Abstract
Study objectives: The physiological responses of an individual depend on preset limits. They must be able to adapt it to changing environmental conditions, modifying the thresholds. We propose a regulatory function of biological responses during REM sleep. Responses previously developed during wakefulness, are evaluated and regulated for integration into the repertoire of responses during sleep. The aims of this study were to evaluate the impact of the restoration of REM sleep in patients with Parkinson disease by stimulation of D2 receptors and to evaluate the symptomatic benefit of this approach. Methods: Ten parkinsonian patients underwent a polysomnography study using nocturnal apomorphine subcutaneous administration at the beginning of each REM detected along all night recording. Results: This therapeutic approach led to a significant benefit for patients in all of three UPDRS scores. The mean UPDRS III motor examination “On” scores (mean ± SD) were reduced by 9.4 ± 8.5 points (p<0.0001). For patients in the UPDRS II scores a total difference of 12 ± 4.22 to 5.2 ± 5.22 (p<0.0001) were observed; and in total UPDRS I the difference was of 5.2 points (p<0.0001), with a reduction from 8.4 ± 3.2 to 3.2 ± 3.1. Conclusion: Sleep alteration can be improved by stimulation of D2 receptors. The symptomatic benefits obtained linked to the restoration of REM functions in patients with PD were significant.
Highlights
Neurodegenerative diseases are often characterized by a progressive deterioration in the regulation of motor, cognitive or psychiatric responses and decreasing response to currently available treatments
Ten parkinsonian patients underwent a polysomnography study using nocturnal apomorphine subcutaneous administration at the beginning of each REM detected along all night recording. This therapeutic approach led to a significant benefit for patients in all of three Unified Parkinson's Disease Rating Scale (UPDRS) scores
For patients in the UPDRS II scores a total difference of 12 ± 4.22 to 5.2 ± 5.22 (p
Summary
Neurodegenerative diseases are often characterized by a progressive deterioration in the regulation of motor, cognitive or psychiatric responses and decreasing response to currently available treatments. We know that neuroplasticity depends on adequate cellular resilience, which promotes neurogenesis and sprouting; and these are determined by genetic and environmental factors. The latter can be an important target to future therapeutic options. During normal aging sleep is reduced and fragmented, and this is even more pronounced in neurodegenerative disorders. This disturbed sleep-wake rhythm is probably related to circadian dysregulation appears during normal aging and in a more sharply way in Alzheimer disease (known as hyper-aging) [1]. Some studies have shown that good sleep quality could have a protective effect in those genetically susceptible individuals (APOE genotypes related) to develop Alzheimer's disease [2] decreasing even the associated neuropathological changes [3]
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