Newer treatments can improve the sleep of people with dementia, which may help both patients and caregivers to feel better.
By Regina Patrick, RPSGT
Caretakers of someone with dementia often report that the person sleeps poorly. At night, the person may frequently arouse or sleep for only a very short time (less than 8 hours). The person may also frequently doze throughout the day or have an erratic sleep/wake schedule.
Such poor sleep can be a consequence of the disease that is responsible for the dementia. For example, some brain-damaging diseases hurt the suprachiasmatic nucleus (SCN), the site in the brain of one’s biological clock. This, in turn, can cause delayed or advanced sleep and wake phases, which means that the person with dementia may want to go to sleep very late at night and awaken very late in the morning (ie, delayed phases) or go to sleep very early at night and awaken very early in the morning (ie, advanced phases). Attempts to get the person to go to sleep or awaken at “normal” times may result in insomnia or excessive daytime sleepiness. It can also negatively affect mood (eg, depression), behavior (eg, late afternoon agitated restlessness often called “sundowning”), and cognition (eg, confusion).
Until recently, poor sleep in people with dementia was taken as an irreversible aspect of the disease. Today, however, studies are increasingly showing that sleep quality in people with dementia can indeed be improved, and, consequently, symptoms of poor sleep, such as sundowning, insomnia, and excessive daytime sleepiness, can be diminished.
Sleep and Dementia
Dementia is the progressive destruction of a person’s memory, judgment, abstract thinking, personality, and ability to carry out everyday activities, such as personal grooming and communication. In its early stages, family and friends may note that the person forgets recent conversations or events, repeats himself or herself in conversations, has difficulty grasping new ideas and adapting to changes, finds decision making difficult, or frequently misplaces things. In later stages, a person may need reminders to dress, eat, use the toilet, etc; does not always recognize familiar people or confuses someone familiar with someone else; or becomes easily upset, frustrated, depressed, or angry. In dementia’s last stages, a person may have total memory loss of people, places, and things (although at times there may be brief flashes of memory) and may live in a “time warp” (ie, the person may act and believe that conditions and people, such as long dead parents, still exist as when he or she was young). The progressive brain damage that accompanies dementia may also, in its last stages, result in physical disability so that the person becomes bedridden or wheelchair-dependent, incontinent, unable to communicate with others, unable to use limbs fully, etc, or a person may become restless and increasingly search for something or someone.
The brain damage that causes dementia can be the consequence of neurodegenerative processes (eg, Alzheimer’s disease, dementia with Lewy bodies), vascular damage brought about by blocked or narrowed blood vessels in the brain (ie, vascular dementia), infection (eg, the human immunodeficiency virus [HIV] in HIV-related dementia or prions in Creutzfeldt-Jakob disease, also known as “mad cow disease”), or exposure to toxic substances (eg, ethanol abuse resulting in alcohol-related dementia).
The type of dementia can have unique effects on sleep architecture and other sleep parameters (eg, rapid eye movement [REM] density or spindles). Some research shows that in the early stages of Creutzfeldt-Jakob disease, there is a drastic reduction of slow-wave sleep, abolition of REM sleep, and disappearance of spindles and K-complexes on the EEG waveforms recorded in stage 2 sleep.1 In Alzheimer’s disease, there is a drastic reduction in REM density, a decrease in K-complexes and spindles during stage 2 sleep,2 and a reduction in duration of REM periods.3 In early infection with HIV (during the time it is asymptomatic), there is an increase in the amount of slow-wave sleep, especially in the later portion of the sleep period; frequent REM periods of decreased duration; frequent arousals; and a shortened sleep latency.4-6
These unique effects on sleep may be a reflection of the primary damage occurring in the dementing disease. For example, damage to the SCN may explain some sleep changes that occur in dementias of neurodegenerative origin. The immune response may explain some sleep changes that occur in dementias of infectious origin. For example, studies reveal that people with HIV and Creutzfeldt-Jakob disease have increased blood levels of the peptides tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1 beta).6,7 The levels of these peptides normally increase when infective agents are present. However, a side effect of TNF-alpha and IL-1 beta is that they induce sleep and enhance the duration of slow-wave sleep.
