Objective: To characterize the sleep-related issues in dementia with Lewy bodies (DLB)/Lewy body disease. Materials and Methods: Review of the literature and several clinical studies are presented. Results: Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia manifested by vivid and often frightening dreams associated with simple or complex motor behavior during REM sleep. RBD is frequently associated with the synucleinopathies (e.g., DLB, Parkinson’s disease, and multiple system atrophy) but rarely associated with the amyloidopathies and tauopathies. A double dissociation on neuropsychological testing has been shown, with worse impairment on measures of attention, visual perceptual-organization, and letter fluency for patients with RBD/dementia, while patients with Alzheimer's disease (AD) have worse performance on confrontation naming and verbal memory tasks. More recent analyses indicate that the neuropsychometric performance in patients with dementia and RBD but without parkinsonism or visual hallucinations resembles the performance typical of DLB, and can be differentiated from the dementia of autopsy-proven AD. Therefore, in the absence of visual hallucinations or parkinsonism, the presentation of dementia and RBD may indicate underlying Lewy body disease. Neuropathologic studies to date involving RBD associated with a neurodegenerative disorder (n=15 patients) have demonstrated Lewy body disease or multiple system atrophy in all cases. Thus, although RBD is currently regarded as a supportive feature for the diagnosis of DLB, the recent data suggests that in the setting of degenerative dementia, RBD should be considered a core diagnostic feature for DLB. Polysomnographic data suggests that sleep disorders may contribute to but do not entirely account for fluctuating cognition in DLB. However, since obstructive sleep apnea, periodic limb movement disorder, REM sleep behavior disorder, and insomnia/poor sleep efficiency are potentially treatable, therapies directed toward these sleep disorders could improve fluctuations in arousal and cognition. REM sleep-wakefulness dissociations that are characteristic of narcolepsy (RBD, daytime hypersomnolence, hallucinations, cataplexy), may explain several features of Parkinson’s disease (PD) as well as DLB. Specifically, the sleep attacks of PD may represent REM sleep intrusions into wakefulness, and the visual hallucinations of PD with psychosis may represent the dream imagery of REM sleep intruding into wakefulness. One could expand this concept to hypothesize that the hypersomnolence in some patients with DLB represent REM sleep intrusions into wakefulness, the visual hallucinations of unmedicated DLB patients represent dream imagery intrusions, and the drop attacks or stroke-like episodes of DLB represent cataplexy-like intrusions of muscle atonia into wakefulness. If future research supports the hypothesis that REM sleep dyscontrol underlies hypersomnolence, visual hallucinations, and stroke-like episodes in some patients with DLB, then therapies already used in the management of narcolepsy may be efficacious in patients with DLB. Conclusion: Further characterization of the sleep issues in DLB may provide insights into the symptomatology of DLB and potentially lead to more effective therapies for managing difficult clinical problems in patients with DLB.
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