Current opinion in neurology · 2008
Abnormal sleep and sleepiness in Parkinson's disease.
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Arnulf Isabelle, Leu Smaranda, Oudiette Delphine
Аннотация
PURPOSE OF REVIEW: Sleep problems are frequent and disabling in patients with Parkinson's disease. Recent data provide major advances in the mechanisms and consequences of rapid eye movement sleep behavior disorders, insomnia and narcolepsy-like daytime sleepiness.
RECENT FINDINGS: A large series confirms that rapid eye movement sleep behavior disorders may precede parkinsonism or dementia (particuarly, but not exclusively, Lewy bodies dementia) for several years. In Parkinson's disease, rapid eye movement sleep behavior disorders expose patients to higher risks of dementia and hallucinations. Surprisingly, parkinsonism disappears during rapid eye movement sleep behavior disorders, suggesting basal ganglia are bypassed. The interest for structures controlling atonia during rapid eye movement sleep switches from the pedunculopontine nuclei to the locus subcoeruleus. The neuropathology of hypothalamus in Parkinson's disease indicates a massive hypocretin loss, probably underlying the narcolepsy phenotype. The benefit of the new, 24-h long acting ropinirole and transdermal rotigotine on sleep and sleepiness is modest. Eventually, the dopamine release in the mesocorticolimbic pathway is increased during rapid eye movement sleep, supporting its role in dopaminergic-induced vivid dreams.
SUMMARY: In clinical practice, rapid eye movement sleep behavior disorders should be looked at as heralding neurodegenerative diseases in patients with mild cognitive impairment and as a risk factor for dementia and hallucinations in patients with Parkinson's disease.
RECENT FINDINGS: A large series confirms that rapid eye movement sleep behavior disorders may precede parkinsonism or dementia (particuarly, but not exclusively, Lewy bodies dementia) for several years. In Parkinson's disease, rapid eye movement sleep behavior disorders expose patients to higher risks of dementia and hallucinations. Surprisingly, parkinsonism disappears during rapid eye movement sleep behavior disorders, suggesting basal ganglia are bypassed. The interest for structures controlling atonia during rapid eye movement sleep switches from the pedunculopontine nuclei to the locus subcoeruleus. The neuropathology of hypothalamus in Parkinson's disease indicates a massive hypocretin loss, probably underlying the narcolepsy phenotype. The benefit of the new, 24-h long acting ropinirole and transdermal rotigotine on sleep and sleepiness is modest. Eventually, the dopamine release in the mesocorticolimbic pathway is increased during rapid eye movement sleep, supporting its role in dopaminergic-induced vivid dreams.
SUMMARY: In clinical practice, rapid eye movement sleep behavior disorders should be looked at as heralding neurodegenerative diseases in patients with mild cognitive impairment and as a risk factor for dementia and hallucinations in patients with Parkinson's disease.