Abstract
The aim of this study was to identify changes of sleep spindles (SS) in the EEG of patients with Parkinson's disease (PD). Five sleep experts manually identified SS at a central scalp location (C3-A2) in 15 PD and 15 age- and sex-matched control subjects. Each SS was given a confidence score, and by using a group consensus rule, 901 SS were identified and characterized by their (1) duration, (2) oscillation frequency, (3) maximum peak-to-peak amplitude, (4) percent-to-peak amplitude, and (5) density. Between-group comparisons were made for all SS characteristics computed, and significant changes for PD patients vs. control subjects were found for duration, oscillation frequency, maximum peak-to-peak amplitude and density. Specifically, SS density was lower, duration was longer, oscillation frequency slower and maximum peak-to-peak amplitude higher in patients vs. controls. We also computed inter-expert reliability in SS scoring and found a significantly lower reliability in scoring definite SS in patients when compared to controls. How neurodegeneration in PD could influence SS characteristics is discussed. We also note that the SS morphological changes observed here may affect automatic detection of SS in patients with PD or other neurodegenerative disorders (NDDs).
Highlights
Parkinson’s disease (PD) is a neurodegenerative disorder (NDD) characterized primarily by motor symptoms, including bradykinesia, rigidity, postural instability, and tremor
For the SS included in the group consensus, it was found that patients with PD show SS that are significantly different from controls in terms of duration, oscillation frequency and max peak-to-peak amplitude
Based on a group consensus of manually scored SS from five independent sleep experts, this study investigates morphological changes of SS in a central EEG lead of patients with PD compared to age- and sex-matched control subjects
Summary
Parkinson’s disease (PD) is a neurodegenerative disorder (NDD) characterized primarily by motor symptoms, including bradykinesia, rigidity, postural instability, and tremor. The disease process in PD is not restricted to a specific brain area, these symptoms are mostly caused by the loss of dopaminergic neurons in the substantia nigra pars compacta resulting in a reduction or depletion of dopamine (Galvin et al, 2001). Lewy body aggregations of alpha-synuclein in the brain are a central feature of PD pathology (Galvin et al, 2001). These inclusions typically start in caudal areas of the brain and progress anteriorly (Braak et al, 2003), and may take place years prior to involvement of the substantia nigra and associated development of motor symptoms.
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