Sleep-Disordered Breathing and Cognitive Impairment in Elderly Japanese-American Men

Foley, Daniel J.; Masaki, Kamal; White, Lon R.; Larkin, Emma K.; Monjan, Andrew A.; Redline, Susan

doi:10.1093/sleep/26.5.596

Cited by 95 publications

(82 citation statements)

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“…Such findings are not surprising as associations between OSA and some cognitive impairment are well established in multiple studies including sleep disorders clinic patients, older adults, patients with Alzheimer disease, and nursing home patients. [71][72][73][74][75][76][77][78][79] We also found that OSA treatment improves nighttime sleep in PD. 80 OSA treatment is therefore clinically indicated, as it may also reduce NMS impairment and improve quality of life.…”

supporting

confidence: 52%

Effects of Sleep Disorders on the Non-Motor Symptoms of Parkinson Disease

Neikrug

Maglione

Liu³

et al. 2013

Journal of Clinical Sleep Medicine

102

106

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Study Objectives: To evaluate the impact of sleep disorders on non-motor symptoms in patients with Parkinson disease (PD). Design: This was a cross-sectional study. Patients with PD were evaluated for obstructive sleep apnea (OSA), restless legs syndrome (RLS), periodic limb movement syndrome (PLMS), and REM sleep behavior disorder (RBD). Cognition was assessed with the Montreal Cognitive Assessment and patients completed self-reported questionnaires assessing non-motor symptoms including depressive symptoms, fatigue, sleep complaints, daytime sleepiness, and quality of life. Setting: Sleep laboratory. Participants: 86 patients with PD (mean age = 67.4 ± 8.8 years; range: 47-89; 29 women). Interventions: N/A. Measurements and Results: Having sleep disorders was a predictor of overall non-motor symptoms in PD (R 2 = 0.33, p < 0.001) while controlling for age, PD severity, and dopaminergic therapy. These analyses revealed that RBD (p = 0.006) and RLS (p = 0.014) were signifi cant predictors of increased non-motor symptoms, but OSA was not. More specifi cally, having a sleep disorder signifi cantly predicted sleep complaints (ΔR 2 = 0.13, p = 0.006), depressive symptoms (ΔR 2 = 0.01, p = 0.03), fatigue (ΔR 2 = 0.12, p = 0.007), poor quality of life (ΔR 2 = 0.13, p = 0.002), and cognitive decline (ΔR 2 = 0.09, p = 0.036). Additionally, increasing number of sleep disorders (0, 1, or ≥ 2 sleep disorders) was a signifi cant contributor to non-motor symptom impairment (R 2 = 0.28, p < 0.001). Conclusion: In this study of PD patients, presence of comorbid sleep disorders predicted more non-motor symptoms including increased sleep complaints, more depressive symptoms, lower quality of life, poorer cognition, and more fatigue. RBD and RLS were factors of overall increased non-motor symptoms, but OSA was not. S C I E N T I F I C I N V E S T I G A T I O N SP arkinson disease (PD) is a progressive neurodegenerative disorder primarily characterized by motor symptoms and increasing motor-related disability, including bradykinesia, rigidity, and tremor.1 Non-motor symptoms (NMS) such as sleep dysfunction, sleepiness, fatigue, pain, and depressive symptoms, are common in PD. In a large multicenter study, NMS were reported by 99% of 1072 PD patients.2 The presentation of NMS in PD is highly variable, and the understanding of such heterogeneity in PD is limited and incomplete.3,4 Chaudhuri et al. 4 suggested that NMS dominate the clinical picture in patients with PD and contribute to the severe disability these patients experience, impair quality of life, and even shorten life expectancy. Studies have suggested that NMS, more than motor symptoms, may impact caregiver distress, quality of life, institutionalization rates, and overall costs related to PD .4-6 A 15-year follow-up study of patients with PD reported that the NMS that did not respond to dopamine therapy (e.g., dementia, sleep disruption) were "more disabling than endof-dose failure or dyskinesia" and were the major cause of morbidity and mortality. Sixty to 98% of pati...

