Abstract
Sleep complaints are frequent and substantially impair quality of life in patients with Parkinson's disease (PD). Severely disrupted sleep and rapid-eye movement (REM) sleep disturbances are early signs of neurodegeneration with involvement of the brainstem with Lewy bodies. REM sleep behavior disorder (RBD) may be a preclinical and premotor sign of PD or other Parkinson syndromes. The behavioral, respiratory, and motor system phenomena accompanying the disease may produce nocturnal symptoms. The medications used as treatment may induce new symptoms, such as nightmares, nocturnal movements or increased wakefulness. Abnormalities of the mesocorticolimbic dopamine system, as well as the mesostriatal system, are apparent in PD and may contribute to sleep–wake disturbances. The administration of a dopamine D 1 -receptor agonist produces electroencephalographic (EEG) desynchronization and behavioral arousal. Low doses of apomorphine also induce sleep when injected into the ventral tegmental area, an effect that is blocked by dopamine receptor autoantagonists, suggesting that dopamine D 2 autoreceptors play a role in the mediation of sleep through autoinhibition of the firing rate of ventral tegmental dopaminergic neurons.
Published Version
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