ABSTRACT
BACKGROUND: Over 50% of persons with idiopathic REM sleep behavior disorder (RBD) will develop Parkinson disease (PD) or dementia. At present, there is no way to predict who will develop disease. Since polysomnography is performed in all patients with idiopathic RBD at diagnosis, there is an opportunity to analyze if baseline sleep variables predict eventual neurodegenerative disease. METHODS: In a longitudinally studied cohort of patients with idiopathic RBD, we identified those who had developed neurodegenerative disease. These patients were matched by age, sex, and follow-up duration to patients with RBD who remained disease-free and to controls. Polysomnographic variables at baseline (i.e., before development of neurodegenerative disease) were compared between groups. RESULTS: Twenty-six patients who developed neurodegenerative disease were included (PD 12, multiple system atrophy 1, dementia 13). The interval between polysomnogram and disease onset was 6.7 years, mean age was 69.5, and 81% were male. There were no differences between groups in sleep latency, sleep time, % stages 2-4, % REM sleep, or sleep efficiency. However, patients with idiopathic RBD who developed neurodegenerative disease had increased tonic chin EMG activity during REM sleep at baseline compared to those who remained disease-free (62.7 +/- 6.0% vs 41.0 +/- 6.0%, p = 0.020). This effect was seen only in patients who developed PD (72.9 +/- 6.0% vs 41.0 +/- 6.0%, p = 0.002), and not in those who developed dementia (54.3 +/- 10.3, p = 0.28). There was no difference in phasic submental REM EMG activity between groups. CONCLUSIONS: In patients with REM sleep behavior disorder initially free of neurodegenerative disease, the severity of REM atonia loss on baseline polysomnogram predicts the development of Parkinson disease.
Subject(s)
Parkinson Disease/diagnosis , Parkinson Disease/physiopathology , REM Sleep Behavior Disorder/diagnosis , REM Sleep Behavior Disorder/physiopathology , Aged , Cohort Studies , Female , Follow-Up Studies , Humans , Longitudinal Studies , Male , Middle Aged , Parkinson Disease/etiology , Polysomnography/methods , Predictive Value of Tests , REM Sleep Behavior Disorder/complications , Severity of Illness Index , Sleep, REM/physiologyABSTRACT
OBJECTIVE: To compare nondemented patients with Parkinson's disease (PD) with and without REM sleep behavior disorder (RBD) to healthy controls on quantitative EEG characteristics for both wakefulness and REM sleep. METHODS: Fifteen patients with PD (7 patients with polysomnographic-confirmed RBD [PD-RBD] and 8 patients without RBD [PD-NRBD]) and 15 healthy control subjects were studied. Each subject underwent a quantitative EEG analysis of both wakefulness and REM sleep. RESULTS: During wakefulness, patients with PD-RBD showed a higher theta power in frontal, parietal, temporal, and occipital regions in comparison to patients with PD-NRBD and control subjects. Moreover, a slowing of the dominant occipital frequency was observed only in patients with PD-RBD (p < 0.02). Patients with PD-NRBD did not present any slowing of the EEG. No between-group difference in quantitative REM sleep EEG was observed. CONCLUSIONS: This study demonstrates that the EEG slowing reported during wakefulness in nondemented patients with PD is strongly related to the presence of RBD.
Subject(s)
Electroencephalography , Parkinson Disease/physiopathology , REM Sleep Behavior Disorder/physiopathology , Aged , Case-Control Studies , Cerebral Cortex/physiopathology , Female , Humans , Male , Middle Aged , Parkinson Disease/complications , Polysomnography , REM Sleep Behavior Disorder/etiology , Wakefulness/physiologyABSTRACT
OBJECTIVE: To determine the frequency of REM sleep behavior disorder (RBD) among patients with PD using both history and polysomnography (PSG) recordings and to further study REM sleep muscle atonia in PD. BACKGROUND: The reported occurrence of RBD in PD varies from 15 to 47%. However, no study has estimated the frequency of RBD using PSG recordings or analyzed in detail the characteristics of REM sleep muscle atonia in a large group of unselected patients with PD. METHODS: Consecutive patients with PD (n = 33) and healthy control subjects (n = 16) were studied. Each subject underwent a structured clinical interview and PSG recording. REM sleep was scored using a method that allows the scoring of REM sleep without atonia. RESULTS: One third of patients with PD met the diagnostic criteria of RBD based on PSG recordings. Only one half of these cases would have been detected by history. Nineteen (58%) of 33 patients with PD but only 1 of 16 control subjects had REM sleep without atonia. Of these 19 patients with PD, 8 (42%) did not present with behavioral manifestations of RBD, and their cases may represent preclinical forms of RBD associated with PD. Moreover, the percentage of time spent with muscle atonia during REM sleep was lower among patients with PD than among healthy control subjects (60.1% vs 93.2%; p = 0.003). CONCLUSIONS: RBD and REM sleep without atonia are frequent in PD as shown by PSG recordings.
Subject(s)
Muscle Hypertonia/complications , Muscle Hypertonia/diagnosis , Parkinson Disease/complications , REM Sleep Behavior Disorder/complications , REM Sleep Behavior Disorder/diagnosis , Aged , Electroencephalography , Female , Humans , Interviews as Topic , Male , Middle Aged , Muscle Tonus , Parkinson Disease/diagnosis , Parkinson Disease/physiopathology , Polysomnography , Predictive Value of Tests , REM Sleep Behavior Disorder/physiopathologyABSTRACT
OBJECTIVES: Few studies have quantified the various characteristics of sleep spindles (SS) in groups of normal human subjects. The aim of the present study was to look at the effects of age on the number, density, duration, intra-spindle frequency, and periodicity of SS during stage 2 sleep in normal subjects of different age groups. METHODS: Thirty-six healthy subjects participated in the study. They were divided into 6 age groups: 10-19, 20-29, 30-39, 40-49, 50-59 and 60-69 years. RESULTS: The results show that there is a progressive decrease in SS number, density, duration and a progressive increase in intra-spindle frequency with age. These changes occur mainly in the first 4 decades, except for SS number and density, for which the changes seem to continue until the sixth decade. The present study also reveals a clear periodicity of SS in human sleep. SS occur every 3-6 s, and the modal value of inter-spindle intervals increases with aging. CONCLUSIONS: The progressive decrease in the number of SS and slow-wave sleep time with age suggests that SS are part of sleep promoting mechanisms. The negative correlation found between SS density and sleep efficiency in the present study is congruent with the sleep maintenance role of SS.