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Behavioural and psychological symptoms of dementia (BPSD) are commonly present in patients with Alzheimer’s disease (AD). Disturbed sleep quality is also observed in AD patients. However, the effects of memantine on sleep architecture have not been investigated. The purpose of this study was to investigate the effects of memantine on polysomnography (PSG) variables and BPSD.
In total, 12 patients with AD (mean age: 79.0±4.1 years old) were enrolled in this study. The following tests were performed: the Neuropsychiatric Inventory for the assessment of BPSD, the Mini-Mental State Examination (MMSE) for cognitive function, and PSG for evaluation of sleep architecture. After baseline examinations, patients were treated with memantine according to a standard prescription protocol. After being treated with 20 mg/day of memantine for 4 weeks, examinations were carried out again.
All subjects completed the trial. The mean MMSE and NPI scores were 22.6±3.4 and 13.8±12.9, respectively. Treatment with memantine significantly decreased the NPI score (5.8±4.3, p<0.01). There were significant decreases in the scores of subscales for anxiety (p=0.04) and irritability/lability (p=0.04). PSG demonstrated a longer total sleep time (TST) (p<0.01), increases in sleep efficiency (p<0.01) and time spent in stage II (% TST, p=0.02), and decreases in nocturnal awakening (p<0.01), the periodic limb movement index (p<0.01), and time spent in stage I (% TST, p=0.02).
Memantine was effective for reducing fragmented sleep and improving BPSD, and was well tolerated.
This chapter focuses on formulating an integrated position on sleepiness in long sleepers. It reviews studies conducted through a pathology lens, where long sleepers frequently include individuals in poor physical or psychological health, who are often older and experience poor nocturnal sleep quality, including insomnia. Most epidemiological studies investigating sleepiness and the behavioral and psychological characteristics of long sleepers have examined the extremes of sleep duration relative to each other. Existing empirically supported models of sleep regulation postulate that duration and timing of sleep are regulated by an interaction between a circadian pacemaker, which programs daily cycles in sleep propensity, and a sleep homeostat, which tracks increases in sleep pressure. Investigations conducted outside the U-shaped pathology lens have also found that long sleepers who do not have insomnia are no sleepier than midrange sleepers.