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Neurobiol Aging. 2015 Feb;36(2):1083-90. doi: 10.1016/j.neurobiolaging.2014.09.009. Epub 2014 Sep 18.

Sleep spindles in Parkinson's disease may predict the development of dementia.

Author information

1
Centre for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montreal, Quebec, Canada; Department of Psychology, Université de Montréal, Montreal, Quebec, Canada.
2
Centre for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montreal, Quebec, Canada; Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada.
3
Centre for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montreal, Quebec, Canada; Department of Psychology, Université du Québec à Montréal, Montreal, Quebec, Canada.
4
Unité des troubles du mouvement André Barbeau, Centre Hospitalier de l'Université de Montréal, Montreal, Quebec, Canada.
5
Centre for Advanced Research in Sleep Medicine, Hôpital du Sacré-Cœur de Montréal, Montreal, Quebec, Canada; Department of Psychology, Université du Québec à Montréal, Montreal, Quebec, Canada. Electronic address: gagnon.jean-francois.2@uqam.ca.

Abstract

Sleep disturbances and cognitive impairment are common non-motor manifestations of Parkinson's disease (PD). Recent studies suggest that sleep spindles and slow waves play a role in brain plasticity mechanisms and are associated with cognitive performance. However, it remains unknown whether these sleep parameters could serve as markers of cognitive decline in PD. Therefore, we examined whether alterations in sleep spindles and slow waves at baseline visit were associated with increased likelihood of developing dementia at follow-up in PD. Sixty-eight nondemented PD patients (64.9 ± 8.8 years old; 46 men) participated in the study, along with 47 healthy individuals (65.0 ± 10.6 years old; 30 men). All participants underwent baseline polysomnographic recording and a comprehensive neuropsychological assessment. Sleep spindles (12-15 Hz) and slow waves (>75 μV and <4 Hz) were automatically detected on all-night non-rapid eye movement sleep electroencephalography. At follow-up (mean: 4.5 years later), 18 PD patients developed dementia (70.2 ± 7.6 years old; 13 men) and 50 remained dementia-free (63.0 ± 8.5 years old; 33 men). Sleep spindle density and amplitude were lower in PD patients who converted to dementia compared with both patients who remained dementia-free and controls, mostly in posterior cortical regions (p < 0.05). Dementia-free PD patients were intermediate between dementia patients and controls, with lower baseline sleep spindle density in all cortical areas compared with controls (p < 0.01). In demented PD patients, lower sleep spindle amplitude in parietal and occipital areas was associated with poorer visuospatial abilities. Although slow wave amplitude was lower in PD patients compared with controls (p < 0.0001), no difference was observed between those who developed or did not develop dementia. Results demonstrate non-rapid eye movement sleep electroencephalographic abnormalities in PD patients. Sleep spindle activity was particularly impaired in PD patients who developed dementia, with a more posterior topographic pattern. Sleep spindle alterations are associated with later development of dementia in PD, and thus may serve as an additional marker of cognitive decline in these patients.

KEYWORDS:

Cognition; Dementia; Electroencephalography; Non-rapid eye movement sleep; Parkinson's disease

[Indexed for MEDLINE]

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