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  • Updated 12.17.2023
  • Released 09.09.1993
  • Expires For CME 12.17.2026

Sleep and dementia



Disordered sleep and dementia are two neurologic issues that are found in many of the same patients and may indeed interact. Insomnia, hypersomnia, circadian rhythm disorders, and sleep-disordered breathing are more prevalent in patients with dementia than in age-matched controls. REM sleep behavior disorder can herald a synucleinopathy, such as dementia with Lewy bodies or Parkinson disease. The treatment of excessive daytime sleepiness and insomnia in patients with dementia is not well described because many medications have risks that outweigh their benefits. Nevertheless, REM sleep behavior disorder has been shown to respond to both clonazepam and melatonin in clinical trials. Continuous positive airway pressure therapy can improve cognition in some cases of obstructive sleep apnea.

Key points

• Various sleep problems such as insomnia, hypersomnia, longer napping duration, circadian rhythm disorders, sleep-disordered breathing, and REM sleep behavior disorder are more prevalent in patients with dementia than in age-matched controls.

• In the preclinical stages of Alzheimer disease, excessive daytime sleepiness and poor sleep efficiency appear to be associated with greater cerebral beta-amyloid burden, as measured by amyloid PET imaging. Excessive daytime sleepiness is also associated with greater cerebral Lewy body burden and more atrophy in the basal forebrain, as documented in autopsy studies.

• Polysomnography is valuable as a diagnostic tool in dementia patients with sleep disorders, as relatively common sleep disorders, such as obstructive sleep apnea and REM sleep behavior disorder, are diagnosed based on the sleep study results.

• Bright light therapy, walking with family members, and melatonin have all been used effectively to manage the sundown syndrome and poor sleep quality, which are relatively common complaints in patients with dementia with Lewy bodies, Alzheimer disease, Parkinson disease, and other dementing illnesses.

• REM sleep behavior disorder is more common in patients with synucleinopathies such as dementia with Lewy bodies and Parkinson disease. In combination with excessive daytime sleepiness and objective signs of napping, idiopathic REM sleep behavior disorder is a predictor for mild cognitive impairment and motor dysfunction after 2 to 12 years of follow-up.

• Melatonin and clonazepam are both effective in reducing symptoms of REM sleep behavior disorder. Melatonin can improve sleep quality in patients with mild to moderate Alzheimer disease and Parkinson disease.

Historical note and terminology

Sundown syndrome. “Sundowning,” or the nocturnal exacerbation of delirium, agitation, and aggressiveness has been recognized since the time of Hippocrates. Cameron first explored sundowning experimentally and reported that patients with dementia brought into a dark room during the daytime were likely to become agitated and confused (20). The terms “sundown syndrome” or “cognitive fluctuations” are now broadly used to describe a set of neuropsychiatric symptoms that begin in the afternoon or early evening, including confusion, inattention, anxiety, pacing, wandering, and resistance to redirection (147; 21; 90).

Hypersomnia. Excessive daytime sleepiness is common in the synucleinopathies, such as Parkinson disease and dementia with Lewy bodies (161; 81), or it can be associated with sleep disordered breathing or idiopathic REM sleep disorder (108; 111; 43). In Parkinson disease, hypersomnia can be related to the disease process itself, advanced age, dopaminergic medications, or to other sleep disorders such as restless legs syndrome (163; 77). Longer napping duration (for greater than 120 min/d, measured by actigraphy) was noted to be associated with greater cognitive decline in a large group of older men who were followed cognitively over a 12-year period (91).

Insomnia. Chronic insomnia is the most prevalent sleep disorder in the general population. It is manifested by difficulty in getting to sleep, staying asleep, and in reduced quality of sleep with daytime consequences. Parkinson disease and insomnia can be aggravated by mood disorders, tremors, and nocturia (161). Some authors have pointed out that insomnia symptom subtypes can assist in predicting signs of prodromal neurodegeneration (156). They showed, for example, that older people with sleep-onset insomnia at baseline were more likely to develop motor (poor balance and slowed gait) and cognitive problems in follow-up.

REM sleep behavior disorder (RBD). This condition is either primary or secondary. Idiopathic REM sleep behavior disorder was initially described in humans in 1985 (121). It is manifested by violent behaviors, dream re-enactment, vocalizations, or involuntary leg movements during rapid eye movement (REM) or dreaming sleep. Secondary REM sleep behavior disorder has been strongly linked to a set of neurodegenerative disorders known as the synucleinopathies, which include Parkinson disease, dementia with Lewy bodies, and multiple system atrophy (73; 50; 86).

Restless legs syndrome (RLS). This condition is either primary or secondary. Patients with restless legs syndrome feel the urge to move their legs whenever they sit down or lie down. Idiopathic restless legs syndrome does not predispose patients to develop Parkinson disease or one of the synucleinopathies in the way that REM sleep behavior disorder does. Secondary restless legs syndrome occurs in 21% of Parkinson disease patients. Compared to idiopathic restless legs syndrome, it begins later in life, is less likely to be associated with a positive family history and is less likely to be associated with a low serum ferritin level (106).

Periodic limb movements of sleep (PLMS). These sleep-related involuntary limb movements can be associated with restless legs syndrome, sleep apnea, and REM sleep behavior disorder. In a study of 146 older stroke-free adults who had a polysomnogram and an MRI within 6 months of each other, a PLMS index of 15/hr or more was recorded in 33% of participants (36). Moderate to severe white matter hyperintensities were present in 23%, and more than 10 basal ganglia enlarged perivascular spaces were present in 30%. In a fully adjusted model, there was no association between PLMS index and any of the neuroimaging signatures of small vessel disease.

Sleep-disordered breathing. Symptoms of obstructive apnea or sleep-disordered breathing can vary from significant snoring with frequent arousals to complete airway obstruction with apneas. There has been mixed evidence in the past concerning the association of sleep-disordered breathing with dementia because it is hard to know about the directionality of the association (89). The difficulty with the older studies was their cross-sectional design. Prospective studies have documented a cause-and-effect relationship between sleep-disordered breathing, intermittent hypoxemia, and the risk of mild cognitive impairment and dementia (108; 57; 102; 124; 05; 119).

Slow-wave sleep. There is now evidence that deep nonrapid eye movement (NREM) slow-wave sleep might play a protective role in certain neurodegenerative disorders, such as Alzheimer disease and Parkinson disease (74; 62). Slow-wave sleep is thought to counteract the accumulation of beta-amyloid, and possibly also alpha-synuclein, in the brain. When 129 Parkinson patients with motor testing were retrospectively examined with polysomnography, a higher power of slow-wave sleep was shown to be associated with slower motor progression over a mean of 4.6 years (122). When participants in the Framingham Heart Study were followed with polysomnography over a 5-year period, researchers found that each percentage point decrease in slow-wave sleep was associated with a 27% increase in incident dementia (HR=1.27; CI=1.06-1.54; p=0.01) (62). Others have shown that reduction in slow-wave sleep is associated with an increase in white matter hyperintensities related to cerebrovascular disease (23).

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