The objective of this cross-sectional study was to test the hypothesis that patients with Parkinson disease (PD) and freezing of gait (PD+FOG) would demonstrate sleep disturbances comparable to those seen in patients with REM sleep behavior disorder (RBD) and these changes would be significantly different from those in PD patients without FOG (PD-FOG) and age-matched controls.
We conducted overnight polysomnography studies in 4 groups of subjects: RBD, PD-FOG, PD+FOG, and controls. Tonic and phasic muscle activity during REM sleep were quantified using EMG recordings from the chin, compared among study groups, and correlated with disease metrics.
There were no significant differences in measures of disease severity, duration, or dopaminergic medications between the PD+FOG and PD-FOG groups. Tonic muscle activity was increased significantly (p < 0.007) in the RBD and PD+FOG groups compared to the PD-FOG and control groups. There was no significant difference in tonic EMG between the PD+FOG and RBD group (p = 0.364), or in tonic or phasic EMG between the PD-FOG and control group (p = 0.107). Phasic muscle activity was significantly increased in the RBD group compared to all other groups (p = 0.029) and between the PD+FOG and control group (p = 0.001), but not between the PD+FOG and PD-FOG groups (p = 0.059).
These findings provide evidence that increased muscle activity during REM sleep is a comorbid feature of patients with PD who exhibit FOG as a motor manifestation of their disease.
[Show abstract][Hide abstract] ABSTRACT: Freezing of gait (FOG) is a common, debilitating feature of Parkinson disease (PD), substantially affecting the patient's quality of life by limiting independence and causing falls. Although it occurs most frequently in the later stages of PD, it is also seen in 26% of early-stage patients not yet exposed to levodopa.(1) Since FOG lacks correlation with bradykinesia,(2) a nondopaminergic mechanism may explain this affliction. This concept is supported by the failure of dopaminergic therapies to relieve FOG, except for the category of "off" period FOG.(3) REM sleep behavior disorder (RBD), a condition characterized by potentially injurious disruptive behaviors during sleep, and REM sleep without atonia (RSWA), a condition defined by polysomnography, are both strongly associated with PD and may antedate the onset of motor symptoms.(4) Two previous studies have shown an increase in the frequency of FOG in PD patients with RBD,(5,6) suggesting a shared pathophysiologic link between these 2 conditions.
[Show abstract][Hide abstract] ABSTRACT: In summary, degeneration of PPN cholinergic neurons and their thalamic projections associates with the important clinical phenomena of RBD, falls, and abnormal sensory integration during postural control. These specific motor and non-motor features may be the clinical signature of a combined dopaminergic-brain cholinergic denervation phenotype in PD that is associated with increased risk of dementia. A subgroup of PD subjects with prominent cholinergic PPN neuron degeneration may be preferred targets for some form of cholinergic augmentation therapy to mitigate falls. The emergence of the cholinergic PPN-thalamus system as a brain center related to some of the disabling motor and non-motor features of Parkinson's disease calls for new clinical trials using preferably nicotinic receptor agonist drugs in selected patients based on cholinergic hypofunction.
[Show abstract][Hide abstract] ABSTRACT: In his initial description of shaking palsy, James Parkinson first noted that sleep became disturbed with advancing paralysis agitans. More recent studies have confirmed that the majority of patients with Parkinson's disease (PD) suffer from some sleep disturbances. This can manifest as difficulty in falling or staying asleep, fractionated sleep, specific parasomnias, and daytime sleepiness. In this article, we will explore the pathophysiology of these varied sleep disorders. In most cases, however, the definitive etiology is debated, and phenotypes are often felt to be multifactorial. Some of these may be associated with dopaminergic dysfunction, some presumed to arise from varied non-dopaminergic PD pathology, and some from PD treatments.
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