Behavioral consequences of poor sleep quality in people with dementia are increased confusion, worsening mood (eg, increased depression), and, the most troublesome, sundowning. Rather than settling down for the night, people with dementia who exhibit sundowning become restless—walking around aimlessly, rocking, pacing, etc. During this time, they may also exhibit belligerence ranging from a stubborn refusal to go to bed to striking out at caregivers. For a tired caregiver, this sudden burst of energy—which can last for hours or even all night—can be incredibly frustrating and can negatively impact the quality of care.
Activity monitoring (eg, actigraphy) offers a clue to why sundowning occurs. Studies8,9 reveal that persons with dementia often suffer from an advanced sleep phase or a delayed sleep phase. In persons with an advanced sleep phase, early evening is when they are most tired. If caregivers attempt to keep them awake in the early evening so that they will be sleepy enough to stay in bed all night, they may become belligerent due to frustration at being prevented from sleeping when they want to. In persons with delayed sleep phase, they will still be alert and undergoing their biorhythmic “day” at early evening. If caregivers attempt to put them to bed at a socially “normal” time in the evening, they may become belligerent because people are trying to force sleep on them.
A Bright Idea
In recent years, bright-light therapy has shown some promise in reducing sundowning and improving sleep quality in people with dementia. Bright-light therapy can induce a shift in a person’s circadian phases so that the “sleep” phase occurs at night and the “wake” phase occurs during the day. This in turn can reduce problems with sundowning, sleepiness, insomnia, etc. Normally, morning bright-light therapy causes one’s sleep and wake phases to shift to an earlier time the following day. Evening bright-light therapy has the opposite effect (ie, sleep and wake phases take place at a later time the following day).
Researcher Sonia Ancoli-Israel and her colleagues10 compared the effect of morning bright-light therapy vs evening bright-light therapy on shifting phases in residents with dementia living in a residential setting. They found that the rhythmicity of the residents’ cycles improved when the residents had been exposed to either morning bright-light therapy or evening bright-light therapy.
They noted, however, that neither morning nor evening bright-light therapy improved the subjects’ alertness or sleep quality. Ancoli-Israel and her colleagues theorized that no improvement may have occurred in these criteria because no distinction was made between subjects who had Alzheimer’s disease and subjects whose dementia was caused by other illnesses. It may be that dementing diseases that affect the SCN respond differently to bright-light therapy than diseases that do not affect the SCN.
The results of a study by Mishima et al11 support the speculation that different diseases may respond differently to bright-light therapy. In the Mishima study, the researchers compared the nighttime activity of people with vascular dementia with that of people with Alzheimer’s disease after both groups had been treated with morning bright-light therapy. The researchers found that people with vascular dementia had less physical activity at night after therapy while the nighttime activity level of people with Alzheimer’s disease remained the same. They concluded that bright-light therapy may be more effective in improving sleep in someone with vascular dementia than in someone with Alzheimer’s disease.
The Behavioral Approach
Besides bright-light therapy, another nondrug approach to improving sleep quality in people with dementia may be behavior modification and sleep hygiene. Researcher Susan M. McCurry and her colleagues9 examined the efficacy of using these techniques to improve sleep quality in people with dementia who were still being cared for by family members at home. The researchers proposed that, if successful, behavior modification and sleep hygiene could be used to improve sleep quality in a person with dementia, allowing caretakers to care for the person at home for a longer period of time.
The McCurry study involved 31 patient-caretaker dyads; 17 dyads underwent behavioral modification and implemented sleep hygiene while 14 dyads acted as a control. The study lasted 2 months after which the dyads continued either the test condition (ie, behavior modification and sleep hygiene) or maintained the control condition (ie, no behavior modification or sleep hygiene).
