Article

Progressive sleep “destructuring” in Parkinson’s disease. A polysomnographic study in 46 patients. Sleep Med 6:313-318

Department of Neuroscience, Centre Hospitalier de Luxembourg, 4, rue Barblé, L-1210 Luxembourg, Luxembourg.
Sleep Medicine (Impact Factor: 3.15). 08/2005; 6(4):313-8. DOI: 10.1016/j.sleep.2005.03.011
Source: PubMed

ABSTRACT

Sleep abnormalities in Parkinson's disease (PD) are frequent, but it is unknown whether or not there is progressive loss of physiological sleep architecture or what the causes could be.
Retrospective review of medical records and polysomnographic data from 46 non-demented PD patients.
Sleep latency was correlated with disease duration (F1,44=4.87, P=0.03). Total sleep time (F1,44=8.54, P=0.005), deep sleep time (F1,44=4.06, P=0.05), REM sleep time (F1,44=9.15, P=0.004) and sleep efficiency (SE) (F1,44=10.20, P=0.003) were inversely correlated with disease duration. The same sleep parameters were independent from the degree of motor impairment, dosage of the dopaminergic medications, and age. Subjective sleep complaints could only partially predict abnormalities in polysomnographic (PSG) studies.
In PD nocturnal sleep 'destructuring' is linked to disease duration and evolves independently from other major disease parameters.

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    • "Neurodegeneration and/or dysfunction in DA and multiple non-DA circuits [7] [183] "
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    ABSTRACT: Parkinson disease is one of the neurodegenerative diseases that benefited the most from the use of non-human models. Consequently, significant advances have been made in the symptomatic treatments of the motor aspects of the disease. Unfortunately, this translational success has been tempered by the recognition of the debilitating aspect of multiple non-motor symptoms of the illness. Alterations of the sleep/wakefulness behavior experienced as insomnia, excessive daytime sleepiness, sleep/wake cycle fragmentation and REM sleep behavior disorder are among the non-motor symptoms that predate motor alterations and inevitably worsen over disease progression. The absence of adequate humanized animal models with the perfect phenocopy of these sleep alterations contribute undoubtedly to the lack of efficient therapies for these non-motor complications. In the context of developing efficient translational therapies, we provide an overview of the strengths and limitations of the various currently available models to replicate sleep alterations of Parkinson's disease. Our investigation reveals that although these models replicate dopaminergic deficiency and related parkinsonism, they rarely display a combination of sleep fragmentation and excessive daytime sleepiness and never REM sleep behavior disorder. In this light, we critically discuss the construct, face and predictive validities of both rodent and non-human primate animals to model the main sleep abnormalities experienced by patients with PD. We conclude by highlighting the need of integrating a network-based perspective in our modeling approach of such complex syndrome in order to celebrate valid translational models. Copyright © 2015 Elsevier Ltd. All rights reserved.
    No preview · Article · Feb 2015 · Sleep Medicine Reviews
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    • "Furthermore, improvement of motor performance in the morning is frequently mentioned by patients, principally in those with a long history of the disease and motor fluctuations (Bateman et al., 1999). Parallel to the disease progression, a progressive change in the physiological sleep architecture is observed, which includes a significant decrease in the amount of NREM sleep (Diederich et al., 2005; Rye and Jankovic, 2002). "
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    ABSTRACT: Levodopa-induced dyskinesia (LID) represents a major challenge for clinicians treating patients affected by Parkinson's disease (PD). Although levodopa is the most effective treatment for PD, the remodeling effects induced by disease progression and the pharmacologic treatment itself cause a narrowing of the therapeutic window because of the development of LID. Although animal models of PD provide strong evidence that striatal plasticity underlies the development of dyskinetic movements, the pathogenesis of LID is not entirely understood. In recent years, slow homeostatic adjustment of intrinsic excitability occurring during sleep has been considered fundamental for network stabilization by gradually modifying plasticity thresholds. So far, how sleep affects on LID has not been investigated. Therefore, we measured synaptic downscaling across sleep episodes in a parkinsonian animal model showing dyskinetic movements similar to LID. Our electrophysiological, molecular, and behavioral results are consistent with an impaired synaptic homeostasis during sleep in animals showing dyskinesia. Accordingly, sleep deprivation causes an anticipation and worsening of LID supporting a link between sleep and the development of LID. Copyright © 2015 Elsevier Inc. All rights reserved.
    Full-text · Article · Dec 2014 · Neurobiology of Aging
    • "Sleep disturbances in Parkinson's disease (PD) have been mentioned since the first descriptions by James Parkinson's Essay on the Shaking Palsy in 1817, but only recently they have become the subject of attention.[1] Sleep abnormalities in PD is possibly due to progressive sleep restructuring.[2] Sleep disorders seen in PD include insomnia, hypersomnia, and parasomnia. "
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    ABSTRACT: Objective: We studied the changes in Polysomnographic (PSG) profile in drug-naïve patients of Parkinson's disease (PD) who underwent evaluation with sleep overnight PSG. Materials and Methods: This prospective study included 30 with newly diagnosed levodopa-naïve patients with PD, fulfilling the UK-PD society brain bank clinical diagnostic criteria (M:F = 25:5; age: 57.2 ± 10.7 years). The disease severity scales and sleep related questionnaires were administered, and then patients were subjected to overnight PSG. Results: The mean duration of illness was 9.7 ± 9.5 months. The mean Hoehn and Yahr stage was 1.8 ± 0.4. The mean Unified Parkinson's Disease Rating Scale (UPDRS) motor score improved from 27.7 ± 9.2 to 17.5 ± 8.9 with sustained usage of levodopa. Nocturnal sleep as assessed by Pittsburgh Sleep Quality Index (PSQI) was impaired in 10 (33.3%) patients (mean PSQI score: 5.1 ± 3.1). Excessive day time somnolence was recorded in three patients with Epworth Sleepiness Scale (ESS) score ≥ 10 (mean ESS score: 4.0 ± 3.4). PSG analysis revealed that poor sleep efficiency of <85% was present in 86.7% of patients (mean: 68.3 ± 21.3%). The latencies to sleep onset (mean: 49.8 ± 67.0 minutes) and stage 2 sleep (36.5 ± 13.1%) were prolonged while slow wave sleep was shortened. Respiration during sleep was significantly impaired in which 43.3% had impaired apnoea hyperpnoea index (AHI) ≥5, mean AHI: 8.3 ± 12.1). Apnoeic episodes were predominantly obstructive (obstructive sleep apnea, OSA index = 2.2 ± 5.1). These patients had periodic leg movement (PLM) disorder (56.7% had PLM index of 5 or more, mean PLMI: 27.53 ± 4 9.05) that resulted in excessive daytime somnolence. Conclusions: To conclude, sleep macro-architecture is altered in frequently and variably in levodopa-naïve patients of PD and the alterations are possibly due to disease process per se.
    No preview · Article · Jul 2014 · Annals of Indian Academy of Neurology
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