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supporting

confidence: 52%

Effects of Sleep Disorders on the Non-Motor Symptoms of Parkinson Disease

Neikrug

Maglione

Liu³

et al. 2013

Journal of Clinical Sleep Medicine

102

106

View full text Add to dashboard Cite

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“…11,39 It is plausible that poor sleep differentially affects executive function by disrupting corticalsubcortical connections within the prefrontal cortex through vascular damage. 3,19,30,40 This study has several important limitations. We were unable to rule out potential selection bias; it is plausible that those with the greatest cognitive decline were less likely to return for a follow-up assessment.…”

Section: Resultsmentioning

confidence: 96%

Sleep disturbances and cognitive decline in the Northern Manhattan Study

et al. 2016

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Objective: To examine frequent snoring, sleepiness, and sleep duration with baseline and longitudinal performance on neuropsychological (NP) battery. Methods:The analysis consists of 711 participants of the Northern Manhattan Study (NOMAS) with sleep data and NP assessment (age 63 6 8 years, 62% women, 18% white, 17% black, 67% Hispanic) and 687 with repeat NP testing (at a mean of 6 6 2 years). The main exposures were snoring, sleepiness, and sleep duration obtained during annual follow-up. Using factor analysis-derived domain-specific Z scores for episodic memory, language, executive function, and processing speed, we constructed multivariable regression models to evaluate sleep symptoms with baseline NP performance and change in performance in each NP domain.

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“…Of the remaining 1,473, 49% completed the PSG. 11 Of these 718 men, 502 died through 2010, and, of these, 167 were included in the autopsy substudy and in this analysis. Data were made available through the National Institute on Aging.…”

Section: Methods Study Population the Honolulu-asia Agingmentioning

confidence: 99%

“…Details of the PSG protocol have been described. 11 We examined apnea-hypopnea index (AHI), duration of apnea or hypopnea, duration of hypoxemia, minimum oxygen saturation during REM and non-REM sleep, duration of slow-wave (SWS, non-REM stage N3) and REM sleep, and arousals. SWS scoring was based on strict amplitude and frequency criteria.…”

Section: Methods Study Population the Honolulu-asia Agingmentioning

confidence: 99%

Associations of brain lesions at autopsy with polysomnography features before death

et al. 2015

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Objective: To determine how sleep-disordered breathing, nocturnal hypoxia, and changes in sleep architecture in the elderly may be related to the development of the neuropathologic correlates of dementia.Methods: The Honolulu-Asia Aging Study is a prospective cohort study of Japanese American men in Honolulu, HI. We examined brain lesions at autopsy (Braak stage, neurofibrillary tangle and neuritic plaque counts, microinfarcts, generalized brain atrophy, lacunar infarcts, Lewy bodies [LBs], neuronal loss and gliosis in the locus ceruleus) in 167 participants who underwent polysomnography in 1999-2000 (mean age, 84 years) and died through 2010 (mean 6.4 years to death). Polysomnography measures included the apnea-hypopnea index, duration of apnea or hypopnea, duration of hypoxemia, minimum oxygen saturation (SpO 2 ), duration of slow-wave sleep (SWS, non-REM stage N3), and arousals.Results: Sleep duration with SpO 2 ,95% was associated with higher levels of microinfarcts (adjusted odds ratio [OR] 3.88, 95% confidence interval [CI] 1.10-13.76, comparing the highest to lowest quartiles of %sleep with SpO 2 ,95%). Greater SWS duration was associated with less generalized atrophy (adjusted OR 0.32, 95% CI 0.10-1.03, comparing highest to lowest quartiles of %sleep in SWS). LBs were less common with greater %sleep with SpO 2 ,95% (adjusted OR 0.17, 95% CI 0.04-0.78, comparing highest to lowest quartiles). Higher minimum SpO 2 during REM sleep was associated with less gliosis and neuronal loss in the locus ceruleus. Cognitive scores declined less among men with greater SWS duration. LRT 5 likelihood ratio test; NFT 5 neurofibrillary tangle; NP 5 neuritic plaque; OR 5 odds ratio; OSA 5 obstructive sleep apnea; PSG 5 polysomnography; SBP 5 systolic blood pressure; SDB 5 sleep-disordered breathing; SpO 2 5 oxygen saturation as measured by pulse oximetry; SWS 5 slow-wave sleep. Conclusions:Sleep-disordered breathing (SDB), 1 nocturnal hypoxia, 1 and changes in sleep architecture 2,3 may lead to dementia in the elderly. A causal association is supported by the finding that continuous positive airway pressure treatment in patients with obstructive sleep apnea (OSA) may improve cognition, even after dementia has developed. 4 It remains unclear how SDB, nocturnal hypoxia, and sleep architecture may be related to the development of brain lesions associated with dementia. Hypoxia and altered brain perfusion during sleep may cause neuronal injury, leading to impaired cognitive functioning. Alternatively, abnormalities in regions such as the locus ceruleus may alter sleep architecture or control

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Sleep-Disordered Breathing and Cognitive Impairment in Elderly Japanese-American Men

Cited by 95 publications

References 0 publications

Effects of Sleep Disorders on the Non-Motor Symptoms of Parkinson Disease

Effects of Sleep Disorders on the Non-Motor Symptoms of Parkinson Disease

Sleep disturbances and cognitive decline in the Northern Manhattan Study

Associations of brain lesions at autopsy with polysomnography features before death

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