For behavior modification, the caretakers of the 17 test dyads were instructed to take daily 30-minute outdoor walks with their patients, to have the patients sit for 1 hour in front of a 2,500 lux light box (ie, bright-light therapy) within 3 hours of the patients’ bedtimes, and to reduce nocturnal light exposure by using only night lights in the patients’ bedrooms or other rooms, such as bathrooms, that the patients might frequent at night. For sleep hygiene, the caregivers of the 17 test dyads were instructed to maintain specific bedtimes for the patients and to try not to vary from those times by more than 30 minutes. They were also told to limit patients’ naps to 30 minutes, to not allow patients to nap past 1 pm, and to identify and, if possible, eliminate triggers for patients’ nocturnal arousals (pets, a bed partner’s snoring, street noise, etc).
Actigraphic monitoring measured the activity of all 31 dyads for 1 week at the outset of the study (baseline), for 1 week at the end of the 2-month study, and, finally, for 1 week 6 months after the study. The researchers found that a combination of bright-light therapy and daily walking improved symptoms of sleepiness, decreased nocturnal awakenings, and decreased nocturnal wake time in patients in the test dyads. By contrast, these criteria worsened in the patients in the control dyads. Six of the patients in the control group were later institutionalized, but none of the patients in the test dyads were institutionalized. McCurry and her colleagues concluded that behavior modification and use of sleep hygiene could improve the sleep of someone with dementia.
Hormonal/Pharmaceutical Treatment
Some research has investigated using melatonin to improve sleep in people with dementia. Melatonin is a sleep-promoting hormone that plays a role in both the initiation and maintenance of sleep. It is produced by the pineal gland and reaches its highest levels during the dark of evening and falls to its lowest levels during the light of day. However, this rhythmic rise and fall is impaired in some forms of dementia (eg, Alzheimer’s disease),12,13 which in turn impairs the rhythmicity of one’s sleep and wake cycles. Studies13 show that exogenous administration of melatonin induces sleep, helps to maintain sleep, and strengthens the circadian rhythm in people with dementia. Additionally, melatonin treatment can reduce sundowning and slow the decline in mental functioning.14,15
Despite the promising results of bright-light therapy, behavior modification, sleep hygiene, and melatonin treatment, people with dementia are often prescribed hypnotics and sedatives to counteract insomnia and sundowning. A consequence of hypnotic/sedative use can be next-day residual sedation. As a result, a person may sleep or act “spaced out” on the day following use of a hypnotic/sedative. In some people with dementia, this residual sedation may worsen problems a person is already having with confusion and memory. Additionally, hypnotic/sedative treatment can impair muscle coordination leading to a greater risk of falls. Bright-light therapy, behavior modification, sleep hygiene, and melatonin treatment have the benefit of avoiding this aspect of drug therapy while improving sleep. Research continues into learning how these nondrug therapies can be most effectively used in people with dementia. Because nondrug therapies may not be effective in the later stages of dementia, scientists also continue investigating how to effectively use hypnotics, sedatives, or other drugs that have a sedating effect, such as antidepressants to improve sleep quality while reducing side effects, such as next-day residual sedation.
Improved sleep means an improved quality of life for a person with dementia through increased alertness, decreased sleepiness, and reduction in behavioral problems. These beneficial consequences have a positive impact on a caregiver’s quality of life and the quality of care the caregiver is able to give. Normally, a caregiver’s own sleep quality begins to suffer as the caregiver deals with a wandering or belligerent person. A moment of inattentiveness on a tired caregiver’s part can potentially allow the person with dementia to get into dangerous situations. Persistent poor sleep quality can cause the caregiver to suffer negative mood changes, such as depression, anger, hopelessness, etc, which in turn can negatively impact the quality of care the person is able to give someone with dementia. Poor sleep quality and its impact on the caregiver may be the most common factor leading caretakers to institutionalize a person with dementia. However, as the McCurry study suggests, improving sleep quality in a person with dementia may delay having to place the person in a institutional setting and improve quality of life of not only the person with dementia but also that of the caregivers.
Regina Patrick, RPSGT, is a contributing writer for Sleep Review.
References
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