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Sleep dysfunction in Alzheimer’s disease and other dementias

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Changes in sleep architecture and circadian rhythms, including increased sleep latency and nighttime awakenings, decreased slow-wave sleep, rapid eye movement sleep, and total sleep time, and increased daytime napping are widespread in people with dementia. In addition, cyclic agitation episodes (“sundowning”), nightmares or hallucinations, sleep attacks, and nocturnal behavioral outbursts are associated with specific dementia syndromes. Sleep hygiene recommendations, particularly those aimed at reducing daytime sleep and improving the sleep environment and routine, can offset the circadian disturbances of some dementia patients. However, they can be burdensome for caregivers to implement, and must be targeted to the specific patterns of sleep disturbances patients are experiencing. Pharmacologic treatments may be useful for symptomatic treatment of insomnia and nighttime behavioral disturbances in dementia patients, but there have been few controlled trials demonstrating their efficacy or long-term safety. Clonazepam is highly effective for treating the nighttime behaviors associated with rapid eye movement behavior disorder. For most dementia patients, however, the side effect risks of prolonged use of sedating medications must be weighed against the potential benefits. Dementia patients should be evaluated for common primary sleep disorders that may contribute to nighttime behavioral disturbances and impact treatment decisions. Continuous positive airway pressure, the gold standard for treating obstructive sleep apnea, can be tolerated by mild to moderately demented individuals with support from supervising caregivers. Increased daily light exposure and physical activity may help normalize circadian restactivity rhythms in some dementia patients, although the frequency and dose needed to maintain treatment effects is currently not known.

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McCurry, S.M., Ancoli-Israel, S. Sleep dysfunction in Alzheimer’s disease and other dementias. Curr Treat Options Neurol 5, 261–272 (2003). https://doi.org/10.1007/s11940-003-0017-9

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