications are indicated, the National Institutes of Health (NIH) State of the Science Conference on Insomnia (38)

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