Human Sleep and Cognition Part IIClinical and Applied by Hans P.A. Van Dongen and Gerard A. Kerkhof (Eds.)

By Hans P.A. Van Dongen and Gerard A. Kerkhof (Eds.)

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Not surprisingly, the etiology underpinning sleep–wake disturbance in PD is likely to be multifactorial. , dopamine agonists, the “wearing off” phenomenon), pain, discomfort, and nocturia may all be compounding the effects of neurodegenerative changes on the sleep–wake brain systems. Despite the fact that there have been an abundance of studies investigating the nature of sleep–wake disturbance in PD, surprisingly, few studies have examined in detail the relationship of these features with performance on neuropsychological test batteries.

Dysfunction in the ascending arousal system can be incurred by hemorrhagic or ischemic lesions at the level of the reticular formation and brainstem generally, which has widespread noradrenergic, cholinergic, and histaminergic cortical connections (with projections originating from the locus coeruleus, reticular substance, and posterior hypothalamus, respectively). Additionally, thalamic lesions have been associated with insomnia and hypersomnia while pontine lesions have been associated with changes to both REM and NREM sleep.

2009 for discussion). , 2009 for review). from that related to motor symptomatology. , 2009). Circadian disturbance To date, there is not strong evidence for circadian disruption in PD. , 1991). , 2009), suggesting a lesser role for circadian disruption than that seen in AD. , 1993). However, these studies often include cases with advanced PD, who are receiving chronic high-dose L-dopa treatment. Thus, circadian disturbance in PD may well be related to dopaminergic medications and their indirect modulation of the circadian system, rather than to the underlying neurodegenerative process per se.

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