Elsevier

Sleep Medicine

Volume 6, Issue 4, July 2005, Pages 313-318
Sleep Medicine

Original article
Progressive sleep ‘destructuring’ in Parkinson's disease. A polysomnographic study in 46 patients

https://doi.org/10.1016/j.sleep.2005.03.011Get rights and content

Abstract

Background

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.

Methods

Retrospective review of medical records and polysomnographic data from 46 non-demented PD patients.

Results

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.

Conclusion

In PD nocturnal sleep ‘destructuring’ is linked to disease duration and evolves independently from other major disease parameters.

Introduction

Sleep abnormalities in Parkinson's disease (PD) are frequent and partially due to nocturnal recurrence of PD motor symptoms and side effects of pharmacotherapy. There is also increasing evidence that the disease underlying degenerative process accounts by itself for impairment in the expression of wakefulness and REM sleep, which could be due to the primary degeneration of sleep-regulating centers such as the locus coeruleus [1], [2] and the involvement of non-dopaminergic transmitters [3]. It should also be noted that dopamine neurons show state-dependent fluctuations in their activity [4]. So far there have been no polysomnographic (PSG) studies that have examined whether or not the loss of the physiological sleep architecture is progressive with longer disease duration, and if such is the case, whether it could similarly be linked to the progression of motor impairment and the increase of dopaminergic medication. Thus the objective of the present study has been to search for potential links between PSG-proven sleep abnormalities in non-demented PD patients and these major disease parameters.

Section snippets

Methods

We retrospectively reviewed the medical records and PSG data of 56 consecutive patients with parkinsonian syndrome (PS) and various sleep complaints. The PS was classified using established consensus criteria [5], [6]. Fifty-four patients were suffering from levodopa-responsive PS, defined as idiopathic PD in 49 patients, Lewy body dementia (LBD) in 2 patients and multiple system atrophy (MSA) in 3 patients. Two patients were suffering from levodopa-resistant PS, classified as progressive

Demographics

The patient sample was composed of 36 men and 10 women. The mean age was 64.26 (9.40) [range: 44–78] years, the Hoehn and Yahr stage 2.34 (0.86) [range:1–4], the disease duration 7.01 (4.60) [range: 0.5–20] years, and the Epworth sleepiness score (data from 36 patients) 8.53 (4.78) [range: 0–18]. Eighty-five percent (39 patients) expressed one or more sleep complaints. M-RBD were reported by 12 (26%) patients, M-H by 9 (20%), M-EDS by 19 (41%) and M-I by 16 (35%).

Descriptive polysomnographic data

For the whole sample, sleep

Discussion

From our retrospective PSG study evolves the novel finding that in PD there is progressive nocturnal sleep ‘destructuring’ (SD). With this neologism we want to express that over time there is gradual loss of the physiological nocturnal sleep architecture, but not yet overt disintegration or dissolution of the major sleep components. Thus, with longer disease duration Parkinsonian patients of our cohort had lower sleep efficiency and reduced percentages of total sleep, deep sleep and REM sleep.

Acknowledgements

We are grateful to Dr Cynthia L. Comella, MD, Department of Neurological Sciences, Rush University, Chicago for fruitful discussions on the design of this study.

References (29)

  • H. Braak et al.

    Staging of brain pathology related to sporadic Parkinson's disease

    Neurobiol Aging

    (2003)
  • J. Mouret

    Differences in sleep in patients with Parkinson's disease

    Electroencephalogr Clin Neurophysiol

    (1975)
  • K. Jellinger

    New developments in the pathology of Parkinson's disease. [Review]

    Adv Neurol

    (1990)
  • D.B. Rye et al.

    Emerging views of dopamine in modulating sleep/wake state from an unlikely source: PD

    Neurology

    (2002)
  • I. Litvan et al.

    Accuracy of clinical criteria for the diagnosis of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome)

    Neurology

    (1996)
  • I. Litvan et al.

    Accuracy of the clinical diagnoses of Lewy body disease, Parkinson disease, and dementia with Lewy bodies: a clinicopathologic study

    Arch Neurol

    (1998)
  • V.S. De Bruin et al.

    Nocturnal and respiratory disturbances in Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy)

    Postgrad Med J

    (1996)
  • J.B. Grace et al.

    A comparison of sleep profiles in patients with dementia with Lewy bodies and Alzheimer's disease

    Int J Geriatr Psychiatr

    (2000)
  • R. Vertrugo et al.

    Sleep disorders in multiple system atrophy: a correlative video-polysomnographic study

    Sleep Med

    (2004)
  • C.G. Goetz et al.

    Progression of gait, speech and swallowing deficits in progressive supranuclear palsy

    Neurology

    (2003)
  • Y. Ben-Shlomo et al.

    Survival of patients with pathologically proven multiple system atrophy: a meta-analysis

    Neurology

    (1997)
  • Diederich NJ, Vaillant M, Leischen M, et al. Sleep apnea syndrome in Parkinson's disease. A case-control study in 49...
  • J. Gagnon et al.

    REM sleep behavior disorder and REM sleep without atonia in Parkinson's disease

    Neurology

    (2002)
  • Cited by (114)

    View all citing articles on Scopus

    This work has been partly presented at the 128th Annual Meeting of the American Neurological Association, San Francisco, October 20-24, 2003.

    View full text